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Healing with Freshman Medical School Physiology (How the Body is designed to Work) Jerry Tennant, MD Tennant Institute for Integrative Medicine 01.02.07 1 Tennant Institute for Integrative Medicine 5601 N. MacArthur Blvd. Suite 200 Irving, TX 75038 972-580-1156 [email protected] © Copyright 2005 All Rights Reserved This book is written for those with chronic disease and those wishing to avoid chronic disease. There are those who just want instructions on what to do to get well and don’t really care why or how it works. This first section is written for those. Others want to know all the details about what they are doing and why. The second part of the book is written for those. If you don’t want/need to know the why and how, you can skip the second part of the book. Another use for the second part of the book is information for those who think you are crazy for doing something other than “traditional medicine”. That includes friends, spouses, relatives, and some of your doctors. The things that we recommend are primary from freshman medical school physiology. For the benefit of your doctors, we have included a bibliography at the back of this booklet with the medical references about the things we are recommending. When we doctors go to medical school, we are taught basic physiology the first year. That teaches us how the body normally works. The second year we are taught what goes wrong with the body. The third and fourth years, we are taught to forget most of the first two years and memorize symptom complexes as “diseases”. We are then taught which drugs cover up the symptoms of those diseases. When that doesn’t work, we are taught to attempt to remove the offending part. After we get into practice, control of the patient is taken from the doctor by the insurance companies. When a doctor makes a diagnosis, he/she must select a code number for whatever diagnosis is made. That code number activates what are called “standards of practice”. That means that a computer programmed by an insurance company is now in control of your medical care. It tells the doctor what drugs must be prescribed and whether you can have surgery. It tells the doctor when you can be hospitalized and how many days you can stay there. Unless your doctor can justify another diagnosis code, you are controlled by the first one. Most HMO’s and PPO’s also set standards for doctors as far as when you can see a specialist and how many patients must be seen by the doctor daily. I know a family 01.02.07 2 practice doctor that is required to see 60 patients/day or lose his job. Under such circumstances, there is little time to talk to patients about the basics of diet and other things needed to stay well. There is no time to do anything but quickly write you another prescription and get you out the door. We do not accept any insurance. With that policy, the insurance companies cannot dictate the length of time we spend figuring out what is wrong with you. Neither do they dictate what we can do to attempt to make you well. What we do is basic freshman medical school physiology plus oriental medicine combined with modern electronics. There is nothing strange or unusual about what we do except that oriental medicine is not recognized by the FDA and insurance companies and thus is not commonly used or understood. Our clinic and doctor(s) do not replace your personal physician(s). We are simply consultants in Integrative Medicine doing things that your doctor may not have time to do. We are not your primary physician, and you must look to your primary physician as your basic and final advisor for medical care. You must consult with your primary physician for emergencies. We do not treat emergencies. The Basics The key to making chronic disease better is making a single cell work. If you give the body the things a single cell needs to work, the body often has the power to heal all of the cells of the body. That means you get well! A cell is made up of a cell membrane and the inside called the cytoplasm. The cell membrane is made of fats. It controls the cell and is consider the “brain” of the cell. That means you must have the proper fats to make those membranes. About 20% of your body is this fat, so if you weigh 200 pounds, you need 40 pounds of perfect fat to be healthy. Since cells replace themselves on an average of about 8 weeks, you would need to absorb about five pounds of fat per week to stay healthy! The cytoplasm of the cell is made up of proteins. There are eight proteins that the body can’t make (ten in children). Thus they are called essential proteins. You must eat enough protein to fill this need. To be used, proteins and fats need vitamins and minerals. To date, I have never seen a patient with a chronic disease that is not mineral deficient, and most are vitamin deficient as well. Cells need the following to be healthy: 1. Water with voltage (alkaline water) 2. Fats to make cell membranes 01.02.07 3 3. Proteins to make the cytoplasm (the “machinery”) inside cells. 4. Vitamins to allow the body to make the fats and proteins work. 5. Minerals to make the fats and proteins work and as On-Off switches and keep your pH in the operating range. 6. Oxygen 7. Sunshine 8. Voltage is the same as pH. The body must have voltage to function (the same as saying you must have an alkaline pH). The body normally runs at pH of 7.2 which is the same as -22 mV. We will be giving you these things as a part of getting you well. The next important thing to recognize is the importance of your liver/gallbladder. The gallbladder is a storage tank for the bile made by the liver. It often becomes filled with sludge and doesn’t function normally. This sludge becomes a breeding ground for all sorts of infections. They produce poisons called “neurotoxins” that make you sick. However, you need your gallbladder because the liver can’t make bile fast enough to allow you to absorb the fat you need to keep healthy. The key is to clean it---not to remove it. (If you have already had it removed, you will need to take bile supplements the rest of your life). The liver is in charge of: 1. Processing your digested food so that it can be used by the body to make new cells and to keep things working. 2. Getting the toxic things out of your body. 3. Controlling the immune system so you can keep infections under control. If your liver is sick, you lose these processes chronic disease. http://images.google.com/imgres?imgurl=http://www.bnaiyer.com/health/liver3.jpg&imgrefurl=http://www.bnaiyer.com/health/liver2.html&h=324&w=277&sz=24&tbnid=PShU2hJ6LYwJ:&tbnh=114&tbnw=97 &hl=en&start=5&prev=/images%3Fq%3Dliver%2Bcells%26svnum%3D10%2 6hl%3Den%26lr%3D%26sa%3DG The liver contains 35,000 square meters (about the surface of seven football fields) of membrane surface used to accomplish these things. These membranes are made of fat. If you don’t eat enough fat of the proper kind or if you eat fats that have been processed so they are similar to plastic, these membranes don’t work correctly. (These “plastic fats” are called “partially hydrogenated” fats and Canola Oil.) 01.02.07 4 http://www.abdn.ac.uk/emunit/emunit/temcells/images/liver.jpg http://www.greenhouse.gov.au/lgmodules/wep/hvac/t raining/components/images/filter.jpg When the liver gets clogged up with debris because the membranes are made of plastic, it tries to wash itself with cholesterol. A high cholesterol means your liver is trying to clean itself---much like you would try to clean the filter from your air conditioner. If you interfere with that process with drugs and continue to give your body only plastic fats to repair itself, you are doomed to chronic diseases of all types. Once the liver cleans itself and repairs itself, the rest of the body can begin to heal. The liver will begin to supply the nutrients needed, begin to remove toxic chemicals (pesticides, pharmaceuticals, etc.) and turn on the immune system to get rid of infections. Thus our initial efforts will be to clean up and repair your liver/gall bladder. It normally takes eight to sixteen weeks for the liver to replace itself with all new cells. Remember that the leading cause of death in the U.S. is reactions to pharmaceuticals. Just listen to the drug advertisements on TV and you will realize that all drugs have side effects. You should have the goal of getting off your drugs. However, do not do that without guidance. Stopping drugs suddenly often causes the body to have a bad reaction. The primary exception is anti-cholesterol drugs. You should stop them immediately. They are all liver toxic and prevent the liver from cleaning itself. Your cholesterol level will go to normal as we clean the liver and give it the fat it needs to repair itself. To be healthy, you must stop eating anything that says, “Partially hydrogenated” or Canola Oil. You will have to stop eating fried foods and cheese in restaurants because these almost always are made of partially hydrogenated oils. In addition, you must stop using all forms of artificial sweeteners such as aspartame, Splenda, saccharine, xylitol and others ending in “–ol”. All of these are severe neurotoxins that the body doesn’t know how to get rid of. Stop MSG as it is also a neurotoxin. Stop smoking. Stop eating soy. Stop drinking coffee, tea, and alcohol. Eat lots of raw milk, butter and eggs. If they make you nauseated, that means your liver isn’t making enough bile to absorb them. You will need to take ox bile and digestive 01.02.07 5 enzymes with each meal until your liver can make bile on its own. You will be able to eat fats without trouble when we get your liver working again. Eat things that don’t have the toxins listed above. Try to vary your diet, with 1/3 protein, 1/3 fat, and 1/3 carbohydrates with the carbs from fruits and vegetables. So that’s the summary. You will be given specific instructions in the office according to your findings. If You Want To Know The Details, Read The Following: So you are sick and tired of being sick and tired. This workbook will be your guide to getting well. Let’s assume that you have bought an old house that hasn’t been lived in for several years. However, you love that old house and want to return it to its former glory. You dream of living in that wonderful house and all the fun you will have in it. Well----your body is that house. Now we have to start the process of returning it to normal. It won’t happen overnight, and there are no miracle pills to make it normal. In fact, medications are simply paint. If you paint over a board eaten by termites, you may not see the holes in the board for awhile, but they are still there and the rotting goes on. Medications cover up the symptoms, but the degeneration in your body continues. If you have arthritis and you take medication, the degeneration in your joints continues. You just don’t feel the pain while the joints continue to rot. So now you own the old house. What must be done before you can move in? First you will want to restore the utilities. You will need water, sewage, and electricity. So let’s get started on those: WATER 01.02.07 6 The body is about 70-80% water. Thus it is the basis of who you are and how healthy you are. Unfortunately, you have probably been lead to believe that drinking things containing water is the same as drinking water-----not so. When things are put into water to make them into some other drink, it changes how the water reacts in the body. If you take good water from a well or an uncontaminated stream, it will be alkaline (finding good water anywhere in the world is getting harder because of chemical contaminations). That means it contains electrons available for your body to use in its metabolism. However, if you put chlorine and/or fluoride in it, it becomes acidic. Anything that is acidic is an electron stealer. Anything that is alkaline is an electron donor. Drinking acidic water steals electrons from your cells and damages them. Drinking water that has been made into carbonated beverages is drinking acid that is so concentrated, you can use it to clean the grease off your engine or clean out your toilet! Can that possibly be good for you? Your cells are composed of water, but it is also what your body uses to wash the inside of your body to clean away the garbage that gets into the body. Would you wash your car with coffee? Then consider washing the inside of your body with coffee or tea or sodas. In addition, zinc is one of the most important elements in the body. Without zinc, you can’t make stomach acid. Without stomach acid, you can’t digest your food. Without nutrition, the body can’t repair itself. In addition, without zinc, you can’t make neurochemicals like serotonin, dopamine, norepinephrine and epinephrine. Zinc is blocked by alcohol, coffee, and tea. (Alcohol also blocks selenium.) Trying to get your fluids by drinking these substances will almost guarantee that you will become depressed. Is it any wonder so much of our population is depressed? Many think it is healthy to drink distilled water; it is not. Distilled water pulls minerals out of your cells and into the water. You can kill yourself drinking distilled water. For example, if you put one drop of distilled water inside an eye, the cornea immediately becomes opaque and the cells inside the eye are killed as the minerals are pulled out of them. 1 7 Another problem is bottled water. Bottled water is almost always city water that has been put through a filter. It is perhaps cleaner than city water, but it is still acidic and contains many other chemicals. Many cities have tap water that has toxic levels of copper. Copper is also a zinc antagonist. 7 If you look on the bottom of bottled water you buy most places, you will see a triangle that contains the number one. That number relates to the kind of plastic used to manufacture the bottle. A number one usually relates to a clear plastic that is not totally polymerized. If you leave such a bottle in the sun, the polymers from the bottle will enter the water and poison it. You probably have noticed that bottled water left in the sun tastes like plastic. What most of us didn’t realize is that that plastic acts like estrogen in our bodies causing hormonal imbalances and blocking zinc. Estrogen Unopposed by Progesterone blocks zinc, magnesium and vitamin B6 and leads to: 1. Increases in heart attacks and strokes, 2. Aging, 3. Anxiety, 4. Allergies, 5. Asthma, 6. Breast cancer, 7. Cervical cancer, 8. Cold hands and feet, 9. Decreased sex drive, 10. Dry eyes, 11. Endometriosis, 12. Fat gain around hips, 13. Fatigue, 14. Fibrocystic breasts, 15. Foggy thinking 16. Gall bladder disease, 17. Hair loss, 18. Headaches, 19. Hypoglycemia, 20. Increased blood clotting 21. Autoimmune disorders. You should drink your water from a bottle made of glass or from a plastic bottle with at least a number two in the triangle. Most sports water bottles have a number seven in the triangle. Perhaps the best water system is the one invented by Viktor Schauberger in Switzerland. It attaches to the main entering your home and provides good water for the entire house. It costs about $2,000 plus installation. Ask us for detail if you want to get one of these systems. 8 For those who can’t afford the Shauberger system, I recommend the system developed by Nikken. Their explanation of how the system works may not be totally accurate, but I have personally tested the pH, Redox potential, rH2, and conductivity of tap water before and after it has gone through the Nikken system. The water coming out of the system is much better than that going in. The cost of the system is about $300-$400 and you can make gallons and gallons of water before having to replace the filters. It is much cheaper than buying bottled water. Put it in your sports bottle (number two or greater in the triangle on the bottom) if you need to be away from home. My recommendation is that you avoid drinking anything but water. If you must drink something else, know that it is toxic to your system and be prepared for the consequences. When people are sick, they often have decreased minerals in their body. Drinking water dilutes the minerals even more reduction in the voltage feel worse. The answer is to restore the minerals and voltage and that allows you to drink the necessary amount of water. Sometimes I see doctors tell their patients to drink less water because some lab test shows they have too little of something in their blood such as sodium. If you dehydrate the patient, the lab test will come back to normal but the patient feels worse. Let’s assume you have two glasses of tea each containing eight ounces. One is very dark and the other is very light. If I put the light colored one out in the sun and let some of the water evaporate, soon both glasses of tea will be the same color. If I ran a lab test on both glasses, the test might show a “normal” amount of tea in each. However, there might not be enough volume left in the dehydrated glass to do much with. If we do that to patients, we cause their blood pressure to be too low or the inside of the cells to become too thick to function. We must correct lab results by looking at total body water, intracellular water, and extracellular water. Then we know if the patient has too much or too little water or too much or too little “stuff” in the water. One can tell that using a device called the Biological Impedance Analysis device. How much water to drink is always a question. The only sure way to know is to measure with the BIA device shown above. However, a good rule of thumb is to drink water every time you feel hungry. If you still feel hungry a few minutes 9 after drinking, then eat. The sense of hunger is often the signal the body really wants more water. So in our old house analogy, you will begin by washing out the debris inside and outside your house. Minerals Minerals play an important role in the body. If you think about the battery in your car, you know that if you put distilled water in it, it won’t hold a charge. So it is with your body. In addition, mineral acts as On-Off switches in the body. This is particularly true of calcium and magnesium. For example, to contract a muscle, calcium is necessary. To relax the muscle, magnesium is necessary. Calcium turns things on and magnesium turns things off. If you run out of one of them, you get stuck in either on or off. Minerals and vitamins are also important in manufacturing of things you need. An example is neurochemicals. To make serotonin from the protein L-tryptophan, you must have: 1. Folate 2. Calcium 3. Iron 4. Vitamin B3 5. Zinc 6. Vitamin B6 7. Magnesium 8. Vitamin C To make dopamine and norepinephrine from the amino acid L-phenylalanine, one needs the following: 1. Folate 2. Iron 3. Zinc 4. Magnesium 5. Copper 6. Vitamin B3 7. Vitamin B6 8. Vitamin C If you don’t have calcium, magnesium zinc, iron, copper, and the necessary vitamins, you can’t make serotonin. If you don’t have serotonin, you will become depressed. The other problem is that the minerals need to be balanced. If you simply take a lot of the above minerals, you may be so out of balance that things don’t work correctly. The easiest way to tell if you need a particular mineral is to taste that mineral in solution. You will need to purchase this mineral testing/treatment kit. Ten minerals are dropped onto your tongue. If it tastes like water or sweet, 10 you are deficient in it. If it tastes metallic or bitter, you don’t need it. Place the ones that don’t taste really bad in your morning juice. Recheck every week until each mineral deficiency is corrected. When one of the minerals starts tasting really bad, you don’t need it anymore. Recheck your mineral level at least once every 3-4 months. Because our soils are so depleted of minerals, you will need to replace them periodically. Some of the most commonly consumed water substitutes are coffee, tea, and alcohol. All three block zinc and alcohol blocks selenium. Look at the symptoms caused by a deficiency of these minerals: Alcohol intolerance Zinc (30) Asthma Zinc (30) Belching Zinc (30) Bloating Zinc (30) Boils Zinc (30) Brittle nails Zinc (30) Bronchitis Zinc (30) Colds Zinc (30) Conjunctivitis Zinc (30) Delayed healing Zinc (30) Depression Zinc (30) Dermatitis Zinc (30) Disrupted sleep Zinc (30) Dry skin Zinc (30) Ear infections Zinc (30) Early graying hair Zinc (30) Eczema Zinc (30) Fidgeting Zinc (30) Frequent sore throats Zinc (30) Gastric-esophageal reflux disease (GERD) Zinc (30) Gastroenteritis Zinc (30) Hair Loss Zinc (30) Hay fever Zinc (30) Hyperactivity Zinc (30) Increased cholesterol Zinc (30) Infertility Zinc (30) Itchy skin Zinc (30) Joint pain Zinc (30) Joint stiffness Zinc (30) Loss of libido Zinc (30) Low blood sugar (hypoglycemic) Zinc (30) Low white blood cell count Zinc (30) Lung infections Zinc (30) Missed periods Zinc (30) Moodiness Zinc (30) 11 Pimples Pneumonia Poor coping with stress Poor memory Pre-dinner tantrums Prolonged infections Psoriasis Runny nose Sinusitis Stomach ulcers Stretch marks Temper outbursts Thrush (mouth fungus) Tinea (athlete's foot) Warts Arthritis Asthma Autoimmune diseases Cancer Cardiomyopathy Depression Diabetes Heart disease Hypothyroid Increased cholesterol Increased infections Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Zinc (30) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Selenium (34) Note: zinc has an atomic number of 30 and selenium 34. Drinking coffee, tea, and/or alcohol make you susceptible to the misery of all of these things = everything from athlete’s foot to cancer! Now doesn’t drinking water make more sense? It is also important to remember that taking antacids or drugs that block stomach acid production causes you to be deficient in zinc. This makes you susceptible to all of the above things noted with zinc deficiency. pH and Calcium pH stands for “Potential Hydrogen”. It is a way of talking about the amount of acid and base in our bodies. It is also a way of talking about the amount of voltage in our body. pH is measured on a log rhythmic scale where 0 is the most acidic and 14 is the most alkaline. Seven (7) is considered neutral. Water (H2O) ionizes into hydrogen (H+) and hydroxyl (OH-) ions. When these 12 ions are in equal proportions, the pH is a neutral 7. When there are more H+ ions than OH- ions then the water is said to be "acid". If OH- ions outnumber the H+ ions then the water is said to be "alkaline". The pH scale goes from 0 to 14 and is logarithmic, which means that each step is ten times the previous. In other words, a pH of 4.5 is 10 times more acid than 5.5, 100 times more acid than 6.5 and 1,000 times more acid than 7.5. pH is also a measure of voltage. A pH of 0 is the same as +400 mVolts. A pH of 14 is the same as -400 mVolts. Cells normally operate at about pH of 7.2 or -22 mVolts. Chronic disease and pain are almost always associated with an acidic pH which is the same as saying that chronic disease and pain are almost always associated with a loss of voltage. Health is associated with the presence of voltage which is the same as saying that healthy people have an alkaline pH. In the body, being able to hold a charge of voltage is associated with minerals in general and calcium in particular. 13 When you begin your day, you “turn on the body machinery”. This creates a byproduct of carbonic acid. This acid must be eliminated from the body or the body loses its charge (becomes acidic). This is accomplished partly by having the carbonic acid dissociate into carbon dioxide and water. The carbon dioxide is breathed out through the lungs. However, one cannot breathe fast enough to get rid of all the necessary carbon dioxide, so some of it is removed by combining with ammonia from the liver and intestine to form urea nitrogen. That is eliminated through the kidneys. Daytime is a time of running the “machinery” and creating acids. Nighttime is a time of replacing worn out cells and eliminating the acids you created through the day that you didn’t get rid of through the day. Measurement of the salivary pH gives you a good indication of how the cellular pH. You can think of it as how much voltage is stored in your cellular batteries. It should never be lower than 6.5. Measurement of the urinary pH gives you an indication of how much acid is being dumped out by the kidneys. It should also be about 6.5 after you get rid of your first morning urine. (The first morning urine represents the acid you got rid of during the night). However, if your daytime urine pH is less than 6.5, you are dumping more acid because your tissue has become too acidic. To be accurate, your salivary pH must be tested either the first thing when you wake up before you drink any water or two hours after a meal. Test it with pH strips. Here is the color code that tells you your pH: Sometimes it is difficult to decide which color is the correct one on the strip. If you want to have a more accurate way to measure pH, meters are available for about $100. IF YOUR URINE OR YOUR SALIVARY pH FALLS BELOW 6.5, YOU NEED MORE CALCIUM. However, you can’t just take any calcium. Calcium citrate is acidic. If you take it, you will make yourself more acidic. Calcium carbonate is alkaline with a pH of about 10. It will cause your system to become more alkaline. A good source of calcium carbonate is from coral. In addition to the calcium, you get trace minerals as well. Coral calcium is about 1/5 calcium carbonate. For example, 565 mg of coral calcium would contain about 110 mg of calcium carbonate. 14 A guide for the amount to take is: pH <6.0 Coral calcium Calcium carbonate 7700 mg (fourteen capsules/day) 110 mg x 14 = 1540 mg 6.0-6.5 5500 mg (ten capsules/day) 110 mg x 10 = 1100 mg. 7.0-7.5 3300 mg (six capsules/day) 110 mg x 6 = 660 mg. >7.5 None None Note that this recommendation has you taking some calcium even if your pH is above 6.5. This is advantageous if you are dealing with serious illness because microorganisms can’t grow in an alkaline pH. Cancer cells have trouble growing with alkaline pH as well. A salivary pH of 6.5 suggests a cellular pH of 7.2. Thus one has to adjust the cellular pH numbers by about 0.7. The normal human cell has a lot of molecular oxygen and a slightly alkaline pH. The cancer cell has an acid pH and lack of oxygen. Cancer cells cannot survive in an oxygen rich environment. At a pH slightly above 7.4 (salivary pH 6.7) cancer cells become dormant and at pH 8.5 (salivary pH 7.8) cancer cells will die while healthy cells will live. Again, the higher the pH reading, the more alkaline and oxygen rich the fluid is. Cancer and all diseases hate oxygen / pH balance. http://home.bluegrass.net/~jclark/coral_calcium.htm Thus it is sometimes advantageous to push the pH above 6.5 if you are trying to overcome a chronic illness. Neurochemicals and Plankton There are two basic theories of how to get people with chronic disease well and keep them that way. One is that we must find a drug that will substitute for a broken “gear” in the body or to repair the “gears” mechanically (surgery). The other is the give the body the things it needs to manufacture new cells and let it heal itself. For those wishing to support the latter theory, it has been difficult to determine what is actually needed to make new cells. People are always saying things like they have a new herb from Africa or a fruit from China that will magically heal everything. Such findings are often useful for some but not predictable for most. My feeling has always been that Heavenly Father would not design a body that requires unusual potions from far-away places to make us healthy. There are very few products that provide all or even most of the raw materials to make new cells and sustain the existing ones. The problem is that we need ALL of them at the same time for things to work. My practice is one of Integrative Medicine where we see 15 primarily people who have been sick for years and who “have tried it all”. I personally suffered from viral encephalitis and a bleeding disorder that kept me incapacitated for seven years. What I have come to appreciate is that one must provide the raw materials for the body to make new cells. If one does that, even severely and chronically ill patients can heal. So what are those raw materials?: 1. 2. 3. 4. 5 Water: The body is about 75% water. It needs to be clean water that is alkaline (contains voltage). Fat: Every cell membrane in the body is made of two layers of fats called phospholipids. Proteins: Every cell in the body contains “machinery” made up of proteins that do the work of the cell. Carbohydrates: Needed primarily to provide vitamins and minerals. A. Vitamins: To use the fats and proteins, cells need vitamins. B. Minerals: To use the fats and proteins, cells need minerals. Minerals are also used by the body as “On-Off” switches. Voltage: Voltage is stored in the cell membrane of every cell to give cells the energy to work. 16 There are very few products that provide all or even most of the raw materials to make new cells and sustain the existing ones. The problem is that we need ALL of them at the same time for things to work. For example, one needs a protein You may get a few of the things you need to called tryptophan to make the brain chemical called serotonin. However, be healthy from a it takes eight vitamins and minerals for this to work. If you are missing product you are taking one of them, e.g., zinc, you can’t make serotonin. You may get a few of this month and a few the things you need to be healthy from a product you are taking this from the product you month and a few from the product you take next month but neither works take next month but neither works because because you didn’t get them all at the same time! you didn’t get them all at the same time! One of those rare products that contains almost everything you need for life (and the rebuilding of a healthy life) is phytoplankton. It contains the ten amino acids that the body cannot make and must be consumed in our diet (essential amino acids). The essential fatty acids are also present (Omega 3 and Omega 6). Vitamins A (beta-carotene), B1 (thiamine), B2 (riboflavin), B3 (niacin), B5 (pantothenic acid), B6 (pyridoxine), B12 (cobalamin), C, and D (tocopherol) and major and trace minerals are all present in phytoplankton. In short, it contains almost everything one needs to sustain life. Therefore, it contains almost everything one needs to restore health by providing the raw materials to make new cells that function normally. This is particularly true if one stops putting toxic materials such as artificial sweeteners and Trans fats (partially hydrogenated fats) into our body. It is exciting to find something that seems to contain most of the things necessary to get well and stay well. It is likely that phytoplankton will change the way we think about health. I have also found that one can replace neurochemicals with phytoplankton even when the liver is too sick to allow the person to take products with just the amino acids and vitamins/minerals necessary to make them. Blood Pressure Blood pressure is related to water. Any fluid system needs---fluids! Having a normal pressure inside your vascular system is key to feeling well. The upper number of your blood pressure is called “systolic”. It is a measure of the highest pressure in your system. It is the result of the heart contracting and pushing blood into the vessels. The second number is called “diastolic” pressure. It is a measure of the lowest pressure in the system and is the pressure present when the heart is between beats and is refilling itself with blood for the next pulse. It is the most important number because a persistently high pressure can damage the vessels. It should be between 80-90. It is often said that blood pressure cannot be too low unless you have symptoms. That is not true. If the blood pressure is too low, you will not have enough pressure to get enough blood to your brain and you will have symptoms of chronic fatigue. When the diastolic pressure is below 80, you will often have symptoms. Blood pressure is much like tire pressure for your car. “Cold” pressure is the pressure in your tires when the car has not been moving. It is the minimum operating pressure to make your tires work 1 7 correctly. When the tire starts rolling, the heat created increases the pressure in the tires and is called the “hot” pressure. It is the maximum pressure experienced by the tires. If that is too high, it will damage the tire walls. Think of systolic blood pressure as “hot” pressure and diastolic blood pressure as “cold” pressure. Your tires are designed to operate within these ranges. Too high or too low means the tires will not function correctly. So it is with blood pressure. A major recommendation from the National Institutes of Health was published in May, 2003. The National High Blood Pressure Education Program is coordinated by the National Heart, Lung, and Blood Institute (NHLBI) at the National Institutes of Health. Copies of the JNC 7 Report are available on the NHLBI Web site at http://www.nhlbi.nih.gov or from the NHLBI Health Information Center, P.O. Box 30105, Bethesda, MD 20824-0105; Phone: 301-592-8573 or 240629-3255 (TTY); Fax: 301-592-8563. Published Abstract: The purpose of the Seventh Report of the Joint Evaluation, and Treatment of High Blood Pressure (JNC 7) is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: In those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP Beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg Those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension Prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD. For uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes. This report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers.) Two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm hg, or <130/80 mm hg) for patients with diabetes and chronic kidney disease. For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered. Regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan.. 1 8 “Because of the new data on lifetime risk of hypertension and the impressive increase in the risk of cardiovascular complications associated with levels of BP previously considered to be normal, the JNC 7 report has introduced a new classification that includes the term “prehypertension” for those with BPs ranging from 120–139 mmHg systolic and/or 80–89 mmHg diastolic. This new designation is intended to identify those individuals in whom early intervention by adoption of healthy lifestyles could reduce BP, decrease the rate of progression of BP to hypertensive levels with age, or prevent hypertension entirely. Cumulative incidence of cardiovascular events in women (panel A) and men (panel B) without hypertension, according to blood pressure category at the base-line examination. Vertical bars indicate 95 percent confidence intervals. Optimal BP is defined here as a systolic pressure of <120 mmHg and a diastolic pressure of <80 mmHg. Normal BP is a systolic pressure of 120–129 mmHg or a diastolic pressure of 80–84 mmHg. High-normal BP is a systolic pressure of 130–139 mmHg or a diastolic pressure of 85–89 mmHg. If the systolic and diastolic pressure readings for a subject were in different categor ies, the higher of the two categories was used.” The recommendations from the Committee on Prevention and Treatment of High Blood Pressure are: Treat to a BP of <140/90 unless you have diabetes or chronic kidney disease. In that case, treat to <130/80. For those with BP from 120/80 to 140/90, start behavior modifications for dietary choices, exercise, stop smoking, etc. For those over 140/90 (or diabetics or kidney disease with >130/80), start with a diazide diuretic as first choice medication. 1 9 Add additional medications as needed to reach goal BP. Since most physicians have to see so many patients per day, it has been my experience that many skip step one of behavior modification and often start drug therapy in all patients whose blood pressure is >120/80. Also, they often choose drugs other than diuretics as the beginning medication. It has been my experience that many people with diastolic pressures <80 will have mental fog and/or dizziness because there isn’t enough pressure to get adequate blood to the brain. Several of my family members have been treated this way. When they report the symptoms to their physicians, they are told to keep taking the medications. This is the common practice of physicians treating lab results and not the patient. If a patient can’t work because you have lowered their blood pressure too low, you haven’t really served the patient. I find that most patients will have a normal blood pressure in 4-6 months after starting the program of restoring voltage and nutrition. One of the principle causes of too low blood pressure is dehydration. If you don’t have enough fluid in the system, you can’t create enough pressure. Another cause is mineral deficiency, particularly sodium and magnesium. Low blood pressure can be a symptom of a deficiency of Vitamin B5 = pantothenic acid. It can also be due to adrenal insufficiency. If your blood pressure drops instead of increasing as you stand up, that is a sign that your adrenals are not working correctly. Unstable blood pressure is often due to a lack of magnesium and/or Vitamin B1 = thiamine. Sewage As we clean up our old house now and in the future we will wash out the debris and need a functional sewage system to get rid of the toxic and waste materials. One of the most important systems in the body is the large intestine. We will start our cleanup by flushing out the large intestine to remove the debris that has accumulated there. We will give you the instructions in the office. For some reason, people seem to fear this simple process. Very few people find it uncomfortable or distressing. It just means you need to be at home for a few hours. Probiotics The word “probiotic” refers to bacteria that normally live in our intestines and help with digestion. They are an important part of the digestive process and need to be replaced if they are diminished in numbers by the use of antibiotics. In addition to digestion, they are believed to assist with: Competition against harmful micro-organisms including Candida, preventing colonization of pathogens through the production of inhibitory substances including acids and hydrogen 2 0 peroxide and natural antibiotics; Enhancement of digestion of lactose (milk sugar); Immune enhancement, including enhanced macrophage activity; Reduction in the levels of and deactivation of potential cancer causing chemicals, particularly in the colon and direct anti-tumor activity of certain strains; Reduction in liver toxicity; Enhancement of peristalsis, digestion, regularity and re-absorption of nutrients, In infants, promotion of healthy digestive tract colonization; Enhancement and balance of estrogen levels, prevention of osteoporosis through increased calcium uptake; Protection against food poisoning, travelers' diarrhea, allergies, skin problems; Enhancement of vitamin status (B, K), digestion of proteins, fats, carbohydrates. Electricity Now that you have the water and sewage working in your old house, you need electricity. So it is with our body. When two hydrogen atoms join with an oxygen atom to form water, the first thing they do is exchange electrons. When electrons move from one place to another, that is called an electric current. All of the chemical reactions in the body depend upon voltage (movement of electrons). Every cell has its own battery pack---the cell membrane---that stores voltage and provides it to the cell as needed to keep it working. Take a voltmeter that reads in millivolts. Place one electrode on your right temple and one on your left temple. It will read voltage. In your house, there is a circuit breaker box that goes to the various circuits throughout the house. Different appliances and switches are on each circuit. When one of those quits working, you can measure the circuit to see what is happening with the voltage in that circuit. Our bodies work much the same way. We have twelve paired circuits on which our organs are attached. These circuits provide voltage to our organs and move the voltage from place to place. These circuits are known as acupuncture meridians. By measuring the voltage or impedance (resistance to flow of electrons) in each circuit, we can determine if each organ has enough voltage to work correctly. We use a device called Meridian Energy Analysis Device (MEAD) to take these measurements. If we find a circuit that isn’t working, we use various electronic devices to place voltage into that circuit and recharge the cells. Note: The FDA has not yet approved these devices for this purpose nor considered these 2 1 statements. In this chart, we look at the total body voltage and then at the voltage in each circuit. Normal is when all of the bars are between the top and bottom red lines. One of the devices we use to restore voltage to the body is the Tennant Biomodulator™. We may also use a variety of low-level lasers, infra-red, and other devices that can carry voltage into the body. COOKING OILS This is one of the most important parts of getting well. If you don’t stop putting Trans Fats (“Plastic Fats”) into your body, you will never get well! Please pay particular attention to this section. The summary of this section is as follows: Food suppliers recognized that the major loss of profits was from spoilage. In order to stop spoilage and increase their profits, they did two things. 1. They added chemicals to the food to keep it from spoiling. These chemicals not only preserve food, they preserve the person who eats them. 2. They began to cook the fats in the food. Cooking fats at 350-380 degrees for 5-6 hours changes the fats into something that is one carbon atom away from plastic. You can tell if this is what you are eating if the label says, “Partially Hydrogenated-----“. These partially 2 2 hydrogenated fats are called “Trans Fats”. When a cell in your body is worn out, it makes a new one. It looks around to see what building materials you have provided to make a new cell. If all you have given your body is plastic fat, it makes a new cell out of plastic. Remember that the cell membrane that surrounds every cell is made of fat. If you make that out of plastic, the cell doesn’t work very well. It is like wrapping all your cells in cellophane. The cell sends a message to your brain that it’s hungry. Your body sends the cell some glucose and insulin. However, the glucose can’t get through the “cellophane” and the cell keeps complaining that it’s hungry. The body keeps sending more insulin and glucose. Much of it gets put into fat cells. Your cells keep complaining that they are hungry. Your brain keeps you eating to try to solve the hunger, but not much gets through the cellophane to the cells. Soon you are obese and your pancreas is worn out from making so much insulin. With all that glucose in your blood stream, you are diagnosed with Type II diabetes. Drugs lower the levels of sugar in your blood, but your cells are still coping with being made of plastic. Soon they began to wear out and you get symptoms of worn out cells = heart attacks, strokes, liver failure, kidney failure, blindness, chronic fatigue, etc. Most restaurants use plastic fats for frying food. If you eat out, you must stop eating fried food or choose a restaurant that doesn’t use plastic fats. Most cheese is made from plastic fats. Thus cheeseburgers and French fries are major sources of plastic fats. Fast food isn’t dangerous because it’s fast---it is dangerous because it’s plastic. The point you must understand is that if you insist on feeding your body plastic fats, you will never get well! However, if you give your body good fat and the other things it needs, your body will build a new you that is vibrant and healthy! Cells need the following to work: 1. 2. 3. 4. 5. Water with voltage (alkaline water) Fats to make cell membranes Proteins to make the cytoplasm (the “machinery”) inside cells. Vitamins to allow the body to make the fats and proteins work. Minerals to make the fats and proteins work and as On-Off switches and keep your pH in the operating range. 6. Oxygen 7. Sunshine 8. Voltage is the same as pH. The body must have voltage to function (the same as saying a normal body has an alkaline pH). The body normally runs at a pH of 7.2 inside cells which is the same as -22 mV. There is a lot of confusion about the type of fat to eat. Many people are becoming toxic from too much Omega-3 fats (from fish oil, etc.). Your cell membranes are like your home. They need to be strong enough to be substantial but have doorways and windows to let things in and out. If you build your house out of concrete blocks with no windows or doors, it will be strong but won’t work 2 3 because you can’t get in or out. If you build it with mostly doors and windows, the next storm will take it down. In cells, saturated fats are strong and unsaturated fats are porous. You need saturated fat (animal fat for example) to make strong cells and unsaturated fats (fish oils for example) for doors and windows. The ratio needs to be 4/1 meaning that you need to eat four times as much saturated fat as unsaturated fats = four times as many bricks as doors and windows. Saturated fats have gotten a bad reputation because plastic fats are saturated. There is a difference between plastic fats and normal saturated fats. The following discussion is for those who don’t understand this problem and insist that eating fat is harmful. Remember that your body should contain about 20% fat since all of your cell membranes and most of your nervous system is fat. That means you need to give your body 24 pounds of good fat to replace the fat in your system if you weigh 120 pounds. If you weigh 200 pounds, you will need to give your body 40 pounds of good fat to get healthy! Remember the following: There is no proven connection between cholesterol and heart disease. In fact, those dying from heart attacks generally have the lowest cholesterol levels and often have low “bad cholesterol (LDL) levels. Eating good fat doesn’t affect your cholesterol or make you obese. The liver makes as much or as little cholesterol as it wants. Eating plastic fat (Trans fats) makes you obese and produces a liver and other cells that cannot function. The liver uses cholesterol to clean itself. A high cholesterol means your liver filtration system is dirty and filled with toxic materials. (Why would you want to interfere with the liver’s ability to clean itself by taking cholesterol-lowering drugs?) A very low cholesterol means the liver is too sick to clean itself and you will suffer major illness or death soon. To get well, you will need to eat at least 20% of your body weight in good fat. If you weigh 200 pounds, you will need to eat at least 40 pounds of good fat to get well! Seventyfive percent of that needs to be saturated fat like animal fat and twenty-five percent needs to be polyunsaturated fat like fish oil. Eating lots of butter and eggs (a stick of butter and 6-12 eggs per day) will help you get well much faster. If eating fat makes you nauseated, it means your liver is too sick to use it. We will have to treat your liver so it can restore itself before you can get well. The following is reproduced with permission from Sally Fallon with Pat Connolly and Mary G. Enig, Ph.D. Nourishing Traditions: The Cookbook that Challenges Politically Correct Nutrition and the Diet Dictocrats. ProMotion Publishing. 800-231-1776, and Sally Fallon. "Why butter is good for you (health aspects of dietary fat)." (Cover Story), Consumers' Research magazine. 03-01- Vol.79 (1996) pp 10(6). COPYRIGHT 1996 Consumers' Research Inc. Why Butter is Good for You (health aspects of dietary fat) Sally Fallon, et al 2 4 Politically correct nutrition is based on the assumption that we should reduce our intake of fats, particularly saturated fats from animal sources. Fats from animal sources contain cholesterol, presented as the villain of the civilized diet. Yet the textbooks tell us that fats from animal and vegetable sources provide a concentrated source of energy in the diet; they also provide the building blocks for cell membranes, for hormones, and for prostaglandins (substances that mediate important chemical processes in the body). In addition, they act as carriers for the important fat-soluble vitamins A, D, E, and K. Dietary fats are needed for conversion of carotene to vitamin A and for a host of other processes. The theory—and it is only a theory—that there is a direct relationship between the amount of saturated fat in the diet and the incidence of coronary heart disease, as well as certain types of cancer, was proposed by a researcher named Ancel Keys in the late 1950s. Numerous subsequent studies have questioned his data and conclusions. Nevertheless, Keys' articles received far more publicity than those contradicting him. The vegetable oil industry and food processing industries, the main beneficiaries of the saturated fat/heart disease connection, began promoting and funding further research designed to support Keys' theories. The most well-known advocate of the low fat diet was Dr. Nathan Pritikin. Actually, Pritikin advocated eliminating sugar, white flour, and all processed foods from the diet and recommended the use of fresh raw foods, whole grains, and a strenuous exercise program; but it was the low fat aspects of his regimen that received the most attention in the media. Adherents found that they lost weight and that their blood cholesterol levels and blood pressures declined. The success of the Pritikin diet was probably due to a number of factors having nothing to do with a reduction in dietary fat—weight loss alone, for example, will precipitate a reduction in blood cholesterol levels—but Pritikin soon found that the fat-free diet presented many problems, not the least of which was the fact that people just could not stay on it. Those who possessed enough will power to stay fat-free for any length of time developed a variety of health problems including low energy, difficulty in concentration, depression, weight gain, and signs of mineral deficiencies. After problems with the no-fat regimen became apparent, Pritikin introduced a small amount of fat from vegetable sources into his diet—something like 10 percent of the total caloric intake. Today the "diet dictocrats"—essentially the public health establishment, including primarily the large health charities and the federal government—advise us to limit fats to 25-30 percent of the caloric intake (12-15 percent of the diet by weight). A careful reckoning of daily fat intake, and avoidance of animal fats, is presented as the key to perfect health. The experts assure us the theory that animal fat consumption causes coronary heart disease is backed by abundant evidence. Most people would be surprised to learn that there is, in fact, very 2 5 little evidence to support the contention that a diet low in cholesterol and saturated fat actually reduces death from heart disease or in any way increases one's life span. Consider the following: Before 1920, coronary heart disease was rare in America, so rare that when a young internist named Paul Dudley White introduced the German electrocardiograph to his colleagues at Harvard University, they advised him to concentrate on a more profitable branch of medicine. The new machine revealed the presence of arterial blockages, thus permitting early diagnosis of coronary heart disease; but in those days clogged arteries were a medical rarity, and White had to search for patients who could benefit from his new technology. During the next forty years, however, the incidence of coronary heart disease rose dramatically, so much so that by the mid'50s, heart disease was the leading cause of death among Americans. Today, heart disease causes 40 percent of all U.S. deaths. If, as we have been told, heart disease results from consumption of saturated fats, one would expect to find a corresponding increase in animal fat in the American diet. Actually the reverse is true. During the sixty-year period from 1910 to 1970, the proportion of traditional animal fat in the American diet declined from 83 to 62 percent, and butter consumption plummeted from eighteen pounds per person per year to four pounds. During the past eighty years, dietary cholesterol intake has increased only one percent. During the same period the percentage of dietary vegetable fat in the form of margarine, shortening, and refined oils increased about 400 percent, and the consumption of sugar and processed foods increased about 60 percent. The Framingham Heart Study is often cited as proof of the cholesterol/animal fat theory. This study began in 1948 and involved about 6,000 people from the town of Framingham, Massachusetts. Two groups were compared at five-year intervals— those who consumed little cholesterol and saturated fat and those who consumed large amounts. Today, after 40 years, the current director of this study admits: "In Framingham, Mass., the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person's serum cholesterol. . . . [W]e found that the people who ate the most cholesterol, ate the most saturated fat, and ate the most calories weighed the least and were the most physically active." The study did show that those who weighed more and had higher blood cholesterol levels were more at risk for future coronary heart disease; but weight gain and cholesterol levels had an inverse correlation with fat and cholesterol intake in the diet. The Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT), which cost 150 million dollars, is the study most often cited by the experts to justify the low fat diet. Actually, dietary cholesterol and saturated fat were not tested in this study as all subjects were already on a low-cholesterol, low-saturated fat diet. Instead, the study tested the effects of a cholesterol lowering drug. Statistical analysis of the results indicated a 24 percent reduction in the rate of coronary heart disease in the group taking drugs compared with the placebo group; however, nonheart disease deaths in the drug group increased—deaths from cancer, stroke, violence, and suicide. Even the claim that a diet low in saturated fat and cholesterol reduced heart disease is 2 6 suspect. Independent researchers who tabulated the results of this study found no significant statistical difference in the coronary heart disease death rate between the two groups. However, both the popular press and medical journals touted the LRC-CPPT survey as the long-sought proof that animal fats are the cause of heart disease, America's number one killer. Mother's milk contains a higher proportion of cholesterol than almost any other food. It also contains over 50 percent of its calories as fat, much of it saturated fat. Both cholesterol and saturated fat are essential for growth in babies and children, especially in development of the brain. (Yet, the American Heart Association is now recommending a low-cholesterol, low fat diet for children.) Most commercial formulas are low in saturated fats and some are almost completely devoid of cholesterol. A recent study linked a low fat diet with failure to thrive in children. As a final example, consider the French. The French diet is loaded with saturated fats in the form of butter, eggs, cheese, cream, liver, meats, and rich pates. Yet the French have a lower rate of coronary heart disease than many other western countries. In the United States, 315 of every 100,000 middle-aged men die of heart attacks each year; in France the rate is 145 per 100,000. In the Gascony region, where goose and duck liver form a staple of the diet, this rate is a remarkably low: 80 per 100,000. This phenomenon has recently gained international attention and has been dubbed the paradox francais. Clearly, something is wrong with the theories we read in the popular press (and used to bolster sales of low fat concoctions and cholesterol-free foods). The notion that saturated fats per se cause heart disease as well as cancer is not only not facile, it is just plain wrong. But it is true that some fats are bad for us. In order to understand which ones, we must know something about the chemistry of fats. Fat Chemistry. Most fat in our bodies and in the food we eat is in the form of triglycerides, that is, three fatty acid chains attached to a glycerol molecule. Elevated triglycerides in the blood have been positively linked to proneness to heart disease but these triglycerides do not come directly from dietary fats; they are made in the liver from any excess sugars that have not been completely burned. The source of these excess sugars is any food containing carbohydrates, but particularly refined sugar and processed carbohydrates. In simple terms, fatty acids are chains of carbon atoms with hydrogen linkages. A fatty acid is called saturated when all available carbon bonds are occupied by a hydrogen atom. Monounsaturated fatty acids have one pair of carbon atoms double bonded to each other and therefore lack two hydrogen atoms. The monounsaturated fatty acid most commonly found in our food is oleic acid, the main component of olive oil. Polyunsaturated fatty acids have two or more pairs of carbon double bonds and therefore lack four or more hydrogen atoms. The two polyunsaturated fatty acids found most frequently in our foods are double unsaturated linoleic acid with two double carbon bonds (also called omega-6) and triple unsaturated linolenic acid with three double bonds (also called omega-3). All fats and oils, whether of vegetable or animal origin, are some combination of saturated fatty 2 7 acids, monounsaturated fatty acids (oleic acid), and the polyunsaturates linoleic and linolenic acid. In general, animal fats such as butter, lard, and tallow contain about 50 percent saturated fat and are solid at room temperature. Vegetable fats from northern climates contain a preponderance of polyunsaturated fatty acids and are liquid at room temperature. But vegetable oils from the tropics are highly saturated. Coconut oil, for example, is 92 percent saturated. These fats are liquid in the tropics, but hard as butter in northern climes. Highly saturated tropical oils such as coconut and palm oil are not harmful, as the popular press would lead us to believe. These fats and oils have nourished healthy populations, free of heart disease, for millennia. Vegetable oils are more saturated in hot climates because the increased saturation helps maintain stiffness in plant leaves. Olive oil with its preponderance of oleic acid is the product of a temperate climate. It is liquid at warm temperatures but hardens when refrigerated. Researchers classify fatty acids not only according to their degree of saturation but also by their length. 1. Short-chain fatty acids have four to six carbon atoms (butter and coconut) 2. Medium-length fatty acids have eight to twelve (butter and coconut) 3. Long-chain fatty acids have 14 to 18 carbon atoms (beef fat) 4. Very-long-chain fatty acids have 20 to 24 carbon atoms (fish oils, organs) Saturated fats vary in length from short to long. Butter and coconut oil contain a large portion of short- and medium-chain fatty acids, while stearic acid, the main component of beef fat, is a longchain fatty acid with 18 carbons. Oleic acid, linoleic acid, and linolenic acid also have 18 carbons. Very-long-chain fatty acids, such as those found in fish oils and organ tissues, tend to be highly unsaturated, with four, five, and even six double bonds. Short- and medium-chain fatty acids have several interesting properties. 1. Longer chain fatty acids are absorbed by the lymph system and must be acted on by bile salts. 2. Short-chain fatty acids (butter and coconut) are absorbed directly through the portal vein to the liver. As they do not need to be acted upon by the bile salts, these short-chain fatty acids supply quick energy. In general, the body uses the longer chain fatty acids, including the longer chain saturated fatty acids, to construct membranes and vital hormone-like substances, to create electric potentials, and to move electric currents. It is the longer chain fatty acids that are stored in the adipose tissue, particularly oleic and linoleic acid. Thus butter and coconut oil, which contain a significant portion of short- and medium-chain fatty acids, do not contribute to weight gain as much as olive and vegetable oil. The short- and 2 8 medium-chain fatty acids also have antimicrobial and antifungal properties in the intestinal tract; they have anti-tumor properties and help strengthen the immune system, while an excess of polyunsaturated fatty acids stimulate tumor growth. Summary: (JLT) 1. Short-chain fatty acids have four to six carbon atoms (butter and coconut) a. Do not contribute to weight gain as much as olive and vegetable oil b. Have antimicrobial and antifungal properties in the intestinal tract c. Have anti-tumor properties and help strengthen the immune system, 2. Medium-length fatty acids have eight to twelve (butter and coconut) a. Do not contribute to weight gain as much as olive and vegetable oil b. Have antimicrobial and antifungal properties in the intestinal tract c. Have anti-tumor properties and help strengthen the immune system, 3. Long-chain fatty acids have 14 to 18 carbon atoms (beef fat) a. Absorbed by the lymph system and must be acted on by bile salts b. Used to construct membranes and vital hormone-like substances, to create electric potentials, and to move electric currents c. Stored in the adipose tissue, particularly oleic and linoleic acid 4. Very-long-chain fatty acids have 20 to 24 carbon atoms (fish oils, organs) a. Absorbed by the lymph system and must be acted on by bile salts b. Used to construct membranes and vital hormone-like substances, to create electric potentials, and to move electric currents c. Stored in the adipose tissue, particularly oleic and linoleic acid; an excess of polyunsaturated fatty acids stimulate tumor growth. Too Many Polyunsaturates. Unsaturated omega-3 and omega-6 fatty acids are called essential fatty acids, or EFAs, because the body cannot manufacture them, at least not in the form in which they occur. Researchers vary in their estimates of the amount of polyunsaturated fatty acids needed in the diet, giving figures as low as 0.5 percent and as high as 15 percent, but recent scientific evidence supports the lower range and has led knowledgeable researchers to recommend limiting our intake of polyunsaturates to 4 percent of the caloric total, in approximate proportions of 1.5 percent omega-3 fatty acid and 2.5 percent omega-6. (More recently, Yehuda et al have proven that the proper ratio is 4:1 of omega-6 to omega-3 of the lower order linoleic and linolenic acids. JLT). What we find in the American diet is a high intake of polyunsaturates—something like 10 to 30 percent of the total caloric intake. Worse, most of these polyunsaturates are in the form of 2 9 omega-6 linoleic acid, with very little of vital omega-3 linolenic acid. Recent research has revealed that too much omega-6 in the diet can interfere with the enzymes that produce longer chain, highly saturated fatty acids, which are the precursors of important prostaglandins. These are localized tissue hormones that direct many processes in the cells. When the production of prostaglandins is compromised by excess omega-6 in the diet, coupled with too little omega-3, serious problems result including inflammation, hypertension, irritation of the digestive tract, depressed immune function, sterility, cell proliferation, cancer, and weight gain. Other studies indicate that excessive unsaturated fatty acids in the diet of infants can interfere with brain development and with learning and behavior. In contrast, dietary saturated fats (e.g., coconut, palm, beef, butter, eggs) contribute to optimal utilization of essential fatty acids. Thus, although not called essential, saturated fats are absolutely necessary in the diet, not only for the role they play in enhancing EFA utilization, in supplying quick energy, and in their immune system enhancing characteristics, but also because of the important vitamins they carry. A Serious Problem. A serious problem with the polyunsaturate family, and particularly omega-3 (fish, flax, hemp), is its instability. With their double carbon bonds, these fatty acids tend to polymerize, that is, bond with each other and bond with other molecules. They are also more easily rendered rancid when subjected to heat, oxygen, and moisture as in cooking and processing. Rancid oils are characterized by free radicals in the double bond, that is, single atoms or clusters with an unpaired electron in an outer orbit. These compounds are extremely reactive chemically. They have been characterized as "marauders" in the body, for they attack cell walls and red blood cells and cause damage in DNA/RNA strands, thus triggering mutations in tissue, blood vessels, and skin. Free radical damage to the skin causes wrinkles and premature aging; free radical damage to the tissues and organs sets the stage for tumors. Is it any wonder that tests and studies have repeatedly shown a high correlation between cancer and the consumption of polyunsaturates? New evidence links exposure to free radicals with premature aging, with autoimmune diseases such as arthritis, and to Parkinson's disease, Lou Gehrig's disease, Alzheimer's, and cataracts. (Note that recent work shows that many sources of omega-3 like cod liver oil are severely contaminated with chemical toxins in the ocean. It is critical to only buy and use molecularlydistilled omega-3 oils that have removed these carcinogens. Most health food stores do not sell these as it takes 100 pounds of cod livers to produce 10 pounds of toxin-free oil = more expensive. Use only molecularly-distilled omega-3 supplements. JLT) It is important to understand that of all substances ingested by the body, it is polyunsaturated oils that are most easily rendered dangerous by food processing, especially unstable omega-3 linolenic acid. Consider the following processes inflicted upon naturally occurring fats before they appear on our tables: Extraction. Oils naturally occurring in fruits, nuts, and seeds must first be extracted. In the old days this extraction was achieved by a slow-moving stone press. But oils processed in large factories are obtained by crushing the oil-bearing seeds and heating them to 230 degrees Fahrenheit. The oil is then squeezed out at pressures from 10 to 20 tons per inch, thereby generating more heat. During this process the oils are exposed to damaging light and oxygen. 3 0 High-temperature processing causes the weak carbon bonds of the unsaturated fatty acids, especially triple unsaturated linolenic acid, to break apart, thereby creating dangerous free radicals. In addition, antioxidants including fat soluble vitamin E, which protect the body from the ravages of free radicals, are neutralized or destroyed by high temperatures and pressures. (There is a safe modern technique for extraction that drills into the seeds and extracts the oil and its precious cargo of antioxidants under low temperatures, with minimal exposure to light and oxygen. These unrefined oils will remain fresh for a long time if stored in the refrigerator in dark bottles. Extra virgin olive oil is produced by crushing olives between stone or steel rollers. This process is a gentle one that preserves the integrity of the fatty acids and the numerous natural preservatives in olive oil. If the olive oil is packaged in an opaque container, it will retain its freshness and precious store of antioxidants many months.) Hydrogenation. This is the process that turns polyunsaturates (margarine and shortening) normally liquid at room temperature, into a fat that is solid at room temperature. To produce them, manufacturers begin with the cheapest oil (soy, corn, or cottonseed) already rancid from the extraction process. These oils are then mixed with tiny metal particles—usually nickel oxide. Nickel oxide is very toxic when absorbed and is impossible to eliminate totally from margarine. (Nickel is a severe neurotoxin. JLT) The oil with its nickel catalyst is then subjected to hydrogen gas in a high-pressure, high-temperature reactor. Next, soap-like emulsifiers and starch are squeezed into the mixture to give it a better consistency. The oil is yet again subjected to high temperature when it is steam cleaned. This removes its horrible odor. Margarine's natural color, an unappetizing grey, is removed by bleach. Coal tar dyes and strong flavors must then be added to make it resemble butter. Finally the mixture is compressed and packaged in blocks or tubs, ready to be spread on your toast. (and make “plastic cell membranes” JLT) Forget Margarine. Margarine and other partially hydrogenated oils are even worse for you than the highly refined vegetable oils from which they are made because of chemical changes that occur during the hydrogenation process. Under high temperatures, the nickel catalyst causes the hydrogen atoms to change position on the fatty acid chain. Before hydrogenation, two hydrogen atoms occur together on the chain, causing the chain to bend slightly and creating an electron cloud at the site of the double bond. This is called the "cis" formation, the configuration most commonly found in nature. With hydrogenation, one hydrogen atom is moved to the other side so that the molecule straightens. This is called the "trans" formation, rarely found in nature. These man-made trans-fats are toxins to the body, but unfortunately your digestive system does not recognize them as such. Instead of being eliminated, the trans-fats are incorporated into the body's cell membranes as if they were cis-fats; your cells actually become hydrogenated. Once in place, trans-fatty acids with their misplaced hydrogen atom wreak havoc in cell metabolism. These altered fats actually block the utilization of essential fatty acids, causing many deleterious effects ranging from sexual dysfunction, increased blood cholesterol, and paralysis of the immune system. In the 1940s, researchers found a strong correlation between cancer and the consumption of fat, but the fats used were hydrogenated fats, not naturally saturated fats. (Until recently, the confusion between hydrogenated fats and naturally saturated fats has persisted not only in the popular press, but in scientific data bases, resulting in much error in study results.) 3 1 Consumption of hydrogenated fats is associated with a host of other serious diseases, not only cancer but also atherosclerosis, diabetes, obesity, immune system dysfunction, low birth weight babies and birth defects, sterility, difficulty in lactation, and problems with bones and tendons. Yet, hydrogenated fats continue to be promoted as health foods. Margarine's popularity represents a triumph of advertising over common sense. Your best defense is to avoid it like the plague. Go Butter. The media's constant attack on saturated fats is extremely suspect. Claims that butter causes chronic high cholesterol values have not been substantiated by research, although some studies show that butter consumption causes a small temporary rise. (Other studies have shown that stearic acid, the main component of beef fat, actually lowers cholesterol.) Margarine, on the other hand, provokes chronic high levels of protective cholesterol and has been linked to both heart disease and cancer. Butter has received so much adverse propaganda that we have lost sight of the fact that it has long been a valuable component of many traditional diets containing the following vital nutrients: Fat-Soluble Vitamins These include vitamins A (retinol), D, and E, as well as all their naturally-occurring constituents needed to obtain maximum effect. Butter is America's best source of these essential vitamins. In fact, vitamin A from butter is more easily absorbed and utilized than from other sources. (These fat-soluble vitamins are relatively stable and survive the pasteurization process.) These vitamins act as catalysts to mineral absorption. Without them, we are not able to utilize properly the minerals we ingest, no matter how abundant they may be in our diets. The only good source of fat-soluble vitamins in the American diet, one sure to be eaten, is butterfat. Butter added to vegetables and spread on bread, and cream added to soups and sauces ensures proper assimilation of the minerals and water-soluble vitamins in vegetables, grains, and meat. Arachidonic Acid This is a polyunsaturate containing four double carbon bonds and is found in small amounts in animal fats, but not in vegetable fats. Arachidonic acid is a precursor to important prostaglandins and other vital substances. (Arachidonic acid makes up 17% of cell membranes and there is no vegetable source for it = total vegans cannot have normal cells. JLT) Short- and Medium-Chain Fatty Acids Butter contains about 15 percent short-and medium-chain fatty acids. This type of saturated fat, as mentioned, is absorbed directly from the small intestine to the liver, where it is converted to energy. These fatty acids also have antimicrobial, anti-tumor, and immune system supportive properties, especially 12-carbon lauric acid, a medium-chain fatty acid not found in other animal 3 2 fats. Highly protective lauric (coconut and palm oil) should be called a conditionally essential fatty acid because it is one saturated fat that the body does not make itself. We must obtain it from one of two dietary sources: butter or tropical oils. Propionic acid and butyric acid, very-short-chain fatty acids, are all but unique to butter. These have antifungal properties as well as anti-tumor effects. Omega-6 and Omega-3 Polyunsaturates These occur in butter in small but equal amounts. This balance between linoleic and linolenic acid prevents the kind of problems associated with over-consumption associated with omega-6 (or omega-3 JLT) fatty acids. Conjugated Linoleic Acid Butterfat also contains a form of rearranged linoleic acid called CLA that has strong anticancer properties. Lecithin Lecithin is a natural component of butter. It is known to assist in the proper assimilation and metabolization of cholesterol and other fat constituents. Cholesterol Mother's milk is high in cholesterol because it is essential for growth and development. Cholesterol is also needed to produce a variety of steroids that protect against cancer, heart disease, and mental illness. Glycosphingolipids This special category of fat protects against gastrointestinal infections, especially in the very young and the elderly. For this reason, children who drink skim milk have diarrhea at rates three to five times greater than children who drink whole milk. Trace Minerals Many trace minerals are incorporated into the fat globule membrane of butterfat, including manganese, zinc, chromium, and iodine. In mountainous areas far from the sea, iodine in butter protects against goiter and other thyroid problems. Butter is extremely rich in selenium, a vital antioxidant, containing more per gram than herring or wheat germ. In summary, our choice of fats and oils is one of extreme importance. Most people, especially infants and growing children, benefit from more fat in the diet rather than less. But the fats we eat 3 3 must be chosen with care. Avoid all processed foods containing partially hydrogenated fats and polyunsaturated oils. Instead use extra virgin olive oil and unrefined flaxseed oil in salad dressings. Acquaint yourself with the merits of coconut oil for baking. And finally, use good old-fashioned butter, not margarine, with the happy assurance that it is a wholesome—indeed, an essential— food for you and your whole family. COPYRIGHT 1996 Consumers' Research Inc. "Why Butter Is Good For You (Health Aspects of Dietary Fat)." (Reproduced here with permission of Ms. Fallon; JLT) Common Name Caprylic Capric Lauric Myristic Palmitic Stearic Oleic (Omega-9) Linoleic (LA) (Omega-6) Gamma-linolenic (GLA) (Omega-6) Alpha-linolenic (ALA) (Omega-3) Arachiodonic (AA) (Omega-6) Eicosapentaenoic (EPA) (Omega-3) Docosahexaenoic (DHA) (Omega-3) Foods Coconut Coconut, palm Coconut, palm Palm, beef, mutton, butter, cocoa, lard, eggs Cocoa, beef, mutton, eggs, palm, lard Safflower (high oleic), olive, canola, sesame, rice, butter, corn Safflower, Sunflower, soy, oat, peanut, lard, corn Borage, primrose, black currant, hemp Flax, canola, soy, hemp Eggs, butter, beef, mutton, shellfish Fish oil, cold water fish Fish oil, cold water fish Nomenclature 8:00 10:00 10:00 12:00 16:00 18:00 18:1, ώ-9 18:2, ώ-6 18:3, ώ-6 18:3, ώ-3 20:4, ώ-6 20:5, ώ-3 22:6, ώ-3 Type Saturated (SFA) Saturated (SFA) Saturated (SFA) Saturated (SFA) Saturated (SFA) Saturated (SFA) PUFA PUFA PUFA PUFA HUFA HUFA HUFA Effect on membrane Rigidity Rigidity Rigidity Rigidity Rigidity Rigidity Fluid Fluid Fluid Fluid Fluid Fluid Fluid PUFA = 2-3 double bonds HUFA = >3 double bonds Polyunsaturated fats (PUFA) are extremely vulnerable to damage from heat, so they are not suitable for high-temperature cooking. These oils are best used in salad dressings, sauces, and dips. To add flavor to grains and stir-fry dishes, sprinkle the cooked food with flaxseed oil just before serving. For high temperature cooking, use extra virgin olive oil or organic coconut butter. In July 2002, the National Academy of Sciences’ Institute of Medicine, which advises the government on health policy, made official what many researchers have argued for years: Trans fat worsens blood-cholesterol levels and almost surely increases the risk of heart disease. The institute concluded that people should consume as little Trans fat as possible. That report has helped push the government and the food industry to start taking aggressive steps to address this long-neglected threat to public health. The Food and Drug Administration (FDA) could be close to finalizing a rule that would require trans-fat labeling on packaged foods. Canada instituted such a requirement early this year as part of its mandatory nutrition-labeling system. Labeling not only will help consumers cut back on trans, it will also be "a profound disincentive for manufacturers" to use partially hydrogenated oils, says Marion Nestle, Ph.D., professor and chair of New York University’s department of nutrition and food studies, and author of "Food Politics: How the Food Industry Influences Nutrition and Health." To figure the amount of Trans-Fatty Acid in packaged food by using the new U.S. labels Find the amount of "Total Fat" on the label. Find the amounts of "Saturated Fat", "Polyunsaturated Fat" and "Monosaturated Fat". (These are found on the label, listed directly under "Total Fat" and slightly indented. If one 3 4 or the other is not listed, that particular food does not contain it.) Add theses three together. If there are only two listed, add them together or use one amount if only one is listed. Subtract the total amount of #3 from the amount of #1. The answer is the amount of Trans-fatty Acid in that product. Frito-Lay has said that it would eliminate Trans fat from Cheetos, Doritos, and Tostitos chips. Even the fast-food industry, which generally does not have to label its foods, is starting to cut back: McDonald’s has said that in late spring of this year, its French fries would have 48 percent less trans fat--a significant improvement, though the fries will apparently still have a fair amount of trans and saturated fat. Jason's Deli has eliminated partially hydrogenated oils from every food item at all of its 137 restaurants nationwide and all 1.6 million box lunches provided to schools annually. http://www.bantransfats.com/ Trans fats are one carbon atom away from being plastic. This “near-plastic” fat ends up in your cell membranes. Thus when you eat Trans fats, you become mostly plastic! Is it any wonder why your cells don’t work well and you don’t feel good when your cells are made of “near-plastic”? http://www.consumerreports.org/main/detailv2.jsp?CONTENT%3C%3Ecnt_id=300681&FOLDER%3C%3Efolder_id =162689 http://www.bantransfats.com/images/cigs.gif Here is a summary of a few facts regarding Canola Oil: It is genetically engineered rapeseed. Canada paid the FDA the sum of $50 million to have rape seed registered and recognized as "safe". (Source: Young Again and others) 3 5 Rapeseed is lubricating oil used by small industry. It has never been meant for human consumption. It is derived from the mustard family and is considered a toxic and poisonous weed, which when processed, becomes rancid very quickly. It has been shown to cause lung cancer It is very inexpensive to grow and harvest. Insects won't eat it. Some typical and possible side effects include loss of vision, disruption of the central nervous system, respiratory illness, anemia, constipation, increased incidence of heart disease and cancer, low birth weights in infants and irritability. Here is a review article about Canola Oil (rapeseed oil) and its toxic effects from a Swedish Medical Journal: Physiopathological effects of rapeseed oil: a review. Borg K Acta Med Scand Suppl (1975) 585:5-13 ISSN: 0365-463X Rapeseed oil has a growth retarding effect in animals. Some investigators claim that the high content of erucic acid in rapeseed oil alone causes this effect, while others consider the low ratio saturated/monounsaturated fatty acids in rapeseed oil to be a contributory factor. Normally erucic acid is not found or occurs in traces in body fat, but when the diet contains rapeseed oil erucic acid is found in depot fat, organ fat and milk fat. Erucic acid is metabolized in vivo to oleic acid. The effects of rapeseed oil on reproduction and adrenals, testes, ovaries, liver, spleen, kidneys, blood, heart and skeletal muscles have been investigated. Fatty infiltration in the heart muscle cells has been observed in the species investigated. In long-term experiments in rats erucic acid produces fibrosis of the myocardium. Erucic acid lowers the respiratory capacity of the heart mitochondria. The reduction of respiratory capacity is roughly proportional to the content of erucic acid in the diet, and diminishes on continued administration of erucic acid. The lifespan of rats is the same on corn oil, soybean oil, coconut oil, whale oil and rapeseed oil diet. Rats fed a diet with erucic acid or other docosenoic acids showed a lowered tolerance to cold stress (+4 degrees C). In Sweden erucic acid constituted 3-4% of the average intake of calories up to 1970 compared with about 0.4% at present. Generally rapeseed has a cumulative effect, taking almost 10 years before symptoms begin to manifest. It has a tendency to inhibit proper metabolism of foods and prohibits normal enzyme function. Canola is a Trans Fatty Acid, which has shown to have a direct link to cancer. These Trans Fatty acids are labeled as hydrogenated or partially hydrogenated oils. Avoid all of them! According to John Thomas' book, Young Again, 12 years ago in England and Europe, rape seed was fed to cows, pigs and sheep that later went blind and began attacking people. There were no further attacks after the rape seed was eliminated from their diet. Source: David Dancu, N.D. http://www.karinya.com/canola.htm 3 6 Milk One of the few total foods capable of supporting life is raw milk. However, when milk is heated to pasteurize it, the proteins are destroyed. When it is homogenized, it is blown through nozzles to break the long fat chains into short broken pieces of fat. Thus pasteurized, homogenized milk is no longer milk but instead contains toxic proteins and fat particles. Most people who think they are “lactose intolerant” are really just sensitive to the toxic brew we call milk that is available in grocery stores. The state of Maryland was considering prohibiting people who own cows from drinking their own milk or from forming cooperatives so people who buy a portion of a cow could consume raw milk. This rebuttal letter written by Sally Fallon puts it all into perspective. I reproduce it here with her permission. RESPONSE TO LETTER FROM TED ELKINS, DEPUTY DIRECTOR, OFFICE OF FOOD PROTECTION AND CONSUMER HEALTH SERVICES, MARYLAND DEPARTMENT OF HEALTH AND MENTAL HYGIENE The following are comments and clarifications to a letter from Ted Elkins, Deputy Director, Office of Food Protection and Consumer Health Services, sent to citizens who submitted comments to oppose the Notice of Proposed Action to amend Regulation .06 under COMAR 10.15.06.Production, Processing, Transportation, Storage and Distribution of Milk. Mr. Elkin ’s statements are in green; our rebuttals are in black. To summarize, Mr. Elkin has made a series of statements unsupported by references and scientific studies. He has ignored many relevant findings concerning the safety and health benefits of raw milk and the increasing evidence of disease caused by pasteurized milk. He has not reported on evidence of bias in reports on alleged problems with raw milk and has withheld discussion of the numerous incidents of foodborne illness in many commonly consumed foods, thus perpetuating the double standard that uninformed health officials have applied to raw milk. The citizens of Maryland deserve accurate information, not unsubstantiated boilerplate allegations. “The State of Maryland and other federal and state health agencies have documented a long history of the risks to human health associated with the consumption of raw milk. Clinical and epidemiological studies from the Food and Drug Administration (FDA), state health agencies, and others have established a direct causal link between gastrointestinal disease and the consumption of raw milk.” While several incidents of food-borne illness in recent years have been attributed to the consumption of raw milk, no positive correlation in these cases was established and government reports on these cases show strong evidence of bias. For example, in 1983, a reported outbreak of Campylobacter in raw milk led to the passage of anti-raw milk legislation in the state of Georgia. However, extensive testing failed to find Campylobacter or any other pathogens in any milk products from the dairy. All safety measures had been followed faithfully. In spite of this lack of evidence, the author of the official report concluded: “The only means available to ensure the public’s health would be proper pasteurization before consumption.” 3 7 (American Journal of Epidemiology, 1983 Vol 114, No 4). Ironically, just 4 years later, a massive outbreak of over 16,000 culture-confirmed cases of antimicrobial-resistant Salmonella typhimurium was traced to pasteurized milk from one dairy in Georgia (JAMA 1987 Dec 11 ;258(22):3269-74). Yet health officials still allow the sale of pasteurized milk in Georgia. Another example concerns a November 2001 outbreak of Campylobacter in Wisconsin, which local health officials and the Centers for Disease Control blamed on raw milk from a cow-share program in Sawyer County. According to an official report, posted on the CDC website, 70-75 persons became ill from Campylobacter infection during the 12 weeks following November 10, 2001. However, independent investigators determined that the number of afflicted was over 800. Only 24 of 385 cow-share owners became ill. Most had consumed hamburger at a local restaurant. There was no illness in the remaining 361 cow-share owners and most of those who became ill did not consume raw milk. Health workers at local hospitals showed a clear evidence of bias by testing only those who said they had consumed raw milk; others who reported in sick but had not drunk raw milk were sent home without investigation. Most importantly, independent lab tests found no Campylobacter in the raw milk (www.realmilk.com). This outbreak is one that health officials almost always emphasize when arguing against the consumption of raw milk; yet the evidence of the case points to the fact that raw milk was not the cause of the outbreak. “The microbial flora of raw milk may include human pathogens present on the cow's udder and teats.” Standard sanitary procedures can completely eliminate the presence of human pathogens in human milk. Organic Pastures Dairy in California produces raw milk for retail sales. The dairy and the state have conducted routinely tests for several years and have never found a human pathogen in the raw milk they produce (www.organicpastures.com). The intrinsic safety of raw milk stands in sharp contrast to the dangers inherent in other foods. For example, a 1978 survey found Salmonella in many “health food” products, including soy flour, soy protein powder and soy milk powder. The authors of the report concluded that “The occurrence of this pathogen in three types of soybean products should warrant further investigation of soybean derivatives as potentially significant sources of Salmonella (Applied and Environmental Microbiology, Mar 1979, pp 559-566). While raw milk often gets the blame for food-borne illnesses, Campylobacter is best known for contaminating meats. For example, a study carried out during 1999-2000 found that 70.7 percent of chicken and 14.5 percent of turkey samples from Washington, DC grocery stores was infected with Campylobacter. (Zhao C, et al. Applied and Environmental Microbiology, 2001:67(12):5431-5436). Maryland law does not require pasteurization of chicken and turkey, which is highly likely to contain human pathogens, yet has taken steps to deny access to raw milk, which seldom if ever contains human pathogens. If the goal of the state of Maryland is to eliminate our exposure to human pathogens, perhaps health department officials should take steps to ban the use of coins and cookware. E. Coli has been shown to survive on coins for 7-11 days at room temperature; Salmonella enteritidis can survive 1-9 days on pennies, nickels, dimes and quarters; and Salmonella enteritidis can also survive on glass and Teflon for up to 17 days (Jiang and Doyle. Journal of Food Protection 1999;62(7):805-7). The truth is that humans are exposed to pathogens on a daily basis—on surfaces, in our water and in the food we eat. To single out raw milk as a source of pathogens shows extreme bias against the only food that is intrinsically safe and that furthermore contains many components that support our immunity to pathogens. “Further, the intrinsic properties of milk, including its pH and nutrient content, make it an excellent medium for the survival and growth of pathogenic bacteria.” This statement reveals the complete ignorance of over 40 years of science indicating that raw milk does not support the survival and growth of pathogenic bacteria. Milk contains numerous components that fight against pathogens and strengthen the immune system. These include: 3 8 Lactoperoxidase, an enzyme that uses small amounts of H2O2 and free radicals to seek out and destroy bad bacteria. It is found in all mammalian secretions, such breast milk, tears and saliva. Lactoperoxidase levels are much higher in the milk of animals than humans. For example, lactoperoxidase levels are 10 times higher in goat milk than in human breast milk. So effective is lactoperoxidase in fighting pathogens that other countries are looking into using lactoperoxidase instead of pasteurization to ensure safety of commercial milk (British Journal of Nutrition (2000), 84, Suppl. 1. S19-S25; Indian Journal Exp Biology Vol. 36, August 1998, pp 808-810; 1991 J Dairy Sci 74:783-787; Life Sciences, Vol 66, No 23, pp 2433-2439, 2000) Lactoferrin, an enzyme that steals iron away from pathogens and carries it through the gut wall into the blood stream and also stimulates the immune system. Lactoferrin also ensures complete assimilation of iron by the infant. Polysaccharides, special sugars that encourage the growth of good bacteria in the gut; protect the gut wall Medium-Chain Fatty Acids, special types of fats that disrupt cell walls of bad bacteria; levels are so high in goat milk that the test for the presence of antibiotics had to be changed. Enzymes that disrupt bacterial cell walls. Antibodies that bind to foreign microbes and prevent them from migrating outside the gut; initiate immune response (British Journal of Nutrition (2000) 84. Suppl. 1, S3-S10, S11-S17). White blood cells that produce antibodies against specific bacteria, producing immunity for life in the infant. B-lymphocytes, compounds that kill foreign bacteria and call in other parts of the immune system Macrophages, components that engulf foreign proteins and bacteria Neutrophils, which kill infected cells; mobilize other parts of the immune system T-lymphocytes, components that multiply if bad bacteria are present, while producing immunestrengthening compounds. Lysosyme, which kills bad bacteria by digesting their cell walls. Hormones & growth factors, which stimulate the maturation of gut cells thereby preventing “leaky” gut. Mucins, which adhere to bad bacteria and viruses, preventing those organisms from attaching to the mucosa and causing disease. Oligosaccharides, special types of sugars which protect other protective components from being destroyed by stomach acids and enzymes; they bind to bacteria and prevent them from attaching to the gut lining and have other functions just being discovered. B12 binding protein, a component that reduces the levels of vitamin B12 in the colon, which harmful bacteria need for growth. This compound also ensures complete assimilation of B12 by the infant. Bifidus factor is a complex of good bacteria which promotes growth of Lactobacillum bifidis, a helpful bacteria in baby’s gut, which helps crowd out dangerous germs Fibronectin, which increases antimicrobial activity of macrophages and helps to repair damaged 3 9 tissues (J Pediatr 1994 Feb; 124(2): 193-8; Curr Med Chem 1999 Feb;6(2): 117-27). Most of these components are completely inactivated by pasteurization (Scientific American, December 1995; The Lancet, Nov 17, 1984), making pasteurized milk highly susceptible to contamination. Mr. Elkin’s statement, that “the intrinsic properties of milk, including its pH and nutrient content, make it an excellent medium for the survival and growth of pathogenic bacteria,” applies only to pasteurized milk, not to raw milk. It is of interest to note that until recently, the medical profession claimed that breast milk was sterile. Research conducted over the last 20 years indicates that breast milk contains pathogens, often at very high levels. It is actually beneficial for breast milk to contain pathogens because the bioactive components in milk program the baby to have immunity for life to any pathogens with which he comes in contact (J Appl Microbiol. 2003;95(3):471 -8; Neonatal Netw. 2000 Oct; 19(7)21-5; J Hosp Infec. 2004 Oct;58(2): 146-50; J Nutr. 2005 May; 135(5): 1286-8; Curr Med Chem. 1999 Feb;6(2): 117-27; Adv Exp Med Biol. 2004;554: 14554; Scientific American, December 1995; Lancet. 1984 Nov 1 7;2(841 2): 111-3; Lancet. 1984 Nov 17;2(8412):111-3; Cent Afr J Med. 2000 Sep;46(9):247-51; Eur J Pediatr. 2000 Nov; 159(11 ):793-7; J Dairy Sci 1991 ;74:783-787). Maryland health officials do not require breastfeeding mothers to pasteurize their milk before giving it to their babies; yet these same officials discourage mothers who are unable to breastfeed from giving their infants the most appropriate and immune-building substitute—raw milk from another mammal such as a cow or goat. A 1994 study found that premature infants fed raw human milk had lower rates of infection compared to those fed pasteurized human milk (Lancet November 17, 1984). In fact, pasteurization of human milk for babies carries considerable risk. A recent outbreak of Pseudomonas aeruginosa in a neonatal intensive care unit caused by a contaminated milk bank pasteurizer resulted in 31 cases of infection and 4 deaths (Arch Dis Child Fetal Neonatal Ed 2003 Sep;88(5):F434-5). The intrinsic safety of raw milk has been proven in several published reports showing that raw milk passes the “challenge test.” That is, when pathogenic bacteria are introduced to raw milk, their numbers rapidly decline; subsequent testing reveals no pathogens even though they were introduced in large numbers. For example, Lactoperoxidase in raw milk has been shown to kill added fungal and bacterial agents (Life Science 2000 66(25):2433-9; Indian Journal of Experimental Biology 1998;36:808-1 1). In a challenge test, raw goat milk killed Campylobacter jejuni (Hygiene (London) 1985 Feb;94(1):31-44). When Campyloba cter was added to raw milk at 4 degrees C at levels of 13,000,000 per ml, levels were less than 10 per ml nine days later (Doyle, et al. Applied and Environmental Microbiology, 1982;44(5):1 154-58). The anti-microbial properties of raw milk are even more active when milk is not refrigerated. Researchers found that bovine strains of Campylobacter were decreased by 100 cells per ml and poultry strains decreased by 10,000 cells per ml in 48 hours in raw milk at room temperature (37 degrees C) (Diker KS. Mikrobiyol Bul 1987 Jul;21(3):200-5). Most recently, the University of California conducted challenge tests on Organic Pastures raw milk in California, finding that pathogens added to raw milk disappeared completely within 36 hours (www.organicpastures.com). “On August 10, 1987, FDA published 21 CFR Part 1240.61, a final regulation mandating the pasteurization of all milk and milk products in final package form for direct human consumption. This regulation addresses milk shipped in interstate commerce and became effective September 9, 1987. In the Federal Register notification for the final rule to 21 CFR Part 1240.61, FDA made a number of findings including the following: ‘Raw milk, no matter how carefully produced, may be unsafe.’ ” This statement may be part of the official record but it contradicts other statements published by the US government. A study carried out over 19 years and posted on the Centers for Disease Control website gives the incidence of food-borne illness from raw milk at 1.9 cases per 100,000 people, 1973-1992 (American Journal Public Health Aug 1998, Vol 88., No 8). This report cites many incidents reputed to be caused by 4 0 raw milk but not necessarily proven; the actual rate of illness caused by raw milk, on a per-consumer basis, may in fact be much lower. Based on the same CDC website, the incidence of food-borne illness from all foods including pasteurized milk during the period 1993-1997 is 4.7 cases per 100,000 people (US Census Bureau 1997 population estimate 267,783,607). Based on CDC website, the incidence of reported food-borne illness from other foods (not including milk) is 6.4 cases per 100,000 people, per year from 1993-1997. Therefore, the incidence of food-borne illness from consuming raw milk is at least 2.5 times lower than the incidence of food-borne illness from consuming pasteurized milk; and at least 3.5 times lower than the incidence of food-borne illness from consuming other foods. Thus the statement published in the FDA register is false; raw milk is safer than any other food in the food supply. If a food is to be taken out of the food supply because it “may be unsafe,” then we would have nothing left to eat. Raw salads, fruits, vegetables, shellfish, eggs and meat, plus pasteurized milk, soy products, baby formula and mayonnaise have all caused proven outbreaks of illness. Yet these foods remain in the food supply, putting the citizens of Maryland at continued risk. According to our government, food-borne diseases cause approximately 76 million illnesses, 325,000 hospitalizations and 5,000 deaths per year; the most common source of these infections is fruits, vegetables and salads. For example, in 1997, there were 1104 reported cases of food-borne illness from salads and 719 from fruits and vegetables while only 23 from milk, mostly pasteurized milk (MMWR Vol 45, No SS-5). "It has not been shown to be feasible to perform routine bacteriological tests on the raw milk itself to determine the presence or absence of all pathogens and thereby ensure that it is free of infectious organisms." This statement would not hold up in a court of law. Today it is completely feasible to perform routine bacteriological tests on raw milk; these can be performed at the farm and are very inexpensive. There is even a test for E. coli O157:H7 that can be carried out on the farm and costs only $8 per test. It is shameful that health officials of the state of Maryland are unfamiliar with these tests. “Opportunities for the introduction and persistence of Salmonella on dairy premises are numerous and varied, and technology does not exist to eliminate Salmonella infection from dairy herds or to preclude reintroduction of Salmonella organisms. Moreover recent studies show that cattle can carry and shed S. dublin organisms for many years and demonstrated that S. dublin organisms cannot be routinely detected in cows that are 'mammary gland' shedders.” This statement applies only to large confinement herds. It has proven completely possible to eliminate pathogens from dairy premises when cows are raised on pasture and reasonable sanitary protocols are followed. Over several years of testing, not a single human pathogen has been found on the premises of Organic Pastures dairy in California, not in the manure and not in the milk (www.organicpastures.com). “During this rulemaking process, the American Academy of Pediatrics and numerous other organizations submitted comments in support of the proposed regulation. In deciding upon mandatory pasteurization, FDA determined that pasteurization was the only means to assure the destruction of pathogenic microorganisms that might be present.” This statement is completely false. Pasteurization does not ensure the destruction of pathogenic microorganisms in milk. A study published in 2002 found evidence of Mycobacterium paratuberculosis in many samples of pasteurized cow’s milk (Appl Environ Microbiol 2002 May;68(5):2428-35). M. paratuberculosis has been associated with Crohn’s disease. Other studies indicate that B. Cereus spores, botulism spores and protozoan parasites survive pasteurization (Elliott Ryser. Public Health Concerns. In: Marth E, Stelle J, eds. Applied Dairy Microbiology, New York, Marcel Dekker, 2001). 4 1 Furthermore, the US government has documented numerous outbreaks of food-borne illness from pasteurized milk. These include: 1945—1,492 cases for the year in the US 1945—1 outbreak, 300 cases in Phoenix, Arizona. 1945—Several outbreaks, 468 cases of gastroenteritis, 9 deaths, in Great Bend, Kansas 1976—Outbreak of Yersinia enterocolitica in 36 children, 16 of whom had appendectomies, due to pasteurized chocolate milk 1978—1 outbreak, 68 cases in Arizona 1982—over 17,000 cases of Yersinia enterocolitica in Memphis, TN 1982—172 cases, with over 100 hospitalized from a three-Southern-state area. 1983—1 outbreak, 49 cases of Listeriosis in Massachusetts 1984—August, 1 outbreak S. typhimurium, approximately 200 cases, at one plant in Melrose Park, IL 1984—November, 1 outbreak S. typhimurium, at sam e plant in Melrose Park, IL 1985—March, 1 outbreak, 16,284 confirmed cases, at same plant in Melrose Park, IL 1985—197,000 cases of antimicrobial-resistant Salmonella infections from one dairy in California 1985—1,500+ cases, Salmonella culture confirmed, in Northern Illinois 1987—Massive outbreak of over 16,000 culture-confirmed cases of antimicrobial-resistant Salmonella typhimurium traced to pasteurized milk in Georgia 1993—2 outbreaks statewide, 28 cases Salmonella infection 1994—3 outbreaks, 105 cases, E. Coli & Listeria in California 1993-1994—outbreak of Salmonella enteritidis in over 200 due to pasteurized ice cream in Minnesota, South Dakota and Wisconsin 1995—1 outbreak, 3 cases in California 1995—outbreak of Yersinia enterocolitica in 10 children, 3 hospitalized due to postpasteurization contamination 1996—2 outbreaks Campylobactor and Salmonella, 48 cases in California 1997—2 outbreaks, 28 cases Salmonella in California The fact that Mr. Elkins does not present the full story, by enumerating the many outbreaks of food-borne illness in pasteurized milk, provides clear evidence of bias on the part of a Maryland health official. “This decision was science-based, involving epidemiological evidence. FDA and the Centers for Disease Control and Prevention (CDC) in Atlanta have documented illnesses associated with the consumption of raw milk, including ‘certified raw milk’ and have stated that the risks of consuming raw milk far outweigh any benefits.” It is obvious that this decision was not science-based and that it contradicts the epidemiological evidence provided by our government agencies. “Based on research, which has failed to demonstrate a significant difference between the nutritional value of pasteurized and unpasteurized milk, the FDA and CDC reiterate that the health risks associated with raw milk consumption far outweigh the benefits.” Mr. Elkins seems to be unaware of numerous studies showing the benefits of raw milk over pasteurized. For example, studies carried out during 1935-1940 at Randleigh Farm, a research facility in upstate New York, found that rats fed raw milk had better growth and denser bones than those fed pasteurized milk. The rats on pasteurized milk developed hairless patches due to vitamin B6 deficiency and on autopsy showed poor integrity of internal organs (Annals of Randleigh Farm). These studies confirm the findings of Francis Pottenger who noted that the organs of cats fed raw milk were in excellent condition, with creamy yellow subcutaneous tissue of high vascularity. The heart size of rawmilk fed cats was moderate, the liver in good condition, the intestines firm and the uterus well supported. By contrast the internal organs of pasteurized-milk fed cats were inferior, with slight fatty atrophy of the liver, 4 2 inferior condition of the heart, lack of intestinal tone and moderate distention of the uterus. The skin of the pasteurized-milk fed cats had a purplish discoloration due to congestion and the fur was of poor quality (Pottenger’s Cats, Price-Pottenger Nutrition Foundation). During 1930-31, Dr. Ernest Scott and Professor Lowell Erf of Ohio State University carried out rat studies that compared the effects of a diet of whole raw milk with one of whole pasteurized milk. Rats fed whole raw milk had good growth, sleek coats and clear eyes. The rats had excellent dispositions and enjoyed being petted. By contrast, rats fed whole pasteurized milk had rough coats, slow growth, anemic, and loss of vitality and weight. They were very irritable, often showing a tendency to bite when handled (Jersey Bulletin 1931 50:210-21 1;224-226, 237). Studies of guinea pigs carried out by Dr. Rosalind Wulzen and Paul N. Harris, Department of Zoology, Oregon State College are particularly revealing. Animals fed whole raw milk had excellent growth and no abnormalities. By contrast, those fed pasteurized milk had poor growth, muscle stiffness, emaciation and weakness and death within one year. Autopsy revealed atrophied muscles streaked with calcification and calcium deposits under the skin, in the joints, the heart and other organs (American Journal of Pathology Vol XX VI, Jul-Nov 1950 pp 595-615). As for pasteurized milk, many recent studies document the association of pasteurized milk with diabetes (Br J Nutr 2006 Mar;95(3):603-8;Diabetes 2000 Jun;49(6):91 2-7), frequent ear infections (J Pediatr Rio J 2006 mar-Apr;82(2):87-96; Rev Alerg Mex 2001 Sep-Oct;48(5):141-4; Acta Paediatr 2000 Oct;89(10):1 174-80; Acta Otolaryngol 1999;1 19(8):867-73) and asthma (Ann Allergy Asthma Immunol 2002 Dec;89(6 Suppl 1):33-7; J Allergy Clin Immunol 2001 Nov; 108(5):720-5; West J Nurs Res 1996 Dec;18(6):643-54; Pediatr Pulmonol Suppl 1995;1 1:59-60). Of interest is a 2002 study showing that “farm milk,” that is raw milk, had a protective effect against this debilitating and even lift-threatening condition (Lancet 2002 Feb 1 6;359(9306):623-4). The scientific literature contains many case histories of recovery from these conditions by eliminating pasteurized milk from the diet. Meanwhile, reports of recovery from these and other conditions by consuming raw milk are accumulating. The growing numbers of Maryland consumers—especially growing children—who cannot tolerate pasteurized milk deserve to have a choice for raw milk. “Numerous documented outbreaks of milk borne disease involving Salmonella and Campylobacter infections have been directly linked to the consumption of raw milk in the past twenty years. Since the early 1980's, cases of raw milk-associated campylobacteriosis have been reported in the states of Arizona, California, Colorado, Georgia, Kansas, Maine, Montana, New Mexico, Oregon, and Pennsylvania. An outbreak of salmonellosis, involving 50 cases was confirmed in Ohio in 2002. Recent cases of E. coli O1 57:H7, Listeria monocytogenes and Yersinia enterocolitica infections have also been attributed to raw milk consumption.” It would be helpful if Mr. Elkins would provide references so that they could be evaluated for legitimacy and bias. Given the double standard applied to raw milk, it is likely that many of these cases were merely reported, not proven. The 2002 Ohio outbreak that he cites was a case in which health officials demonstrated clear evidence of bias. According to the CDC report, “The source for contamination was not determined; however, the findings suggest that contamination of milk might have occurred during the milking, bottling or capping process.” There were many possible of vectors of illness on the dairy besides raw milk—besides providing raw milk, the dairy also operated a petting zoo. There have been several incidences of illness contracted by children visiting a petting zoo, cases that have nothing to do with raw milk. Based on this one incident, in which raw milk was not proven the culprit, the dairy, which had been in business for decades without incident, caved in to health department pressure and stopped the sale of raw milk. “State health and agricultural agencies utilize the U.S. Public Health Service/FDA Pasteurized Milk Ordinance (PMO) as the basis for the regulation of Grade ‘A’ milk production and processing. The PMO has been sanctioned by the National Conference on Interstate Milk Shipments (NCIMS) and provides a national standard of uniform measures that is applied to Grade ‘A’ dairy farms and milk processing facilities to assure safe milk and milk products. Section 9 of the PMO specifies that only Grade ‘A’ pasteurized milk be sold to the consumer.” 4 3 This issue is a red herring. The individual states do not need to follow the PMO. The PMO is a choice, not an obligation. California, the top milk-producing state, does not follow the PMO but created its own regulations. Furthermore, the state can accept the PMO but have exceptions in certain areas, as does Colorado. In any event, PMO regulations do not prohibit consumers from drinking raw milk. It must be stressed that neither the federal government nor the individual states prohibit the consumption of raw milk. Such laws would be inherently unconstitutional, depriving citizens the right to liberty and property without due process of law. “In summary, since raw milk may contain infective doses of human pathogens, its consumption increases the risk of a variety of illnesses. Even when milk is produced and handled under sanitary conditions, the only proven, reliable method of reducing the level of human pathogens in milk and milk products to safe levels is pasteurization. The FDA has strongly advised against the consumption of raw milk. As the State agency responsible for health of the citizens of Maryland, the Department of Health and Mental Hygiene cannot, in good conscience, condone or encourage the sale of raw milk.” As we have demonstrated in this letter, raw milk does not contain “infective doses of human pathogens” and its consumption does not “increase the risk of a variety of illnesses.” Pasteurization does not guarantee a safe product and the risk of contracting food-borne illness from raw milk is lower that the risk of contracting food-borne illness from pasteurized milk. The statements made in writing by Mr. Elkins would not hold up in a court of law and are an insult to Maryland consumers. But in any event, Maryland consumers are not asking for legalization of the sale of raw milk, but only confirmation of the right to drink the raw milk from their own cows, which is a public policy of the state of Maryland. Maryland consumers are not asking the Department of Health and Mental Hygiene to condone or encourage the sale of raw milk, but merely insisting that the state of Maryland support the rights of its citizens to enter into contractual agreements guaranteed by Maryland law (title 16, Section 401), which recognizes the right of an owner of dairy livestock to contract with another for the boarding and care of that livestock. MDHMH is interfering in areas where it has no jurisdiction whatsoever and is overstepping the bounds of its regulatory authority. Sally Fallon, President The Weston A. Price Foundation May 23, 2006 Phosphatidylcholine DESCRIPTION Phosphatidylcholine is a phospholipid that is a major constituent of cell membranes. Phosphatidylcholine is also known as 1, 2-diacyl-: ussn: ue-glycero-3-phosphocholine, PtdCho and lecithin. It is represented by the following chemical 44 structure: Phosphatidylcholine The term lecithin itself has different meanings when used in chemistry and biochemistry than when used commercially. Chemically, lecithin is phosphatidylcholine. Commercially, it refers to a natural mixture of neutral and polar lipids. Phosphatidylcholine, which is a polar lipid, is present in commercial lecithin in concentrations of 20 to 90%. Most of the commercial lecithin products contain about 20% phosphatidylcholine. Lecithins containing phosphatidylcholine are produced from vegetable, animal and microbial sources, but mainly from vegetable sources. Soybean, sunflower and rapeseed are the major plant sources of commercial lecithin. Soybean is the most common source. Plant lecithins are considered to be GRAS (generally regarded as safe). Egg yolk lecithin is not a major source of lecithin in nutritional supplements. Eggs themselves naturally contain from 68 to 72% phosphatidylcholine, while soya contains from 20 to 22% phosphatidylcholine. The fatty acid makeup of phosphatidylcholine from plant and animal sources differs. Saturated fatty acids, such as palmitic and stearic, make up 19 to 24% of soya lecithin; the monounsaturated oleic acid contributes 9 to 11%; linoleic acid provides 56 to 60%; and alpha-linolenic acid makes up 6 to 9%. In egg yolk lecithin, the saturated fatty acids, palmitic and stearic, make up 41 to 46% of egg lecithin, oleic acid 35 to 38%, linoleic acid 15 to 18% and alpha-linolenic 0 to 1%. Soya lecithin is clearly richer in polyunsaturated fatty acids than egg lecithin. Unsaturated fatty acids are mainly bound to the second or middle carbon of glycerol. Choline comprises about 15% of the weight of phosphatidylcholine. (See monograph on Choline.) ACTIONS AND PHARMACOLOGY ACTIONS Phosphatidylcholine may have hepatoprotective activity. 45 Phosphatidylcholine is important for normal cellular membrane composition and repair. Phosphatidylcholine is also the major delivery form of the essential nutrient choline. Choline itself is a precursor in the synthesis of the neurotransmitter acetylcholine, the methyl donor betaine and phospholipids, including phosphatidylcholine and sphingomyelin among others. Phosphatidylcholine is involved in the hepatic export of very-low-density lipoproteins. MECHANISM OF ACTION Phosphatidylcholine's role in the maintenance of cell-membrane integrity is vital to all of the basic biological processes. These are: information flow that occurs within cells from DNA to RNA to proteins; the formation of cellular energy and intracellular communication or signal transduction. Phosphatidylcholine, particularly phosphatidylcholine rich in polyunsaturated fatty acids, has a marked fluidizing effect on cellular membranes. Decreased cell-membrane fluidization and breakdown of cellmembrane integrity, as well as impairment of cell-membrane repair mechanisms, are associated with a number of disorders, including liver disease, neurological diseases, various cancers and cell death. PHARMACOKINETICS Phosphatidylcholine is absorbed into the mucosal cells of the small intestine, mainly in the duodenum and upper jejunum, following some digestion by the pancreatic enzyme phospholipase, producing lysophosphatidylcholine (lysolecithin). Reacylation of lysolecithin takes place in the intestinal mucosal cells, reforming phosphatidylcholine, which is then transported by the lymphatics in the form of chylomicrons to the blood. Phosphatidylcholine is transported in the blood in various lipoprotein particles, including very-low-density lipoproteins (VLDL), low-density lipoproteins (LDL) and high-density lipoproteins (HDL); it is then distributed to the various tissues of the body. Some phosphatidylcholine is incorporated into cell membranes. Phosphatidylcholine is also metabolized to choline, fatty acids and glycerol. The fatty acids and glycerol either get oxidized to produce energy or become involved in lipogenesis. Choline is a precursor of acetylcholine. Serum choline levels peak between 2 to 6 hours after oral intake. INDICATIONS AND USAGE Phosphatidylcholine may be indicated to help restore liver function in a number of disorders, including alcoholic fibrosis, and possibly viral hepatitis. It may also be indicated for the treatment of some manic conditions. There is some evidence that Phosphatidylcholine may be useful in the management of Alzheimer's disease and some other cognitive disorders. A possible future role in cancer therapy is also suggested by recent research. It may also be indicated in some with tardive dyskinesia. (Recent studies by Kane and Kane have found it critical in most chronic diseases including Lou Gehrig’s disease, Alzheimer’s, Lyme disease, autism, etc. JLT) 46 RESEARCH SUMMARY Clinical studies have demonstrated that choline is essential for normal liver function. Phosphatidylcholine is a better delivery form and is also more tolerable than choline. But, in addition, research has shown that phosphatidylcholine, independent of its choline content, has striking hepatoprotective effects. In two animal studies using baboons fed diets high in alcohol, some supplemented with a soy-derived polyunsaturated lecithin (60% phosphatidylcholine) and some unsupplemented, both fibrosis and cirrhosis were largely prevented in the phosphatidylcholine group. Most of the unsupplemented animals in these studies, which continued for up to eight years, developed fibrosis or cirrhosis. Because these researchers had previously found that choline, equal in amounts contained in the phosphatidylcholine-rich lecithin they subsequently used, had no comparable protective effects on the liver, they concluded that the polyunsaturated phospholipids themselves may have been responsible for the benefits observed. In vitro studies have shown that these phospholipids increase hepatic collagenase activity and may thus help prevent fibrosis and cirrhosis by encouraging collagen breakdown. Several other mechanisms under investigation may also contribute. Others have reported similarly encouraging results in animal models. Clearly, human trials are warranted. In addition, phosphatidylcholine has demonstrated other protective effects in nonalcoholic liver disorders, including protection against various other toxic substances. Its benefits in viral hepatitis were reported some years ago by several different research groups in Europe and elsewhere. In one of these studies, individuals suffering from hepatitis type A and B were given 1.8 grams of phosphatidylcholine daily. Compared with unsupplemented controls, the phosphatidylcholine group enjoyed quicker recoveries, fewer relapses and quicker normalization of liver function tests. Researchers in Great Britain treated chronic active hepatitis C patients with 3 grams daily of phosphatidylcholine in double-blind fashion. The phosphatidylcholine patients had significantly reduced symptoms, compared with controls. All histological evidence of the disease disappeared in some cases. These researchers, like others, have hypothesized that phosphatidylcholine's possible antiviral effects are related to the supplement's apparent ability to increase cellular membrane fluidity and repair the membranes of liver cells. Phosphatidylcholine may help some with tardive dyskinesia, a neurological disorder characterized by defective cholinergic nerve activity. Both supplemental choline and phosphatidylcholine were found to reduce the muscular hyperactivity of this disorder by about 50% in some studies. However, one significant trial did not see a beneficial effect. There is some very preliminary evidence that phosphatidylcholine may help control manic symptoms in some. There has been hope, for some time, that phosphatidylcholine would demonstrate clearcut benefits in cognitive disorders, such as age-related memory loss and Alzheimer's 47 disease. There are a few reports that supplemental choline can improve short-term memory skills and enhance the memories of those who are initial poor learners. Those with Alzheimer's disease have a diminished ability to synthesize and/or utilize the neurotransmitter acetylcholine, particularly in those areas of the brain related to memory, thus the hope that supplemental choline/phosphatidylcholine might be of benefit. A few studies have suggested some small benefit in memory restoration, but most have not. Research continues. Recently it has been suggested that phosphatidylcholine might eventually have some therapeutic role in some cancers. There is no evidence of this to date, but animal studies indicate that deficiencies in choline and phosphatidylcholine may disrupt cell membrane signal transduction in ways that could lead to various cancers. There is ample evidence that liver cancer is promoted in various animals by choline-deficient diets, and it has been shown that excess choline can protect against liver cancer in a mouse model. Phosphatidylcholine has been used to lower serum cholesterol levels, based on the premise that lecithin cholesterol acyltransferase (LCAT) activity has an important role in the removal of cholesterol from tissues. A few studies have shown reduction in serum cholesterol with phosphatidylcholine intake. The results were quite modest, and most studies have not shown any significant cholesterol-lowering activity. CONTRAINDICATIONS, PRECAUTIONS, ADVERSE REACTIONS CONTRAINDICATIONS There are no reported or known contraindications of phosphatidylcholine supplementation. PRECAUTIONS Those with malabsorption problems may develop diarrhea or steatorrhea when using phosphatidylcholine supplements. Those with the antiphospholipid-antibody syndrome should exercise caution in the use of phosphatidylcholine supplements. ADVERSE REACTIONS No major side effects have been reported. Mild side effects have been noted occasionally such as nausea, diarrhea and increased salivation in some. This holds for all forms of phosphatidylcholine. INTERACTIONS There are no known interactions. OVERDOSAGE 48 There are no reports of overdosage. DOSAGE AND ADMINISTRATION There are several forms of phosphatidylcholine supplements. Typical commercial lecithin supplements contain 20 to 30% phosphatidylcholine. Softgel capsules containing 55% and 90% phosphatidylcholine are available. Liquid concentrates containing 3 grams of phosphatidylcholine per 5 milliliters (one teaspoon) are also available. Recommended doses range from 3 to 9 grams of phosphatidylcholine daily in divided doses. LITERATURE Atoba MA, Ayoola EA, Ogunseyinde O. Effects of essential phospholipid choline on the course of acute hepatitis-B infection. Trop Gastroenterol. 1985; 6:96-9. Buko V, Lukivskaya O, Nikitin V, et al. Hepatic and pancreatic effects of polyenoylphosphatidylcholine in rats with alloxan-induced diabetes. Cell Biochem Funct. 1996; 14:131-137. Canty DJ, Zeisel SH. Lecithin and choline in human health and disease. Nutr Rev. 1994; 52:327-339. Cohen BM, Lipinski JF, Altesman RI. Lecithin in the treatment of mania: double-blind, placebo-controlled trials. Am J Psychiatry. 1982; 139:1162-1164. Gelenberg AJ, Dorer DJ, Wojcik JD, et al. A crossover study of lecithin treatment of tardive dyskinesia. J Clin Psychiatry. 1990; 51:149-153. Growdon JH, Gelenberg AJ, Doller J, et al. Lecithin can suppress tardive dyskinesia. N Engl J Med. 1978; 298:1029-1030. Hanin I, Ansell GB, eds. Lecithin. Technological, Biological and Therapeutic Aspects. New York and London: Plenum Press; 1987. Hirsch MJ, Growdon JH, Wurtman RJ. Relations between dietary choline or lecithin intake, serum choline levels, and various metabolic indices. Metabolism. 1978; 27:953960. Jackson IV, Nuttall EA, Ibe IO, Perez-Cruet J. Treatment of tardive dyskinesia with lecithin. Am J Psychiatry. 1979; 136:1458-1460. Jenkins PJ, Portmann BP, Eddleston AL, Williams R. Use of polyunsaturated phosphatidylcholine in HBsAg negative chronic active hepatitis: results of prospective double-blind controlled trial. Liver. 1982; 2:7-81. 49 Kosina F, Budka K, Kolouch Z, et al. Essential cholinephospholipids in the treatment of virus hepatitis. Cas Lek Cesk. 1981; 120:957-960. Lieber CS, Leo MA, Aleynik SI, et al. Alcohol Clin Exp Res. 1997; 21:375-379. Lieber CS, De Carl LM, Mak KM, et al. Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin. Hepatol. 1990; 12:1390-1398. Little A, Levy R, Chuaqui-Kidd P, Hand D. A double-blind, placebo-controlled trial of high-dose lecithin in Alzheimer's disease. J Neur Neurosurg Psych. 1985; 48:736-742. Visco G. Polyunsaturated phosphatidylcholine in association with vitamin B complex in the treatment of acute viral hepatitis B. results of a randomized double-blind clinical study. Clin Ter. 1985; 114:183-188. Wurtman RJ, Hefti F, Melamed E. Precursor control of neurotransmitter synthesis. Pharmac Rev. 1981; 32:315-335. Wurtman RJ, Hirsch MJ, Growdon JH. Lecithin consumption raises serum-free-choline levels. Lancet. 1977; 2(8028):68-69. TOXINS Now that we have the utilities turned on, we are ready to start cleaning. Over time, several undesirable things are likely to be present. There are likely to be bacteria, fungus, roaches, spiders, ants, mice, termites, etc. present. These things must be removed for us to live happily in our remodeled home. We live in a toxic society. We have been in the process of poisoning ourselves to death for years. We have been lead to believe that scientists know everything and that the government agencies would not allow companies to do anything that will harm us. The recent episodes of Vioxx, Bextra, NutraSweet and many others show us that isn’t true. We used DDT as a pesticide for years until finally it killed most of our eagles by poisoning the fish they eat. Now we have a new syndrome where harmless amoebae in our lakes and rivers have turned into meat-eating pathogens that cause chronic fatigue because the apple, orange, and tobacco farmers are using pesticides that kill the algae that the amoebae used for a food supply. When aspartame (NutraSweet) was first tested, it was given to seven monkeys. One died and five had seizures. When given to mice, over 40% developed brain tumors. Still the government now allows it to be put into most of our food. MSG causes monkey to have holes in their brains. However, the government allows it to be put into children’s vitamins, seasonings, crackers, potato chips, etc. You cannot depend on the government to protect you from things that aren’t healthy. One of the unsuspected problems with these various toxins is that the body becomes ADDICTED to them. Food manufactures know this. That is why they put known neurotoxins like aspartame and MSG in their products. You become addicted. That makes you want to use more of their product and have trouble when you try to stop using 50 it. It is not likely that many of us would think about being addicted to Diet-sodas or corn chips! Because stopping addictions is difficult and uncomfortable, you will find giving up these toxic things difficult. Therefore I recommend you eliminate these toxic things one at a time. Check them off the list each time you can go for a couple of weeks without craving each item or being tempted to eat them when others are doing so. Here is the list. Think of these things as spiders, rodents, termites and other things you don’t want in your house: 1. All forms of tobacco. 2. All artificial sweeteners. That includes aspartame (NutraSweet, Equal), Splenda, Saccharine, sorbitol, mannitol, etc. Use Stevia if you must have a sweetener. Go through your pantry and throw out anything that contains any artificial sweeteners. 3. Mono Sodium Glutamate (MSG). Go through your pantry and throw out anything that contains MSG. Don’t forget to look at vitamins, spices, etc. 4. Trans Fats. Look for “hydrogenated” or “partially hydrogenated” oil or “Canola Oil” on the label. Try not to eat in restaurants that use Trans fats. Use real butter instead of margarine. 5. Drink raw whole milk instead of 2% or skim milk. You should know that heating milk to pasteurize it changes its proteins to toxic ones. Homogenization is accomplished by forcing the milk through nozzles under pressure. That fractures the fats into abnormal small chains that are water soluble. These are often toxic. That is why so many people have trouble with milk products. Unfortunately, only California allows raw milk to be sold, so you will have to have it shipped to you unless you own an interest in your own cow. In many states you can join a club so you can get raw milk that isn’t pasteurized or homogenized. 6. Sugar. Processed sugar has been separated from the minerals that make it less harmful. In addition, it causes the release of an enzyme that destroys cells (phospholipase A2, PLA2) 7. Toothpaste. Just read the label on any major brand toothpaste or mouthwash. You'll see they are loaded with dangerous toxins and chemicals such as sodium fluoride, triclosan, FD&C Blue Dye #1 and 2, sodium lauryl sulfate, and hydrated silica. All of these common ingredients have been found to be harmful to humans. That is why your toothpaste tube has a poison warning on it! Instead, use 2/3 baking soda and 1/3 sea salt. http://www.oramd.com/hiddendangers.htm If you don’t like the baking soda, use essential oils, e.g., Shine. 8. Aluminum. You will find it in white flour and Extra-dry antiperspirants. Stop using aluminum cookware, aluminum foil, and drinking from aluminum cans. 9. Copper. Copper toxicity is a problem from exhaust fumes, tap water (copper pipes), pesticides, etc. Copper blocks zinc, a critical element in over 350 metabolic processes. 10. Antiperspirants that contain aluminum, polyethylene glycol, or propylene glycol. Ethylene glycol and propylene glycol are clear liquids used in antifreeze and deicing solutions. Exposure to large amounts of ethylene glycol can damage the 51 kidneys, heart, and nervous system. Use a deodorant instead of an antiperspirant. An example is Roll. 11. Coffee. Even decaffeinated coffee blocks zinc depression. 12. Tea. Same as coffee. 13. Alcohol. Same as coffee. Deodorants vs. Antiperspirants Most people think that antiperspirants and deodorants are the same thing, but they aren’t. Antiperspirants work by clogging, closing, or blocking the pores with powerful astringents such as aluminum salts so that they can’t release sweat. (Note that aluminum can accumulate in the brain.) Deodorants work by neutralizing the smell of the sweat and by antiseptic action against bacteria. Deodorants are preferable because they don’t interfere with sweating, a natural cooling and detoxifying process. Baking Soda Simple Solution Baking soda works wonders because it neutralizes the odor of sweat. Just sprinkle a light covering of baking soda onto a damp washcloth. Pat on. Don’t rinse. This tip—just using baking soda—has saved me on many occasions, especially when traveling. Basic Deodorant Powder 1/2 cup baking soda 1/2 cup cornstarch a few drops essential oils such as lavender or cinnamon Place the ingredients in a glass jar. Shake to blend. Sprinkle a light covering of the powder on a damp washcloth. Pat on. Don’t rinse. Basic Liquid Deodorant 1/4 cup each witch hazel extract, aloe vera gel, and mineral water 1 teaspoon vegetable glycerin a few drops antibacterial essential oils such as lavender (optional) Combine the ingredients in a spray bottle. Shake to blend. Makes 3/4 cup Shelf Life: Indefinite http://www.care2.com/channels/solutions/consumer_guides/114 If you don’t want to make your own deodorant, use ROLL Natural Organic Quench Scented Deodorant and ROCK by Forever Green. As your liver gets sicker, the immune system becomes weaker. There are always over 1,000 types of pathogenic organisms in your body just waiting to eat you when you immune system fails. These infectious organisms feed on carbohydrates and must have 52 an acidic medium (voltage deficient). Thus if your liver is so sick you get nauseated when you eat fat, you will need to avoid feeding these infections by avoiding carbohydrates until you can get your liver/immune system working again. If you are so sick you are disabled, you will need to avoid other possible sources of increased toxins that you body will not be able to manage. In addition you will need to avoid carbohydrates (increase destruction of cells). The Intense Detoxification Diet includes the following and must be followed for two months if you are disabled by your illness. If you eat in restaurants, eat ½ the amount of these items you might otherwise eat: REMOVE THESE FROM THE DIET IF YOU ARE DISABLED BY YOUR ILLNESS AND/OR YOU GET NAUSEATED WHEN YOU EAT FAT: 1. No grains 2. No pasta 3. No starchy vegetables (potato, carrot, parsnip, beet, radish, peas, corn) 4. No fruit or fruit juice 5. No beans 6. No corn syrup, dextrose, sucrose, honey, sugar, maltodextrin. 7. No fast foods 8. No carbonated drinks 9. No artificial sweeteners. 10. No hydrogenated oils. 11. No MSG 12. No Canola oil or mayonnaise 13. No peanuts or peanut butter 14. No mustard. Mustard seeds contain goitrogens, naturally occurring substances in certain foods that can interfere with the functioning of the thyroid gland. Individuals with already existing and untreated thyroid problems may want to avoid mustard seeds for this reason. Cooking may help to inactivate the goitrogenic compounds found in food. However, it is not clear from the research exactly what percent of goitrogenic compounds get inactivated by cooking, or exactly how much risk is involved with the consumption of mustard seeds by individuals with pre-existing and untreated thyroid problems. http://www.whfoods.com/genpage.php?tname=foodspice&dbid=106 15. No spinach. Spinach contains oxalic acid. Oxalic acid is corrosive to tissue. When ingested, oxalic acid removes calcium from the blood. Kidney damage can be expected as the calcium is removed from the blood in the form of calcium oxalate. The calcium oxalate then obstructs the kidney tubules. Persons with preexisting skin disorders or eye problems, or impaired kidney or respiratory function may be more susceptible to the effects of the substance. 16. No cashews. See corn. 17.Absolutely No Corn (Aflatoxicosis is poisoning that results from ingestion of aflatoxins in contaminated food or feed. The aflatoxins are a group of structurally related toxic compounds produced by certain strains of the fungi Aspergillus flavus and A. parasiticus. Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the liver in a number of animal species; no animal species is resistant to the acute toxic effects of aflatoxins; hence it is logical to assume that 53 humans may be similarly affected. In the United States, aflatoxins have been identified in corn and corn products, peanuts and peanut products, cottonseed, milk, and tree nuts such as Brazil nuts, pecans, pistachio nuts, and walnuts. Other grains and nuts are susceptible but less prone to contamination. http://www.cfsan.fda.gov/~mow/chap41.html 18.Cleaning Up the Pests In our house analogy, it is likely that the rats have built a nest in our old home. There will be spider webs, ants, mice, crickets, termites etc. These pests will damage our home and steal our food if we don’t get rid of them. So it is with our body. Heavy metals in our tissues and biotoxins (chemicals that damage our cells) will have concentrated in our liver and gall bladder because those organs try to remove these pests from our body---often unsuccessfully. Most of these toxic things are fatsoluble (dissolved in the fat of our bodies). This is particularly true of our cell membranes and our brain, endocrine glands and liver. Since they are fatsoluble, they tend to get stored and concentrated in our liver and gall bladder. Bacteria, viruses and fungi then tend to grow in our gall bladder and produce more toxins. In this manner, our liver and gall bladder become a “rat’s nest” that must be cleaned out for us to start feeling better. 54 GALL BLADDER There are many misconceptions about the gall bladder. Note the following facts: 1. The gall bladder is a very important organ---not something to be disposed of if it annoys you. The same symptoms of pain, bloating and heartburn occur in 50-100% after you have had your gall bladder removed as before. More than 500,000 North Americans have their gall bladder removed every year. 2. The liver makes 1 ½ quarts of bile per day to digest fats. Since the liver can’t make bile fast enough to digest a fatty meal, the gall bladder is necessary to store bile. Without the gall bladder, you can’t do a good job of digesting fats. Since every cell membrane in the body is made of fat, if you can’t digest the fats, you can’t repair your cells (heal) without help. 3. Forty percent of Americans have abdominal pain, bloating, loose stools, and symptoms often thought to be from the stomach (heartburn due to gas pushing stomach acid into esophagus), fever and chills, nausea and vomiting, and yellowing of the skin----all due to gall bladder malfunction. 4. The most likely people to make gallstones are Fair complexion, Female, Fat, Fertile (previous pregnancies), and over Forty (the Five F’s). 5. Gall stones are more common in people who eat a low fat diet, obesity, take oral contraceptives, take calcium, estrogen, antibiotics, and nonsteroidal anti-inflammatory drugs. To help clean the gall bladder, you will take: 1. Taurine is an amino acid needed to make bile. You will need to take 1000 mg. /day. In studies, 100% of those taurine-deficient developed gallstones. In those given taurine supplements, the formation of gallstones dropped to zero. 2. Vitamin C: Take 2000 mg. /day. You should plan on taking vitamin C long term. If you have had your gallbladder removed, you will need to take Bile Salts (Ox Bile) 500 mg. each time you eat. You can use Digestabs = contain bile and digestive enzymes. You will be given an appointment for us to begin the process of cleaning your gallbladder. Attempting to do it on your own using herbal remedies, lemonade, etc. will often give you significant pain. 55 LIVER CLEANUP: The liver, the largest solid organ, is the body’s detoxification center and a vast center for metabolic activity including: 1.Lipid/carbohydrate/protein metabolism 2.Blood synthesis 3.Bilirubin metabolism 4.Urea cycle 5.Ammonia detoxification 6.Biliary processes 7.Bile and cholesterol synthesis 8.Oxidative energy metabolism 9.Hormone metabolism 10. Immune function (Kupffer cells) 11. Clearance of drugs (pharmaceuticals) 12. Processing of nutrients, toxins, and bile acids from the intestine. The liver’s detoxification processes has three distinct phases. The purpose is to change fat-soluble toxins into water-soluble products that can be excreted from the body. Conversion of cholesterol into bile is a primary process in the elimination of wastes. Thus a high cholesterol is a symptom of the liver attempting to clear toxins from the body and should not be interrupted with anti-cholesterol drug therapy: Phase I: polarity is increased by a process called oxidation or hydroxylation using enzymes called PP450 oxidases. It requires oxygen as toxins are burned or oxidized. Elevation of very long chained fatty acids is indicative of interruption of Phase I. Phase II: toxins are made more water-soluble using oxidation, reduction, hydrolysis, dehalogenation, methylation, sulfation, glucuronidation, peptide conjugation, acetylation, and glutathione conjugation. Phase III: toxins ported from cells for removal via gallbladder and kidneys. When detoxification is occurring, nitrogen may be retained involving albumin, uric acid, BUN or Creatinine. Ammonia levels rise due to impaired ability to convert ammonia into urea. Oral butyrate therapy addresses both control of nitrogen in states of increased blood ammonia and interruption of abnormal lipid metabolism. It also clears what are called “renegade fats” from the liver. To accomplish this cleanup, you will be given instructions in our office: 56 REBUILDING BEFORE AFTER From Extreme Home Makeover With our old house, now that we have the water, sewage, electricity on (pure water, large intestine, Biomodulator therapy) and have cleaned up the pests (gall bladder and liver cleanse), we are ready to start rebuilding our old house. We start removing rotten boards and replacing broken windows, lost shingles, etc. The “brain” of every cell is the cell membrane. Cell membranes interact with the environment, communicate with other cells, allow nutrients to enter the cell and waste to exit the cell, store voltage for the needs of the cell, etc. Every cell membrane is made primarily of fatty acids called phospholipids. Since most toxins in the body are fat-soluble, they are stored in the cell membranes. These toxins interfere with the function of the cell. If you eat Trans Fats (nearly plastic), your cells function as if they were made of plastic. You must stop eating them and then consume good fats so you can replace all of your cells with membranes that work. Cells normally die and replace themselves. Some cells replace themselves every 48 hours and some cells only replace themselves every eight months. Thus it will take up to eight months to rebuild yourself. Phosphatidylcholine (PC): This is the most abundant phospholipid (fat) of the cell membrane and protects the liver’s 33,000 square meters of membrane. It protects the liver against damage from alcohol, pharmaceuticals, pollutants, drugs and infections due to viral, bacterial and fungal infections (Lieber). PC is most effective when given intravenously but can also be given orally. If you are disabled, you may choose to use both IV and oral until you are better and then continue with oral until you are well or at least functional. Generally speaking, disabled people will require 5-40 IV injections of PC. They are usually given daily for at least a week and until you can tolerate oral fats. The liver cells are completely replaced every two months. The skin is replaced every six weeks. Nerve cells take months to be replaced. The capsules are 57 taken for 6-12 months. Heavy Metals Many people have accumulated heavy metals like mercury (silver fillings, seafood), lead (paint, gasoline), cadmium (auto exhaust, zinc-depleted soil), etc. These metals also accumulate in cell membranes and short-out the systems. One molecule of mercury can inhibit 2000 molecules of zinc! The way to determine if you have heavy metal poisoning is with a hair test since only 1-5% remains in the blood and the rest is in your tissue. If you have heavy metals in your system, we can give you a liquid that contain both phosphatidylcholine and EDTA, a material that will slowly release the metals from the cells. This is called DetoxMax Plus. We also use a light (Collins Light) that provides missing electrons to help the metals release from the cells and an infrared sauna to help release the metals from the cells. Proteins An essential amino acid for an organism is an amino acid that cannot be synthesized by the organism from other available resources, and therefore must be supplied as part of its diet. Eight amino acids are generally regarded as essential for humans: tryptophan, lysine, methionine, phenylalanine (or tyrosine), threonine, valine, leucine, isoleucine. Two others, histidine and arginine are essential only in children. http://en.wikipedia.org/wiki/Essential_amino_acid Two of the essential amino acids, lysine and tryptophan, are poorly represented in most plant proteins. Thus strict vegetarians should ensure that their diet contains sufficient amounts of these two amino acids. Without tryptophan, you will become severely depressed. The symptoms of lysine deficiency include anemia, enzyme disorders, lack of energy, hair loss, bloodshot eyes, weight loss and retarded growth as well as reproductive problems, poor appetite and poor concentration. EGGS Eggs are one of nature's most nutritious foods. One large egg contains only 70 calories and an incredible amount of nutrition. An egg is one of the few foods that contain everything necessary for life. The other is plankton. Lutein and zeaxanthin are important for maintaining good vision. Studies have shown that these antioxidants help prevent age-related macular degeneration-the leading cause of blindness in people over 65, and help decrease the risk of cataracts. According to the American Heart Association, lutein also protects against the progress of early heart disease. A great source of these is Wolf Berries. Recognized as an essential nutrient, choline has been shown to play a strong role in brain development and function. One egg provides half your daily requirement of choline. 58 Protein is essential for building and repairing body tissue. Muscles, organs, skin, hair as well as antibodies, enzymes, and hormones are all made from protein. Protein is composed of 20 different amino acids. There are 8 essential amino acids that the body cannot make, and so they must come from foods. Eggs are one of the few foods considered to be a complete protein because they provide all eight essential amino acids. You should eat 2-4 eggs per day. Some worry about cholesterol. As noted above, the liver makes cholesterol when it is trying to clean itself of toxins. Thus the relationship of heart disease to cholesterol is simply the presence of toxins that cause inflammation. It is well known that measurements of inflammation (like C-reactive Protein) is much more related to heart attacks and strokes than cholesterol. Ansel Keyes who first proposed that there might be a relationship between cholesterol and heart disease has often said that there is no relationship between what you eat and your blood cholesterol levels unless you are a rabbit or a rat. If you eat a diet that has no cholesterol in it, your blood cholesterol won’t change 5%. If you eat buckets of cholesterol, your blood cholesterol won’t change 5%. Thus the idea that you should avoid eating eggs, whole raw milk, fatty meats, etc. is pure nonsense and was proposed primarily to sell cholesterol-lowering drugs. Restricting these fat sources in children is particularly harmful since their brain (mostly fat) is developing and needs enormous amounts of fat to develop normally. Seventeen percent (17%) of the normal cell membrane is a fat called Arachidonic acid. The primary source of that is eggs. If you don’t eat eggs, it is hard to make good cell membranes = you will be sick because you don’t have normal cells. There is no vegetarian source of Arachidonic acid, so it is very difficult for total vegetarians to be healthy. Remember that eating good fats doesn’t make you fat! It makes you healthy. Eating Trans fats (almost plastic) makes you fat because “plastic” cell membranes won’t react correctly to insulin. In an effort to get glucose into your plastic cells, the body makes more and more insulin (we call that insulin-resistant). Insulin locks fat inside of fat cells and it cannot be used as long as insulin is present. Thus eating more and more Trans fats makes us obese and diabetic because our cells are “plastic”. Thus-----eat eggs along with other fats to get the proteins and fats you need to make neurochemicals and good cells. You want free-range eggs, not eggs from chickens not allowed to move and fed 24 hours a day until they can no longer produce. 59 Juicing for Those Who are Disabled If you are disabled (for example, you get nauseated when you eat fat), you need to juice vegetables. There are several reasons for this: 1. You need the nutrients available in their natural form in vegetables. 2. The water available from inside the vegetables is perfect for getting inside your cells. 3. When you digest vegetables in their whole form, you have to spend energy (voltage) to digest the fiber. Fiber is good for scraping debris from your intestine, but you don’t have the extra energy it requires to move it along your intestine. We have already cleaned out your intestine, so you don’t need the fiber while we are getting you feeling better, but you do need the nutrition in the vegetables. 4. Most toxins in vegetables stick to the fiber. Getting rid of the fiber means your fragile liver doesn’t have to deal with more toxins right now. 5. If you need fiber to keep you from having your stools too loose, we will supply that with FiberNet. It has the added benefit of soaking up the toxins that your body is getting rid of. Juicing is not chopping. Juicing means that you squeeze the juice from the vegetables so that the juice is collected and the fiber (pulp) is removed. You cannot do this with a machine with a spinning blade. That chops the vegetables into little pieces that include the fiber (pulp). Get a real juicer-squeezer if you don’t have one. The Omega is a highly rated brand. Another major issue is heating. Heat destroys many of the nutrients in your food. Bladebased blenders heat up the food. It is okay to put your juice from the juicer into a blender to mix in the items mentioned below like nuts, protein powder, etc, but run it at very low speed so that heat is not a problem. How much do I need? You will need one pound of raw vegetables per 50 pounds of body weight per day. Thus if you are a 200 pound man, you will need to juice four pounds of vegetables per day. You can consume this as a meal or divide it up throughout the day. NOTE: If you are taking anticoagulants, the Vitamin K in the vegetables may thicken your blood. Monitor your INR (coagulation test) weekly until you are sure it is okay. You may need to alter your medication dose when you start juicing and when you stop juicing. Now that you're ready for the benefits of vegetable juice, you need to know what to juice. I recommend starting out with these vegetables, as they are the easiest to digest: Celery 60 Fennel (anise) Cucumbers These aren't as beneficial as the more nutritionally intense dark green vegetables. Once you get used to these, you can start adding the more nutritionally valuable, but less palatable, vegetables into your juice. Vegetables to avoid include carrots and beets. Most people who juice usually use carrots. The reason they taste so good is that they are full of sugar. I would definitely avoid all vegetables that grow underground to avoid an increase in your insulin levels. If you are healthy, you can add about one pound of carrots or beets per week. I do believe that the deep, intense colors of these foods provide additional benefits for many that are just not available in the green vegetables listed above. Step 2: When you've acclimatized yourself to juicing, you can start adding these vegetables: Red leaf lettuce Green Leaf lettuce Romaine lettuce Endive Escarole Spinach Step 3: After you're used to these, then go to the next step: Cabbage Chinese Cabbage Bok Choy An interesting side note: Cabbage juice is one of the most healing nutrients for ulcer repair as it is a huge source of vitamin U. (Vitamin U is not a vitamin. Vitamins are essential nutrients that cannot be synthesized (either at all or in sufficient quantities) by a given organism and therefore must be taken with food for the organism's continued good health. The term "vitamin U" was coined because the compound is very effective in the medical treatment of gastric ulcers. It is found in raw cabbage leaves and other green vegetables.) http://www.althealth.co.uk/services/info/supplements/vitamin_u.php Step 4: When you're ready, move on to adding herbs to your juicing. Herbs also make wonderful combinations, and there are two that work exceptionally well: Parsley Cilantro You need to be cautious with cilantro, as many cannot tolerate it well. If you are new to juicing, hold off. These are more challenging vegetables to consume, but they are highly beneficial. 61 Step 5: The last step: Only use one or two of these leaves, as they are very bitter: Kale Collard Greens Dandelion Greens Mustard Greens (bitter) When purchasing collard greens, find a store that sells the leaves still attached to the main stalk. If they are cut off, the vegetable rapidly loses many of its valuable nutrients. One important note: I prefer to juice my vegetables at room temperature. Lesson 4: Make your juice a balanced meal. Balance your juice with protein and fat. Vegetable juice does not have much protein or fat, so it's very important for you to include these fat and protein sources with your meal. Use eggs. Eggs will add a significant amount of beneficial fats and protein to your meal. An egg has about 8 grams of protein, so you can add two to four eggs per meal. I suggest that you add the whole eggs, raw, into the vegetable pulp (not the juicer). The reason I advocate this is because once you heat the eggs, many of their nutrients become damaged. If you are concerned about salmonella, purchase organic eggs; it's unlikely you'll have any problems. Additionally, if you are not sensitive to milk, you can add some raw milk cheese, as it will improve the flavor. There is a potential problem with using the entire raw egg if you are pregnant. Biotin deficiency, a common concern in pregnancy, could be made worse by consuming whole raw eggs. Incorporate seeds. Raw seeds, freshly ground and alternated regularly, are another great addition to the pulp. The simplest way to grind the seeds is to use an inexpensive coffee grinder. The seeds are full of protein and essential fatty acids that bring a juice into balance beautifully. I recommend pumpkin and flax seeds. Use chlorella. Chlorella is an incredibly powerful nutrient from the sea and is a form of algae. It can be helpful for mercury detoxification as it binds very strongly to mercury to eliminate it from the body. The normal dose is one teaspoon in the juice. However, about 30 percent of people cannot tolerate the chlorella, so if it makes you nauseous you should definitely avoid it. o o o Is a useful source of chlorophyll. Adds magnesium and protein. Binds to heavy metals and pesticides. If you have high iron or vitamin D levels you will want to avoid chlorella though as it is loaded with both of these nutrients. 62 Consider a protein powder. While protein powders are convenient, I believe them to be far inferior to whole food choices like eggs or chlorella. Glutamine is an amino acid and the majority of our skeletal muscle is made of it. You can obtain glutamine powder and add one teaspoon into your drink for a very effective healing addition. You can also use protein powders. Some people are concerned about my milk avoidance suggestion and taking whey protein. Although whey protein is from milk, most people tolerate it quite well as the major protein in milk that causes an allergy is casein. I would strongly advise against the use of soy protein powders. I recommend THUNDER from Forever Green. (JLT) Add some garlic. Don't worry; this won't give you "dragon breath." I like to add one to two cloves of garlic in my juice, as it incorporates the incredible healing potential of fresh garlic. I strongly advise you to do this regularly to balance out your bowel flora. The ideal dose is just below the social threshold where people start to notice that you have eaten garlic. One large clove, two medium cloves or three small cloves is the recommended dose. Add oil. You can add the BodyBio oil to your juice mixture if you prefer to take it this way. (JLT) Lesson 5: Make your juice taste great. If you would like to make your juice taste a bit more palatable, especially in the beginning, you can add these elements: Coconut: This is one of my favorites! You can purchase the whole coconut or use shredded coconut. It adds a delightful flavor and is an excellent source of fat to balance the meal. Coconut has medium chain triglycerides, which have many health benefits. Cranberries: You can also add some cranberries if you enjoy them. Researchers have discovered that cranberries have five times the antioxidant content of broccoli, which means they may protect against cancer, stroke and heart disease. In addition, they are chock full of phytonutrients and help many women avoid urinary tract infections. Limit the cranberries to about 4 ounces per pint of juice. Lemons: You can also add half a lemon (leaving much of the white rind on). If you are a protein metabolic type you will not want to use lemons as they will push your pH in the wrong direction. Fresh ginger: This is an excellent addition if you can tolerate it. It gives your juice a little "kick" 24 carat Chocolate: Dark chocolate has more antioxidants than any other food tested with perhaps the exception of Wolf Berries (Lycium barbarum). This chocolate from Forever Green does not contain wax, fillers, caffeine, and other items that give chocolate a bad reputation. You can add it to your drink. It is already in THUNDER protein powder. (JLT) 63 Wolf berries: Wolfberry contains 19 types of amino acids and 21 trace minerals. It has more beta-carotene than carrots and nearly as much Vitamin C as oranges and protein as bee pollen. Lesson 6: Drink your vegetable juice right away, or store it very carefully. Juicing is a time-consuming process, so you'll probably be thinking to yourself, "I wonder if I can juice first thing and then drink it later?" This isn't a great idea. Vegetable juice is very perishable so it's best to drink all of your juice immediately. However, if you're careful you can store it for up to 24 hours with only moderate nutritional decline. To store your juice: 1. Put your juice in a glass jar with an airtight lid and fill it to the very top. There should be a minimum amount of air in the jar as the oxygen in air (air is about 20 percent oxygen) will "oxidize" and damage the juice. 2. Wrap the jar with aluminum foil to block out all light. Light damages the juice. 3. Store it in the refrigerator until about 30 minutes prior to drinking, as vegetable juice should be consumed at room temperature. Most people juice in the morning, but if that does not work out well for your schedule please feel the freedom to choose whatever meal works out best for your lifestyle. Lesson 7: Clean your juicer properly. We all know that if a juicer takes longer than 10 minutes to clean, we'll find excuses not to do it. I find that using an old toothbrush works well to clean any metal grater. For the Omega 8003, the whole process takes about 5 minutes. Whatever you do, you need to clean your juicer immediately after you juice to prevent any remnants from contaminating the juicer with mold growth. Warning: Don't follow the juicing recommendations that come with the juicer, as they most often emphasize carrot and fruit combinations. http://www.mercola.com/nutritionplan/juicing.htm# Vitamin B12 According to John V. Dommisse, MD, an expert in vitamin B12 (cyanocobalamin) deficiency and therapy, the psychiatric conditions most associated with vitamin B12 deficiency include toxic brain syndrome, paranoia, violence and depression. There is a well documented association between B12 deficiency and dementia. In an article entitled "Subtle Vitamin B12 Deficiency in Psychiatry: A Largely Unnoticed But Devastating Relationship?" published in Medical Hypotheses, 2 Domisse expresses the opinion that most cases of so-called "Alzheimer's dementia" ("idiopathic dementia") are actually cases of B12 deficiency. According to Domisse, B12 deficiency can cause depression and even, 64 in certain cases, bipolar-1 disorder (manic-depressive illness) and, more commonly, bipolar-2 disorder (cyclothymic personality). Says Domisse: "The third most common psychiatric manifestation of this deficiency is violent behavior, yet how often is this deficiency ever sought or treated in criminal cases of violent behavior? I have witnessed numerous cases of rage attacks, temper outbursts, domestic violence, etc., where the violence ceased after the patient's B12 deficiency was diagnosed and properly treated." The fourth and last major psychiatric effect of this deficiency is paranoid ideation and even paranoid psychosis (but not schizophrenia). Fatigue is another symptom of vitamin B12 deficiency but the medical community has been slow to recognize the connection. "Even after major articles, like that of Lindenbaum in the New England Journal of Medicine in 1988," says Domisse, "fatigue is still not recognized as a prominent feature of B12 deficiency syndrome. Peripheral neuropathy is another non-psychiatric condition that can result from this and other B vitamin deficiencies. However, by the time the deficiency is recognized (serum level below 200 pg/ml), just as in the case of the dementia, the neuropathy may well have become irreversible. Then the treating physician will say, 'See, B12 treatment does not reverse dementia (or neuropathy)!'" A major point by this author is that the range used to establish serum vitamin B12 deficiency in conventional medicine (less than 200 to 400 pg/ml) is far too low. When peripheral neuropathy occurs in this range, it is often permanent. The author suggests that 1,000 to 2,000 pg/ml may be the optimal range. The hydroxy- and methyl- forms of vitamin B12 are generally recommended. Cyanocobalamin at high doses has never been shown to be toxic. Oral doses of 1,000 to 5,000 ug daily have been used in cases of pernicious anemia to maintain these patients' vitamin B12 levels. Oral doses of 1,000 to 2,500 ug after both breakfast and supper seem the best way to maintain very high levels of serum vitamin B12 . Any child with violent tendencies, especially when accompanied by fatigue and neuropathy, should be tested for vitamin B12 deficiency. An acute condition can be treated with oral supplements or vitamin B12 injections. In the long term, the best protection is a diet rich in animal foods. http://www.westonaprice.org/children/childviolence.html Symptoms of B12 deficiency include: Anemia Brown spots over joints Bursitis Dementia Depression Diarrhea Dizziness B12 B12 B12 B12 B12 B12 B12 65 Irritability Mood swings Nausea Negative thinking Pale smooth tongue Paranoia Poor Memory Psychosis Restlessness Schizophrenia Sore tongue Temper outbursts Tingling Violence Weakness B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 B12 Replacing Your Cells = A Completely New You The process of rebuilding a new and healthy you is based in the fact that your body is constantly replacing itself. You get new retinal elements every two days. You get an entirely new skin every six weeks. You get a new liver every eight weeks. It takes months to get new nerve cells. As each new cell is built, the process looks for the proper building materials. If all it finds is “plastic” Trans fats, it uses them to build the new cell membranes. Remember the cell membrane is the “brain” of the cell and determines whether that is a healthy or sick cell. That membrane is almost completely fat. The “manufacturing” part of the cell is the cytoplasm. It is almost entirely protein. We have to supply your body with good fats and good proteins so it can make good new cells. If you keep doing what you are doing as far as nutrition is concerned, you will keep making the same quality of cells you have been making. If you are sick, that obviously isn’t very good. DOING MORE OF WHAT ISN’T WORKING DOESN’T MAKE IT WORK BETTER. If your digestion is working well enough to absorb good fats and proteins, you will be able to make good new cells. We have started by cleaning up your digestion organs and providing the voltage to get things working again. Now we are going to give you the fats you need to start making good cells. You will be given a list of things to provide your body with the materials you need to start rebuilding. One issue is whether your digestive system is working well enough to get the fats from your mouth to your cells so they can make new ones. One can give them intravenously so that we know the fats will get to the cells that are making new ones. In addition, we can give glutathione, a material that helps the cells use antioxidants to clean up toxic things called free radicals. 66 Experience shows that getting the digestive system working well enough to absorb fats is difficult because it needs to make new cells so it can work. If the digestive system can’t function well enough to supply the fats needed to rebuild itself, we will have to give the fats intravenously until it can rebuild. If the digestive system is working, we can give the necessary fats orally. Remember that fats and proteins require vitamins and minerals to work, so replacing them is also important. We will help you decide if you need intravenous therapy for awhile or if oral will work. In either case, you will need two months of intensive work to build you a new liver and then several months to finish building the new you from top to bottom. As you can see, there is no magic bullet to cure you in a flash. The only way for you to be healthy is to build a new body with good materials. I can’t control what you put into your mouth----thus the result you will experience is mostly determined by your choices. Those of us in our clinic will guide you, but only you can heal yourself. We look forward to watching for the new you as you rebuild yourself into renewed health. 67 BIBLIOGRAPHY Abbott, B.C., Hill, A.V., and Howarth, J. V. (1958). The positive and negative heat production associated with a si ngle impulse. Proc. Roy. Soc. B. 148: 149-187. Aggeli, A., Bell, M., Boden, N., Keen, ]. N., Knowles, P. P., McLeish, T. C. B., Pitkeathly, M., and Radford, S. E. (1997). Responsive gels formed by the spontaneous self-assembly of peptides into polymeric beta-sheet tapes. Nature 386: 259-262. Alberts, B., Bray, D., -Lewis, ]., Raff, M., Roberts, K., and Watson, ]. D. (1994). Molecular Biology of the Cell, Third edition, Garland, N. Y. Alberts, B., Bray, D., Lewis, ]., Raff, M., Roberts, K., and Watson, ]. D. (1989). Molecular Biology of the Cell, Second edition, Garland, N. Y. Alberts, B., Bray, D., Lewis, )., Raff, M., Roberts, K., and Watson, ]. D. (1983). Molecular Biology of the Cell, First edition, Garland, N. Y. Albin, G., Horbett, T. A., and Ratner, B. D. (1985). Glucose sensitive membranes for controlled delivery of insulin: insulin transport studies. /. Contr. Rel. 2: 153-164. Albrecht-Buehler, G. (1980). Autonomous movements of cytoplas -mic fragments. Proc. Nat'1. Acad. Sci. 77(11): 6139 -6643. Albrecht-Buehler, G. (1985). Is the cytoplasm intelligent too? Cell Motil. and Cytoskd. 6: 1 -21. Albrecht-Buehler, G. (1998). Altered drug resisrance of microrubules in cells exposed to infrared light pulses: Are microrubules the "nerves" of cells? Cell Motil. and Cytoskel. 40:183-192. Albrecht-Buehler, G., and Bushnell, A. (1982). Reversible compres sion of the cytoplasm. Exf. Cell Res. 140:173-189. Alien, R. D., Cooledge, ]. W., and Hall, P. ]. (1960). Streaming in cytoplasm dissociated from the giant amoeba, chaos chaos. Nature 187: 896899. Almdal, 1C, Dyre, ]., Hvidt, S., and Kramer, O. (1993). Towards a phenomenological definition of the term'gel.' Polym. Gels and Ntwks. 1: 5-17. Alonso, A., Nunez-Fernandez, M., Beltramo, D. M., Casale, C. H., and Barra, H. S. (1998). Na, K-ATPase was found to be the membrane component responsible for the hydrophobic behavior of the brain membrane tubulin. Biochem. Biophys. Res. Commun. 253: 824-827. Anisimova, V. I., Deryagin, B. V., Ershova, I. G., Lychnikov, Y. I., Simonova, V. K., and Churaev, N. V. (1967). Prep erati on of structuarally modified water in quartz capillaries. Russ. J. Phys. Chem. 41: 1282-1284. Annaka, M., andTanaka, T. (1992). Multiple phases of polymer gels. Nature 355: 430-432. Asakura, A., Taniguchi, M., and Oosawa, F. (1963). Mechano-chemi-cal behavior of F-actin. /. Mol. Biol. 7: 55- 63. Ault, ]. G., Demarco, A. J., Salmon, E. D., and Rieder, C. L. (1991). Studies on the ejection properties of asters: astral microtubule turnover influences the osciliatoty behavior and positioning of mono -oriented chromosomes. /. Cell Sci. 99:701-710. B Bartels, E. M., and Elliott, G. F. (1985). Donnan potentials from the A- and I-bands of glycerinated and chemically skinned muscles, relaxed and in rigor. Biophys. J. 48: 61-76. Bausch, A. R., Mbller, A., and Sackmann, E. (1999). Measurement of local viscoelasticity and forces in living cells by magnetic tweezers. Biophys. J. 76: 573-579. Beall, P. T. (1980). Water-macromelecular interactions during the cell cycle. Nuclear-cytolasmic Interactions in the Cell Cycle, ed. G. Whitson, Acad. Press, NY. Beall, P. T., Brinkiey, B. R., Chang, D. C., and Hazlewood, C. R (1982). Microtubule complexes correlated with growth rate and wa ter proton relaxation times in human breast cancer cells. Cancer Res, 42: 4124-4130. Bernal, J. D. (1961). Origin of life on the shores of the ocean. Oceanography, ed. M. Sears. AAAS. 67:95-118. Berridge, M. J. (1994). The biology and medicine of calcium signaling. Mol. Cell. Endicrinol. 98: 119-124. Bi, G.-Q., Alderton, ]. M., and Steinhardt, R. A. (1995). Calcium -regulated exocytosis is required for cell membrane resealing. /. Cell Biol. 131: 1747-1758. Bingley, M. S. (1966). Furthet investigations into membrane potentials in amoebae. Exf. Cell Res. 43: 1-12. Block, S. M. (1996). Fifty ways to love your lever: myosin motors. Cell 87: 151-157. Bloodgood, R. A.(1977). Motility occurring in association with the surface of the Chlamydomonas flagellum. /. Cell BioL 75: 983-989. Bloodgood, R. A. (1978). Unidirectional motility occurring in association with the axopodial membrane of Echinosphaerium nucleophilum. CellBiol. Int. Rep. 2: 171-176. Bloodgood, R. A., Leffler, E. M., and Bojczuk, A. T. (1979). Reversible inhibition of Chlamydomonas flagellar surface motility. / Cell Biol. 82: 664-674. Blyakhman, R, Shklyat, T., and Pollack, G. H. (1999). Quantal length changes in single contracting sarcomeres. /. Muscle Res. Cell Mitol. 20: 529-538. Boyle, P. J., and Conway, E. J. (1941). Potassium accumulation in muscle and associated changes. /. Physiol. 100: 1-63. Brand t, P. W., Diamond, M. S., and Schachat, F. H. (1984). The thin filament of vertebrate skeletal muscle co-operatively activates as a unit. /. Mo 1. Biol. 180: 379-384. Bratton, C. B., Hopkins, A. L., and Weinberg, J. W. (1965). Nuclear magnetic resonance studies of living muscle. Science 147: 738- 739. Bray, D. (1992). Cell Movements, Garland, NY. Brooks, S. C. (1940). The intake of radioactive isotopes by living cells. Cold Spring Harbor Symp. Quant. Biol. 8: 171-180. Brummer, S. B., Bradspies, J. I., Entine, G., Leung, C., and Lingertat, H. (1972). Polywater, an organic contaminant. / Phys. Chem. 76: 457-458. Bungenberg de Jong, H. (1932). Die Koazervation und ihre Bedeutung fiir die Biologic. Protoplasma 15: 110-173. Buxbaum, R. E., Dennerll, T, Weiss, S., and Heidemann, S. R. (1987). F-actin and microtubule suspensions as indeterminate fluids. Science 235: 1511-1514. C Ca m eron, I. E. (1 9 8 8 ). U lt ra s t ru c t u ra l observations on the transectioned end of ftog skeletal muscles. Physiol. Chem. Phys. Med. NMR. 20: 221 -225. Cameron, E E. , Kanal, K. M., Keener, C. R., and Ftillerton, G. D. (1997). A mechanistic view of the non- ideal osmotic and motional behavior of intracellular water. Cell Biol. Int'l. 21(2): 99-1 13. Cameron, I. E. Cook, K. R., Edwards, D., Fullerton, G. D., Schatten, G., Schatten, H., Zimmerman, A. M., and Zimmerman, S. (1987). /. Cell. Physiol. 133: 14-24. Cameron, I. E., Cook, K. R., Edwards, D., Fullerton, G.D., Schatten, G., Schatten, H., Zimmerman, A. M., and Zimmerman, S. (1997). Cell cycle changes in watet p r o p e r ti e s in sea utchin eggs. J. Cell Physiol. 133(1): 99-113. Cameron, E E.,Fullerton, G. D., and Smith, N. K. R. (1988). Influence of cytomatrix proteins on water and on ions in cells. Scanning Microscop. 2(1): 275-288. 68 Cameton, E E., Hardman, W. E., Fullerton, G. D., Miseta, A., Koszegi, T, Eudany, A., and Kellermayer, M. (1996). Maintenance of ions, proteins and water in lens fiber cells before and after treatment with non-ionic detergents. Cell Bio. Int. 20(2): 127-137. Canny, M. J. (1998). Transporting water in plants. Am. ]. Sci. 86: 152-159. Carmeliet, E. (1992). A fuzzy subsarcolemmal space for intracellular Na in cardiac cells? Cardiovasc. Res. 26: 433-442. Casademont, J., Carpenter, S., and Karpati, G. (1988). Vacuolation of muscle fibers near sarcolemmal breaks represents T tubule dilatation secondaty to enhanced sodium pump activity. /. Neuropath. Exp. Neural. 47: 618-628. Challice, C. E. (1965). Studies on the microstructute of the heart. /. Roy. Microsc. Soc. 85: 1-21. Chanutin, A. and Hermann, E. (1969). The interaction of organic and inorganic phosphates with hemoglobin. Arch. Biochem. Biophys. 131: 180-184. Chaudhury, M. K., and Whitesides, G. M. (1992). How to make watet run uphill. Nature 256:1539- 1541. Chen, W. T. (1981). Mechanism of retraction of the trailing edge during fibroblast movement. /. CellBiol. 90(1): 187-200. Cheng, Y.-P. (1971). The ultrastructute of the rat sino -arrial node. Acta. Anat. Nippon. 46: 339-358. Choi, D. W. (1988). Glutamate neuortoxicity and diseases of the nervous system. Neuron 1:623-34. Chou, K. C. (1992). Energy-optimized structure of antifreeze pro t ei n and its bindin g mechanism. /. Mol. Biol. 223: 509-517. Clarke, M. S. F., Caldwell, R. W., Miyake, K., and McNeil, P. E. (1995). Contraction-induced cell wounding and release of fibroblast growth factor in heart. Circ. Res. 76: 927-934. Clegg, J. S. (1982). Interrelationships between water and cell metabolism in Attemia cysts. IX. Evidence for organization of soluble cjtoplasmic enzymes. Cold Spring Harbor Symp. Quant. Biol. 46(Pt. 1): 23-37. Clegg, J. S. (1 984). Intracellular water and the cytomatrix: some methods of study and cutrent views. /. CellBiol. 99: 167s-171s. Clegg, J. S. (1988). On the internal environment of animal cells. Microcompartmentation, CRC Press, Boca Raton. Clegg, J. S., and Drost-Hansen, W. (1991). On the biochemistry and cell physiology of water. Biochem. and Mol. Biol. of Fishes, Vol. 1, ed. Hochachka, and Mommsen, Elsevier, N. Y. Clegg, J. S., and Jackson, S. A. (1988). Glycolysis in permeabilized L-929 cells. Biochem.]. 255:335 -344. Cohn,W. E., and Cohn, E. T. (1939). Permeability of red corpuscles of the dog to sodium ion. Proc. Soc. Exf. Biol. 41: 445-449. Collins, E. W., Jr. and Edwards, C. (1971). Role of Donnan equilibrium in the testing potentials in glycerol-extracted muscle. Am. J. Physiol. 22(4): 1130-1133. Collins, K. D. (1995). Sticky ions in biological systems. Proc. Nat'1. Acad. Sci. 92: 5553 -5557. Cooke, R. (1997). Actomyosin interaction in striated muscle. Physiol. Rev. 77(3): 671-697. Cope, F. W. (1969). Nuclear magnetic resonance evidence using D,,0 for structured water in muscle and brain. Biophys. J. 9: 303-319. Curran, M. J., and Brodwick, M. S. (1991). Ionic control of the size of the vesicle matrix of beige mouse mast cells. /. Gen. Physiol. 98: 771-790. Cussler, E. E., Stokar, M. R., and Varberg, J. E. (1984). Gels as size selective exttaction solvents. AIChE Journal 30(4): 578-582. D Damadian, R. (1971). Tumor detection by nuclear magnetic reso nance. Science 171: 1151-1153. Dayhoff, J., Hameroff, S., Lahoz- Beltra, R., and Swenberg, C. E. (1994). Cytoskeletal involvement in neuronal learning: a review. Eur. Biophys. J. 23: 79-93. Dean, R.(1941). Theories of electrolyte equilibrium in muscle. Biol. Symp. 3: 331-348. deBeer, E. L, Sontrop, A., Kellermayer, M. S. Z., and Pollack, G. H. (1998). Actin-filament motion in the in vitro motility assay is periodic. CellMotil. and Cytoskel. 38: 341-350. DeDuve, C. (1995). Vital Dust, Basic Books Press, New York. Delay, M. J., Ishide, N., Jacobson, R. C., Pollack, G. H., and Tirosh, R. (1981). Stepwise sarcomere shortening: Analysis by high-speed cinemicrography. Science 213: 1523-1525. Dempster, J. A., Van Hoek, A. N., and Van Os, C. H. (1992). The quest for water channels. NIPS 7: 172-176. Derjaguin, B. V. (1966). Effects of lyophilic sutfaces on the properties of boundary liquid films. Disc. Frad. Soc. 42: 109-119. DeVries, A. L. (1982). Fish glycopeptide and peptide antifreezes: then interaction with ice and water. Biophysics of Water, ed. F. Franks, and S. Mathias, Wiley Interscience, N. Y. Discher, E. E., Mohandas, N., and Evans, E. A. (1994). Molecular maps of red cell deformation: hidden elasticity and in situ connectiv ity. Science 266: 1032-1035. Dos Remedies, C. G., and Moens, P. D. (1995). Actin and the acto-myosin intetface: a review. Biochim. Biophys. Acta. 1228(2-3): 99-124. Doyle, D. A., Cabral, J. M., Pfuetzner, R. A., Kuo, A., Gulbis, J. M., Cohen, S. E., Chait, B. T, and MacKinnon, R. (1998). Structute of thepotassium channel: molecular basis of K conduction and selectivity. Science 280: 69-77. Draper, M. H., and Weidmann, S. (1951). Cardiac resting and action potentials recorded with an inttacellulat electrode. /. Physiol. 115: 74-94. Drummond, D. R., Peckham, M., Sparrow, J., and White, D. C. (1990). Alteration in kinetics caused by mutations in actin. Nature 348: 440-442. Dujardin, F. (1835). Stir les pretendus estomacs des animalcules infusoires et sur une sustance appelee satcode. part 2 of "Recherche sur les organismes inferieur." Ann. De Sci. Natur, part. Zool. 2d Ser., 4. Dusek, K. and Pattetson, D. (1968). A transition in swollen polymer networks induced by intramolecular condensation. /. Polymer Sci. A-2 6: 1209-1216. Edelmann, L. (1978). Vizualization and x -ray microanalysis of p o tassium tracers in freeze-dried and plastic embedded frog muscle. Microsc. Acta. Suppl. 2: 166-174. Edelmann, E. (1980). Preferential localized uptake of K and Cs over Na in the A -band of freeze-dried embedded muscle section: de tection by x -ray microanalysis and laser microprobe mass analysis. Physiol. Chem. Phys. 12(6): 509-514. Edelmann, E. (1983). Electron probe x-ray microanalysis of K, Rb, Cs, and Ti in cryosections of striated muscle. Physiol. Chem. Phys. Med. NMR. 15(4): 337-344. Edelmann, E. (1988). The cell water problem posed by election microscopic studies of ion binding in muscle. Scanning Microsc. 2(2): 851-865. Ehrenpries, S.(1967). Discussion on P. G. Waser: Receptor localization by autoradiographic techniques. Ann. N. Y. Acad. Sci. (Discussion). 144: 754(1). Endo, (1972). Length dependence of activation of skinned muscle fibers by calcium. Symp. on Quant. Biol. Cold Spring Harbor, N.Y. Endo, S., Sakai, H., a n d Matsumoto, G. (1979). Microtubules in squid giant axon. Cell Struct. Funct. 4: 285-293. Ernst, E. (1970). Bound water in physics and biology. Acta Biochim et Biophys. Acad. Sci. Hung. 5(1): 57-69. 69 Fenn, W. O. (1953). Introduction to a symposium on the metabolism of potassium. Lancet 73: 163-166. Fenn, W. O., and Cobb, D. M. (1934). The potassium equilibrium in muscle. /. Gen. Physiol. 17:629-656. Fernandez, J. M., Villalon, M., and Verdugo, P. (1991). Reversible condensation of mast cell secretory products in vitro. Biophys. J. 59: 1022-1027. Fischer, M. H., and Moore, G. (1907). On the swelling of fibrin. Am. J. Physiol. 20: 330-342. Fisher, H. F. (1964). A limiting law relating the size and shape of protein molecules to their composition. Proc. Natl. Acad. Sci. USA. 51: 1285-1291. Fisher, I. R., Gamble, R. A., and Middlehurst, J. (1981). The Kelvin equation and the condensation of water. Nature 290: 575-576. Fishman, H. M., Tewari, K. P., and Stein, P. G. (1990). Injury-induced vesiculation and membrane redistribution in squid giant axon. Biochim. Biophys. Acta. 1023: 421-435. Fleischer, S., Fleischer, B., and Stoeckenius, W. (1965). The struc-tute of whole and fragmented mitochondria after lipid depletion. Fed. Proc. 24: 296-298. Fletcher, N. H. (1970). Chemical Physics of he, Cambridge, London. Frank, H. S. and Wen, W. Y. (1957). Structural aspects of ion-solvent interaction in aqueous solutions: a suggested pictrue of water structure. Discuss. Faraday Soc. 24: 133-140. Frommet, M. A., and Lancet, D. (1972) Freezing and non-freezing water in cellulose acetate membranes. /. Appl. Polymer Sci. 16: 12951303. Fushime, K., and Verkman, A. S. (1991). Low viscosity in the aque ous domain of cell cytoplasm measured by picosecond polarization microfluorimetry. /. Cell Biol. 112:719- 725. Gabriel, C., Sheppard, R. J., and Grant, E. H. (1983). Dielectric properties of ocular tissues at 37 degrees C. Phys. Med. Biol. 28(1): 4349. Garamvolgyi, N. (1959). Kontraktion isolierter Muskelfibtillen. Acta. Physiol. Acad. Sci. Hung. 16: 139-146. Garrigos, M., Morel, ]. E., and Garcia de la Torre, J. (1983). Rein vestigation of the shape and state of hydration of the skeletal myosin stibfragment 1 monomer in solution. Biochem. 22: 4961-4969. Gary-Bobo, C. M., and Lindenberg, A. B. (1969). The behavior of nonelectroytes in gelatin gels. /. Colloid and Interface Sci. 29(4): 702-709. Gershon, N. D., Porter, K. R., andTrus, B. L. (1985). The cytoplas-mic matrix: its volumes and surface area and the diffusion of molecules through it. Proc. Natl Acad. Sci. USA. 82(15): 5030-5034. Ginzburg, B. Z., and Cohen, D. (1964). Calculation of internal hydrostatic pressure in gels from the distribution coefficients of nonelectrolytes between gels and solutions. Trans. Faraday Soc. 60: 185-189. Glynn, I. M., and Karlish, S. J. D. (1975). The sodium pump. Ann. Rev. Physiol. 37:13-55. Gomez, A. M., Kerfant, B. G., and Vassort, G. (2000). Mictotubule disruption modulates Ca2 signaling in rat cardiac myocytes. Circ. Res. 86: 30-36. Goodsell, D. S. (1991). Inside a living cell. Trends Biochem. Sci. 16(6): 206-210. Graham. T. (1833). TitlePhil. Mag. 2:175,269,351. Granick, S. (1991). Motions and telaxations of confined liquids. Science 253: 1374-1379. Granzier, H. L. M., Myers, J. A., and Pollack, G. H. (1987). Stepwise shortening of muscle fiber segments. /. Mus. Res. Cell Motil, 8: 242251. H Hagiwara, S., Chichibu, S., and Naka K. (1964). The effects of vari ous ions on resting and spike potentials ofbarnacle muscle fibers. /. Gen. Physiol. 48: 163-179. Hardy, W. (1932). Problems of the boundary state. Phil. Trans. Roy. Soc. London Ser. A. 230: 1-37. Harrington, W. F. (1979). On the ot igin of the contractile fotce in skeletal muscle. Proc. Natl. Acad. Sci. 76(10): 5066-5070. Hatano, S. (1972). Conformational changes of plasmodium actin polymers formed in the presence of Mg . /. Mech. Cell Motil. 1: 75-80. Hatano, S., Totsuka, T., and Oosawa, F. (1967). Polymerization of plasmodium actin. Biochim. Biophys. Acta. 140: 109-122. Hatoti, K., Honda, H., and Matsuno, K. (1996a). ATP dependent fluctuations of single actin filaments in vitro. Biophys. Chem. 58: 267-272. Hatori, K., Honda, H., and Matsuno, K. (1996b). Communicative intetaction of myosins along an actin filament in the presence of ATP. Hatori, K., Honda, H., Shimada, K., and Matsuno, K. (1998). Propagation of a signal coordinating force generation along an actin filament in actomyosin complexes. Biophys. Chem. 75:81-85. Hazlewood, C. F. (1979). A view of the significance and understanding of the physical properties of cell-associated water. Cell-Associated Water, ed. W. Drost-Hansen, and J. S. Clegg, Acad. Press, N. Y. Hazlewood, C. E, Nichols, B. L, and Chamberlain, N. F. (1969). Evidence for the existance of a minimum of two phases of ordered water in a skeletal muscle. Nature 222: 747-750. Hazlewood, C. P., Singer, D. B., and Beall, P. (1979). Electron microscope examination of common red cell ghosts: cytoplasmic con tamination. Physiol. Chem. Phys. 11(2): 181-184. Heidorn, D. B. (1985). A Quasielectric Neutron Scattering Study of Water Diffusion in Frog Muscle, PhD Thesis, Rice University, Houston, TX. Heimburg, T., and Biltonen, R. L. (1996). A Monte Carlo simulation study of protein-induced heat capacity changes and lipid-induced protein clustering. Biophys. ]. 70: 84-96. Hennessey, E. S., Drummond, D. R., and Sparrow, J. C. (1993). Molecular genetics ofactin function. Biochem. ]. 282:657-671. Heppel, L. (1939). The electrolytes of muscle and liver in potassium-depleted tats. Amer. J. Physiol. 127:385-392. Heppel, E. (1940). The diffusion of radioactive sodium into the muscles of potassium-depleted rats. Amer. J. Physiol. 128: 449-454. Hille, B. (1973). The permeability of the sodium channel to metal cations in myelinated nerve. /. Gen Physiol. 59: 637-658. Hille, B. (1984). Ionic Channels of Excitable Membranes, Sinauer, Sunderland, MA. Hille, B. (1992). Ionic Channels of Excitable Membranes, Second edition, Sinauer, Sunderland, MA. Hillman, H. (1994). New considerations about the structure of the membrane of the living animal cell. Physiol. Chem. and Med. NMR. 26:55-67 Hirokawa, N. (1998). Kinesin and dynein superfamily proteins and the mechanism of organelle transport. Science279: 519 -524. Hodgkin, A. E, and Katz, B. (1949). The effect of sodium on the electrical conductivity of the giant axon of the squid. /. Physiol. 108: 37-77. Hodgkin, A. E., and Horowicz, P. (1959a). Movements of Na and K in single muscle fibres. /. Physiol. 145: 405-432. 70 Hodgkin, A. E., and Horowicz, P. (1959b). The influence of potas sium and chloride ions on the membrane potential of single muscle Hoenger, A., and Milligan, R. A. (1997). Motor domains of kinesin and Ho/interact with microtubule protofilaments with the same binding geometry. /. Mol. Biol. 265(5): 553-564. Hoeve, C. A. J., Willis, Y. A., and Martin, D. J. (1963). Evidence for a phase transition in muscle contraction. Biochem. 2: 282-286. Hoffman, A. S. (1991). Conventional and environmentally-sensitive hydrogels for medical and industrial uses: a review paper. Polymer Gels 268(5): 82-87. Holstein, T, and Tardent, P. (1984). An ultrahigh -speed analysis of exocytosis: nematocyst discharge. Science 223: 830-833. Horn, R. G., and Israelachvili, J. (1981). Direct measurement of structural forces between two surfaces in a nonpolar liquid. /. Chem. Phys. 75(3): 1400-1411. Howard, J. (1997). Molecular motors: structural adaptations to cel lular functions. Nature 389: 561-567. Hubley, M. J., Rosanske, R. C., and Moerland, T. S. (1995). Diffu sion coefficients, of ATP and creatine phosphate in isolated muscle: Pulse gradient P NMR. of small biological samples. NMR. in Biomed. 8: 72-78. Hutchings, B. E. (1969). Tetracycline transport in Staphylococcus Aureus H. Biochim. Biophys. Acta. 174:734-748. Huxley, A. P., and Niedergerke, R. (1954). Structural changes in muscle during contraction: Interference microscopy of living muscle fibres. Nature173: 971-973. Huxley, A. P., and Niedergerke, R. (1958). Measurement of the stria-tions of isolated muscle fibres with the interference microscope. /. Physiol. 144: 403-425. Huxley, H. E.(1996). A personal view of muscle and motility mechanisms. Ann. Rev. Physiol. 58: 1-19. Huxley, H. E., and Hanson, J. (1954). Changes in the cross stria-tions of muscle during contraction and stretch and their structural interpretation. Nature 173: 973-976. Hyman, A. A., and Karsenti, E. (1996). Morphogenetic properties of microtubules and mitotic s pindle assembly. Cell 84:401 -410. I Inoue, L, Kobatake, Y, and Tasaki, I. (1973). Excitability, instability, and phase-transition in squid axon membrane under internal per-fusion with dilute salt solutions. Biochem. Biophys. Acta. 307: 471-477. Inoue, S., and Salmon, E. D. (1995). Force generation by microtubule assembly/disassembly in mitosis andrelated movements. Mol. Biol. of Cell 6:1619-1640. Irving, M., St.-C., Alien, T., Sabido-David, C., Craik, J. S., Brandmeler, B., Kendrick-Jones,J., Corrie, J. E. T., Trentham, D. R., and Goldman, Y. E.(1995). Tilting of the light-chain region of myo-sin during step length changes and active force generation in skeletal muscle. Nature 375: 688-691. Ishijima, A., Doi, T., Sakurada, K., and Yanagida, T. (1991). Sub-piconewton force fluctuations of actomyosin in vitro. Nature 352: 301-306. Israelachvili, J. N., and McGuiggan, P. M. (1988). Forces between surfaces in liquids. Science 241: 795-800. Israelachvili, J., and Wennerstrom, H. (1996). Role of hydration and water srructure in biological and colloidal interactions. Nature 379: 219-225. Ito, T., Suzuki, A., and Stossel, T. P.(1992). Regulation of water flow by actin-binding protein-induced actin gelation. Biophys.J. 61: 1301-1305. J Jacobs, W. P. (1994). Caulerpa. Set. Amer. 271(6): 100-106. Jhon, M. S., and Andrade, J. (1973). Water and hydrogels. /. Biomed. Mater. Res. 7: 509-522. Jordan-Lloyd, D., and Shore, A. (1938). The Chemistry of Proteins, Second edition, J. A. Churchill, London. Joseph, N. R., Engel, M. B., and Catchpole, H. R. (1961). Distribu tion of sodium and potassium in certain cells and tissues. Nature 4794: 11751178. K Kamitsubo, E. (1972). Motile protoplasmic fibrils in cells of the Characeae. Protoplasma 74: 53-70. Kamiya, N. (1970). Conrractile properties ofthe plasmodial strand. Proc. Jpn. Acad. 46:1026-1031. Kas, J., Strey, H., and Sackmann, E. (1994). Direct imaging of reptation for semi-flexible actin filaments. Nature 368: 226-229. Kasturi, S. R., Hazlewood, C. F., Yamanashi, W. S., and Dennis, L. W. (1987). The nature and origin of chemical shift for intracellular water nuclei in Anemia cysts. Biophys. J. 52: 249-256. Katayama, E. (1998). Quick-freeze deep -etch electron microscopy of the actin-heavy meromyosin complex during the in vitro motility assay. /. Mol. Biol. 278: 349-367. Katayama, E., and Nonomura, Y. (1979). Electron microscopic analysis of tropomyosin paracrystals. /. Biochem. 86: 1511-1522. Katchalsky, A., and Zwick, M. (1955). Mechanochemistry and ion exchange /. Polymer Sci. 16: 221-234. Kellermayer, M. S. Z., and Pollack, G. H. (1996). Rescue of in vitro actin motility halted at high ionic strength by reduction of ATP to submicromolar levels.Biochim. Biophys. Acta.. 1277:107-114. Kellermayer, M., Ladany, A.,Jobsr, K., Szucs, G., Trombitas, K., and Hazlewood, C. F. (1986). Cocompartmentation of proteins and K within the living cell. Proc. Natl. Acad. Sci. USA. 83(4): 1011-1015. Kellermayer, M., Ludany, A., Miseta, A., Koszegi, T., Berta, G., Bogner, P., Hazlewood, C. E, Cameron, I. L., and Wheatley, D. N. (1994). Release of potassium, lipids, and proteins from nonionic detergent treated chicken red blood cells. /. Cell. Physiol. 159: 197-204. Kim, E., Bobkova, E., Miller, C. J., Orlova, A., Hegyi, G., Egelman, E. H., Muhlrad, A., and Reisler, E. (1998). Intrastrand cross-linked actin between Gin-41 and Cys-374. III. Inhibition of motion and force generation with myosin. Biochem. 37(51): 17801-17809. Riser, P. R, Wilson, G., and Needham, D. (1998). A synthetic mimic of the secretory granule for drug delivery. Nature 394: 459-462. Kitamura, K., Tokanaga, M., Iwane, A. H., and Yanagida, T. (1999). A single myosin head moves along an acin filament with regular steps of 5.3 nanometers. Nature 397(6715): 129-134. Klenchin, V. A., Sukharev, S. L, Serov, S. M., Chernomordik, L. V., and Chizmadzhev, Yu. A. (1991). Electrically induced DNA uptake by cells is a fast process involving DNA electrophoresis. Biophys ]. 60: 804-811. Klinger, R. G., Zahn, D. P., Brox, D. H., and Frundes, H. E. (1971). Interaction of the hemoglobin with ions. Binding of ATP to human hemoglobin under simulated in vitro conditions. Europ. J. Biochem. 18: 171-177. Kojima, H., Muto, E., Higuchi, H., and Yanagida, T. (1997). Me chanics of single kinesin molecules measured by optical trapping nanometry. Biophys. J. 73: 2012-2022 Kolara, G. B. (1976). Water structure and ion binding: a role in cell physiology? Science 192: 1220-1222. Kolberg, R. (1994). A membrane flip for a bacterial ion channel. / NIHRes. 6: 35-36. Korn, E. D. (1966). Structure of biological membranes. Science 153: 1491-1498. 71 Kraft, T., Messerli, M., Rothen-Rurishauser, B., Perriard, J.-C., Wallimann, T., and Brenner, B. (1995). Equilibration and exchange of fluorescently labeled molecules in skinned skeletal muscle fibers visualized by confocal microscopy. Biophys.J. 69: 1246-1258. Krause, T. L., Fishman, H. M., Ballinger, M. L., and Bittner, G. D. (1984). Exrent and mechanism of sealing in transected giant axons of squid and earthworms. /. Neurosci. 14: 6638-6651. Krauskopf, K. B. (1967). Introduction to Geochemistry, McGraw-Hill, Appendix III. Kull, F. J., Sablin, E. P., Lau, R., Fletterick, R. J., and Vale, R. (1996). Crystal structure of the kinesin motor domain reveals a structural similarity to myosin. Nature 380: 550-555. Kuroda, K. (1 964). Behavior of naked cytoplasmic drops isolated from plant cells. Primitive Motile Systems in Biology, ed. R. D. Alien, and N. Kamiya, Acad. Press, N. Y. Kushmerick, M. J., and Podolsky, R. J. (1969). Ionic mobility in muscle cells. Science 166(910): 1297-1298. L Lehninger, A. L. (1964). The Mitochondrion, Benjamin, Menlo Park, CA. Lev, A. A., Korchev, Y. E., Rostovtseva, T. K., Bashford, C. L., Edmonds, D. T., and Pasternak, C. A. (1993). Rapid switching of ion current in narrow pores: implications for biological ion channels. Proc. Roy. Soc. Land. B. 252: 187-192. Lewis, A., Rousso, I., Khachatryan, E., Brodsky, L, Lieberman, K., and Sheves, M. (1996). Directly probing rapid membrane protein dynamics with an atomic force microscopic: a study oflight -induced conformational alterations in bacteriorhodopsin. Biophys. J. 70: 2380-2384. Ling, G. N. (1 992). A Revolution in the Physiology of the Living Cell. Krieger Pub. Co., Malabar, Fl. Ling, G. N. (1997). Debunking the alleged resurrection of the sodium pump hypothesis. Physiol. Chem. Phys. & Med NMR. 29: 123-198. Ling, G. N., and Ochsenfeld, M. M. (1973). Mobility of potassium ion in frog muscle cells, both living and dead. Science 181: 78-81. Ling, G. N., and Walton, C. L. (1976). What retains water in living cells? Science 191: 293-295. Ling, G. N., Kolebic, T, and Damadian, R. (1990). Low paramagnetic-ion content in cancer cells: its significance in cancel detection by magnetic resonance imaging. Physiol. Chem. Phys. & Med. NMR. 22: 1-14. Ling, G. N., Niu, Z., and Ochsenfeld, M. (1993). Predictions of polarized multilayer theory of solute distribution confirmed from a study of the equilibrium distribution in frog muscle of twenty-one nonelectrolytes including five cryoprotectants. Physiol. Chem. Phys. Med. NMR. 25(3): 177-208. Ling, G. N., Walton, C., and Bersinger T. J. (1980). Reduced solubility of polymer-oriented warer for sodium salts, amino acids a n d other solutes normally maintained at low levels in living cells. Physiol. Chem. Physics 12: 111-138. Lippincott, E. R., Cessac, G. L., Stromberg, R. R., and Grant, W. H. (1971). Polywater - a search for alternative explanations. J. Colloid Interface Sci, 36: 443-460. Lippincott, E. R., Stromberg, R. R., Grant, W. H., and Cessac, G. (1969). Polywater. Vibrational spectra indicate unique stable poly meric sttucture. Science 164: 1482-1487. Lopez-Beltran, E. A., Mate, M. J., and Cerdan, S. (1996). Dynamics and environment of mitochondrial watet as detected by H NMR. /. Biol. Chem. 271(18): 10648-10653. Lowey, S.,and Luck, S. M. (1969). Eq ui li b riu m binding of andenosine diphosphate to myosin. Biochem. 8: 3195-3199. Luby-Phelps, K., Mujumdat, S., Majumdar, R. B., Ernst, L. A., Galbraith, W., and Waggoner, A. S. (1993). A novel fluorescence ratiometric method confirms the low solvent viscosity of the cytoplasm. Biophys. J. 65: 236-242. Luby-Phelps, K., Taylor, D. L., and Lanni, F. (1986). Probing the structure of cytoplasm. J. Cell. Biol. 102(6): 201 5-2022. Luck, W. A. P. (1976). Water in biological systems. Topics Current Chem. 64: 113-180. Ling, G. N. (1952). The role of phosphate in maintenance of the resting potential and selective ionic accumulation in frog muscle cells. Phosphorous Metabolism, 11: 749-795. ed. W. McElroy, and B. Glass, J. Hopkins Press, Baltimore. Ling, G. N. (1955). New hypothesis.for the mechanism of cellular resting potential. Fed. Proc. 14: 93-94. Ling, G. N. (1962). A Physical Theory of the Living State: the Association-Induction Hypothesis, Blaisdell Publ. Co., Waltham, MA. Ling, G. N. (1965). The physical state of water in living cell and model systems. Proc. N. Y. Acad. Set. 125: 401-417. Ling, G. N. (1973). How does ouabain control the levels of cell K and Na ? By interference with a Na pump or by allosteric control of K -Na adsorption on cytoplasm protein sites. Physiol. Chem. and Physics 5: 295-311. Ling, G. N. (1978). Maintenance of low sodium and highpotassium levels investing muscle cells. /. Physiol. 280: 105-123. Ling, G. N. (1984). In Search of the Physical Basts of Life, Plenum Publ. Co., New York. Ling, G. N. (1988). A physical theory of the living state: application to water and solute distribution. Scanning Microsc. 2(2): 899-913. M Maniotis, A., and Schliwa, M. (1991). Microsurgical removal ofcen-trosomes blocks cell reproduction and centriole generation in BSC-1 cells. Cell 67: 495-504. Marsh, D. J., De Bruin, S. H., and Gratzer, W. B. (1977). An investigation of heavy meromyosin-ADP binding equilibria by proton release measurements. Biochem. 16: 1738-1742. Matsumoto, G. (1984). A proposed membrane model for generation of sodium currents in squid giant axons. /. Theor. Biol. 107: 649-666. Matsumoto, G., Ichikawa, I. M., Tasaki, A., Murofushi, H., and Sakai, H. (1984). Axonal microtubules neccessary for generation of sodium current in squid axons: I. Pharmacological study on sodium current by microtubule proteins and 260 K protein. / Membr. Biol. 77: 77-91. Matsumoto, G., Kobayashi, T., and Sakai, H. (1979). Restoration of the excitibility of squid giant axon by tubulin tyrosine ligase and microtubule proteins. /. Biochem.86:1155-1158. Matsumoto, G., Murofushi, H., Endo, S., and Sakai, H. (1982). Bio logical Functions of Microtubules and Related Structures, ed. H. Sakai., H. Mohri, and G. G. Borisy, Academic Press, Tokyo. Matsumoto, G., Murofushi, H., Endo.'S., Kobayashi, T., and Sakai, H. (1983). Structure and Function of Excitable Cells, ed. D. C. Chang, I. Tasaki, W. J. Adelman, and R. H. Leuchtag, Plenum Press, N. Y. Maughan, D., and Lord, C. (1988). Protein diffusivities in skinned frog skeletal muscle fibers. Molecular Mechanism of Muscle Contraction, ed. H. Sugi, and G. H. Pollack, Plenum Press, N.Y. Maughan, D., and Recchia, C. (1985). Diffusible sodium, potassium, magnesium, calcium, and phosphorous in frog skeletal muscle. J. Physiol 368: 545-563. Mclntosh, J. R. (1973). The axostyle of Saccinobaculus. II. Motion of the microtubule bundle and a structural comparison of straight and bent axostyles. J. Cell Biol. 56:324-339. McLachlan, A. D., and Karn, J. (1982). Periodic charge distributions in the myosin rod amino acid sequence match cross-bridge spacings in muscle. Nature 299:226-231. McNeil, P. L, and Ito, S. (1990). Molecular traffic through plasma membrane disruptions of cells in vivo. ]. Cell Sci. 96: 549-556. McNeil, P. L., and Steinhardt, R. A. (1997). Loss, restoration, and maintenance of plasma membrane integrity. /. Cell Biol. 137(1): 1-4. 72 Meaves, H., and Vogel, W. (1973). Calcium i nward currents in inter nally perfused giant axons. /. Physiol. (London) 235: 225 -265. Mehta, A. D., Rock, R. S., Rief, M., Spudich, J. A., Mooseker, M. S., and Cheney, R. E. (1999). Myosin-V is a processive actin -based motor. Nature 400(6744): 590-593. Menetret, J. R, Hoffmann, W., Schroeder, R. R., Rapp, G., and Goody, R. S. (1991). Time-resolved cryo-electron microscopic study of the dissociation of actomyosin induced by photolysis of photolabile nucleotides. J. Mol. Biol. 219(2): 139-144. Mentre, P. (1995). L'Eau dans la Cellule: Une Interface Dynamique et Heterogene des Macromolecules, Masson, Paris. Mentre, P., and Debey, P. (1999). An unexpected effect of an oua-bain-sensitive ATPase activity on the amount of antigen-antibody complexes formed in situ. Cell and Mol. Biol. 45(6): 781-791. Metuzals, J., and Izzard, C. S. (1969). Spatial patterns of thread-like elements in the axoplasm of the giant nerve fiber of the squid (Loligo pealii L.) as disclosed by differential interference microscopy and by electron microscopy. /. Cell Biol. 43:456-479. Metuzals, J., and Tasaki, I. (1978). Subaxolemmal filamentous network in the giant nerve fiber of the squid (Loligo pealei L.) and its possible role in excitability. /. Cell Biol. 78: 597-621. Miki, M., and Koyama, T. (1994). Domain motion in actin observed by fluorescence resonance energy transfer. Biochem. 33: 10171-10177. Miller, D. J. (1979). Are cardiac muscle cells 'skinned' by EGTA or EDTA? Nature 277: 142-143. Mimori, Y., and Miki-Nonumura, T. (1995). Extrusion of rotating microtubules on the dynein-track from a microtubule-dynein gamma-complex. Cell Motil. And Cytoskel. 30:17-25. Miyagishima, Y. (1975). Catecholamine in the myocardium: a fluorecence histochemical study. Jpn. Circ. J. 39: 357-375. Miyano, M., and Osada, Y. (1991). Electroconductive organogel. 2. appearance and nature of current oscillation under electric field. Macromol. 24: 4755-4761. Mond, R., and Amson, K. (1928). Uber die lonenpermeabilitaet des quetgestreiften Muskels. Pfliiger's Arch. Ges. Physiol. 220: 69-81. Morel, J. E. (1991). The isometric force exerted per myosin head in a muscle fibre is 8 pN. Consequence on the validity of the ttaditional concepts of force generation. /. Theor. Biol. 151:285-288. Moriyama, Y, Yasuda, K., Ishiwata, S., andAsai, H. (1996). Ca (2+)-induced tension development in the stalks of glycerinated Vorticella convallaria. Cell Motil. and Cytoskel. 34(4): 271-278. Muto, E., and Yanagida, T. (1997). Cooperative binding of kinesin molecules to a microtubule in the presence of ATP. Biophys. J. 72: A62. N Nanavati, C., and Fernandez, J. M. (1993). The secretory granule matrix: a fast-acting smart polymer. Science 259(5097): 963-965. Natori, R. (1975). The electric potential change of internal membrane during propagation of contraction in skinned fibre of toad skel etal muscle. Jpn. J. Physiol. 25(1): 51-63. Naylor, G. R., Barrels, E. M., Bridgman, T. D., and Elliott, G. F. (1985). Donnan potentials in rabbit psoas muscle in rigor. Biophys. J. 48(1): 4759. Naylor, W. G., and Merrillees, N. C. R. (1964). Some observations on the fine structure and metabolic activity of normal and glycerin -ated ventricular muscle of toad. /. Cell Biol. 22:533-550. Negendank, W. (1982). Studies of ions and water in human lymphocytes. Biochim. Biophys. Acta. 694: 123-161. Neher, E., Sackmann, B., and Steinba'ch, J. H. (1978). The extracellular patch clamp: a method for resolving currents through individual open channels in biological membranes. Pfliiger's Archiv. Ges. Physiol. 375: 219-228. Nickels, J. (1970). Localisation of a microelectrode tip in muscle cell: A light and electron microscopic study. Acta. Physiol. Scand. 80: 360-369. Nickels, J. (1971). A method for localisation of the muscle cell and the motor end plate after in vivo registrarion with a microelectrode. Pfliiger's Archiv. Ges. Physiol. 330: 45-50. Nicklas, R. B. (1997). How cells get the right chromosomes. Science 275: 632-637. Noble, D., and Bett, G. (1993). Reconstructing the heart: a challenge for integrative physiology. Cardiova.se. Res: 27: 1701-1712.. Noda, C., and Yugari, Y. (1973). Effect of catecholamines in restoring the beating of cultured rat heart cells treated with reserpine. Jpn. J. PharmacoL 23(6): 839-846. O Odelblad, E., Bhar, B. N., and Lindstrom, G. (1956). Proton magnetic resonance of human red blood cells in heavy-water exchange experiments. Arch. Biochem. Biophys. 63: 221- 225. Ogata, M. (1996). Hydrodynamic ptoperties of water in myoplasm in resting and acrive states. Proc. Jpn. Acad. Set. B 72(6): 137-141. Okada, Y., and Hirokawa, N. (2000). Mechanism of the single-headed processivity: Diffusional anchoring between the K -loop of kinesin and the C terminus of tubulin. PNAS. 97(2): 640-645. Okuzaki, H., and Osada, Y. (1994). Electro-driven chem omechanical polymer gel as an intelligent soft material. /. Biomater. Sci. Polymer Edn. 5: 485-496. Oosawa, P., Fujime, S., Ishiwata, S., and Mihashi, K. (1972). Dy namic property of F-actin and thin filament. CSHSymposia on Quant. Biol. XXXVII: 277-285. Oparin, A. I. (1971). Routes for the otigin of the first forms of life. Sub-Cell Biochem. 1: 75-81. Oparin, A. I. (1964). The Chemical Origin of Life, ed. C. Thomas; Springfield, 111. Oplatka, A. (1996). The rise, decline, and fall of the swinging crossbridge dogma. Chemtntcts. Bioch. Mol. Biol. 6: 18-60. Oplatka, A. (1997). Critical review of the swinging crossbridge theoryand of the cardinal active role of water in muscle contiaction. Crit. Rev. Biochem. Mol. Biol. 32(4): 307-360. Oplatka, A. (1998). Do the bactetial flagellar motor and ATP syn-thase operate as water rurbines? Biochem. Biophys. Res. Commun. 249: 573-578. Osada, Y, and Gong, J.(1993). Stimuli-responsive polymer gels and their application to chemomechanical systems. Prog. Polym. Sci. 18: 187-226. Osada, Y, and Ross-Murphy, S. (1993). Intelligent gels. Sci. Amer. 268: 82-86. Osterhout, W. J. V., and Hill, S. E., (1938). Calculations of bioelectric potentials. /. Gen. Physiol. 22: 139-146. Overbeek, J. Th. G. (1956). The Donnan equilibrium. Prog. Biophys Biophys Chem. 6: 58-84. Pashley, R. M., and Kitchener, J. A. (1979). Surface forces in adsorbed mmultilayers of water on quartz. /. Colloid and Interface Sci. 71: 491-500. Pauling, L. (1945). The adsorption of water by proteins. J. Am. Chem. Soc. 67: 555-557. Pauling, L. (1959a). A molecular theory of genetal anesthesia. Science134: 15-21. Pauling, L. (1959b).Hydrogen Bonding, ed. L. Hadzi, Pergamon Press, London. Peachey, L. D. (1965). The sarcoplasmic reticulum and transverse tubules of the frog's sartorius. /. Cell Biol. 25: 209- 231. Peters, R.(1984). Nucleo-cytoplasmic flux and intracellular mobility in single hepatocytes measuted by fluorescence microphotolysis. EMBOJ. 3: 1831-1836. 73 Petka, W. A., Harden, J. L., McGrath, K. P, Wirtz, D., andTirrell, D. A. (1998). Reversible hydrogels from self-assembling artificial proteins. Science 281: 389-392. Pfann, W. G. (1962). Zone melting. Science 135:1101-1109. Pfeffer, W. F. (1877). Osmotische Untersuchungen: Studien zur Zell -Mechanik, Engelmann, Leipzig. Pinto da Silva, P., and Branton, D. (1970). Membrane splitting in freeze-ethching. Covalently bound ferritin as a membrane marker. /. CellBiol. 45: 598-605. Pissis, P., Anagnostopoulou-Konsta, A., and Apekis, L. (1987). A dielectric study of the state of water in plant stems. /. Exptl. Bat. 38(194): 1528-1540. Plumb, R. C., and Bridgman, W. B. (1972). Ascent of sap in trees. Science 176: 1129-1131. Pollack, G. H. (1977). Cardiac pacemaking: an obligatoty tole of catecholamines? Science 196: 731-738. Pollack, G. H. (1983). The sliding filament / ctoss-bridge theory. Physiol. Rev. 63: 1049-1113. Pollack, G. H. (1990). Muscle dr Molecules-: Uncovering the Principles of Biological Motion, Ebnet and Sons, Seattle, WA. Pollack, G. H. (1996). Phase transitions and the molecular mechanism of contraction. Biophs. Chem. 59:315-328. Pollack, G. H., Iwazumi, T., ter Keurs, H. E. D. ]., and Shibata, E. F. (1977). Sarcomere shortening in striated muscle occurs in stepwise fashion. Nature 268: 757-759. Pollard, T. (1984). Actin-binding protein evolution. Nature 312(5993): 403. Porter, K. R., Beckerle, M., and McNivan, M. (1983). The cytoplas-mic matrix. Mod. Cell Biol. 2: 259-302. Prausnitz, M. R., Milano, C. D., Gimm, ]. A., Langer, R., and Weaver, ]. C. (1994). Quantitative study of molecular ttansport due to electroporation: uptake of bovine serum albumin by erythrocyte ghosts. Biophys. J. 66(5): 1522-1530. Prochniewicz, E., Zhang, Q., Janmey, P. A., and Thomas, D. D. (1996). Cooperativity in F-actin: binding of gelsolin at the barbed end affects structure and dynamics of the whole filament. /. Mol. Biol. 260(5): 756-766. Pruliere, G., and Dotizou, P. (1989). Sol-gel processing of actin to obtain homogeneous glasses at low temperartires. Biophys. Chem. 34: 311-315. Purcell, E. M. (1977). Life at low Reynolds number. Am. ]. Physics 45(1): 3-11. R Rabenstein, D. L., Ludowyke, R., and Lagunoff, D. (1987). Proton nuclear magnetic resonance studies of mast cell histamine. Biochem Rao, P. N., Hazlewood, C. R, and Beall, P. T. (1982). Cell cycle phase-specific changes in relaxation times and water content in HeLa cells. Cell Growth, ed. C. Nicolini, NATO Adv. Study Inst. Series, Ser. A38: 535-547. Rieder, C. L, and Salmon, E. D. (1994). Motile kinetochores and polar ejection forces dictate chtomosome position on rhe vertebrate mitotic spindle. /. CellBiol. 124(3): 223-233. Rief, M., Gautel, M., Oesterhelt, R, Fernandez, ]. M., and Gaub, H. E. (1997). Reversible unfolding of individual titin immunoglobin domains by AFM. Science 276: 1109-1112. Robinson, G. W., and Cho, C. H. (1999). Role of hydration water in protein unfolding. Biophys.]. 77:3311-3318. Robinson, G. W., Zhu, S.-B., Singh, S., and Evans, M. W. (1996). Water in Biology, Chemistry, and Physics, World Scientific, London. Rorschach, H. E., Bearden, D. W., Hazlewood, C. E, Heidorn, D. B., and Nicklow, R. M. (1987). Quasi-elastic scattering studies of watet diffusion. Scanning Microsc. 1(4): 2043-2049. Rorschach, H. E., Lin, C., and Hazlewood, C. F. (1991). Diffusion of water in biological rissues. Scanning. Microsc. Suppl. 5: S1-S10. Rozycka, M., Gonzalez-Serratos, H., and Goldman, W. (1993). Non-homogeneous Ca release in isolated frog skeletal muscle fibres. /. Mus. Res. Cell Motil. 14: 527-532. Ruch, T. C., and Patton, H. D. (1965). Physiology and Biophysics, Saundets, Philadelphia. Sachs, F., and Qin, F. (1993). Gated, ion-selective channels observed with patch pipettes in the absence of membranes: novel properties of agigaseal. Biophys. J. 65(3): 1101-1107. Sakahibara, H., Kojima, H., Sakai, Y., Katayama, E., and Oiwa, K. (1999). Inner-arm dynein c of Chlamydomonas flagella is a single-headed processive motor. Nature 400(6744): 586-590. Sato, H., Tasaki, L, Carbone, E., and Hallett, M. (1973). Changes in axon birefringence associated with excitation: implications for rhe structure of the axon membrane. /. Mechanochem. Cell Motil. 2:209-217. Sato, M., Wong, T. Z., Brown, T., and Alien, R. D. (1984). Rheo-logical properties of living cytoplasm: a preliminary investigation of squid axoplasm (Loligo pealei). Cell Motil. 4:7-23. Sawahata, K., Gong, J. P., and Osada, Y. (1995). Soft and wet touch-sensing system made of hydrogel. Macromol. Rapid Commun. 16:713-716. Schliwa, M. (1986). The Cyto'skeleton: An Introductory Survey, Springer, N. Y. Schiiltze, M. (1861). Mailer's Arch, fur Anatomie und Physiologic und fur Wissenschaftliche Medicin, Berlin. Schiiltze, M. (1863). Das Protoplasma des Rhizopoden und der Pflanzenzellen. Bin Beitrag zur Theorie der Zelle, Leipzig. Schutt, C. E., and Lindberg, U. (1992). Actin as the generator of tension during muscle contraction. Proc. Natl. Acad. Sci. USA. 89(1):319-333. Schutt, C. E., and Lindberg, U. (1993). A new perspective on muscle contraction. FEES. 325: 59-62. Schutt, C. E., and Lindberg, U. (1998). Muscle contractions as a Markov process I: energetics of the process. Acta. Physiol. Scan. 163: 307-324. Schwann, T. (1 83 9 ) . Mikroskopische Untersuchungen iiber die Ubereinstimmung in der Struktur und dem Wachstum der Thiere und Pfl/tnzen, Berlin. Schwister, K., and Deuticke, B. (1985). Formation and properties of aqueous leaks induced in human erythrocytes by electrical breakdown. Biochim. Biophys. Acta. 816: 332-348. Schwyter, D. H., Kron, S. J., Toyoshima, Y. Y., Spudich, J. A., and Reisler, E. (1990). Subtilisin cleavage of actin inhibits in vitro sliding movement of actin filaments over myosin. /. Cell Biol. I l l : 465-470. Serpersu, E. H., Kinosita, K.,Jr. and Tsong, T. Y. (1985). Reversible and irreversible modification of erythrocyte membrane permeability by electric field. Biochim. Biophys. Acta. 812: 779-785. Slatin, S. L., Qiu, X-Q, Jakes, K. S., and Finkelstein, A. (1994). Identification of a translocated protein segment in a voltage-dependent channel. Nature 371: 158-161., Solomon, A. K. (1960). Red cell membrane structure and ion transport. /. Gen. Physiol. 43: 1-15. Somlyo, A. V., Gonzalez-Serratos, H. G., Shuman, H., McClellan, G., and Somlyo, A. P. (1981). Calcium release and ionic charges in the sarcoplasmic reticulum of tetanized muscle: an electron probe study. / Cell Biol. 90(3): 577-594. Spira, M. E., Benbassat, D., and Dormann, A. (1993). Resealing of the proximal and distal cut ends of transected axons: electrophsiological and ultrastructural analysis./ Neurobiol. 24: 300-316. Spudich, J. A. (1994). How molecular motors work. Nature 372: 515-518. 74 Spyropolous, C. S. (1961). Initiation and abolotion of electric response by thetmal and chemical means. Am. J. Physiol. 200: 203-208. Stebbings, H., and Hunt, C. (1982). The nature of the clear zone around microtubules. Cell and Tissue Res. 227:609-617. Stebbings, H., and Willison, J. H. M. (1973). Stucture of microtubules: a study of freeze-etched and negatively stained microtubules from the ovaries of Notonecta. Z. Zellforsch u. Mikrosc. Anat. 138(3): 387-396. Stein, W. D. (1990). Channels, Carriers, and Pumps: An Introduction to Membrane Transport, Acad. Press, San Diego. Steinbach, B. (1940). Sodium and potassium in frog muscle. /. Biol. Chem. 133: 695-701. Steinberg, I. Z., Oplatka, A., and Katchalsky, A. (1966). Mecha-nochemical engines. Nature 210: 568-571. Stephenson, D. G., Wendt, I. R., and Forrest, Q. G. (1981). Non-uniform iondistributions and electrical potentials in sarcoplasmic regions of skeletal muscle fibres. Nature 289(5799): 690-692. Stillinger, F. A. (1980). Water revisited. Science 209:451-457. Sugitani, M, Kobayashi, T., and Tanaka, T. (1987). Polym. Preprints Jpn. 36: 2876-2878. Suzuki, M. (1994). A new concept of a hydrophobicity motor based on local hydrophobicity transition of functional polymer substrate for micro/nano machines.Polym. Gels and Ntwks. 2:279-287. Szasz, A., van Noon, D., Scheller, A., and Douwes, F. (1994). Water states in living systems. I. Structural aspects. Physiol. Chem, Phys. & d. NMR. 26: 299-322. Szent-Gyorgyi, A. (1951). Chemistry of Muscular Contraction, Acad. Press, N. Y. Szent-Gyorgyi, A. (1960). Introduction to a Submolecular Biology, Acad. Press, N. Y., London. Szent-Gyorgyi, A. (1972). The Living State. With Observations on Cancer, Acad. Press, N. Y. Tabcharani, J. A., Jensen, T.J., Riordan, J.R., and Hanrahan, J.W. (1989). Bicarbonate permiability of the outwardly rectifying anion channel. / Memb. Biol. 112(2): 109-122. Tanaka, T.(1981). Gels. Sci. Amer. 244:110-113. Tanaka, T., Annaka, M., Franck, I., Ishii, K., Kokufuta, E., Suzuki,A., and Tokita, M. (1992). Phase transitions of gels. Mechanics of Swelling. NATO ASI Series Vol H 64, Springer-Verlag,Berlin. Tang, J., and Janmey, P. A. (1998). Two distinct mechanisms of actin bundle formation. Biol. Bull. 194: 406-408. Tang,}., and Janmey, P. A. (1996). Polyelectrolyte nature of F-actin and the mechanism of actin bundle formation. J. Biol. Chem.271(15): 85568563. Taniguchi, Y., and Horigome, S. (1975). The states of water in cellulose acetate membranes. /. Appl. Polymer Sci. 19: 2743-2748. Tasaki, I, Byrne, P. M., and Masumura, M. (1987). Detection of thermal responses of the retina by use of polyvinylidene fluoride multilayer detector.Jpn. ]. Physiol. 37:609-619. Tasaki, I. (1988). A macromolecular approach to excitation phenomena: mechanical and thermal changes in nerve during excitation. Physiol. Chem. and Phys. and Med. NMR. 20: 251-268. Tasaki, I. (1982). Physiology and Electrochemistry of Nerve Fibers, Acad. Press, NY. Tasaki, I. (1998). Repetitive mechanical responses of the amphibian skin to adrenergic stimulation. Jpn. ]. Physiol. 48: 297-300. Tasaki, I. (1999a). Rapid structural changes in nerve fibers and cells associated with their excitation processes. Jpn. J. Physiol. 49(2): 125-138. Tasaki, I. (1999b). Evidence for phase transition in nerve fibers, cells and synapses. Ferroelectric 220: 305-316. Tasaki, I., and Hagiwara, S. (1957). Demonstration of two stable potential states in the squid giant axon under tetraethylammonium chloride. /. Gen. Physiol. 40: 859-885. Tasaki, I., and Byrne, P. M. (1992). Discontinuous volume transitions in ionic gels and their possible involvement in the nerve excitation process. Biopolymers 32: 1019-1023. Tasaki, I., and Byrne, P. M. (1994). Discontinuous'volume transitions induced by calcium-sodium ion exchange in anionic gels and their neurobiological implications. Biopolymers 34: 209-215. Tasaki, I., and Iwasa, K. (1981). Temperature changes associated with nerve excitation: detection by using polyvinylidene fluoride film. Biochem. Biophys. Res. Commun.101: 172-176. Tasaki, I., Kusano, K., and Byrne, P. M. (1989). Rapid mechanical and thermal changes in the garfish olfactory nerve as sociated with a propagated impulse. Biophys.]. 55: 1033-1040. Tasaki, I., Singer, I., and Takenada, T. (1965). Effects of internal and external ionic environment on excitability of squid giant axon: A mac romolecular appraoach. /. Gen. Physiol. 48: 1095-1123. Taylor, S. R., Shlevin, H. H., and Lopez, J. R. (1975). Calcium in excitation -contraction coupling of skeletal muscle. Biochem. Soc. Transact. 1: 759-764. Terakawa, S., Nagano, M., and Watanabe, A. (1977). Intracellular divalent cations and plateau duration of squid giant axons treated with tetraethylammonium. Jpn. J. Physiol. 27: 785-800. Thomas, D. D. (1987). Spectroscopic probes of muscle cross-bridge rotation. Ann. Rev. Physiol. 49: 641-709. Tigyi, J., Kellermayer, M., and Hazlewood, C. F. (1991). The Physical Aspect of the Living Cell, Akad. Kiado, Budapest. Tirosh, R., and Oplatka, A. (1982). Active streaming against gravity in glass microcapillaries of solutions containing acto -heavy meromyo-sin and native tropomyosin. _/. Biochem. 91: 1435-1440. Tokita, M., and Tanaka, T. (1991). Reversible decrease of gel-solvent friction. Science 253: 1121-1123. Toney, M. F., Howard, J. N., Richer, J., Borges, G. L., Gordon, J. G., Melroy, O. R., Wiesler, D. G., Yee, D., and Sorensen, L. B. (1994). Voltage-dependent ordering of water molecules at an electrode -electrolyte interface. Nature 368: 444-446. Trantham, E.G., Rorschach, H. E., Clegg, J. C., Hazlewood, C. F, Nicklow, R. M., and Wakabayashi, N. (1984). Diffusive properties of water in Artemia cysts as determined from quasi-elastic neutron scattering spectra. Biophys. J. 45(5): 927-938. Trautwein, W., and Uchizono, K. (1963). Electron microscopic and electrophysiologic study of the pacemaker in the sino-atrial node of the rabbit heart. Z. Zellforsch. 61: 96-109. Trentham, D. R., Eccleston, J. P., and Bagshaw, C. R. (1967). Kinetic Analysis of ATPase Mechanisms. Quart. Rev. Biophys. 9: 218-281. Trombitas, K., and Pollack, G. H. (1995). Visualization of the transverse cytoskeletal network in insect-flight muscle by scanning-electron microscopy. Cell Motil. and Cytoskel. 32: 226-232. Trombitas, K., and Tigyi-Sebes, A. (1979). The continuity of thick filaments between sarcomeres in honey -bee flight muscle. Nature 281(5729): 319-320. Trombitas, K., Baatsen, P., Schreuder, J., and Pollack, G. H. (1993). Contraction-induced movements of water in single fibres of frog skeletal muscle. /. Mus. Res. Cell Motil. 14: 573-584. Troshin, A. (1948). Salt currents in the complex coascervate: gelatine and gum arabic. Izv. Akad Nauk SSSR ser biol. No 4: 180-185. 75 Troshin, A. (1966). Problems of Cell Permeability, Pergamon Press, Oxford. Troshin, A. S. (1956). Problems of Cell Permeability, English edition: Pergammon Press, Oxford, Translated by W. F. Widdas. Troyer, D. (1975). Possible involvement of the plasma membrane in saltatory particle movement in heliozoan axopods. Nature 254: 696-698. Tskhovrebova, L., Trinick, J., Sleep, J. A., and Simmons, R. M. (1997). Elasticity and unfolding of single molecules of the giant muscle protein titin. Nature 387:308-312. Tsukita, S., Tsukita, S., Kobayashi, T., and Matsumoto, G. (1986). Subaxolemmal cytoskeleton in squid giant axon. II. Morphological identification of microtubule- and microfilament-asociated domains ofaxolerama. /. Cell Biol. 102: 1710-1725. Tuganowski, W., Krause, M., and Dorczak, K. (1973). The effect of dibutyryl 3'5' -cylic AMP on the cardiac pacemaker, arrested with re -serpine and alpha-methyl-tyrosine. Naunyn-Schmiedebergs Arch. Pharmakol. 280: 63-70. U Urry, D. W. (1993). Molecular Machines: How motion and other functions of living organisms can result from reversible chemical changes. Angewandte Chemie Intl. Ed. Engl. 32: 819-841. Uvnas, B., Aborg, C. H., Lyssarides, L., andThyberg, J. (1985). Cation exchanger property of isolated rat peritoneal mast cell granules. Acta. Physiol. Scand. Suppl. 125: 25-31. Uvnas, B., and Aborg, C. H. (1977). On the cation exchanger properties of rat mast cell granules and their storage of histamine. Acta. Physiol. Scand. 100: 309-314." V Vale, R. D., and Toyoshima, Y. Y. (1988). Rotation and transition of microtubules in vitro induced by dyneins from Terahymena Cilia.. Cell 52: 459469. Vale, R. D., Funatsu, T., Pierce, D. W., Romberg, L., Harada, Y, and Yanagida, T. (1996). Direct observation of single kinesin molecules moving along microtubules. Nature 380: 451-453. Valentijn, K., Valentijn, J. A., and-'Jamieson, J. D. (1999). Role of actin in regulated exocytosis and compensatory membrane retrieval: insights from an old acquaintance. Biochem. Biophys. Res. Commun, 266: 652-661. vanIterson, W. (1965). Symposium on the fine structure and replication of bacteria and their parts. Bact. Rev. 29: 299-325. Verdugo, P. (1990). Goblet cells secretion and mucogenesis. Ann.. Rev. Physiol. 52: 157-176. Verdugo, P., and Orellana, M. V. (1995). The secretory granule as a biomimetic model for drug delivery. Proc. Intern. Symp. Control Rel. Bioact. Mater. 22: 25-33. Verdugo, P., Deyrup-Olsen, L, Martin, A. W, and Luchtel, D. L. (1992). Polymer gel-phase transition: the molecular mechanism of product release in mucin secretion? NATO ASI Series Vol. H64, Mechanics of Swelling, ed. T. K. Karalis, Springer, Berlin. Verdugo, P., Orellana, M. V, and Freitag, C. (1995). The secretory granule as a biomimetic model for drug delivery. Proc. Intern. Symp. Control Rel. Bioact. Mater. 22:25. Visscher, K., Schnitzer, M. J., and Block, S. M. (1999). Single kinesin molecules studied with a molecular force clamp. Nature 400(6740): 184-189. Vogler, E. A. (1998). Structure and reactivity of water at biomaterial surfaces. Adv. Colloid and Interface Sci. 74:69-117. Von Hippel, P. H., and Wong, K-Y. (1964). Neutral salts: the generality of the stability of macromolecular conformation. Science 145: 577-580. Von Zglinicki, T. (1988). Monovalent ions are spatially bound within the sarcomere. Gen. Physiol. Biophy. 7: 495-504. W Walczak, E. C., Mitchison, T. J., and Desai, A. (1996). XKCM1: a Xenopus kinesin-related protein that regulates microtubule dynamics during mitotic spindle assembly. Cell 84: 37-47. Walker, M. and Trinick, J. (1986). Electron microscope study of the effect of temperature on the length of the tail of the myosin molecule. /. Mo 1. Biol. 192: 661-667. Walker, R. A., Salmon, E. D., and Endow, S. A. (1990). The Droso-phila claret segregation protein is a minus-end directed motor molecule. Nature 347: 780-782. Walzthony, D., and Eppenberger, H. M. (1986). Melting of myosin rod as revealed by electron microscopy. II. Effects of temperature and pH on length and stability of myosin rod and its fragments. Eur. J. Cell Biol. 41: 38-43. Walzthony, D., Eppenberger, H. M., and Walliman, T. (1986). Melting of myosin rod as revealed by electron microscopy. I. Effects of glycerol and anions on length and stability of myosin rod. Eur. J. Cell Bio. 41: 33-37. Wang, C., Stewart, R. J., and Kopecek, J. (1999). Hybrid hydrogels assembled from synthetic polymers and coiled-coil protein domains. Nature 397: 417-420. Wang,N., Butler, J.P., and Ingber, D.E.(1993). Mechanotransduction across the cell surface and through the cytosk -eleton. Science 260: 11241127. Warner, F. D., and Mitchell, D. R. (1981). Polarity of dynenin-mi-crotubule interactions in vitro: cross-bridging between parallel and antiparallel microtubules. /. Cell Biol. 89:35-44. Washabaugh, M. W, and Collins, K. D. (1986). The systematic characterization by aqueous column chromatography of solutes which affect protein stability. J. Biol. Chem. 261: 12477-12485. Watterson, J. G. (1991). The role of water in cell function. Biofizika. 36(1): 5-30. Watterson, J. G. (1997). The pressure pixel-unit of life? BioSytems 41: 141-152. Weisenberg, R. C., and Cianci, C. (1984). ATP-induced gelation-contraction of microtubules assembled in vitro. /. CellBiol. 99: 1527 -1533. Weiss, R. M., Lazarra, R., and Hoffman, B. R (1967). Potentials measured from glycerinated cardiac muscle. Nature 215: 1305-1307. Wells, A. L, Lin, A. W., Chen, L.-Q., Safer, D., Cain, S. M., Hasson, T., Carragher, B. O., Milligan, R. A., and Sweeney , H. L. (1999). Myosin VI is an actin-based motor that moves backwards. Nature 401: 505-508. Whittam, R. (1961). Active cation transport as a pace-maker of respiration. Nature 19: 603-604. Wiggins, P. M. (1990). Role of water in some biological processes. Microbiol. Rev. 54(4): 432-449. Wiggins, P. M., and van Ryn, R. T. (1990). Changes in ionic selectivity with changes in density of water in gels and cells. Biophys. J. 58: 585-596. Wohlfarth-Botterman, K. E. (1964). Diffetentiations of the ground cytoplasm and their significance for the generation of the motive force of ameboid movement. Primitive Motile Systems in Cell Biology, ed. R. D. Alien, and N. Kamiya, Acad. Press, N. Y. Wojcieszyn, J. W., Schlegel, R. A., Wu, E.-S., and Jacobson, K. A. (1981). Diffusion of injected mactomolecules within cytoplasm of living cells. Proc. Nat'1. Acad. Sci. USA 78(7): 4407-4410. Woodbury, D. (1989). Pure lipid vesicles can induce channel-like conductances in planar bilayers. /. Memb. Biol. 109(2): 145-150. 76 Wordeman, L., and Mitchison, T. J. (1995). Identification and partial characterization of mitotic centromere- associated kinesin, a kinesinrelated protain that associates with centromeres during mitosis. /. Cell Biol. 128: 95-104. X Xie, T-D, Sun, L., and Tsong, T. Y. (1990). Studies of mechanisms of electric field-induced DNA transfection. Biophys. J. 58: 13-19. Xu, X.-H. N, and Yeung, E. S. (1998). Long-range electrostatic trapping of single-protein molecules at liquid-solid interface. Science 281: 16501653. Y Yanagida, T., and Oosawa, R (1978). Polarized fluorescence from ep-silon-ADP incorporated into F-actin in a myosin-free single fiber: conformation of F-actin and changes induced in it by heavy meromyosin. / Mol. Biol. 126: 507-524. Yanagida, T., Nakase, M., Nishiyama, K., and Oosawa, R (1984). Direct observation of motion of single F-actin filaments in the ptesence ofmyosin. Nature 307:58-60. Yang, P., Tameyasu, T,, and Pollack, G. H. (1998). Stepwise shortening in single sarcomeres of single myofibrils. Biophys. J. 74: 1473-1483. Yano, M., Yamada, T., and Shimizu, H. (1978). Studies of the chemo-mechanical conversion in artificially produced streamings. /. Biochem. 84: 277283. Yano, M., Yamamoto, Y, and Shimizu, H. (1982). An actomyosin motor. Nature 299: 557-559. Yasunaga, H., and Ando, I. (1993). Effect of ctoss-linking on the molecular motion of water in polymer gel as studied by pulse H NMR and PGSR H NMR.Polym Gels and Ntwks 1: 267-274. Yasunaga, H., Kobayashi, M., Matsukawa, S., Kurosu, H., and Ando, I. (1997). Structures and dynamics of polymer gel systems viewed from NMR. spectroscopy. NMR. in Polymer Science, Acad. Press, London. Yawo, H., and Kuno, M.(1985). Calcium dependence of membrane sealing at the cut end of the cockroach giant axon. /. Neurosci. 5: 1626-1632. Yen, T. J., Li, G., Cshaar, B. T., Szilak, L, and Cleveland, D. W. (1992). CENP-E is a putative kinetochore motor that accumulates just before mitosis. Nature 359: 536-539. Yoshizaki, K., Seo, Y, Nishikawa, H., and Morimoto, T. (1982). Application of pulsed-gradient 31P NMR on frog muscle to measure the diffusion rates of phosphorous compounds in cells. Biophys. J. 38: 209-211. Yuan, S., and Hoffman, A. S. (1995). Synthetic sulfonated microspheres as drug delivery carriers. Proc. Int ern. Symp. Control Rel. Bioact. Mater. 22: 26-27. Zimmermann, U., Zhu, ]. J., Meinzer, R C., Goldstein, G., Schneidet, H., Zimmermann, G., Benkert, R., Thurmer, F., Melcher, P., Webb, D., and Haase, A. (1994). High molecular weight organic compounds in the xylem sap of mangroves: implications for long -distance water transport. Bot. Acta. 107:218-22 Yamada, T. (1998). H-NMR spectroscopy of the intracellular water of testing and rigor frog skeletal muscle. Mechanisms of Work Production and Work Absorption in Muscle, ed. H. Sugi, and G. H. Pollack, CopperReferences: 1] Aggett P. J., Fairweather-Tait. Adaptation to High and LowCopper Intakes: Itsrelevanceto Estimated Safe and adequate daily dietary intakes. Am J ClinNut.67:1061S 63.1998 2] Allcroft R. &UvarovO. Parenteral Administration ofCopperCompoundstoCattle with SpecialReferenceto Copper Glycine (Copper Amino-acetate). Vet. Rec. 71: 797-810.1959 3] Aminoff M.J. Pharmacologic management of Parkinsonism and other movement disorders. In: Katzung, B.G. (editor), Basic & Clinical Pharmacology (sixth edition). Prentice-Hall International, London. 419-431,1995 4] ArnonD.I. &StoutP.R. TheEssentialityofCertain Elementsin MinuteQuantityforPlants, with SpecialReference to Copper. Plant Phvsiol. 14:371-5,1939 5] Barber R.S. et al. Further Studies on Antibiotic and Copper Supplements for Fattening Pigs. Brit. J. Nutr. 1170-79,1957 6] Baumslag N., et al. Trace metal Content of maternal and neonate hair. Arch Environ Health. 29,1974 7] BaxterJ.H. & Wyk J.S. Van ABone Disorder Associated with Copper Deficiency. Bull. Johns Hopk. Hosp.93:1 -23, 1953 8] Bennets H.W., et al.Studies on Copper Deficiencyin Cattle:the Fatal Termination (Falling Disease). Aust. VetJ. 18:50-63, 1942 9]Beshgetoor L. &HambridgeM. Clinicalconditionsalteringcoppermetabolisminhumans. AmJClin Nutr.67:1017S-21S, 1998 10] Boccuzzi G., etal. Protective effect of dehydroepiandrosterone against copper -induced lipid peroxidation in Calves. Anim. Prod. 4: 303-7,1962 71] Nakakoshi T. Copper andhepatocellular carcinoma. Radiology (United States), Jan. 214(1) p304 -6,2000 72] Narasaka S. Studies in the Biochemistry of Copper. XX. Thyroid as a Factor in the Regulation of Blood Copper Level. Jap. J. Med. Sci. 4: 33-36,1938 73] Neelakantan V. & Mehta B.V. Copper Status of Soils in Western India. Soil Sci. 91: 251-6,1961 74] Nolan K.R. Copper toxicity syndrome. J Orthomol Psych. 12:270-282,1983 75] O'Dell B.L.Biochemistry of Copper. The Medical Clinics of North America 60. Saunders Press. 1960 76] Osiecki Henry The Nutrient Bible. Bio Concepts Publishing. 1998 77] Owen C. A,Copperdeficiency and toxicity: Acquired and inherited in plants, animalsand man. Park Ridge NJNoyesPub. 1981 77 78] Pfeiffer C. Mental and Elemental Nutrients. Keats New Canaan. 1975 79] Pirrie R.Serum Copper and its Relationship to Serum Iron in Patients with Neoplastic Disease. J Clin. Path. 5: 190-3, 1952 80] Polukhina 1.N.& Masljanaja H.K. Influence of Nitrogen and Copper on the Anatomical Structure of Oat Stemsin Relation tothe Resistance of Oats on Peat Soils. (English translation), Izv. Timir. Sol. Shokh Akad., No.l, 205-8, 1961 81 ] Pratt W.B. Elevated haircopperin idiopathic scoliosisand ofnormalindividuals. Clin Chem. 24,1978 82] Ramaswamy M.S. Copper in Ceylon Teas. Tea Quart. 31: 76-80,1960 83] Reavley Nicola The New encyclopaedia of Vitamins. Minerals. Supplements and Herbs. Bookman Press. 1998 84] Robertson H. A. & Broome A.W.J. Factors Influencing the Blood Copper Level of Sheep: the Effect of change in Basal Metabolic Activity. J.Sci. Fd. Agric. (Supp. Issue), 8, s. 82-s. 87,1957 85] Roelofsen H., Wolters H., Van Luyn M.J., et al. Copper-induced apical trafficking ofATP7B in polarized hepatoma cells provides a mechanism for biliary copper excretion. Gastroenterology (United States), Sep. 119(3):782-93, 2000 86]SandsteadHH. Copper bioavailability and requirements.American Journal of Clinical Nutrition. 35:809814, 1982 87] Schultze M.O. The Effect of Deficiencies in Copper and Iron on the Cytochrome Oxidase of Rat Tissues. J. Biol. Chem. 129: 729-37,1939 88] Shore D., etal.CSF copper concentrations in chronic schizophrenia. American Journal of Psychiatry. 140:754-757, 1983 89] SidhuK. S., etal. Need to revise the national drinking water regulation for copper. RegulToxicol Pharmacol. 22(1): 95-100,1995 90] Solioz M. et alCopper pumping ATPases: common concepts in bacteria and man. FEBS Lett. 346:44-7, 1994 91] Stine J.B., et al. Copper and Cheddar Flavour.Dairy World, Chicago. 32:10-14,1953 (Chemical Abstracts, 48,900) 92] Sugimoto Y, et al Cations inhibit specifically type 1 5 alpha-reductase found in human skin. J Invest Dermatol. 104(5): 775-778,1995 93] Takamiya K. Anti-tumour Activities of Copper Chelates. Nature. 185:190-1,1960 94] TimberlakeC.F. Complex Formation between Copperand some Organic Acids. Phenols and Phenolic Acids Occurring in Fruit. J. Chem. Soc. 2795-8,1959 95] Tumlund et al. Copper absorption, excretion and retention by young men consuming low dietary copper determined by using stable isotope 65Cu. AM J Clin Nut. 67: 1219-1225,1998 96] Van Campen D.R. Zinc interference with copper absorption in rats. Journal of Nutrition. 91:473,1967 97] Van den Berg G.J., et al.Dietary ascorbic acid lowers the concentration of soluble copper in the small intestinal lumen of rats. BrJNutr. 71(5): 701-707,1994 98] Van Koetsveld E.E.The Manganese and Copper contents ofhair as an indication of the feeding condition of cattle regarding manganese and copper. Tijdschr. Dieregeneesk. 83: 229,1958 99] Vir et al. Serum and hair concentrations of copper during pregnancy. Am J ClinNutr. 34: 2382-2388,1981 Metals and Glucose Control I] Abraham A. S., et al. The effects of chromium supplementation on serum glucose and lipids in patients with and wi thout non-insulin dependent diabetes. Metabolism. 41:768-771,1992 78 2] Anderson R., et al.Beneficial effects of chromium for people with Type II Diabetes. Diabetes. 45(Suppl. 2): 124A/454,1996 , 3] Anderson R.A., Roussel A-M, Zouari N., et al. Potential antioxidant effects of zinc and chromium supplement in people with type II diabetes mellitus. J Am Coll Nutr. 20(3):212-218.2001 4] Anderson R. A., et al. Chromium supplementation of human subjects: Effects on glucose, insulin, and lipid variables. Metabolism. 32:894899,1983 5] Anderson R. A., et al. Supplemental chromium effects on glucose, insulin, glucagon. and urinary chromium losses in subjects consuming low-chromium diets. American Journal of Clinical Nutrition. 54:909-916,1991 6] Anderson R. A., et al. Elevated intakes of supplemental chromium improve glucose and insulin variables in individuals with ;type 2 diabetes. Diabetes. 46:1786-1791,1997 7] Anderson R. A. Nutritional factors influencing the glucose/insulin system: chromium. J Am Coll Nutr. 16(5):404-410,1997 ; 8] Baly P.. et al. Effect of manganese deficiency on insulin binding, glucose transport & metabolism in rat adipocytes. J Nutr. 120:1075-1079,1990 9] Boden G., et al.Effects of vanadyl sulfate on carbohydrate and lipid metabolism in patients with non-insulin-dependent diabetes mellitus. Metabolism. 45:1130-1135,1996 10] Boyd S. G., et al. Combined dietary chromium picolinate supplementation and an exercise program leads to a reduction of serum cholesterol and insulin in college-aged subjects. J Nutr Biochem. 9:471-475,1998 II] Cam M. C., et al. Distinct glucose lowering and beta cell protective effects of vanadium and food restriction in streptozotocin-diabetes. Eur J Endocrinol. 141(5):546-554,1999 12]Chanetal. The role of copper, molybdenum selenium and zinc in nutrtion and health. Clin Lab Med. 18(4): 673-85,1998 13] Chauser A. Zinc. Insulin and Diabetes. J of American College ofNutrition 17(2): 109-115,1998 14] Cohen N., et al. Oral vanadyl sulfate improves hepatic and peripheral insulin sensitivity in patients with non-insulin-dependent diabetes mellitus. Journal of Clinical Investigations. 95(6):2501-2509,1995 15] Combs G.F. and Combs S.B. The Role of Selenium in Nutrition. Academic Press, Inc., Orlando, USA, 1986 16] Corica F.. Allegra A.. Di Benedetto A., et al. Effects of oral magnesium supplementation on plasma lipid concentrations of patients with non-insulin-dependent diabetes mellitus. Magnes Res. 7:4347,1994 17] Davies S.,etal. Age-related decreases in chromium levels in 51.665 hair, sweat, and serum samples from 40.872 patients -implications for the prevention of cardiovascular disease and type II diabetes mellitus. Metabolism. 46(5):469-473,1997 18] Evans G. W. The effect of chromium picolinate on insulin controlled parameters in humans. Int J Biosocial Medical Research. 11:163-180,1989 19] Evans G. W., et al. Chromium picolinate increases membrane fluidity and rate of insulin internalization. J Inorg Biochem. 46(4):243-250,1992 20] Fugii S., Takemura T., Wada M., et al. Magnesium levels in plasma, erythrocyte. and urine in patients with diabetes mellitus. HormMetabRes. 14:161-162,1982 21] Haglund et al. Evidence of a relationship between childhood onset type 1 diabetes and low groundwater concentration of zinc. Diabetes Care Aug. 19:8 873-5,1996 22] Jing M.A., Folsom A.R., Melnick S.L., et al. Associations of serum and dietary magnesium with cardiovascular disease, hypertension, diabetes, insulin, and carotid arterial wall thickness: the ARIC study. J Clin Epidemiol. 48:927-940,1995 23]KellyG.S. Insulin resistance: lifestyle and nutritional interventions. Alternative Medicine Review. 5(2):109-132,2000 24] Leach R.M.Jr. Metabolism & Function of Manganese. Trace elements in Human Health & Disease. Vol.III. 25] Lee N. A., et al. Beneficial effect of chromium supplementation on serum triglyceride levels in NIDDM. Diabetes Care. 17(12):1449-1452,1994 26]Mather H. M., etal. Hypomagnesemia in diabetes. Clin Chem Acta. 95:235-242,1979 27] McNeillJ. Enhanced in vivo sensitivity of vanadyl-treated diabetic rats to insulin. Canadian Journal of Physiology and Pharmacology. 68(4):486491,1996 28]MechegianiE.,etal. Zinc-dependent low thymic hormone level in type I diabetes. Diabetes. 12:932-937,1989 29]MertzW., etal. Present knowledge of the role of chromium. Federation Proceedings. 33:2275-2280,1974 30]NakamuraT.,etal. Kinetics of zinc status in children with IDDM. Diabetes Care. 14:553-557,1991 31] Niewoener C. B.. et al. Role of zinc supplementation in type II diabetes mellitus. Am J Med. 63-68,1988 32] Paolisso G., et al. Improved insulin response and action by chronic magnesium administration in aged NIDDM subjects. Diabetes Care. 12(4):265-269,1989 33] Paolisso et al. Hypertension, diabetes and insulin resistance: the role of intracellular magnesium. Am J Hypertens. 10:3 346-55,1997 34] Pepato M. T., etal. Effect of oral vanadyl sulfate treatment on serum enzymes and lipids of streptozotocin -diabetic young rats. Mol Cell Biochem. 198(1-2):157-161,1999 35]PidduckH.G.,et al. Hyperzincuria of diabetes mellitus and possible genetic implications of this observation. Diabetes. 19:240-247,1970 36]PreussH.G.,etal.Chromium update: examining recent literature 1997-1998. Ciirr Opin Clin Nutr Metab Care. 1:509-512,1998 37]Poucheret P.. et al. Vanadium and diabetes. Mol Cell Biochem. 188(l-2):73-80,1998 38] Prout I.E., et al. Zinc Metabolism in Patients with Diabetes Mellitus. Metabolism. 9:109-17,1960 39] Pryor K. Nutritional approaches to optimal blood glucose and insulin levels: key factors in longevity and resistance to 79 : diabetes and other degenerative diseases.Vitamin Research News. April 2000 40] Rabinowitz M. B., et al. Effects of chromium and yeast supplements on carbohydrate and lipid metabolism in diabetic men. Diabetes Care. 6(4):319-327,1983 43]RaoK.V.R., etal. Effect of zinc sulfate therapy on control and lipids in type I diabetes. JAPI. 35:52,1987 44]RaymanM.P. The importance of selenium to human health. Lancet. 356(9225): 233-241,2000 45]ReavenG. Role of insulin resistance in human disease. Diabetes. 37:1595-1607,1998 46] Resnick L. Magnesium in the pathophysiology and treatment of hypertension and diabetes mellitus: where are we in 1997? Am J Hypertension. 10:368-370,1997 47] Rubinstein A.H. Manganese-induced hypoglycemia. The Lancet. 2:1348-1351,1962 48] Rubenstein A.H.. et al. Hypoglycemia induced by manganese. Nature. 194:188-9,1962 49] SakuraiH., etal. Insulin-like effect of vanadyl ion on streptozotocin-induced diabetic rats. JEndocrinol. 126(3):451-459, 1990 50] SeeligM.S..et al. Low Magnesium: A Common Denominator in Pathologic Process in Diabetes Mellitus. Cardiovascular Disease and Eclampsia. Journal of the American College of Nutrition. October: 11(5): 608/Abstr39,1992 51] Sjogren A., etal. Oral administration of magnesium hydroxide to subjects with insulin-dependent diabetes mellitus. Magnesium. 121:16-20,1988 52] Sjogren A. et al. Magnesium, potassium and zinc deficiency in subjects with type II diabetes mellitus. Acta Med Scand. 224(5):461-466,1988 53] Singh R.B., et al. Current zinc intake and risk of diabetes and coronary artery disease and factors associated with insulin resistance in rural and urban populations of North India. J Am Coll Nutr. 17:564-570,1998 54] Stapleton S.R. Selenium: an insulin-mimetic. Cell Mol Life Sci. 57(13-14): 1874-1879,2000 55] Striffler J. S.,etal. Chromium improves insulin response to glucose in rats. Metabolism. 44:1314-1320,1995 56] Striffler J. S.,etal. Dietary chromium decreases insulin resistance in rats fed a high-fat, mineral-imbalanced diet. Metabolism. 47:396-400,1998 57] Striffler J.S., etal. Overproduction of insulin in the chromium-deficient rat. Metabolism. 48:1063-1068,1999 58] Toplack H., et al. Addition of chromium picolinate to a very low calorie diet improves the insulin-glucose ratio after weight reduction. International Journal of Obesity. 19(2):s057,1995 59]UeharaS.,etal. Clinical significance of selenium level in chronic pancreatitis. J Clin Biochem Nutr. 5:201-207,1988 60] Wallace E. C. Diabetic epidemic. Energy Times. 9(4):24-28 1999 61] Watts D.L. The nutritional relationships of manganese. J. Orthomol. Med. 5(4):219-22,1990 Heavy Metal References: 1] Abe T., et al. High hair and urinary mercury levels offish eaters in the nonpolluted environment of Papua New Guinea. Arc Environ Health. 50:367-373,1995 2] Abraham J.E., Svare C.W. & Frank C. W. The effect of dental amalgam restorations on blood mercury levels.J Dent Res. 63:71-73 1984 3] Alexander. The uptake of lead by children in differing environments. Environ Hlth Prospectus. 1974 4] Aller A. J. The clinical significance of beryllium. J Trace Elements and Electrolytes in Health and Dis. 4,1,1990 5] Altmann P., et al. Disturbance of cerebral function by aluminum in haemodialysis patients without overt aluminum toxicity Lancet. Jul, 1989 6] Ames B.N. Dietary carcinogens and anticarcinogens. Science. 221:1256-1264,1983 7] Annest J.I., et al. Chronological trend in blood lead levels between 1976 and 1980. N.E.J.M. 308,23,1983 8] Anthony H., et al. Environmental Medicine in Practice. Southhamptom: BSAENM Publications. 204-208,1997 9] Aposhian H.V.DMSA and DMPS-water soluble antidotes for heavy metal poisoning. Ann Rev Pharmacol Toxicol. 23:193-215 1983 10] Aschner M., et al. Interactions of methylmercury with rat primary astrocyte cultures: inhibition of rubidium and glutamat uptake and induction of swelling. Brain Res. 530:245-250,1990 11] Ashby J., et al. Studies on the genotoxicity of beryllium sulphate in vitro and in vivo. Mutation Res. 240,3,1990 12] Atchison W.D. & Hare M.F. Mechanisms of methylmercury-inducedneurotoxicity. FASEB J. 8:622-629,1994 13] Baaumslag N., et al. Trace metal content of maternal and neonate hair. Zinc, copper, iron and lead. ArchEnviron. Hlth. 29,197 14] Baker E.L., etal. A nationwide survey of heavy metal absorption in children living near primary copper, lead and zinc smelter. An J Epidemiology. 206,4,1977 15] Bapu C., Rao P. & Sood P.P.Restoration of methylmercury inhibited adenosine triphosphatases during vitamin and monothio 80 therapy. J Environ Path Toxicol Oncol. 17:75-80,1998 16] Barregard L., Sallsten G. & Jarvholm B. People with high mercury uptake from their own dental amalgam fillings. QccupEnviron Med. 52:124-128,1995 17] Barth G..ed. The Lewis and Clark Expedition. Selections from the Journals Arranged by Topic. New York: Bedford St. Martins 158-162,1998 18] Batuman V.. et al. Contribution of lead to hypertension with renal impairment. N.E.J.M. 309.1.1983 19] Beattie J.H. & Peace H.S.The influence of a low-boron diet and boron supplementation on bone, major mineral and sex steroi metabolism in postmenopausal women. Brit J Nutr. 69,3,1993 20] Bhat R.K., et al.Trace elements in hair and environmental exposure. Sci Total Environ. 22(2): 169-178,1982 21] Bigazzi P.E.Lessons from animal models: the scope of mercury-induced autoimmunity. Clin Immunol Immunopathol. 65:81-! 1992 22] Birchall J.D. & Chappell J.S. Aluminum, chemical physiology and Alzheimer's disease. Lancet. Oct. 1988 23] Blakley B.R., Sisodia C.S. & Mukkur T.K. The effect of methylmercury. tetraethyl lead, and sodium arsenite on the humora immunity response in mice.Toxicol Appl Pharmacol. 52:245-254,1980 24]BlumerW. & Reich T. Leaded gasoline-a cause of cancer. Environmental International. 3:456-471,1980 25] Bonhomme C.. et al. Mercury poisoning by vacuum-cleaner aerosol. Lancet. 347:115,1996 26] Boogaard P.J., et al. Effects of exposure to elemental mercury on nervous system and the kidneys in workers producing natura gas^Arch Environ Health. 5:108-115,1996 27] BoyceB.F., et al. Hypercalcaemic osteomalacia due to aluminum toxicity. Lancet. Nov, 1982 28] BoydN.D.. et al. Mercury from dental "silver" tooth fillings impairs sheep kidney function. Am J Phvsiol. 261 :R1010-R1014.199 29] Capel I.D., etal. Assessment of zinc status by the zinc tolerance test in various groups of patients. Clin Biochem. 15(2):257-260 1982 30] Cavalleri A. & Gobba F. Reversible color vision loss in occupational exposure to metallic mercury. Environ Res. 77:173-177,1998 31] Chang L.W. Neurotoxic effects of mercury. A review. Environ Res. 14:329-373,1977 32] Cheraskin E. & Ringsdorf W.M. The distribution of lead in human hair. J Of Med Assoc of Alabama. April, 1979 33] Cheraskin E. & Ringsdorf W.M. Prevalence of possible lead toxicity as determined by hair analysis. J Orthomol Psych. 8,2. Am JIndMed. 2,1,5-14,1981 34] Cianciola M.E., et al. Epidemiologic assessment of measures used to indicate low-level exposure to mercury vapor. J Toxicol Environ Health. 52:19-33,1997 35] Cimino J.A. & Demopoulos H.B. Introduction: Determinants of cancer relevant to prevention, in the war on cancer. J Environ Path. &Toxi.3:l-10,1980 36] Clarke N.E., Clarke C.N. & Mosher R.E. The "in vivo" disolution of metastatic calcium: An approach to athero-sclerosis. Ami MedSci. 229:142-149,1955 40] Coccini T., et al. Low-level exposure to methylmercury modifies muscarinic cholinergic.receptor binding characteristics in rat brain and lymphocytes: physiologic implication and new opportunities in biological monitoring. Environ Health Perspect. 108:29 33,2000 41] Collipp P.J., et al. Hair zinc levels in infants. Clin Pediatr. 22(7):512-513,1983 42] Cooper G.P. & Manalis R.S. Influence of heavy metals on synaptic transmission: a review. Neurotoxicology. 4:69-83,1983 43] Cornell C.R., Markesbery W.R. & Ehmann W.D. Imbalances of Irace elements related to oxidative damage in Alzheimer's disease brain. Neurotoxicology. 19:339-346,1998 44] Crapper-McLaughlin D.R. Aluminum loxicily in senile dementia: Implications for treatment. Read be fore the Fall Conference, American Academy of Medical Prevenlics, Las Vegas, NV, Nov 8,1981 45] Cranlon E.M.. el al. Standardization and interpretation of human hair for elemental concentrations. J Holistic Med. 4:10-20,1982 46] Crinnion W. J. Unpublished research. Healing Naturally. Kirkland, WA. 1999 47] David O., el al. Lead and hyperaclivity. behavioral response to chelalion: A pilol study. Am J Psychiatry. 133:1155 -1158,1976 48] De Souza Queiroz M.L., et al. Abnormal antioxidanl system in erythrocytes of mercury exposed workers. Human & Exp Toxicol. 17:225-230,1998 49] Del Maestro R.F. An approach to free radicals in medicine and biology. Acta Physiol Scand. 492(suppl):153-168,1980 50] Diamond G. & Zalups R.K. Understanding renal loxicity of heavy metals. Toxicol Pathol. 26:92-103.1998 51] Dieter M.P., et al. Immunological and biochemical responses in mice treated wilh mercuric chloride. Toxicol Appl Pharmacol. 68:218-228,1983 52] Dirks M.J., el al. Mercury excretion and inlravenous ascorbic acid. ArchEnviron Health. 49:49-52,1994 53] Dix Y. Metabolism of polycyclic aromatic hydrocarbon derivatives to ultimate carcinogens during lipid peroxidation. Science. 221:77,1983 81 54] Dormandy T.L. Free-radical reaction in biological systems. Ann R Coll Surg Engl. 62:188-194,1980 55] Dormandy T.L. Free-radical oxidation and antioxidants. Lancet. i:647-650,1978 56] Druel P., el al. Immune type glomerulonephrilis induced by HgC 12 in Brown-Norway rat. Ann Immunol (Inst Pasteur). 129C:777 792,1978 57] Durham H.D., Minotti S. & Caporicci E. Sensitivity of platelel microlubles lo disassembly by methylmercury. J Toxicol Enviro Health. 48:57-69, 1997 58] Ely J.T., et al. Urine mercury in micromercurialism: a bimodal distribution and its diagnostic implications. Unpublished. 59] Ely D.L., el al. Aeromelric and hair trace metal conlenl in learning-disabled children. Environ Res. 25(2):325-339,1981 60] EmerickR.J. & Kayongo-Male H. Silicon facilitation of copper utilization in the rat J Nutr Biochem. 1,1990 61] Enestrom S. & Hultman P. Immune-mediate glomerular nephritis induced by mercuric chloride in mice. Experientia. 40:1234-1240, 1984 63] Enestrom S. & Hullman P. Dose-response sludies in murine mercury-induced autoimniunity and immune-complex disease. Toxicol Appl Pharmacol. 113:199-208,1992 64] Engqvisl A., Colmsjo A. & Skare I. Specialion of mercury excreted in feces from individuals wilh amalgam fillings. Arch Environ Health. 53:205-213,1998 65] Erickson, el al. Tissue mineral levels in victims of Sudden Infanl Deallh Syndrome 1. Toxic melals - lead and cadmium. Fed Res. 17,10,1083 66] Falconer M.M.. et al. The molecular basis of microtuble stability in neurons. Neurotoxicology. 15:109-122,1994 67] FiedlerN., el al. Neuropsychological and slress evaluation of residential mercury exposure. Enviro Heallh Perspect 107:343-347, 1999 68] Florence T.M.. Lilley S.G. & Slauber J.L. Skin absorption of lead. Lancet Jul. 16,1988 69] Foli M.R., Hennigan C. & Errera J. A comparison of five toxic melals among rural and urban children. Environ Pollul Ser A Ecol Biol. 29:261-270,1982 70] Fukuda Y., et al. An analysis of subjective complainls in a populalion living in a methylmercury-polluted area. Environ Res. 81:100-107,1999 71] GalsterW.A. Mercury in Alaskan Estimo mothers and infants. Environ Heallh Perspect 15:135-140,1976 72] Ganther H.E. Selenium: relation to decreased loxicity of methylmercury in diels conlaining luna. Science. 175:1122,1972 73] Ganlher H.E. Modification of methylmercury toxicily and melabolism by selenium and vilamin E: possible mechanisms. Environ Heallh Perspect 25:71-76,1978 74] Garrell P.J., et al.Aluminum encephalopalhy: Clinical and immunological features. Quart J Med. 69,258, 1988 75] Gibson R.S. & Gage L. Changes in hair arsenic levels in breast and bottle fedinfanls during Ihe firsl year of infancy. Sci Tolal Environ. 26:33-40,1982 76] Goldberg R.L., Kaplan S.R. & Fuller G.C.Effecl of heavy melals on human rheumatoid synovial cell proliferation and collagen synthesis. Biochem Pharmacol. 32:2763-2766,1983 77] Grandjean P., et al. Methylmercury neurotoxicily in Amazonian children downslream from gold mining.Environ Heallh Perspect 107:587-591,1999 78] Grandjean P., el al. Relation of a seafood diet to mercury, selenium, arsenic and polychlorinated biphenyl and other organochlorine concentrations in human milk. Environ Res. 71:29-38. 1995 79] Giaziano J.H., Lolacono N.J. & Meyer P. Dose-response sludy of oral 2.3-dimercaptosuccinic acid in children wilh elevated blood lead concentrations. J Pediatr. 113:751-757,1988 80] Giaziano J.H. Role of 2.3-dimercaptosuccininc acid in the treatment of heavy metal poisoning. Med Toxicol. 1:155 -162,1986 81] Grazino J.H. & Blum C. Lead exposure from lead crystal. Lancet. 337,1991 82] Gunderson E.L. PDA Total Diet Study. April 1982-April 1986. Dietary intake of pesticides, selected elements and other chemicals. Distributed by: Association of Official Analytical Chemists. Arlington, VA. 83] Hahn L.J., et al. Dental "silver" tooth fillings: a source of mercury exposure revealed by whole-body image scan and tissue analysis. FASEB J. 3:2641-2646.1989 84] Hahn L. J., et al. Whole body imaging of the distribution of mercury released from dental fillings into monkey tissue. FASEB J. 4:3256-3260,1990 85] Halbach S., et al. Compartmental transfer of mercury released from amalgam. Hum Exp Toxicol. 16:667-672,1997 86] Halbach S., et al. Systemic transfer of mercury from amalgam fillings before and after cessation of emisson. Environ Res. 77:115123,1998 87] Hansen J.C., Christensen L.B. & Tarp U. Hair lead concentration in children with minimal cerebral dysfunction. Danish Med Bull. 27:259-262,1980 88] Harada M., et al. The present mercury contents of scalp hair and clinical symptoms in inhabitants of the Minamata area. Environ 82 Res. 77:160-164,1998 89] Harnly M., et al. Biological monitoring for mercury within a community with soil and fish contamination. Environ Health Perspect. 105:424-429,1997 90] Harrison W., Yurachek J. & Benson C. The determination of trace elements in human hair by atom ic absorption spectroscopy. ClinChimActa.23(l):83-91,1969 91 ] Herrstrom P., et al. Dental amalgam, low-dose exposure to mercury, and urinary proteins in young Swedish men. Arch Environ Health. 50:103-110,1995 92] Hibberd A.R., Howard M.A. & Hunnisett A.G. Mercury from dental amalgam fillings: studies on oral chelating agents for assessing and reducing mercury burdens in humans. J Nutr Environ Med. 8:219-231.1998 93] Homma-Takeda S., et al. Selective induction of apoptosis of renal tubular cells caused by i norganic mercury in vivo. Environ Toxicol Pharmacol. 7:179-187,1999 94] Huel G., Boudene C. & Ibrabim M.A. Cadmium and lead content of maternal and newborn hair: Relationship to parity, birth weight and hypertension. Arch Environ Health.,35(5^):221-227.1981 95] Hunt C.D., Shuler T.R. & Mullen L.M'. Concentration of boron and other elements in human foods and personal-care products. J Am Diet Assoc. 91,5,1991 96] Hurry V.J. & Gibson R.S. The zinc, copper and manganese status of children with malabsorption syndromes and in -born errors ofmetabolism. Biol Trace Element Res. 4:157-173.1982 97] InSug O., et al. Mercuric compounds inhibit human monocyte function by reactive oxygen species, development of rmtochondrial j membrane permeability transition and loss ofreductive reserve. Toxicology. 124;211-224,1997 98] Jenkins D. W. Toxic TraceMetals in Mammalian Hair and Nails.US Environmental Protection Agencypublication No. (EPA)600/4-79-049. EnvironmentalMonitoringSystems Laboratory. 1979 99]JenkinsD. W.Biologicalmonitoringoftoxic tracemetals Vol. 1.Biologicalmonitoringand surveillance. EPA600/3-80-089,1980. ClinChem.36,3,1990 100] Jones R.J. The continuing hazard of lead in drinking water. Lancet. Sept 16,1989 101] Kanematsu N., et al. Mutagenicity of cadmium, platinum and rhodium compounds in cultures mammalian cells. Gifu Shika Zasshi. 17,2,1990 102] KingN., et al. The effect of in ovo boron supplementation on bone mineralization of the vitamin D-deficient chicken embryo. BiolTraceElement Res.31,1,1991 103] Kissel K.P.Teens fall ill after taking, playing with mercury. The Seatle Times: January 15,1998 104] Klevay L. Hair as a biopsy material-assessment of copper nutriture. Am J ClinNutr. 23(8): 1194-1202,1970 105] Kolata G. Newsuspect in bacterial resistance:amalgam. The NewYork Times: April24,1993 106] Kopito L., et al. Chronic plumbism in children. Diagnosed by hair analysis. J.A.M.A. 209,2,1969 107] Langworth S., BlinderC.G. &SundqvistK.G. Minoreffects oflowexposuretoinorganic mercuryon thehumanimmunesystem ScanJ Work Environ Health.19:405-413,1993 108] Lebel J., Mergler D. & LucotteM. Evidence of early nervous system dysfunction in Amazonian populations exposed to low-. levels of methylmercury. Neurotoxicology. 17:157-167,1996 109] Levine S.A. & Reinhardt J.H.Biochemical-pathology initiated by free radicals, oxidant chemicals and therapeutic drugs in the etiology of chemical hypersensitivity disease. J Orthomol Psychiatr. 12(3):166-183,1983 110] Lichtenberg H. Symptoms before and after proper amalagam removal in relation to serum-globulin reaction to metals. J orthomolec Med.11:195-204,1996 112] Lieb J. & Hershman D. Isaac Newton: mercury poisoning or manic depression. Lancet. 1479-1480,1983 113]MagourS.,MaserH. & Grein H.The effect of mercury and methylmercury on brain microsomal Na+, K+ ATPase after partial delipidisation with Lubrol. Pharmacol Toxicol. 60:184-186,1987 114] Maloney S.R.. Phillips C.A. & Mills A. Mercury in the hair of crematoria workers. Lancet. 352:1602,1998 115] Marlowe M.,etal.Increased lead burdens and trace mineral status in mentally retarted children. J SpecEduc. 16:87-99,1982 116] Marlowe M., et al. Lead and mercury levels in emotionally disturbed children. J Orthomol Psychiatr. 12(4):260-267,1983 117] Marlowe M. & Mood C. Hair aluminum concentration and nonadaptive classroom behavior. J of Advancement in Med. 1,3, 1988 118] Matte T.D., et al. Acute high-dose lead exposure from beverage contaminated by traditional Mexican pottery. Lancet. 344,8929, 1994 119] Matthews A.D. Mercury content of commercially important fish of the Seychelles and hair mercury levels of a selected part of the population. Environ Res. 30:305-312.1983 120] Medeiros D.M. & BorgmanR.F. Blood pressure in young adults as associated with dietary habits, body conformation and hair element concentrations. NutrRes. 2:455-466.1982 121] Medeiros D.M, Pellum L.K. & Brown B.J. The association of selected hair minerals and anthropometric factors with blood 83 pressure in a normotensive adult population. Nutr Research. 3:51-60,1983 122] Medeiros D.M. & Pellum L.K.Elevation of cadmium, lead and zinc in the hair of adult black female hypertensives. Bull Environ Toxicol.32,1984 123] Miettinen J.K. Absorption and elimination of dietary mercury (2+) ion and methylmercury in man. In: Miller MW, Clarkson T.W., eds. Mercury, Mercurials and Mercaptans. Proceedings 4th International Conference on Environmental Toxicology. New York: Plenum Press; 1973 124] Miller O.M., Lund B.O. & Woods J.S.Reactivity of Hg(II) with superoxide: evidence for the catalytic dismutation of superoxide bv Hg<m J Biochem Toxicol. 6:293-298,1991 125] Miura K., et al. The involvement of microtubular disruption in methylmercury-induced apoptosis in neuronal and nonneuronal cell lines. Toxicol Appl Phamacol. 160:279-288,1999 126] Moser P.B., Krebs N.K. & Blyler E. Zinc hair concentrations and estimated zinc intakes of functionally delayed normal sized and small-for-age children. Nutr Research. 2:585-590.1982 127] Musa-Alzudbaidi L., et al. Hair selenium content during infancy and childhood. Eur J Pediatr. 139:295-296,1982 128] Nakatsuru S., et al.Effect of mercurials on lymphocyte functions in vitro. Toxicology. 36:297-305,1985 129] Narang A.P.S., et al. Arsenic levels in opium eaters in India. Trace Elements in Med. 4,4,1987 130] Ngim C.H., et al.Chronic neurobehavioral effects of elemental mercury in dentists. Br J Indust Med. 49:782-790,1992 131] Niculescu T., et al. Relationship between the lead concentration in hair and occupational exposure. Brit J Industrial Med. 40,67, 1983 132] Ninomiya T., et al. Expansion of methylmercury poisoning outside of Minamata: an epidemiological study on chronic methylmercury poisoning outside Minamata. Environ Res. 70:47-50,1995 133] Nolan K.R.Copper toxicity syndrome. J Orhtomol Psychiatr. 12(4):270-282,1983 134] Nordlind K. Inhibition of lymphoid-cell DNA synthesis by metal allergens at various concentrations. Effect on short-time cultured non-adherent cell compared to non-separated cells. Int Arch Allergy Appl Immunol. 70:191-192,1983 135] Nriagu J.O. Lead and Lead Poisoning in Antiquity. Wiley N.Y. 1983 136] Orloff K.G.. et al. Human exposure to elemental mercury in a contaminated residential building. Arch Environ Health. 52:169-172. 1997 137] OrtegaH.G., et al. Neuroimmunological effects of exposure to methylmercury forms in the Sprague -Dawley rat. Activation of the hypothalamic-pituitary-adrenal axis and lymphocyte responsiveness. Toxicol Indust Health. 13:57 -66,1997 138] Oskarsson A., et al. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Arch Environ Health. 51:234-241,1996 139] OudarP, Caillard L. & Fillon G. In vitro effects of organic and inorganic mercury on the serotonergic system. Pharmacol Toxicol. 65:245-248,1989 140] Patterson J.E., Weissberg B. & Dennison P.J. Mercury in human breath from dental amalgam. Bull Environ Contam Toxicol. 34:459-468,1985 141] Pearl D.P., et al. Intraneuronal aluminum accumulation in Amyotrophic Lateral Sclerosis and Parkinsonism -Dementia of Guam. Science. 217,1982 142] Pendergrass J.C., et al. Mercury vapor inhalation inhibits binding of GTP to tubulin in rat brain: similarity to a molecular lesion in Alzheimer's disease brain. Neurotoxicity. 18:315-324,1997 143] Pendergrass J.C. & Haley B.E. Mercury-EDTA complex specifically blocks brain beta-tubulin-GTP interactions: similarity to observations in Alzheimer's disease. In: Friberg L.T., Scrauzer G.N., eds. Status Quo and Perspectives of Amalgam and other Dental Materials. Stuttgart: GeorgThieme Verlag.98-105,1995 144] Peters H. A. Trace minerals, chelating agents and the por-phyrias. Fed Proc. 20(3)(Part II)(suppl 10):227-234.1961 145] Peters H.A.. et al. Arsenic, chromium and copper poisoning from burning treated wood. N Engl J Med. 308(22): 1360-1361,1983 146] Peters H.A.. et al. Seasonal arsenic exposure from burning treated wood. J.A.M.A. 11;25,18,2393-2396,1984 147] Peto R.. et al. Can dietary beta-carotene materially reduce human cancer rates? Nature. 290:201.1981 148] Rajanna B. & Hobson M. Influence of mercury on uptake of dopamine and norepinephrine by rat brain synaptosomes. Toxicol Lett. 27:7-14,1985 149] Rajanna B., et al. Effects of cadmium and mercury on Na+. K+ ATPases and the uptake of 3H-dopamine in rat brain synaptosomes. Arch Int Physiol Biochem. 98:291-296,1990 150] Redhe O. & Pleva J. Recovery from Amyotrophic Lateral Sclerosis and from allergy after removal of dental amalgam filling. IntJ Risk Safety Med. 4:299236,1994 151] Rees E.L. Aluminum poisoning of papua New Guinea natives as shown by hair testing. J Orthomol Psychiatr. 12(4):312-313, 1983 152] Salonen J.T., et al. Intake of mercury from fish, lipid peroxidation. and the risk of myocardial infarction and coronary, cardiovascular. and any death in eastern Finnish men. Circulation. 91:645-655,1995 84 153] Schroeder H. A. & Perry H.M. Jr. Antihypertensive effects of metal binding agents. J Lab Clin Med. 45:416,1955 154] Seven M.J. & Johnson L.A. (eds). Metal Binding in Medicine: Proceedings of a Symposium Sponsored by Hahnemann Medical College and Hospital. Philadelphia. Philadelphia. J.B. LippincottCo., 1960 155] Sharp D.S. & Smith A.H. Elevated blood pressure in treated hypertensives with low-level lead accumulation. Arch Environ Hlth. 44,1,1989 156] Shenker B.J., Guo T.L. & Shapiro I.M. Low-level methylmercury exposure causes human T -Cells to undergo apoptosis: evidence of mitochondrial dysfunction. Enviro Res. 77:149-159.1998 157] SiblerudR.L. The relationship between mercury from dental amalgam and mental health. Am J Psychotherapy. 43:575-587.1989 158] Sitprija V., et al. Metabolic problems in northeastern Thailand: possible role of vanadium. Mineral and Electrolyte Metabol. 19,1,1993 159] Skerfving S. Mercury in women exposed to methylmercury through fish consumption, and in their newborn babies and breast milk. Bull Environ Contam Toxicol. 41:475-482,1988 160] Stopford W. & Goldwater L.J. Methylmercury in the environment: a review of current understanding. Environ Health Perspect. 12:115-118,1975 161] Stortebecker P. Mercury Poisoning from Dental Amalgam. A Hazard to Human Brain. Stockholm: Stortebecker Foundation for Research. 24,1985 162] Szylman P., et al. Potassium-wasting nephropathy in an outbreak of chronic organic mercurial intoxication. Am J Nephrol. 15:514-520,1995 163] Thatcher R.W., et al. Effects of low levels of cadmium and lead on cognitive functioning in children. Arch Environ Health, 37(3):159-166,1982 164] Thimaya S. & Ganapathy S.N. Selenium in human hair in relation to age, diet, pathological condition and serum levels. Sci Total Environ. 24:41-49,1982 165] Thompson C.M., et al. Regional brain trace-element studies in Alzheimer's disease. Neurotoxicology. 9:1-8,1988 166] Ting K.S.. et al. Chelate stability of sodium dimercaptosuccinate on the intoxication from many metals. Chinese Med J. 64:1072 1075,1965 167] Tollefson L. & Cordle F. Methylmercury in fish: a review of residue levels, fish consumption and regulatory action in the United States. Environ Health Perspect. 68:203-208,1986 168] TrepkaM.J., et al. Factors affecting internal mercury burdens among East German children. Arch Environ Health. 52:134-138, 1997 169] Vanderhoff J.A., et al. Hair and plasma zinc levels following exclusion of biliopancreatic secretions from functioning gastrointestinal tract in humans. Dig Pis Sci. 28(41:300-305.1983 170] Vimy M.J. & Lorsheider F.L. Intra-oral air mercury released from dental amalgams. J Dent Res. 64:1069-1071,1985 171] Vimy M.F. & Lorsheider F.L. Serial measurements of intra-oral air mercury: estimation of daily dose from dental amalgams. J DentRes. 64:1072-1075,1985 172] Walker P.R., LeBlanc J. & Sikorska M. Effects of aluminum and other cations on the structure of brain and liver chromatin. Biochem. 28,9,1989 173] Watanabe C. & Satho H. Evaluation of our understanding of methylmercury as health threat. Environ Health Res. 104:367-378, 1996 174] Watts D.L. Prevalence of lead in environment threatens children. Hlth Freedom News. Oct, 1985 175] Watts D.L. Implications of lead toxicity. TEI Newsletter. 1,2,1985 176] Wedeen R.P., Mallik D.K. & Batuman V. Detection and treatment of occupational lead nephropathv. Arch Intern Med. 139:5357,1979 177] Welsh S.O. & Scares J.H. Jr. The protective effect of vitamin E and selenium against methylmercury toxicity in the Japanese quail. Nutr Rep Int. 13;43,1976 178] Westhoff D.D., et al. Arsenic intoxication as a cause of megaloblastic anemia. Blood. 75,45,2.241-246. 179] Willett W.C.. et al. Prediagnostic serum selenium and risk of cancer. Lancet. 2(83431:130-134.1983 180] Wilson R.L. Iron, zinc, free radicals and oxygen tissue disorders and cancer control, in Iron Metabolism. Ciba Foundn Symp 51 (new series). Amsterdam, Elsevier. 331-354,1977 181] Yamanaka S., Tanaka H. & Nishimura M. Exposure of Japanese dental workers to mercury. Bull Tokyo Den Coll. 23:15-24,1982 182] Yokel R.A. Hair as an indicator of excessive aluminum exposure. Clin Chem. 28,4,1982 183] Zalups R.K. & Cernichiari E.2.3-dimercapto- 1-propanesulfonic acid (DMPS) as a rescue agent for the nephropathy induced by mercuric chloride. The Toxicologist. 10:271(Abstractonly), 1990 184] Zalups R.K. & Lash L.H. Interactions between glutathione and mercury in the kidney, liver and blood. In: Chang L.W., ed.Toxicology of Metals. BocaRaton: CRC Press. 145-163,1996 185] Zheng W.. et al. Choroid plexus protects cerebrospinal fluid against toxic metals. FASEB J. 5:2188-2189.1991 85 Copyright 2005 Jerry Tennant, MD All Rights Reserved Price $24.95 USD 86