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Health Education 345 Health Promotion and Disease Prevention Lecture notes Spring 2010 Dr. Gordon Chalmers Dept. of PEHR Western Washington University 2010, Gordon Chalmers, Ph.D. Communicable Diseases VOLUME 3 ISSUE 12 September 15, 2006 Wash your hands Does it work? Just 30 seconds of simple handwashing with soap and water reduces the bacterial count on health care workers’ hands by 58%. And there is an even better way: Alcohol-based handrubs (discussed below) reduce counts by 83%. A two-year study of Navy recruits shows that handwashing pays big dividends. A simple soap and water handwashing campaign reduced clinic visits for respiratory infections by 45%, and the sailors who washed most often enjoyed the greatest protection. What’s best? Soap and water is the time-honored technique, and it does work. In fact, it’s still the best way to remove visible soilage and particulate material. But as the public has become concerned about the risk of infection, soaps with antibacterial additives have gradually taken over 45% of the market. It’s understandable, but it’s not helpful; antibacterial soap is no better than ordinary soap, and the additives actually increase the risk of allergic reactions and other side effects. The only exception is that the spores of the anthrax bacillus are more susceptible to antimicrobial soap than ordinary soap. Unless the bioterrorism of 2001 resurfaces, however, that’s not a worry for ordinary folks. Plain soap will do the job — and so will plain water. Tap water is excellent, and cool or lukewarm temperatures serve as well as hot water. In fact, excessively warm water may do more harm than good by damaging skin. If soap and water are not available, antibacterial wipes can help. Although they are not as effective, they will reduce bacterial counts. Antibacterial towelettes are particularly convenient for travel and picnics. Washing with soap and water is the best way to remove dirt, but waterless, alcohol-based handrubs are even better at killing germs. Handrubbing is faster and more convenient than handwashing, and it’s also easier on the skin. Hospitals are switching to handrubs because they kill more bacteria and viruses and they are used more regularly. Alcohol-based rubs and gels are also available for use at home. The best products contain 60%–95% isopropanol or ethanol. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 2 updated 3/17/2010 Communicable Diseases When and how Do it early and often. Wash your hands before each trip to the dining room and after each trip to the bathroom. Wash after handling diapers and animals. Wash before and after you handle food. Wash after you take out the trash, work in the yard, clean the house, repair the car, or do other messy chores. Wash before and after sex. Wash after you come in contact with anyone who is sick, particularly if they have a respiratory infection or diarrhea. Wash your hands whenever they look or feel dirty, but use common sense. If you follow reasonable guidelines you’ll be washing often, but you won’t become obsessive or compulsive. Be careful, not fearful. How should you wash? Liquid, bar, powdered, and lather forms of plain soap are all acceptable. Wet your hands with water, then apply the soap to your palms. Rub your hands together briskly for at least 15 seconds before rinsing. In most cases, removing jewelry is not necessary. If your nails are dirty, scrub under them with a nailbrush, but unless you are a surgeon preparing to operate, don’t scrub your skin. Whenever possible, use a disposable towel to dry your hands thoroughly, and use the towel to turn off the faucet. Alcohol-based handrubs are preferred for health care workers, and you should consider using them at home when dirt is not an issue but infection is a particular worry. Apply the recommended amount of the gel or rub to the palm of one hand, then rub your hands and fingers until your hands are dry. If your hands dry in less than 15 seconds you have not used enough rub; if it takes 30 seconds or longer, you’ve applied more than you need. Skin care is also important. Alcohol-based rubs are easy on the skin, but if you use a lot of soap and water, your skin may get dry, itchy, or cracked. Soaps that contain bath oil may help, but the best protection is to apply a moisturizer after each wash. What is a communicable disease? A disease that we catch from somebody (or something) else = INFECTIOUS DISEASE. Why are they of concern to me? What causes communicable diseases? GERMS = pathogens = disease causing organisms bacteria, virus, spirochetes, protozoa, fungi (& others) bacteria = single celled microorganism virus = non-living particle of genetic material spirochetes = type of bacteria fungus = plant like microorganism How do PATHOGENS work to make me sick? HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 3 updated 3/17/2010 Communicable Diseases All infectious diseases follow a TRANSMISSION cycle which allows them to be passed from one person (or thing) to the next person. LYME DISEASE EXAMPLE Lyme disease PATHOGEN? RESERVOIR supply of the PATHOGEN, a good place for it to survive, in some cases the site of reproduction. Lyme disease causing spirochete RESERVOIR? other reservoirs for a variety of pathogens: animals (including people), soil, air, water, inanimate objects = virtually everything around you (you can’t avoid the reservoirs) Period of COMMUNICABILITY Time period when pathogen is most easily transmitted from the reservoir. e.g., a cold is most easily transmitted during it’s early phases other pathogens have specific phases when they can most likely be transmitted (e.g., genital herpes, Most likely transmitted during outbreak, at other times risk is low) Lyme disease causing spirochete Period of COMMUNICABILITY? Place of EXIT Route of pathogen out of reservoir toward the person to be infected. Lyme disease causing bacteria exit from reservoir? Place of EXIT for some other common infectious agents: moisture droplets from mouth & nose, feces or direct physical contact Mode of TRANSMISSION How pathogen moves from reservoir to the person to unsuspecting recipient. Lyme disease causing spirochete Mode of TRANSMISSION? Mode of TRANSMISSION for some other common infectious agents: air or surface carried moisture droplets from mouth & nose, or direct physical contact, carried in dirt , food, water that is them ingested Portal of ENTRY How pathogen gets into recipient’s body. Lyme disease causing spirochete Portal of ENTRY? Portal of ENTRY for some other common infectious agents? SUSCEPTIBILITY of host Recipient of pathogen may not become sick if body is able to resist the infection by specific or nonspecific body responses to pathogens e.g., inflammatory response & immunity HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 4 updated 3/17/2010 Communicable Diseases Lyme disease causing spirochete SUSCEPTIBLE hosts? Which groups in the population are very susceptible hosts to infections? INCUBATION PERIOD Time between pathogen entry and symptom appearance Lyme disease causing spirochete INCUBATION PERIOD? varies greatly between pathogens e.g., 1-3 day for cold overlap with period of communicability varies DISEASE 1 incubation symptoms communicability DISEASE 2 incubation symptoms communicability What is a special challenge to stopping disease #2? What diseases fit this category? SELECT A COMMUNICABLE DISEASE AND… WORK OUT EACH STEP IN THE DISEASE CYCLE IDENTIFY WHERE IN THE CYCLE THE SPREAD OF THE DISEASE CAN BE ADDRESSED HOW DOES THE BODY DEFEND AGAINST PATHOGENS? PART A: NONSPECIFIC DEFENSES AGAINST BROAD CATEGORIES OF PATHOGENS = NONSPECIFIC IMMUNITY 1) NOT BE SUSCEPTIBLE TO THE PATHOGEN some pathogens are only able to infect certain species e.g, some viruses that infect animals will not infect humans due to differences in genetic material 2) MECHANICAL BARRIER The intact skin and gut lining have tight junction between cells to prevent many pathogens from passing easily to the interior of the body (remember, something inside the gut is not yet inside the body) Cilia “sweep” foreign pathogens from respiratory tract. 3) ENZYMES HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 5 updated 3/17/2010 Communicable Diseases Enzymes in the stomach and tears destroy some pathogens trying to enter the body through this route AFTER A PATHOGEN HAS ENTERED YOUR BODY, WHAT CAN YOUR BODY DO? 4) INTERFERONS proteins produced by cells infected by viruses, will reduce the chance of other cells getting infected (a mechanism not well understood yet) 5) INFLAMMATION & PHAGOCYTOSIS A tissue response to pathogenic injury (or mechanical) that prevents the spread of the infectious agents, then removes the foreign material and killed cells EXAMPLE OF NONSPECIFIC DEFENSE PROCESS: pathogen enters body (e.g., through a cut) macrophages & leukocytes are chemically attracted to the site (chemotaxis) complement proteins in the blood promote destruction of bacteria macrophages remove the foreign pathogen by phagocytosis if infection is sufficiently large: redness & warmth due to increased blood flow swelling due to increased fluid movement into tissues as capillaries become more permeable to allow leukocytes to move into tissue from blood stream pus due to accumulation of dead leukocytes fever due to chemical release from leukocytes some believe that a mild to moderate fever is beneficial during a bacterial infection, inhibiting bacterial growth if infection is small, then the nonspecific immune response described above may be sufficient to eliminate the pathogen if infection is sufficiently large, then SPECIFIC IMMUNE RESPONSE IS INITIATED, to allow antibodies specific to the invading pathogen to be produced HOW DOES THE BODY DEFEND AGAINST PATHOGENS? PART B: DEFENSES AGAINST SPECIFIC PATHOGENS = SPECIFIC IMMUNITY HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 6 updated 3/17/2010 Communicable Diseases BONE MARROW erythrocytes LEUKOCYTES (WHITE BLOOD CELLS) platelets stem cell IMMATURE LYMPHOCYTES (one class of leukocytes) Lymphocyte maturation in BONE produces B-LYMPHOCYTE (bone derived) Lymphocyte maturation in THYMUS produces T-LYMPHOCYTE (thymus derived) T-cell Release to blood and accumulation in lymph nodes & spleen (70-80% Tlymphocytes, most of the rest are B-lymphocytes) Two types of lymphocytes for our immune response: B-cell = B-lymphocytes: combat bacterial & some viral infections secrete antibodies into blood & lymph = humoral immunity = antibody-mediated immunity T- cell = Tlymphocytes: combat host cells infected with viruses or fungi, transplanted human cells, and cancer cells do not secrete antibodies, must come physically close to the cell to be attacked = cell-mediated immunity B-cell 80% of lymphocytes are T-cells. These are critical for immunity, transplant rejection, cancer and other situations. But we will focus on B-cells, because these are involved in the development of immunity, our focus of discussion. HOW B-LYMPHOCYTES & ANTIBODIES PROTECT YOU FROM INFECTIONS BREAK IN SKIN ALLOWING BACTERIA ENTRY SKIN ANTIGEN = molecule that stimulates antibody production usually a protein, e.g., protein on the surface of a foreign bacteria ANTIGEN ON SURFACE B-lymp hocyte with antibod ies on all surfaces = recep tors for foreign (non-self) antigens bacteria with foreign (to the host) p rotein on the surface Exposure of a B-Lymphocyte to an antigen it is sensitive to results in multiple cell divisions to produce: 1) plasma cell: which produces HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 7 updated 3/17/2010 Communicable Diseases antibodies which attach to the antigen 2) memory cell: produce antibodies for the antigen faster next time Next: a ntigen on ba cter ia binds to a ntibodies on B-lymphocyte B-lymphocyte w ith a ntibodies on a ll sur fa ces = r eceptor s for a ntigens ba cter ia w ith for eign (to the host) pr otein on the sur fa ce Next: B-lymphocyte divides many time to produce PLASMA CELLS & MEMORY CELLS, both of which are specific to the specific antigen (on the foreign pathogen) which arrived Memory cell Plasma cell PLASMA CELL: produce about 2 thousand antibodies per second during 5-7 day life. Antibodies are specific to bind with antigen on foreign material (protein in this example). MEMORY CELL: ready to produce antibodies specific for the foreign protein antigen (on the foreign bacteria in this example) if that foreign protein shows it’s face (i.e., it’s antigen) again. Memory cell Plasma cell When antibodies bind to foreign antigen on invading pathogen, they do not kill the pathogen, BUT THEY IDENTIFY IT AS A FOREIGN BODY, and this stimulates COMPLEMENT proteins to kill the foreigner. Complement proteins also stimulate MAST CELLS (a connective tissue cell type) to release HISTAMINE. HISTAMINE causes increased local blood flow, attracts more phagocytes to the area to the area, and increased capillary permeability, causing edema (now you know why you take antihistamines, see HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 8 updated 3/17/2010 Communicable Diseases Next: Antibodies a tta ch to the specific a ntigen (on the for eign pa thogen), to ma r k for for a tta ck by complement (C) pr oteins. Complement stimula tes HISTAM INE r elea se. M emor y cells w a it for next inva ision by sa me pa thogen. M emor y cell Pla sma cell M emor y cell C there are 100 million trillion (1020) antibodies in each person, representing specificity for a few million different antigens C C ba cter ia C HISTAMINE RELEASE discussion of allergies later) MAST CELL C C C Q: WHAT IS THE BIG DIFFERENCE BETWEEN THE FIRST & SUBSEQUENT EXPOSURES TO A PATHOGEN? DEVELOPMENT OF MEMORY CELLS WITH FIRST EXPOSURE, ALLOWING FASTER RESPONSE TO NEXT EXPOSURE TO PATHOGEN IS TERMED DEVELOPING IMMUNITY TO THAT PATHOGEN IMMUNITY = protected from getting a disease because immune system can destroy the pathogen before disorder & symptoms in the host HOW DOES YOUR SPECIFIC IMMUNITY DEVELOP (IS IT ACTIVE OR PASSIVE IMMUNITY)? ACTIVE IMMUNITY You ACTIVELY develop antibodies specific to a certain antigen through exposure to the antigen #1) NATURALLY ACQUIRED ACTIVE IMMUNITY Exposure to the actual antigen, and you get the disease. (process discussed above) E.G., You get exposed to the mumps virus (from a sibling), you have the disease, but in the process you develop antibodies to the virus. These antibodies (blueprint for them actually) are stored in the memory cells specific for mumps. If the HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 9 updated 3/17/2010 Communicable Diseases mumps virus invades your body again, your immune system is able to act quickly and specifically to destroy the virus BEFORE it infects the body again. YOU HAVE IMMUNITY TO THE MUMPS VIRUS, and will not get mumps again #2) ARTIFICIALLY ACQUIRED ACTIVE IMMUNITY = you develop immunity WITHOUT going through the disease Exposure to the actual antigen accompanying weakened or dead pathogen = VACCINATION. E.G., Oral (Sabin) polio vaccine contains living polio viruses, which are attenuated (too weak to cause disease). They have the protein antigens, so an immune response is developed, and memory cells formed (YOU DEVELOP IMMUNITY TO THE PATHOGEN) to combat successfully any subsequent exposure to the polio virus. BUT, the attenuated virus in the vaccine will not give you the actual polio disease (in almost all cases). other examples of vaccinations: diphtheria, pertussis (whopping cough), tetanus, polio, rubella, measles, mumps, cholera, typhoid fever, hepatitis B You should have a list of specific dates of your documented infection with these diseases, or immunization schedule. Check with your physician/nurse to see that you are up to date with the immunizations you need • tetanus immunizations (actually tetanus & diphtheria booster) must be updated every 10 years • was Hep B given to you? Probably not, the safe recombinant form is only a few years old! Now recommended for all children. Strongly recommended for health care workers, sexually active gay men, heterosexuals with multiple partners (transmitted by contact with infected body fluids). (Both Hep A & B cause liver damage) • Hep A: a new vaccine. Needed by persons traveling in Mexico, Latin America, Africa, eastern Europe, & other places where Hep A is common (due to fecal contamination of food & water). Also persons with liver disorders and those who have anal sex. • new developments in the science of immunization mean that old immunizations may be determined to be not as good as what is available currently, so get the updated vaccine PASSIVE IMMUNITY You do not develop antibodies specific to a certain antigen, you get them ADDED to your system to fight pathogens in your system #1) ARTIFICIALLY ACQUIRED PASSIVE IMMUNITY HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 10 updated 3/17/2010 Communicable Diseases The antibodies for a specific pathogen are injected into your system, they last a few days to a few weeks. You have not developed your own immune response. E.G., snake bite or tetanus antiserum (antitoxin) #2) NATURALLY ACQUIRED PASSIVE IMMUNITY The antibodies for a specific pathogen are passed from mother to baby. Baby has not developed it’s own immune response. E.G., Some of mother’s antibodies cross the placenta, last approximately 1 month after birth. Some of mother’s antibodies are carried in the mother’s first milk (the colostrum) HOW DOES YOUR IMMUNE SYSTEM DISTINGUISH BETWEEN SELF AND FOREIGN ANTIGENS? Why do you not develop antibodies against yourself? In the first month of life, when the immune system is developing, the immune system learns to recognize “self” antigens and does not produce B & T cells for them In some disorders, the immune system attacks self antigens as though they are foreign = autoimmune disorders e.g., rheumatoid arthritis, multiple sclerosis, insulin dependent (type I) diabetes mellitus, myasthenia gravis, systemic lupus erythematosus • the body produces antibodies or presents self tissue to T-lymphocytes, that try to destroy the body’s own tissue • cause unknown FINAL COMMENTS ON A FEW SPECIFIC PATHOGENS: : WHY DO WE KEEP GETTING COLDS & FLUS? IS OUR IMMUNE SYSTEM NOT WORKING? FLU (influenza): Kills 20,000 U.S. residents in a typical year. Caused by a virus that is always changing shape (mutations), so no permanent vaccine is possible now. New flu viruses are always developing, typically where humans live very close to animals, especially pigs, Southern China is a major breeding ground for new flu viruses. But a vaccine for the strain common that year can be developed and taken. Immunity useful for that strain only. People who would really suffer (the elderly, people with immune deficiency) from the flu should get the vaccine. COLD: caused by a virus, so antibiotics don’t help. Cold viruses keep changing surface antigens, so while we develop immunity to the cold virus that just made our week miserable, a new virus comes along the next week, so we get the new cold. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 11 updated 3/17/2010 Communicable Diseases EXERCISE & IMMUNITY With emphasis on Upper Respiratory Tract Infections (URTI) (e.g., cold & flu) The hypothesized relationship between URTI and exercise exertion is a “J” shaped relationship. inactive person has average rate of colds and flu moderate activity levels reduce your rate of infection extreme activity levels increase rates of infection above average. WHAT EVIDENCE IS THERE FOR THIS HYPOTHESIS? STRENUOUS EXERCISE LEVELS acute strenuous exercise: • raises blood epinephrine and cortisol levels • these hormonal alterations depress immune function, lasting hours after exercise (decreases in ALL the following: leukocyte & lymphocyte levels in blood, t-cell proliferation in response to pathogen, b-cell function, antibody levels, complement levels) following strenuous exertion you are more likely to experience a URTI e.g., following marathon run cumulative, repeated day-after-day strenuous physical exertion keeps the immune system depressed Hence: rise in infection rates with chronic high level training WHAT LEVEL OF EFFORT DEPRESSES IMMUNE FUNCTION? no set level, individual responses will vary PLUS, physiological (training) effect COMBINES with mental stressors acting on person (e.g., mental load of training, stress caused by competition) & people will have different mental stressors, and ways of reacting to them. MODERATE EXERCISE LEVELS, do they reduce risk of URTI? FEW TO NO GOOD STUDIES THAT EXAMINE THIS QUESTION & PROVIDE SOLID ANSWERS SHOULD YOU EXERCISE WHEN YOU HAVE AN URTI? MILD EXERCISE DURING SICKNESS: does not appear to be bad UNLESS: infection has spread beyond the URT to other body systems (e.g., fever, extreme tiredness, muscle aches, swollen lymph glands) THEN allow 2-4 weeks before intensive training to ensure virus has been eliminated HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 12 updated 3/17/2010 Communicable Diseases if the virus is systemic, the risk of severe form of viral infection is HIGH e.g., viral cardiomyopathy STRENUOUS EXERCISE DURING SICKNESS: VERY bad idea severe form of viral infection is HIGH e.g., viral cardiomyopathy e.g., military basic training: close quarters, lot of opportunity for viral infections to spread, forced strenuous exercise, some people drop dead during training 1.6 million recruits, 19 sudden deaths, 2/3 (?) viral cardiomyopathy PERSONAL WELLNESS ACTIONS FOR COMMUNICABLE DISEASES AT YOUR WORKSITE HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 13 updated 3/17/2010 Allergies TOPICS: ALLERGIES IMMEDIATE HYPERSENSITIVITY TREATMENT FOR IMMEDIATE ALLERGIC REACTION CAN YOU PREVENT ALLERGIES? DELAYED HYPERSENSITIVITY WELLNESS ACTIONS FOR ALLERGIES ALLERGY = hypersensitivity of the immune response to an antigen in this case the antigen is called an ALLERGEN 2 major forms of allergies: 1) IMMEDIATE HYPERSENSITIVITY Occurs in seconds or minutes after exposure Due to excessive B-lymphocyte response to antigen (allergen) e.g., Hay fever (allergic rhinitis), commonly grass pollen allergin Common allergens: dust mite poop, animal dander carrying animal saliva protein, plant pollens HAY FEVER: allergen is grass or tree pollen, ragweed, mold spores, review of normal (non allergy) immune response to antigen HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 14 updated 3/17/2010 Allergies NORMAL (NON ALL ERGY) IMMUNE RE SPONSE TO ANTIGE N 1) Foreign bacteria with antigen Plasma cell C C C C 2) Prod uct ion of antibodi es to the antigen 3) anti bod ies bind to foreign bod y at antigen sit e, identi fy it as forei gn CAPILL ARY 4) stimulation of compl ement proteins (C) to kil l foreign cel l, & stimulate mast cell to prod uce histamine C Mast cell C C HISTAMINE C 5) Histamine release causes increased capi llary permiabilit y, so more phagocytes can move into ti ssue, and allow l ocal swelli ng 6) Phagocyti c cell s engul f and di gest d ead bacteria Phagocyte STEPS 1-3) FIRST EXPOSURE TO ALLERGIN B-Lym phocyte Plasm a cell 1) Foreign particle with allergin (antigen) 3) IgE antibodies bind to MAST CELL 2) Production of IgE antibodies to the allergin Mast cell HISTAMINE STEP 4) ON SUBSEQUENT EXPOSURE TO ALLERGIN Mast cell MECHANISM of allergic response: allergen stimulates antibody production by B-lymphocyte antibodies to allergen attach to mast cell (because they are IgE, not IgG) not to antigen like in usual response to antigen Mast cell releases histam ine & other chem icals to produce allergic reaction HISTAMINE HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. In a person who Pg. 15 updated 3/17/2010 Allergies SUBSEQUENT EXPOSURE TO ALLERGEN stimulates mast cell to produce HISTAMINE (& other chemicals) HISTAMINE causes itching, sneezing, runny nose (clear thin fluid for allergy) develops the allergy, there is an excessive production of these antibodies, which then allows the following steps. Histamine causes vasodilation & increased leakage of fluids from blood vessels, if excessive blood pressure drops = anaphylactic shock therefore: some allergies CAN be fatal to some people (e.g, allergies to food, stinging insects, drugs) TREATMENT FOR IMMEDIATE ALLERGIC REACTION: treat with antihistamine drug, to reduce histamine release But antihistamines are often sedating (newer, stronger, non sedating antihistamines are available by prescription) FOOD ALLERGIES: only 1% of adults (3% of children) have true allergies to food food allergies have a significant genetic influence (i.e. inherited), breast feeding reduces susceptibility WHY DO WE DEVELOP ALLERGIES? {GENETICS + ENVIRONMENT} There is a genetic component to the development of many allergies A major hypothesis is that sensitization (exposure) to an allergen in early infancy (even in utero) is a major contributor to the subsequent development of the allergy. Therefore, avoiding exposure to allergens when an infant may help subsequent allergies not develop. 2) DELAYED HYPERSENSITIVITY Occurs within 1-3 days after exposure Due to excessive T-lymphocyte response to antigen (allergen) e.g., contact dermatitis (poison ivy, poison oak) but some individuals can give allergic response following exposure to a wide variety of common items (e.g., coins, plastics, cosmetics, leather, rubber, dyed clothing) treatment: corticosteroids HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 16 updated 3/17/2010 Allergies Mysteries of Allergies Studied Sunday, May 19, 2002 12:02 p.m. EDT By JUSTIN GLANVILLE Associated Press Writer You wake up in the morning congested and sniffling. Your eyes itch. The roof of your mouth burns. You sneeze. It's allergy season, and pollen is in the air. Pollen is the archenemy of an estimated 20 million allergy sufferers in the United States alone, according to the Columbia University College of Physicians and Surgeons. Why is your body so upset? How is it that your neighbor can mow the lawn without batting an eye, while the very sight of cut grass sends you running for the medicine cabinet? "There's no simple answer," says Dr. Andrew Saxon , chief of the UCLA School of Medicine's Division of Clinical Immunology and Allergy. On one level, allergies remain a medical mystery. There's nothing truly dangerous about pollen, dust, fur or most other common allergens, so it's uncertain why some people's bodies treat them as invaders. An allergen is anything that triggers an exaggerated, and usually unnecessary, immune response. But over the past several decades, Saxon and other researchers have made significant progress toward explaining why allergies exist and why they have become so common. Hard numbers are not available, but Saxon estimates that about 35 percent of the population of the Western hemisphere suffer some form of allergy - up from about 25 percent in the 1970s. In the early 19th century, hay fever was so rare that it took one early researcher, Jonathan Bostock, nine years to find enough subjects to publish a study. At that rate of increase, it seems clear that factors other than heredity - long identified as a crucial determinant of whether one is allergic - are involved. Pollution may be one important culprit. According to Saxon's research, breathing irritants such as diesel exhaust sets the immune system on edge, increasing the likelihood that it will overreact to potential allergens. "What diesel and other irritants do is kick the immune system in the side, pushing it toward an attack," Saxon says. His experiments, which began about 12 years ago, involved two groups of subjects. One group was exposed only to an allergen. The other group was exposed to the allergen and a whiff of diesel exhaust. Those in the first group had only a "protective" immune response: Their bodies tended not to identify the allergen as a potential threat. Those who also breathed exhaust, on the other hand, were more likely to attack the allergen. Their bodies produced more antibodies and they responded to a smaller amount of the allergen in the future. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 17 updated 3/17/2010 Allergies Air quality has improved markedly in the United States since 1970. However, Saxon has found that inhaling even small amounts of industrial pollution increases the likelihood of an immune reaction. Civilization may also be heightening people's sensitivity to so-called perennial allergens - indoor particles such as dust, roaches, mold and dander (bits of animal skin). They have become a widespread problem only in the last century or so. "We think it may be related to the way homes are being built nowadays," says Dr. Jacqueline Pongracic, acting manager of the division of allergies at Children's Memorial Hospital in Chicago and a professor at Northwestern University. "Homes are tightly sealed, with better systems of heating and cooling and less outside ventilation. That increases the number of indoor allergens," she says. "Also, modern society tends to have cats and dogs as indoor pets, whereas in older times, animals were more outdoors, especially in rural areas." Paradoxically, allergies may also be on the rise because health care for children is improving. How's that? There are two main patterns of immune response - allergic and infectious. In children who face many viral and bacterial infections, their immune systems may "learn" to operate more in infectious mode than in allergic mode. That can be beneficial because the infectious response is more of a destroyer than the allergic response. Faced with an infection, the body identifies viruses and bacteria, tries to kill them outright, and girds the body to eliminate invaders when they re-enter the body. That's why people usually don't suffer the same infection, such as chicken pox, twice. The allergic response is more wishy-washy. The body identifies allergens as threats, but doesn't have any means of protecting itself in the future. So the same allergen usually plagues people for most of their lifetime. All of which begs a question: Why does the allergic response exist in the first place? That remains a mystery. But it might have to do with worms. "The hypothesis is that a long time ago, before civilization, people evolved this hypersensitive response as a way of dealing with parasites," Pongracic says. "But today we don't have much exposure to parasites, so the response shifted to allergens." People sometimes report that they outgrow their allergies in adulthood, but that is usually an illusion, doctors say. Once the body is sensitized to an allergen, it's programmed for life. "The reason a lot of people perceive that they are outgrowing allergies is that they're changing their lifestyles and habits," says Dr. Stanley Goldstein, an allergist in HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 18 updated 3/17/2010 Allergies Rockville Centre, N.Y. and director of Allergy and Asthma Care of Long Island. "Whereas they used to be out in the fields playing sports in high school, once they get to college they're inside studying. Or they move out of their parents' house, where they had once been allergic to the family pet." But symptoms often taper off in old age, due to the general weakening of the immune system - the same process that makes seniors especially vulnerable to disease. The body isn't strong enough to react to allergens with the same gusto it did in childhood and adulthood. "So you get other diseases, but your allergies get better," Goldstein says wryly. Still, according to Saxon, allergies are a small price to pay for improved pediatric health and better home insulation. "Are we that bad off with allergies? No. I mean, in the middle ages, people lived to 32." --On the Net: American Academy of Allergy, Asthma and Immunology: http://www.aaaai.org/ Asthma and Allergy Foundation of America: http://www.aafa.org/ Columbia University School of Medicine: http://www.medsch.ucla.edu/ Copyright © 2002 Associated Press. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed. PERSONAL WELLNESS ACTIONS FOR ALLERGIES & barriers to those actions & hurdles to those barriers Identify the role of the health professional HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 19 updated 3/17/2010 Allergies IMMUNE SYSTEM WITH POTENTIAL TO EXCESSIVELY REACT TO AN ANTIGEN WHY? GENETICS (INHERITED) RANDOM CHANCE (BIOLOGICAL VARAIBILITY) YES NEED: 1ST EXPOSURE TO PRIME MAST CELLS 2ND EXPOSURE TO PRODUCE ALLERGIC RESPONSE FIRST EXPOSURE: FOR SOME ALLERGIES IN SOME PEOPLE THE FIRST EXPOSURE MUST OCCUR WHEN THE IMMUNE SYSTEM IS DEVELOPING (0-6 MONTHS) E. G. , ? POTENTIAL HERE TO PREVENT FIRST EXPOSURE AT CRITICAL TIME TO PREVENT MAST CELL PRIMING IN SOME PEOPLE FOR SOME ALLERGIES, & SOME PEOPLE THE FIRST EXPOSURE CAN OCCUR AT ANY AGE. E. G. , ? HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 20 updated 3/17/2010 Asthma Topics: What is asthma? Exercise induced asthma What is asthma? Asthma = bronchiolar constriction, which increases airway resistance to air flow, and makes breathing (very) difficult. Episodes can vary from mild (& lasting a few minutes) to severe, closing of the airway, leading to unconsciousness & death. typically in children (males mostly) under 10 yrs, but can continue into adulthood results is a few thousand deaths/yr. (4900 in 1992), but rate is increasing CAUSED BY allergic response PLUS influence by psychological factors is common Allergic response: allergen causes allergic response (e.g., dust mites, pollen, food, mold, tobacco smoke, mold) i.e., histamine release and LEUKOTRIENES, the latter causing contraction of smooth muscles in the bronchioles Leukotrienes: chemical released from mast cells not discussed previously Psychological factors: i.e., emotional states make the attack due to an allergic response worst • some asthmatic children improve when removed from stressful family situations • some adult asthmatics experience more attacks when under stress ASTHMA HAS 2 COMPONENTS: 1) Underlying inflammation of airway, not obvious, long term 2) Asthmatic episode, obvious, short lived The ACUTE attack tends to be treated, but the chronic inflammation must also be treated or the attacks will become more frequent and more severe. Treat inflammation with steroids Treat attack with bronchiole dilators Why are rates of asthma increasing? PERSONAL WELLNESS ACTIONS FOR ASTHMA EXERCISE INDUCED ASTHMA (EIA) 10% of people (= 25 million Americans) are affected to some degree by EIA EIA is a mild form of bronchial constriction and difficulty breathing usually begins during exercise, or within 20 min following exercise, usually abates within 30 min EIA is more likely with high intensity exercise, & in cold dry air HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 21 updated 3/17/2010 Asthma WHY DOES EIA OCCUR? • rapid breathing of cold dry air may trigger release of chemicals causing constriction of the bronchioles • air pollutant or allergen may stimulate attack PERSONAL WELLNESS ACTIONS FOR EIA: HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 22 updated 3/17/2010 Arthritis Topics: Arthritis Rheumatoid arthritis OsteoarthritisWellness actions ARTHRITIS strikes 1 in 3 Americans nearly everyone > 40 years shows some signs of osteoarthritis costs the economy 10 billion per year including > 1 billion spent on fraudulent cures (seniors citizens are easy prey) Rheumatoid arthritis (RA) = autoimmune disorder antibodies attack synovial membrane tissues that produce fluids to lubricate the joints, later damage to bone ends & articular cartilage causing: inflammation, stiffness, pain, loss of movement, joint deformity occurs in children, as well as adults (most common onset at ages 20-45), 3X more women than men. 1% of all people like most auto immune disorders, it may flair up, then go into remission, it may onset quickly, or gradually. CAUSES: genetic predisposition?, viral infection in joint? TREATMENT: Pain relief (analgesics, massage, heat), immunosupression drugs, joint replacement, bone fusion Osteoarthritis (OA) = degeneration of the cartilage structures within joint = gradual loss of smooth soft articular cartilage at the joint surface, frequent compensatory overgrowth of bone. Results in: painful range of motion, morning stiffness < 30 min, crepitance HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 23 updated 3/17/2010 Arthritis 85% of people 70-79 years old, especially in weight bearing joints, but also the hand FACTORS WHICH MAY INFLUENCE DEVELOPMENT: age (normal wear & tear?) genetic predisposition (especially of hand OA) direct injury to the joint tissue chronic low level trauma to joint: occupational stress e.g., increased & earlier hip, knee or hand osteoarthritis in: ♀ cleaners, ♀ in clothing industry, ♂ masons, other construction workers, agriculture workers (Rossignol et al., Primary osteoarthritis of hip, knee, and hand in relation to occupational exposure. Occup Environ Med. 2005 Nov;62(11):772-7.) being overweight: A 11 lb loss of weight in heavy people may decrease risk of knee OA by 50% (Collins J., Exercise for the mind: are you joint smart? Semin Roentgenol. 2005 Jul;40(3):201-2) ligament instability which alters the biomechanics of the joint may contribute to premature OA E.G, A SINGLE KNEE INJURY INCREASES RISK OF KNEE OA 5X (Collins J., Exercise for the mind: are you joint smart? Semin Roentgenol. 2005 Jul;40(3):201-2) TREATMENT: generally managed with analgesics, extreme cases require joint replacement or fusion Heat & massage may help symptoms IS PHYSICAL ACTIVITY GOOD FOR OA? HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 24 updated 3/17/2010 Arthritis When pain is controlled, stretching exercises are very important for maintaining range of motion of the joint, maintaining strength of the muscles surrounding the joint is important because the person will tend not to use them. PLUS, person will obtain all the general physiological & psychological benefits of aerobic exercise DOES PHYSICAL ACTIVITY PLAY A ROLE IN PROMOTING THE DEVELOPMENT OF OA? This is suggested by a number of anecdotal evidence & studies that suggested that activity may lead to joint problems later in life. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 25 updated 3/17/2010 Arthritis Studies examining this question must account for the influence of injury during activity and subsequent joint misalignment. BEST ADVICE: Reasonable activity, within limits of comfort, and without previous joint problems, need not lead to joint injury (i.e., OA), and premature wearing out of joints, even over many years. WELLNESS ACTIONS FOR ARTHRITIS PREVENTION ACTIONS FOR THOSE WITH ARTHRITIS HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 26 updated 3/17/2010 Cardiovascular Disease Topics: Assessment of your cardiac risk Normal function of the CV system Cardiovascular (CV) disorders Hardening of the arteries (arteriosclerosis) High blood pressure (hypertension) Heart attack (myocardial infarction) Chest pain (angina pectoris) Stroke (cerebrovascular accident) Wellness actions related to CV disease ASSESSMENT OF YOUR CARDIAC RISK Do the test on the overhead to assess your risk level for cardiovascular disease, and to introduce you to some of the issues we’ll be discussing. question #6: assume total cholesterol is 200 mg, or estimate score based on amount of animal & solid fats in diet SCORE 1 Age 2 Heredity 3 Weight 4 Tobacco smoking 5 Exercise 6 Blood Cholesterol level or % fat in diet 7 Blood pressure 8 Sex, age, shape TOTAL SCORE: 6 - 11 = very low risk 12 - 17 = low risk 18 - 25 = average risk 26 - 32 = high risk 33 - 42 = dangerous risk 43 - 60 = extremely dangerous risk Note: more detailed assessment of CV risk may be obtained using the scoring scales provided by the Framingham heart study. Available: http://www.nhlbi.nih.gov/about/framingham/riskabs.htm CARDIOVASCULAR (CV) DISORDERS HARDENING OF THE ARTERIES (ARTERIOSCLEROSIS) Several conditions (genetic & environmental risk factors) can lead to thickening & hardening of the normally elastic arterial vessel walls as fat, mineral & cellular material accumulates in the vessel wall. The inner diameter of the vessel is reduced. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 27 updated 3/17/2010 Cardiovascular Disease The hardened walls are less compliant to blood flow, and so contributes to hypertension The narrowed lumen is more likely to be occluded by a clot, and so contributes to a heart attack or stroke. The process is a GRADUAL one that progresses over a life time RISK FACTORS: Diet high in fat, especially saturated fat (animal fats and tropical oils (e.g., palm)), high blood pressure, smoking, lack of aerobic exercise, genetic influence HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 28 updated 3/17/2010 Cardiovascular Disease New view of heart disease in women Harvard Health Publications e-Newsletter. VOLUME 4 ISSUE 5 February 15, 2007 A revolution in thinking about coronary blood vessels could change the way women’s heart problems are diagnosed and treated. Discoveries from the WISE study suggest that many women have a form of heart disease called coronary microvascular dysfunction that isn’t detected by standard diagnostic procedures and thus goes unrecognized and untreated. Causes of ischemic heart disease Ischemic heart disease (IHD) is reduced blood flow to the heart. According to the classic model of the disease, trouble begins when plaque builds up inside a coronary artery, which eventually thickens and hardens, obstructing blood flow. The newer view of IHD suggests that the tiny vessels feeding the heart can also become constricted and reduce blood flow. Microvessel disease could also help explain why so few women have the classic crushing chest pain that signals coronary artery disease. Instead, they feel diffuse discomfort, exhaustion, or shortness of breath under stress or even during daily routines — symptoms that are nonspecific and less dramatic than those that herald a blockage caused by a blood clot. As vessels lose their resilience, blood flow is reduced, and the heart muscle, deprived of oxygen, gradually dies, resulting in congestive heart failure. HIGH BLOOD PRESSURE (HYPERTENSION) Blood pressure = pressure exerted on the walls of the arterial vessels by the blood peak pressure due left ventricle contraction = systolic pressure low pressure between contractions = diastolic pressure “typical” = 120/80 mm Hg how many people here have had a BP taken in the last year by a professional (not in a student lab)? HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 29 updated 3/17/2010 Cardiovascular Disease Hardened, narrowed arteries (due to atherosclerosis) offer more resistance to blood flow, which raises blood pressure (since the wall of the vessels don’t give as the blood flows through) this makes the heart need to work harder to push the blood The high blood pressure then helps contribute to the development of further atherosclerosis Hypertension CAUSES OF HYPERTENSION: 90% of cases of hypertension are “essential” = no known cause. 10% of cases related to other disorders (e.g., kidney, diabetes) RISK FACTORS: Heredity (more likely if it is in family history), race (black more likely than whites), high sodium in diet (only 10% of population is sodium sensitive, and so have BP that responds to sodium they consume, but for others there is no reason to consume typical high levels of sodium in diet), obesity, lack of aerobic exercise, alcohol HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 30 updated 3/17/2010 Cardiovascular Disease Date: Feb. 11, 2004 Report Sets Dietary Intake Levels for Water, Salt, and Potassium To Maintain Health and Reduce Chronic Disease Risk WASHINGTON -- The vast majority of healthy people adequately meet their daily hydration needs by letting thirst be their guide, says the newest report on nutrient recommendations from the Institute of Medicine of the National Academies. The report set general recommendations for water intake based on detailed national data, which showed that women who appear to be adequately hydrated consume an average of approximately 2.7 liters (91 ounces) of total water -- from all beverages and foods -- each day, and men average approximately 3.7 liters (125 ounces) daily. These values represent adequate intake levels, the panel said; those who are very physically active or who live in hot climates may need to consume more water. About 80 percent of people's total water comes from drinking water and beverages -- including caffeinated beverages -- and the other 20 percent is derived from food. "We don't offer any rule of thumb based on how many glasses of water people should drink each day because our hydration needs can be met through a variety of sources in addition to drinking water," said Lawrence Appel, chair of the panel that wrote the report and professor of medicine, epidemiology, and international health, Johns Hopkins University, Baltimore. "While drinking water is a frequent choice for hydration, people also get water from juice, milk, coffee, tea, soda, fruits, vegetables, and other foods and beverages as well. Moreover, we concluded that on a daily basis, people get adequate amounts of water from normal drinking behavior -- consumption of beverages at meals and in other social situations -- and by letting their thirst guide them." Regarding salt, healthy 19- to 50-year-old adults should consume 1.5 grams of sodium and 2.3 grams of chloride each day -- or 3.8 grams of salt -- to replace the amount lost daily on average through perspiration and to achieve a diet that provides sufficient amounts of other essential nutrients. Elevated blood pressure, which may lead to stroke, coronary heart disease, and kidney disease, is associated with sodium intake. On average, blood pressure rises progressively as salt intake increases. A tolerable upper intake level (UL) -- a maximum amount that people should not exceed -- is set at 5.8 grams of salt (2.3 grams of sodium) per day. Older individuals, African Americans, and people with chronic diseases including hypertension, diabetes, and kidney disease are especially sensitive to the blood pressure-raising effects of salt and should consume less than the UL. More than 95 percent of American men and 90 percent of Canadian men ages 31 to 50, and 75 percent of American women and 50 percent of Canadian women in this age range regularly consume salt in excess of the UL. To lower blood pressure, blunt the effects of salt, and reduce the risk of kidney stones and bone loss, adults should consume 4.7 grams of potassium per day. However, most American women 31 to 50 years old consume no more than half of the recommended amount of potassium, and men's intake is only moderately higher. Among foods with the highest amounts of potassium per calorie are spinach, cantaloupes, almonds, brussels sprouts, mushrooms, bananas, oranges, grapefruits, and potatoes. Canadians typically eat more potassium than their American counterparts. African Americans in the United States generally get less potassium than non-Hispanic whites, and because they have a higher prevalence of elevated blood pressure, increased potassium intake may have particularly significant benefits for them. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 31 updated 3/17/2010 Cardiovascular Disease The typical Western diet is high in salt and low in potassium -- the opposite of what evidence shows is optimal for good health and reducing the risks of chronic disease, the report says. "Research is needed to find ways to help people select better food choices to reduce their salt intake and boost their potassium consumption," Appel said. In addition, because Americans and Canadians get the majority of their salt -- 77 percent, according to one study -- from prepared and processed foods, research should be done to help food processors develop alternative technologies that can reduce the amount of salt added during processing without impairing taste, shelf-life, or product qualities at an affordable cost. [ This news release and report are available at http://national-academies.org ] Sodium101.ca http://www.sodium101.ca/ Test of 6 foods Top Sodium Sources HEART ATTACK (MYOCARDIAL INFARCTION) Blood, & oxygen, supply to a portion of the myocardium is stopped due to a clot producing an occlusion in the coronary artery Often due to narrowing of the artery with arteriosclerosis The myocardium downstream of the blockage is ISCHEMIC, myocardium dies without oxygen if a major coronary artery is blocked, then large amounts of myocardium dies, and the effect is very serious, or fatal if a minor coronary artery is blocked, then lesser amounts of myocardium dies, and the effect is serious, but may not be fatal. The myocardium may have the opportunity to utilize it’s COLLATERAL vessels to supply blood to the ischemic tissue Major symptoms: severe chest pain, which may radiate to adjacent areas, dizziness, nausea, pale, cold, rapid, shallow pulse Immediately: obtain emergency care, start CPR if heart stops RISK FACTORS: see risk factors for arteriosclerosis CHEST PAIN (ANGINA PECTORIS) HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 32 updated 3/17/2010 Cardiovascular Disease Chest pain occurs when the blood flow (& oxygen supply) to the myocardium is insufficient (but not severe enough to cause a MI) caused by restricted blood flow due to coronary atherosclerosis, combined with period of stress, emotional upset or physical exertion Treatment: drugs to dilate coronary arteries to increase blood flow RISK FACTORS: see risk factors for arteriosclerosis STROKE (CEREBROVASCULAR ACCIDENT) Travelling clot lodges at atherosclerotic development, causes occlusion of an artery supplying nervous tissue in the brain, elimination of oxygen supply causes cells to die. Loss of function will depend on the region of the brain which was damaged, and the extent of the damage. Typically, stoke survivors may have loss of motor function (paralysis), speech, memory, cognitive abilities. Minor occlusions can lead to small strokes TRANSIENT ISCHEMIC ATTACKS (TIA) seen as confusion, minor sensory or motor loss, temporary dizziness Important for the individual, family member, or health care worker to recognize these symptoms and have them seek medical help, because this is an early warning sign of the disease process that will lead to more serious strokes. RISK FACTORS: being black, high blood pressure, existing heart disease (reduces blood flow to brain & increase probability of clots), & diabetes THINK ABOUT: Sate the chances that you will suffer from CV disease PERSONAL WELLNESS ACTIONS FOR CV DISEASE [ANSWER AS A REVIEW OF PREVIOUS MATERIAL BEFORE READING ON] HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 33 updated 3/17/2010 Cardiovascular Disease HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 34 updated 3/17/2010 Cardiovascular Disease RISK FACTORS WE CAN’T INFLUENCE: Heredity, increasing age, being male (at same age prior to female menopause, male has higher risk) genetics environment + disease Smoking, don’t do it. #1 lifestyle factor to contribute to CV disease smoking damages lining of arteries, to contribute to atherosclerosis, it raises total cholesterol & lowers HDL (HDL is the “good” cholesterol, which decreases risk of CV disease), reduces oxygen content of the blood, increases heart rate, may constrict coronary arteries. quitting is not easy due to addiction Hypertension, avoid it, treat it. avoiding hypertension: treat hypertension: must know you have it, so have BP taken regularly, reduce salt intake, maintain optimal body weight / regular exercise Reduce saturated fat intake where do saturated fats come from? saturated fats have the effect of increasing the LDL (low density lipoprotein) cholesterol component in the blood. Reduce trans-fatty acid intake what is an polyunsaturated fat? to make fats more solid to make margarine, or to put them into foods, hydrogen atoms will be added to remove double bonds, fewer double bonds are more solids at room temp look at a food label & look for the word “hydrogenated” Problem is that the process produces TRANS isoforms of fatty acids (cis- isoforms exist in nature) Trans isoforms of fatty acids increases the LDL (low density lipoprotein) cholesterol component in the blood. LDL is the “bad” cholesterol, which increases risk of CV disease. Use nonhydrogenated, or softest (least hydrogenated), margarine possible HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 35 updated 3/17/2010 Cardiovascular Disease AEROBIC EXERCISE Lack of aerobic exercise is an independent risk factor for CV disease, independent from it’s effects on smoking, hypertension, diabetes etc. Typical college students (and North Americans in general) are not active in regular aerobic exercise. THINK ABOUT: list 1 action you have done in the last month to improve your CV health. THINK ABOUT: list 3 actions you can do in the next month to improve your CV health. This must include one dietary action. How easy do you think it will be to make these changes? Why do you think it will be easy or difficult? The following material to the end of this unit will be discussed if there is time in the class. If it is not discussed, it will not be on the exam. DIETARY FAT: recommended: 20-35% of calories from fat HOW CAN YOU TELL? Looking at one food: see food label see: # calories, # fat calories e.g., 120/260 * 100 = 46% but this is one food only, the AVERAGE intake should be <=35% calories from fat. How to figure this average? and, how to do this for all foods your eat, how to do this for nonlabeled food eaten at restaurant? USE A COMMON SENSE, NO CALCULATION APPROACH TO KEEPING YOUR FAT INTAKE LOW (from the Berkeley Wellness Letter): HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 36 updated 3/17/2010 Cardiovascular Disease HOW OFTEN DO YOU EAT THE FOLLOWING FOODS: IF: NEVER, SELDOM, INFREQUENTLY & IN SMALL AMOUNTS % calories from fat likely < 35% hot dogs, sausages, luncheon meats, bacon, fried foods, hamburgers, fatty cuts of meats (regular ground beef, corned beef, spare ribs, prime rib), cheese, donuts, cookies, cakes, pies, pastries, oily or creamy salad dressings, potato chips, butter, margarine, whole milk, premium ice cream, nuts, peanut butter Common sense, no calculation approach #2 to keeping your fat intake low: Learn to read food labels and be aware of content of foods you eat, keep a mental running average If food > 35% calories from fat - limit intake (pulls average up) If food < 35% calories from fat - eat freely (pulls average down) OTHER General Principles for changing eating habits to decrease % fat in diet: Think of meats, poultry & fish as side dishes (not the center of the meal) to be consumed only once per day Increase consumption of grains, fruits & vegetables Switch to nonfat or low fat dairy products What are some of the road block to this? How to overcome them? Does vegetarian food mean healthy? OTHER INFLUENCES ON CV HEALTH BEING STUDIED • 2-3 servings of fish per week, especially cold water fish (e.g., salmon, sardines (not oil packed), lake trout, albacore tuna, whitefish) lower fat & lower saturated fats than meat, omega-3 oils may be of some use in lowering risk of CV disease, (but not as capsules) • ANTIOXIDANTS: Vit E, C, beta carotene, selenium, polyphenols (& others) IN: fruits, grains, vegetables, tea, coffee, wine (& other sources) act as antioxidants, reducing free radicals in the body tissues Free Radicals: cause LDL cholesterol to oxidize which promotes plaque buildup in vessel walls (& free radicals may contribute to aging, cancer and other diseases) • Alcohol: For men, up to 2 drinks per day is associated with reduced CV disease, by raising HDL levels. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 37 updated 3/17/2010 Cardiovascular Disease For women & men, Alcohol increases the risk of cancers of the mouth, pharynx (throat), larynx (voice box), esophagus, liver, and breast, and probably of the colon and rectum. People who drink alcohol should limit their intake to no more than 2 drinks per day for men and 1 drink per day for women. Regular consumption of even a few drinks per week is associated with an increased risk of breast cancer in women, especially in women who do not get enough folate. Women at high risk of breast cancer may want to consider not drinking any alcohol. . HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 38 updated 3/17/2010 Overweight & Obese Why is obesity and overweigh such a prominent health issue today? 1. The incidence of people being obese or overweight is increasing rapidly. 2. There are significant health consequences of being obese or overweight. What is “Overweight” & “Obesity”? How to evaluate if a person is “Overweight” or “Obese” Your body is composed of: 1. Fat-free mass o Bone, water, muscle, connective tissue, organs, teeth 2. Fat mass o Essential Fat Fats in: nerves, brain, heart, glands etc. o Non essential (storage) fat Fats is: fat cells below skin and around organs. How do you determine is someone is “Overweight” or “Obese”? Body Mass Index (BMI) BMI = body weight (kilograms) / height2 (meters) BMI e.g., 5 ft 4 inch & 145 lbs = 64 inches, 145 lbs = 1.62 meters, 66 kg = 66 / 1.62562 BMI = 25 The use of BMI to evaluate if a person is “Overweight” or “Obese” is widely advocated by almost all major health organizations, e.g., CDC What is the BMI definition of “Overweight” & “Obese”? BMI Cut points for Adults (> 18 years) Source: http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult.htm Interpret BMI values for adults with one fixed number, regardless of age or sex, using the following guidelines: HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 39 updated 3/17/2010 Overweight & Obese Underweight OK Overweight Obese BMI less than 18.5 18.5 – 24.9 BMI of 25.0 to 29.9 BMI of 30.0 or more Source: http://win.niddk.nih.gov/publications/understanding.htm#genetic Positive aspects of using BMI to evaluate people? Negative aspects of using BMI to evaluate people? Height 6'3" Weight 220 lbs BMI 27.5 Elderly people with low muscle mass and high body fat may be classified as OK How do you determine is someone is “Overweight” or “Obese”? Body Composition Analysis Body Composition Analysis to determine % body fat Methods? Underwater weighing Skin folds HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 40 updated 3/17/2010 Overweight & Obese Bioelectric impedance How is % body fat interpreted? Percent Body Fat Standards* Men ≤5% 6-14% 15% 16-24% ≥25% At Riska Below Average Average Above Average At Riskb Women ≤8% 9-22% 23% 24-31% ≥32% At risk for diseases and disorders associated with malnutrition a At risk for diseases associated with obesity b *From Heyward, V.h. Advanced Fitness Assessment and Exercise Prescription. Champaign, IL: Human Kinetics. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 41 updated 3/17/2010 Overweight & Obese Source : Measurement for Evaluation in Physical Education and Exercise Science. Baumgartner, Jackson, Mahar, Rowe. 7th ed, McGraw Hill, 2003. What is the incidence of American Adults that are overweight? a) 15% b) 35% c) 65% HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 42 updated 3/17/2010 Overweight & Obese Source: http://www.cdc.gov/nchs/products/pubs/pubd/hestats/obese/obse99.htm Percent of adults ages 20–74* who were at a healthy weight, overweight, or obese† *Data are age-adjusted to the 2000 U.S. standard population. †Healthy weight, body mass index (BMI) = 18.5–24; overweight, BMI = 25–29; obese, BMI = >30. Sources: National Health and Nutrition Examination Survey (National Center for Health Statistics); Cancer Trends Progress Report — 2005 Update (National Cancer Institute 2005). BMI > 30 2003 source: http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 43 updated 3/17/2010 Overweight & Obese Overweight among Children: Source: http://www.cdc.gov/nchs/products/pubs/pubd/hestats/overwght99.htm Consequences for children: Type 2 diabetes, previously considered an adult disease, has increased dramatically in children and adolescents. Overweight and obesity are closely linked to type 2 diabetes. Overweight adolescents have a 70% chance of becoming overweight or obese adults. This increases to 80% if one or more parent is overweight or obese. The most immediate consequence of overweight as perceived by the children themselves is social discrimination. This is associated with poor self-esteem and depression. Source: http://www.surgeongeneral.gov/topics/obesity/calltoaction/fact_adolescents.htm Health risks of people being obese or overweight? Overweight and obese individuals (BMI of 25 and above) are at increased risk for physical ailments such as: Reduced life expectancy by 10-20 years. o o An estimated 300,000 deaths per year may be attributable to obesity. Even moderate weight excess (10 to 20 pounds for a person of average height) increases the risk of death, particularly among adults aged 30 to 64 years High blood pressure, hypertension High blood cholesterol Type 2 (non-insulin dependent) diabetes Insulin resistance, glucose intolerance Hyperinsulinemia Coronary heart disease (even mildly to moderately overweight women have 80% increased risk of CHD) Angina pectoris Congestive heart failure Stroke Gallstones Gout HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 44 updated 3/17/2010 Overweight & Obese Osteoarthritis Obstructive sleep apnea and respiratory problems Some types of cancer (such as endometrial, breast, prostate, and colon) Complications of pregnancy such as; gestational diabetes, gestational hypertension and preeclampsia (A condition of hypertension occurring in pregnancy, typically accompanied by edema and proteinuria.) as well as complications in operative delivery (i.e., c-sections). Poor female reproductive health (such as menstrual irregularities, infertility, irregular ovulation) Bladder control problems (such as stress incontinence) Psychological disorders (such as depression, eating disorders, distorted body image, and low self-esteem). Overweight and obesity were found to be significantly associated with: Diabetes (discussed in another unit) High blood pressure (discussed in another unit) High cholesterol (discussed in another unit) Asthma (discussed in another unit) Arthritis (discussed in another unit) For every 2-pound increase in weight, the risk of developing arthritis is increased by 9 to 13%. Poor health status Sources: http://www.cdc.gov/nccdphp/dnpa/obesity/consequences.htm http://www.surgeongeneral.gov/topics/obesity/calltoaction/fact_consequences.htm $ Cost of Overweight and obesity $78.5 billion (1998) ($92.6 billion in 2002 dollars) Source: http://www.cdc.gov/nccdphp/dnpa/obesity/economic_consequences.htm The Duchess of Windsor once said, 'You can never be too rich or too thin.' Possible negative consequences of excessive leanness. Reproductive disorders Circulatory disorders Immune system disorders Muscle wasting Fatigue Eating disorders HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 45 updated 3/17/2010 Overweight & Obese Causes of overweight & obesity Overweight and obesity are a result of energy imbalance over a long period of time. 1. 2. 3. 4. Causes of Energy in > Energy out, resulting in overweight & obesity Genetic factors Physiological factors Lifestyle factors (=Behavior) Psychosocial factors Causes of overweight & obesity 1. Genetic factors Heredity plays a role in determining how susceptible people are to overweight and obesity (5% - 40% contribution???). “.Heredity plays a large role in determining how susceptible people are to becoming overweight or obese” http://www.cdc.gov/nccdphp/dnpa/obesity/faq.htm#factors Genes also influence how the body burns calories for energy or stores fat. e.g., the weight of an adoptee is more like that of the biological parent than the adoptive parents "Despite obesity having strong genetic determinants, the genetic composition of the population does not change rapidly. Therefore, the large increase in . . . [obesity] must reflect major changes in non-genetic factors." http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm Causes of overweight & obesity 2. Physiological factors o Metabolism o Hormones o Fat Cells METABOLISM: Resting Metabolic Rate (RMR) = 55-75% of daily energy burned HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 46 updated 3/17/2010 Overweight & Obese RMR is higher for: Some people due to genetics (you can’t control this) Men (higher due to increased muscle mass) (you can’t control this) Heavier people (more body tissue) (heavy people want to reduce this) People who exercise ????? HORMONES: Hormones play a role in fat accumulation & distribution; this is obvious at puberty & menopause when sex hormone levels change. LEPTIN – a hormone released by fat cells is thought to be a feedback system, communicating from the fat cells to the brain, telling how large the fat stores are, allowing brain to regulate appetite and metabolic rate. FAT CELLS: There is variation n the # of fat cells people have. It has NOT been demonstrated that having more fat cells is a factor that drives people to eat more. Causes of overweight & obesity 3. Lifestyle factors (=Behavior) A. Eating B. Physical activity C. Environment A.) EATING influences: In America, a changing environment has broadened food options and eating habits. Grocery stores stock their shelves with a greater selection of products. Pre-packaged foods, fast food restaurants, and soft drinks are also more accessible. While such foods are fast and convenient, they also tend to be high in fat, sugar, and calories. Choosing many foods from these areas may contribute to an excessive calorie intake. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 47 updated 3/17/2010 Overweight & Obese Portion size has also increased. People may be eating more during a meal or snack because of larger portion sizes. Examples of common food options and eating habits Bacon Double Cheeseburger Vanilla Shake (Large) French Fries (King) Dutch Apple Pie Calories 570 800 600 300 TOTAL 2270 If you go to your neighborhood McDonald's restaurant and order the Big Xtra meal, you will get a sandwich, a large order of french fries and a large Coke. This meal contains: 710 calories in the sandwich 540 calories in the french fries 310 calories in the drink 630 calories in a M&M McFlurry for dessert TOTAL = 2190 calories The calories required in one day are: 1,600 calories is about right for many sedentary women and some older adults. 2,200 calories is about right for most children, teenage girls, active women, and many sedentary men. Women who are pregnant or breastfeeding may need somewhat more. 2,800 calories is about right for teenage boys, many active men, and some very active women. Source: http://www.pueblo.gsa.gov/cic_text/food/food-pyramid/main.htm B. PHYSICAL ACTIVITY influences: Physical activity is any bodily movement produced by skeletal muscles that results in an expenditure of energy with a range of activities such as HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 48 updated 3/17/2010 Overweight & Obese Occupational work, Carpentry, construction work, waiting tables, farming Household chores, Washing floors or windows, gardening or yard work Leisure time activities, Walking, skating, biking, swimming, playing Frisbee, dancing Structured sports or exercise Softball, tennis, football, aerobics Modernization, the growth of industry and technology, was introduced over 50 years ago in the Western world. and has led to a decrease in overall physical activity In 2000 more than 26% of adults reported no leisure time physical activity. A significant world-wide decrease is observed in Physical Activity practices among young people, especially in poor urban areas. A low level of physical activity is particularly common in teenage girls. It is estimated that in a great number of countries, less than one third of young people are sufficiently active to benefit their present and future health and well-being. Very importantly, physical education and other school-based physical activities are decreasing. http://www.obesity.org/subs/fastfacts/obesity_global_epidemic.shtml http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm http://www.who.int/moveforhealth/about/2004/en/ C. ENVIRONMENT influences: Home, work, school, or community can provide barriers to, or opportunities for, an active lifestyle. Home Schools Work Community Ways to improve environmental factors contributing to weight gain Reduce time spent watching television and in other sedentary behaviors Build physical activity into regular routines Ensure that the school breakfast and lunch programs meet nutrition standards Provide food options that are low in fat, calories, and added sugars Provide all children, from prekindergarten through grade 12, with quality daily physical education Create more opportunities for physical activity at work sites Promote healthier choices including at least 5 servings of fruits and vegetables a day, and reasonable portion sizes Encourage the food industry to provide reasonable food and beverage portion sizes Encourage food outlets to increase the availability of lowcalorie, nutritious food items Create opportunities for physical activity in communities HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 49 updated 3/17/2010 Overweight & Obese Causes of overweight & obesity 4. Psychosocial factors Food may be used in response to, or to regulate emotions, not being controlled by calorie needs. Obesity is more prevalent at lower income levels. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 50 updated 3/17/2010 Overweight & Obese SUMMARY: Causes of Energy in > Energy out, resulting in overweight & obesity Genetic factors Physiological factors Lifestyle factors(=Behavior) Eating Physical activity Environment Psychosocial factors Behavioral and environmental factors are the main contributors to overweight and obesity and provide the greatest opportunities for prevention and treatment. http://www.cdc.gov/nccdphp/dnpa/obesity/faq.htm#why http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm Genetics and the environment may increase the risk of personal weight gain, and may make weight control more of a challenge for some people. However, the choices a person makes in eating and physical activity also contributes to overweight and obesity. http://www.cdc.gov/nccdphp/dnpa/obesity/contributing_factors.htm#Environment Healthy Weight Management Diet & Eating Habits Physical Activity Thinking, emotions, coping strategies Healthy Weight Management Diet & Eating Habits Diet = daily food choices Dieting = some form of food restriction Basis for a healthy diet that allows for weight management: 1. Use the food pyramid as a basis for planning (to be revised Spring 2005) HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 51 updated 3/17/2010 Overweight & Obese 2. To keep energy in balance, pay attention to: Total calories taken in balances energy expenditure Best way to lose weight = moderate calorie restriction + increase in physical activity e.g., A difference of one 12-oz. soda (150 calories) or 30 minutes of brisk walking most days can add or subtract approximately 10 pounds to your weight each year. To watch or reduce your calorie intake, pay attention to: a) Portion size A healthy portion size is usually smaller than the portion size served b) Energy density Consumption of a certain weight &/or volume of food makes you feel full and satisfied. So eat: Food with a low # calories per volume e.g.) increase consumption of: fruits & vegetables reduce consumption of: Meat, ice cream, cookies, chips c) Fat & sugar (carbohydrates) intake Limit fat intake, to < 35% of total calories Consume unsaturated fats (plant and fish fats) DO NOT TRUST BOX LABELS SAYING “LOW FAT” OR “NON-FAT”. While these products will be required by law to be low fat or non-fat, they are often high in calories due to added sugars. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 52 updated 3/17/2010 Overweight & Obese Simple carbohydrates (single or short chain sugar molecules) are broken down quickly by the body to be used as energy. Simple carbohydrates are found naturally in foods such as fruits, milk, and milk products. They are also found in processed and refined sugars such as candy, table sugar, syrups, and soft drinks. Refined sugars are often called "empty calories" because they have little to no nutritional value. Complex carbohydrates are made up of sugar molecules that are strung together in long, complex chains. Complex carbohydrate foods provide vitamins, minerals, and fiber that are important to the health of an individual. Of the recommended 45% - 65% of your calories coming from carbohydrates: The majority of carbohydrates should come from complex carbohydrates (starches) and naturally occurring simple carbohydrates, rather than processed or refined sugars, which do not have the vitamins, minerals, and fiber found in complex and natural carbohydrates. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 53 updated 3/17/2010 Overweight & Obese d) Protein Intake Limit protein intake to recommended 10% - 35% of calories Meat foods high in protein are often high in fat Additional protein is not necessary e) Eating habits Small, frequent meals on a regular schedule. Skipping meals, promotes snacking Healthy Weight Management Physical Activity Increase activity in daily activities (take stairs, park further away & walk more, house work, gardening, etc.) Add in a formal exercise program (aerobic, then resistance training). Healthy Weight Management Thinking, emotions, coping strategies - to help with weight management Developing positive, realistic goals and beliefs about yourself, and developing positive problem solving skills Have adequate and appropriate strategies to cope with life’s stresses and challenges, so you do not rely on eating (or other unhealthy habits) to cope. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 54 updated 3/17/2010 Overweight & Obese Hot Topic: High Fructose Corn Syrup Sunday, December 4, 2005 SUSAN JOUFLAS / THE SEATTLE TIMES High-fructose corn syrup fueling obesity epidemic, doctors say By Carolyn Poirot Knight Ridder Newspapers FORT WORTH, Texas — High-fructose corn syrup isn't completely responsible for the nation's 6 million overweight children — but Dr. George Bray says it's a big part of the problem. Nurture trumps nature in the current childhood-obesity epidemic, says Bray. It's the environment we're creating for our kids that's the problem, and that environment includes increasing numbers of products high in highfructose corn syrup, or HFCS. Bray, who served as founding president of the North American Association for the Study of Obesity and organized the first international congress on obesity in 1973, points out that between 1970 (when HFCS was introduced) and 2000 (when average yearly consumption of the ultra-sweet liquid sugar hit 73.5 pounds per person in this country), the prevalence of obesity more than doubled, from 15 percent to almost one-third of the adult population. And worse, much worse, obesity among children 12 to 19 — who consume a disproportionate amount of the soft drinks, fruit juice, sports drinks and packaged cookies and other baked goods that are sweetened with HFCS — increased from 4.2 percent in 1970 to 15.3 percent in 2000. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 55 updated 3/17/2010 Overweight & Obese American Journal of Clinical Nutrition, Vol. 79, No. 4, 537-543, April 2004 © 2004 American Society for Clinical Nutrition Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity1,2 George A Bray, Samara Joy Nielsen and Barry M Popkin 1 From the Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA (GAB), and the Department of Nutrition, University of North Carolina, Chapel Hill (SJN and BMP). Obesity is a major epidemic, but its causes are still unclear. In this article, we investigate the relation between the intake of high-fructose corn syrup (HFCS) and the development of obesity. We analyzed food consumption patterns by using US Department of Agriculture food consumption tables from 1967 to 2000. The consumption of HFCS increased > 1000% between 1970 and 1990, far exceeding the changes in intake of any other food or food group. HFCS now represents > 40% of caloric sweeteners added to foods and beverages and is the sole caloric sweetener in soft drinks in the United States. Our most conservative estimate of the consumption of HFCS indicates a daily average of 132 kcal for all Americans aged 2 y, and the top 20% of consumers of caloric sweeteners ingest 316 kcal from HFCS/d. The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity. FIGURE 1. Availability of total fructose (•), high-fructose corn syrup (HFCS; ), and free fructose ( ) in relation to obesity prevalence (x) in the United States. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 56 updated 3/17/2010 Overweight & Obese Obes Res. 2004 Nov;12 Suppl 2:124S-9S. Carbohydrates and increases in obesity: does the type of carbohydrate make a difference? Wylie-Rosett J, Segal-Isaacson CJ, Segal-Isaacson A. Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461, USA. [email protected] With the prevalence of obesity increasing in the U.S. and elsewhere, the place of carbohydrates in the diet has recently been under closer examination. This has led to the development of methods for analyzing the effects of dietary carbohydrate. Primary among these methods is the glycemic index, a measure of a food's effect on blood glucose levels, which was initially designed as a method for determining suitable carbohydrates for people with diabetes. However, the glycemic index does not address other metabolic issues related to excess sugar consumption. Prominent among these issues is the use of low glycemic index sweeteners, particularly fructose, which is increasingly present in processed food. Fructose is associated with increased adiposity, which may result from its effects on hormones associated with satiety. Other methods of determining "good" carbohydrates have also been developed. The common theme among them is increased nonstarchy vegetables and higherfiber legumes. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 57 updated 3/17/2010 Overweight & Obese Wellness Facts, September 2004 There is much debate these days about just how bad sugar is, but one thing is not disputed: Americans eat too much of it, 50% more than a half century ago. Say the word sugar and most people think of the refined white granules (sucrose) made from cane or beets. We actually eat much less of this sugar than we used to. What we’re mostly overeating is fructose, the main sugar found naturally in fruit and honey. It’s not that we’re eating lots of fruit, but rather millions of tons of high-fructose corn syrup (HFCS), which is added to so many foods. This sweetener now supplies nearly 10% of all calories consumed by Americans. The figure is closer to 20% for some people, including many children. Those excess daily calories are bad enough. But, in addition, preliminary research suggests that HFCS may be worse for you than regular sugar. HFCS is a liquid sweetener made from corn starch. Corn contains little fructose, but manufacturers use a special process to boost the fructose content and thus make it sweeter. About 70% of HFCS ends up in soft drinks; it’s also used in everything from baked goods and candies to breakfast cereals and pasta sauces. HFCS is so widely used because it is cheap (corn as a crop is subsidized by the government, and we grow more of it than we can use), sweeter than sucrose, and easy to handle and blend with other ingredients. Thirty years ago we consumed almost no HFCS, but now it is pushing refined sugar aside as the No.1 additive in our food supply. The average American consumes more than 62 pounds of it each year. What’s wrong with HFCS, besides the calories The body uses fructose differently than it does other sugars, in part because fructose doesn’t stimulate insulin secretion. This used to be considered a good thing: for instance, small amounts of fructose can help improve blood sugar control in people with Type 2 diabetes. But animal studies have found that large amounts of fructose actually impair blood sugar control, and may promote high blood pressure. Studies on humans suggest that high levels—as in large amounts of HFCS-sweetened soft drinks—can boost triglycerides (fats in the blood) and possibly cholesterol. There’s even some evidence that, in large quantities, fructose may not be as filling as sucrose and thus may encourage overeating. In fact, some researchers point to the increased consumption of HFCS as a prime culprit in the rising obesity rate. And if that isn’t enough, high-fructose diets may have a negative effect on the body’s ability to use calcium, chromium, and other minerals. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 58 updated 3/17/2010 Overweight & Obese IFIC Foundation http://if ic.org July / August 2004 What Do We Know About Fructose And Obesity? Start of article not included here, see web site to obtain full article Because nearly identical amounts of glucose and fructose are found in sucrose and the HFCS used in beverages, similar results would be expected with the types of HFCS commonly used in soft drinks. (i.e. similar biological effects of fructose intake can be expected if sucrose or HFCS were used to sweeten food products because fructose intake will be similar). This remains to be tested. Sucrose (table sugar) = 50% glucose and 50% fructose Disaccharide = 2 bonded monosaccharides High fructose corn syrup 42 (baking) = 42 % fructose, 58 % glucose; HFCS 55 (beverage) = 55 % fructose, 45 % glucose 2 mixed monosaccharides (not chemically bonded) HFCS is produce by a chemical reaction that converts some of the glucose in corn syrup to fructose Obesity is a complex issue with many contributing factors ranging from genetics, social issues, food consumption, and physical activity. As indicated previously in this article, the HFCS in the food supply does not appear to be a major contributor to the increased energy intake of the U.S. population. Many societal as well as dietary changes have occurred since the 1970s that could be contributing to energy imbalance and development of obesity. Changes affecting caloric intake also include: more meals eaten away from home, larger portion sizes, and the relatively inexpensive and abundant food supply. There are also other changes working to reduce energy expenditure: increased reliance on the automobile, cuts in physical education, more “screen time” (television, computers, and video games), more hours working at sedentary jobs, more long distance commuting, and more labor saving devices. Finally, other changes may be contributing to both increased calorie intake and reduced energy expenditure: more sleep deprivation, more night work, certain prescription medicines, and emotional stress. With so many changes, it may be overly simplistic to advocate a major causal role for any one food, food ingredient, or nutrient in the obesity epidemic. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 59 updated 3/17/2010 Overweight & Obese Oregon State University: Food Resource http://food.oregonstate.edu/sugar/hfcs.html “The truth is table sugar and HFCS are both about 50% fructose and 50% dextrose (D-glucose). An analysis of annual HFCS 55 & 42 production would reveal an average content of 49% fructose-nearly identical to the fructose content of sucrose.” i.e., A switch from sucrose to HFCS as a major sweetener does not change fructose intake levels Fructose is sweeter than sucrose (if not heated), but statistics from the USA suggest that people do not cut back sugar use when they use fructose. http://www.medbio.info/Horn/Time%201-2/carbohydrate_metabolism.htm 1) Fructose, insulin resistance, and metabolic dyslipidemia Heather Basciano , Lisa Federico and Khosrow Adeli Nutrition & Metabolism 2005, 2:5 doi:10.1186/1743-7075-2-5 The electronic version of this article is the complete one and can be found online at: http://www.nutritionandmetabolism.com/content/2/1/5 Obesity and type 2 diabetes are occurring at epidemic rates in the United States and many parts of the world. The "obesity epidemic" appears to have emerged largely from changes in our diet and reduced physical activity. An important but not well-appreciated dietary change has been the substantial increase in the amount of dietary fructose consumption from high intake of sucrose and high fructose corn syrup, a common sweetener used in the food industry. A high flux of fructose to the liver, the main organ capable of metabolizing this simple carbohydrate, perturbs glucose metabolism and glucose uptake pathways, and leads to a significantly enhanced rate of de novo lipogenesis and triglyceride (TG) synthesis, driven by the high flux of glycerol and acyl portions of TG molecules from fructose catabolism. These metabolic disturbances appear to underlie the induction of insulin resistance commonly observed with high fructose feeding in both humans and animal models. Fructose-induced insulin resistant states are commonly characterized by a profound metabolic dyslipidemia, which appears to result from hepatic and intestinal overproduction of atherogenic lipoprotein particles. {Chalmers notes: Liver fructose metabolism is the same whether fructose comes from sucrose or HFCS} Thus, emerging evidence from recent epidemiological and biochemical studies clearly suggests that the high dietary intake of fructose has rapidly become an important causative factor in the development of the metabolic syndrome. There is an urgent need for increased public awareness of the risks associated with high fructose consumption and greater efforts should be made to curb the supplementation of packaged foods with high fructose additives. The present review will discuss the trends in fructose consumption, the metabolic consequences of increased fructose intake, and the molecular mechanisms leading to fructose-induced lipogenesis, insulin resistance and metabolic dyslipidemia. 2) Carbohydrate metabolism lesson by Biochemistry professor. http://www.medbio.info/Horn/Time%201-2/carbohydrate_metabolism.htm HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 60 updated 3/17/2010 Overweight & Obese 3) Elliott, S. S., Keim, N. L., Stern, J. S., Teff, K., & Havel, P. J. (2002). Fructose, weight gain, and the insulin resistance syndrome. American Journal of Clinical Nutrition, 76, 911-922. Sources 1, 2, 3 above describe: No difference in metabolism of fructose from sucrose versus from HFCS, both fructose sources grouped and discussed together when fructose metabolism explained. (diagram) Sources 1, 2, 3 above agree that an elevated fructose intake is very bad due to: increased blood lipid levels fructose does not stimulate insulin release, which means lack of insulin mediated leptin release, producing less appetite supression increased body weight insulin resistance and other effects http://www.cdc.gov/nccdphp/dnpa/nutrition/pdf/r2p_sweetend_beverages.pdf CDC 2006: No mention that HFCS offers an increased risk over other sugars present in beverages. Recommended that people “Replace Sugar-Sweetened Beverages with Water or Low-Calorie Beverages” Added sweeteners. Are high-fructose corn syrup and other sweeteners fueling the American obesity epidemic?: Harvard Health Letter. Oct. 2006;31(12):1-3. No mention that HFCS offers an increased risk over other sugars present in a beverage. Recommended that people “Reduce consumption of Sugar-Sweetened Beverages & foods”, including those sweetened with fruit-juice concentrates. Drink water”. American Dietetic Association 2009 Kristine S. Clark, High Fructose Corn Syrup, (2008) Retrieved from: http://www.eatright.org/cps/rde/xchg/ada/hs.xsl/nutrition_19399_ENU_HTML.htm “High fructose corn syrup may be used as a sweetener in processed foods and beverages and is nutritionally equivalent to sucrose. Both sweeteners contain the same number of calories (4 per gram) and consist of about equal parts of fructose and glucose. Once absorbed into the HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 61 updated 3/17/2010 Overweight & Obese blood stream, the two sweeteners are indistinguishable. No persuasive evidence supports the claim that high fructose corn syrup is a unique contributor to obesity, however, like all nutritive sweeteners, it does contribute calories. This is where moderation and portion size become important.” What do George Bray and Barry Popkin NOW say about the role of HFCS in the development of the obesity epidemic? Source: Warner, M., A sweetener with a bad rap, IFIC Foundation, http://ific.org Jan / Feb 2007 HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 62 updated 3/17/2010 Overweight & Obese IS: High-fructose corn syrup fueling obesity epidemic? Chalmers’ conclusion Fructose is metabolized very differently from glucose (remember fructose is not HFCS) Elevated levels of fructose intake in the current diet is a contributing factor to obesity (and associated metabolic disorders) Would we be having the obesity epidemic IF HFCS were never invented? The switch from sucrose to HFCS should not be blamed for the elevated fructose intakes (IFIC article). o If HFCS was never invented, we would be having the same obesity epidemic, if we had the same high eating (and low physical activity) patterns, and food was instead sweetened with sucrose, because fructose intake and metabolic effects of fructose would be the same with sucrose sweetening (IFIC article “this remains to be tested”) “Fuel” for obesity epidemic: a) Increased eating (more total calories = more fats + more sugars) b) Decreased physical activity c) Environmental changes that lead to (a) & (b). HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 63 updated 3/17/2010 Diabetes Diabetes note will be distributed if Dr. Chalmers covers this topic. Otherwise, Dr. Li will cover it in the second half of the class. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 64 updated 3/17/2010 HLED 345: RESEARCH PAPER ON A DISEASE OR HEALTH ISSUE: GRADING SHEET Introduction Yes & good ___(0 points) Weak Facts & detail do not explain issues, or some significant errors. Presentation with very significant errors 2 Comments Yes but weak ___(-2 points) Missing NAMES: Exceptional Good Adequate Obvious extra Correct facts at Facts & detail explain issues, & outstanding sufficient detail to but more detail, easily effort in explain issues, and possible, or some explanation research & presentation without confusing. Presentation with reporting any significant errors some significant errors 5 4 3 5 4 3 2 1 FACTUAL CONTENT (cover in the order listed) TOPIC Needs Help! The term papers are to be turned into the PEHR office (CV 102) by 5 pm on the date they are due. 1 0 No ___(-4 points) Individual Vulnerability. Who is vulnerable-e.g., age, gender, occupation, ethnic origin, SES Suggested and/or established cause(s) Symptoms & severity of the disease/illness Methods / procedures used to diagnose the disease / illness Scientifically proven treatments, to eliminate, reduce severity or control disease Prognosis Suggestions for preventing acquisition and development of the disease / illness PREPARATION OF PAPER Paper and paragraph organization of material, use of headings (listed above) to organize material is REQUIRED. Spelling, punctuation, & sentence structure Minimum nine citations, at least 4 peer reviewed journal articles, all internet sources high quality Citation list and in text citations follow style defined in assignment description (i.e., superscript #s in text, numbered reference list). Neatness of paper: arrangement of margins, spacing, use of headings and quality of font (i.e., blurred, broken or faint printing is not acceptable)._____ 1.5 pages _____ Grading sheet attached _______ (Maximum = 48 points) General Comments (if any) on Reverse. HLED 345 Lecture Notes 2010, Gordon Chalmers, Ph.D. Pg. 65 updated 3/17/2010