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of a definitive series written by SureScreen THE ’PSYCHO-DELICATESSEN’ From starchy Christmas dinners and that warm sleepy feeling of satisfaction during the Bond film, to the “buzz” some of us experience after munching chocolate, there is a definite connection between what we eat and how we feel. That’s why drug users, alcoholics and those with addictive tendencies routinely resort to certain psychoactive foods between fixes to regulate their mood. In Issue 9 we looked at the root causes of addiction, and here we focus on one aspect — nutrition. The role of nutrition is fundamental to human well-being and is often overlooked in addiction. In this bulletin we explore the food-addiction link in identifying a person’s addictions, and offering them nutritional support based on our findings. There is growing concern that the modern diet may be involved in triggering addictions and antisocial behaviour(1). Depression has increased twenty-fold since 1945 and is predicted by the World Health Organisation (WHO) to be the second highest cause of the global disease burden by 2020. WHO also predict that by 2020 childhood mental disorders will rise by 50 per cent. And certain foods might reduce withdrawal symptoms, or even help to steer them away from their addiction altogether. As we shall see, the pantry is a veritable ‘psychodelicatessen’. WHY IS FOOD LINKED TO MOOD? “fruit, or Nutritious food is satisfying because it something releases the brain’s “anti-stress” neurotransmitter dopamine, a chemical which sweet can normally helps us form healthy natural banish dependencies in eating, sex and social interaction. So when dopamine falls to cravings.” low levels, for whatever reason, unhealthy dependencies can arise because of attempts to boost dopamine to ’normal’ levels. We know this because genetic or chemically-induced hypodopaminism (low dopamine) in the brain’s vital mesolimbic “pleasure reward” (PR) pathway leads to irritability, anxiety, depression and a craving for a variety of different substances. And those can lead to addiction. Cravings are very different from simple hunger pangs. In a balanced state of brain chemistry, hunger arises from the body’s need for nutrition and energy; but when it comes to a craving, only specific food or foods will quench it. They are invariably the ones that restore neurotransmitter levels or imbalanced body chemistry back to normal. Some cravings, like crunching ice cubes or lettuce pica might even be strong indicators of various nutritional deficiencies.(2) Although an addicted person’s neurotransmitter chemistry will also be determined by genetics and exposure to drugs, some of these chemicals are directly influenced by what they eat. For example: • Bananas and milk products are rich in the amino acid tryptophan, the precursor for the “mood transmitter” serotonin (5-HT), involved at the beginning of the pleasure-reward pathway. • Dopamine and its breakdown product, the “motivation transmitter” noradrenaline, on the other hand, are influenced by the amount of tyrosine and phenylalanine in the diet from protein sources like meat and cheese. • Eggs and soya, rich in the fatlike compound choline, can turn on the production of the “memory transmitter” acetylcholine. • Vegetable oils are a rich supply of the essential fatty acid (EFA) gamma-linolenic acid (GLA) which governs the formation of the “mania transmitter” prostaglandin E1 (PGE1). • Foods such as peanut butter, and yeast extract that are high in zinc and magnesium, and those that contain vitamins and minerals such as B-vitamins, vitamin C, vitamin E, iron, and copper, may also be of interest to the addicted person because they are used as “assemblyline” workers in the manufacture of neurotransmitters. • Foods containing iron and zinc aid neurotransmitter formation, whilst others rich in Vitamin E will protect neurotransmitters from degradation. Unless neurotransmitters are replenished, and there are adequate amounts of these “helpers” in the diet, the addicted person will experience increased negative after-effects of drug use. Already we can see that some foods help neurochemical production, but unfortunately others are no better than quick fixes which are addictive in themselves. Some cravings could simply replace a chemical addiction by a food addiction. Studying the dietary habits of addicted people can give us a fascinating insight into the psychopharmacology of everyday foods which most of us take for granted. Surprisingly, nutrition and addiction have received little attention, with advice to addicted people mostly being ‘eat healthily’, so this is an ideal topic for our bulletins, which are designed to give you a concise précis of current innovative thinking. In this issue we will focus on a few key nutritional categories of the 21st century diet. - Sugar Dairy products Cereal grains Chocolate Processed and “fast” foods Synthetic additives Curry SUGAR AND THE SUBSTANCE USER Drug users and alcoholics who are genetically or chemically hypodopaminergic, are more likely to snack on sugary foods between drug fixes, in an unconscious effort to raise 5-HT and dopamine levels in the brain’s pleasure-reward pathway. Drug users find that table sugar, sweets and fizzy drinks can lessen their withdrawal symptoms and even produce a short-lived “rush”, similar to the high experienced on narcotic drugs. Soup kitchens and the like get through vast amounts of sugar in tea, coffee and hot chocolate where sugar is a common request. Abstinent smokers attempting to cure their nicotine addiction, for example, learn that a piece of fruit or something sweet can help banish cravings. By temporarily restoring their dopamine levels, the craving subsides, but often at the cost of progressively putting on weight. You are more likely to see a user with a bar of chocolate in his hand than a sausage roll. The neurobiological processes behind the sugar-dopamine connection are very interesting. During abstinence when dopamine levels are low and a user is stressed (as also with fasting), his adrenal gland will automatically release more of the stress steroid corticosterone, which in turn stimulates the hypothalamus to release neuropeptide Y. This increases desire for sweets and carbohydrate-rich foods in the appetite centre. Eating something sweet or starchy returns neuropeptide Y levels to normal and activates the dopamine system to lessen drug withdrawal stress in several ways. Even before it has reached the stomach, sucrose activates sweet taste receptors on the tongue which release the brain’s opiate neurotransmitters, such as methionine enkephalin (ME) and beta-endorphins stored in the A10 neurones of the pleasure-reward pathway. This amplifies the PR signal at the final dopamine-releasing site of the Ventral tegmentum, making the sweet treat instantly enjoyable and reassuring. Interestingly, opioid-blocking drugs like naloxone prevent this instant taste-reward response from developing, thereby causing drug users to lose interest in sweets. Complex carbohydrates, like wholegrain breads and starchy vegetables, do not have an instant reinforcement effect on endorphin levels, nor do they impact blood sugar in the same way. They are broken down into glucose over a longer period, which has a negligible effect on brain opiates. For that reason they do not tend to be craved as much as sweets even though they still satisfy 5-HT needs, and better regulate appetite, pain control and sleep. This is why eating highly processed white bread causes rebound hunger shortly afterwards, while eating wholemeal bread usually satisfies sugar demand until the next SureScreen Diagnostics Ltd www.surescreen.com 1 meal. It could explain why hunger returns more quickly after take- Milk is intended exclusively for newborns, and cow’s milk has only away meals with rice when consumed after alcohol. relatively recently become a mainstay in modern diet. It supplies “feel good” chemicals to ensure that offspring nurse and thrive, and establish Once it is absorbed into the bloodstream, sugar impacts the 5-HT a bond with their mother. By interacting with opioid receptors in the penulsystem and the pleasure-reward pathway directly to ease withdrawal timate “signal amplification” segment of the brain’s PR pathway, it can symptoms and the stress of abstinence. In the case of simple sugars or also mimic the effect of narcotic drugs by temporarily restoring dequickly absorbed refined starches (e.g. white bread or rice), the resulting pleted dopamine levels in the user. It no doubt explains why a pint of full rapid rise in blood glucose will stimulate an insulin spike from the fat milk and a Snicker’s bar is a perennial snacking favourite of opiate pancreas to withdraw competing, larger, neutral amino acids from the users, and why some heroin users can consume many pints of milk bloodstream into muscle cells, allowing brain L-tryptophan levels to rise each day in between fixes. sharply in the hypothalamus, where, (with co-factors vitamin B6 and minerals iron, calcium, zinc and magnesium), it is made into 5-HT in the The downside is that these casomorphins are addictive, produce nasty “starter motor” area of the pleasure-reward circuit the hypothalamus to opiate-like withdrawal symptoms, and have been implicated with the deinitiate the reward-reinforcement cascade. velopment of autism, schizophrenia, ADD, diabetes and skin reactions. Most endogenous (naturally produced in the body) peptide hormones like Free glucose molecules also bind directly to hypothalamic glucose recep- insulin, glucagons, CCK, somatomedin and leptin, for instance, actually tors which links the serotonergic (5-HT) system with the “amplifier” opioid reduce food intake, but beta-casomorphin increases it when taken orally, peptides in the VTA leading to the ultimate release of dopamine and its making milk products, especially cheese (which contains concentrated interaction with D2 receptors at the key reward site of the nucleus accum- milk protein, lactose and whey proteins) habit-forming. Some sensitive bens. This generates a pleasurable reward-reinforcement effect. people report withdrawal symptoms when dairy products are eliminated from the diet including irritability, tantrums and depression. Like caffeine in tea and coffee, and nicotine in cigarettes, sugar may be Autistic children are frequently found to be addicted to dairy products. heavily consumed between fixes to fire that “spark gap” of dopaminerelease in a substance user’s dopamine-depleted brain. Normally, most dietary exorphins are broken down into inactive dipeptides by peptidase enzymes like Depeptidyl pepidase IV (DPPIV) in the intestine, leaving a small amount to travel into the general circulation to Unfortunately the quick “pick-me-up” is produce mild psychoactive effects in the neonate. But this enzyme may equally matched by a quick “let down”, “a2 milk be deficient in autistics and schizophrenics, leading to a dietary overbecause blood sugar levels can drop below load of psychoactive peptides and, consequently, negative behavioural baseline levels. This leads to a sudden and contains less symptoms. BCM7, for instance, is known to bind to the 5-HT2 receptor unpleasant return of drug withdrawal sympBCM-7 and is involved in the genesis of psychotic symptoms. Opioid peptides derived toms, dysphoria (irritability, tiredness and from food proteins have also been found in the urine of autistics and depression), lingering insulin levels and elebetter for women. For these women, postpartum psychosis and ongoing lactation vated neuropeptide Y which triggers off the autistics” are also found to have higher than normal circulating levels of craving cycle; making the user want to eat beta-casomorphin-8 (BCM8) peptide. more sweet food, while also driving the drug cravings once again. Certain milk products may be even more psychoactive, and thereComplex carbohydrates like wholegrain bread and starchy vegetables fore more appealing to the addict than others. The bovine BC milk on the other hand are free of this chemical roller coaster effect. They protein actually exists in two genetic variants, the exorphin-producing A1, produce a softer insulin response and more gradual and sustained glu- and the less active A2 form. Milk sources containing the A1 variant cose, 5-HT, and hence dopamine-raising effect in the user’s PR pathway produce 4 times as much BCM7 as the latter, and are associated with the over the following 60-90 minutes. They tend to produce longer-lasting development of psychiatric disorders. Cow’s milk contains over 300 times feelings of well-being, satiety and pain-tolerance — conducive to recov- more alpha s1 casein than human milk, and its separation product, ery; and give smokers and other addicted people a better chance of BCM7, differs slightly in structure to human sources at kicking their habit. These foods should therefore be incorporated into two amino acid positions, which may explain why dairy products are so psychoactive and appealing to opithe menu in residential treatment centres. ate users. The food industry knows this too, and American dairies are believed to be developing “superCARBS OR PROTEIN? Unlike tryptophan, tyrosine levels rise after a protein-rich meal. cheeses” with higher than normal levels of beta-casein, Because protein is not a strong insulin response trigger, the competing perhaps targeting consumers with a casomorphin habit. larger amino acids are allowed to “fight it out”, and this favours tyrosine And some breeds have been developed to produce absorption across the blood brain barrier. There, with the aid of vitamin more A2, promoted for its health benefits. B6 and C, and minerals iron, zinc, copper and magnesium, tyrosine is converted into dopamine and noradrenaline. Consequently tryptophan CEREAL GRAINS AND THE USER and tyrosine levels tend to oppose one another, dependent on the meal’s Opioids are also available in the gluten protein of grains like wheat, rye, starch or protein content. For tryptophan and 5-HT levels to rise, tyrosine barley, oats and spelt. Gluten is actually a combination of two proteins must be low; conversely, when tyrosine and its neurotransmitters are gliadin and glutenin which together account for up to 80 per cent of the high, tryptophan levels are moderate to low. This peak-trough effect often protein in these cereal grains. In the course of peptic digestion these explains the food choices of drug users. For instance, an amphetamine gluten proteins, like milk protein, break apart yielding the same psychoacuser who has exhausted his dopamine and noradrenaline levels, and tive opiate-like peptides. Glutenin is cleaved into at least 5 gluten exorfeels depressed and unable to think straight, may be drawn to high- phins A4, A5, B4, B5 and C whilst gliadin breaks down into gliadorphin protein, tyramine-rich foods, such as a steak, pizza or a cheese sand- also known as gluteomorphin. All of them bind to the same opioid rewich and a glass of milk. An MDMA or “ecstasy” user experiencing ceptors in the brain as the casomorphins from milk. There are three fatigue, irritability, and aching muscles from dancing all night, would classes of opioid receptor, all with analgesic (painkilling) effects, but subprobably crave something like fish and chips rich in carbohydrates, and tly different actions when activated: the delta receptor which also posa sugar rich drink to temporarily bring the depleted 5-HT levels back up to sesses antidepressant effects, the kappa receptor which has sedative actions and the mu receptor which causes euphoria. Whilst the gluten normal. exorphin B5 peptide is thought to be the most potent at delta opioid receptors, the A5 sequence is possibly the most abundant occurring at least MILK PRODUCT AND THE USER Whole milk, and foods such as ice cream, rice pudding and milk choco- 15 times more in the glutenin protein. late are a favourite with opiate users, because they contain biologically active opioid peptides, derived from cow’s milk proteins alpha-casein, Although it is not known what effects these gluten exorphins have on the beta-casein, alpha-lactalbumin and beta lactoglobulin. Out of all of them dopamine system, it is likely they will mimic the “signal amplification” beta-casein is considered the most potent as a “food hormone” and it also actions of the opiate-releasing A10 neurones in the VTA of the brain’s PR pathway. Users are no stranger to this and are often enticed by the moodhappens to be the most psychoactive. altering effects of refined cereal grains found in pizza, burgers, bagels Peptic digestion of beta-casein breaks this protein into a variety of and the like. psychoactive “exorphins” (opiates from outside the body). These tiny peptide fragments are released during proteolytic digestion, influencing Unfortunately, both gluten exorphins and gliadorphin/gluteomorphin are brain function. They are called beta-casomorphins (BCM), and although themselves addictive. Celiacs, (who are allergic to the gliadin protein) there are at least 21 different varieties, beta-casomorphin–7 (BCM7) is and autistics who are addicted to these grains, experience strong food probably the most centrally active. It binds to the same mu opiod receptor cravings and withdrawal symptoms such as irritability, mental foggias heroin and morphine, and despite having only around one tenth the ness, fatigue and depression in the first few days and weeks of strength of morphine, possesses significant mood-altering anxiolytic (anti- following a strict gluten-free diet. About 70 per cent of celiacs will go through this withdrawal syndrome which makes one wonder to what exanxiety), and analgesic (pain-killing) activity. SureScreen Diagnostics Ltd www.surescreen.com 2 tent these foods keep cereal grain-craving drug users locked into a cycle of highs and lows. Like casomorphins there is also some evidence that these opioid peptides are appetite-regulating and insulinomimetic (insulinreleasing) and possibly involved in the pathogenesis of diabetes. Over-milling of most white flour products ruptures the cell structure and provides an instant surge of glutens, whereas wholemeal products allow the digestive system to slowly break down the cells, providing a ‘slow release’ of glutens, explaining why wholemeal products are better tolerated. It is not only milk and gluten protein that have mood-altering digestion products. Cannabis-smoking vegetarians may consume a lot of soya produce for its own mood-altering digestive products called soymorphins. Red meat that is cooked rare will contain excess amounts of the oxygencarriage protein haemoglobin, which upon degradation by brain proteases, yields its own psychoactive hemorphin-7 peptides. This could explain why certain people like their steaks bloody, and why others prefer the HCAs found in well-cooked meat. Other food addicts can’t get enough spinach in their diet; they will sprinkle it on their pasta, mix it into their casomorphin-rich cheeses and even eat it raw. The answer may lie in the peptic digestion of the ribulose bisphosphate carboxylase enzyme in spinach leaves which is known to produce at least two psychoactive exorphinlike substances rubiscolin 5 and 6. FATTY FOODS AND THE USER Stimulants like amphetamines, cocaine, ecstasy, and appetite suppressants like opiates cause the body to breakdown fat to maintain energy levels. This releases tiny fat fragments (free fatty acids) into the blood that travel to the brain’s appetite centre in the hypothalamus and trigger the release of the nerve chemical galanin. Both stimulant-induced fasting and the stresses of abstinence will increase adrenal corticosterone secretion which, as before with neuropeptide Y, will also increase galanin output. Elevated galanin levels, in turn, trigger cravings for fatty foods; everything from ice cream to hamburgers, in order to replenish long-term fuel sources. These foods are a favourite with addicts because sugars and fats instantly stimulate taste receptors linked to the release of the same enkephalins and endorphins in the PR pathway responsible for restoring dopamine neurotransmission. This makes eating these foods instantly enjoyable and moreish, and only increases a user’s desire for cakes, biscuits, ice cream and other creamy or sugary foods. CHOCOLATE AND THE USER Users will often resort to snacking on chocolate in between “highs” for its calming mildly-euphoric effect. Chocolate is well known for producing a mild empathogenic “love-buzz” effect in its occasional users, and addicts are no exception. Chocolate is in fact, like sugar and many of the other favourite foods of drug users, an addictive substance in its own right with its own class of addict, the “chocoholic”. The actual “love-chemical” constituent of the 300 or so chemicals in raw cocoa, responsible for its muchcoveted behavioural effect, is the subject of long-standing debate. One disputed ingredient is Phenethylamine, an amphetamine-like stimulant also present as a trace amine in the brain responsible for releasing dopamine in the PR pathway during sexual orgasm. It is an attractive theory but unfortunately most, if not all phenethylamine is metabolised by gut monoamine oxidase B (MAOB) enzymes before it reaches the brain. Related psychoactive amines like L-tryptophan, 5-HT, tryptamine, phenylalanine, the DA-derivative salsolsinol, tyramine, octopamine and histamine have also been proposed but many of these exist in higher concentrations in other foods with less appeal than chocolate. The search goes on, however, and recent research has revealed that chocolate also supplies trace quantities of the brain’s own short-lived cannabis-like “bliss chemical” anandamide, and at least two of its chemical cousins N-oleolethanolamine and N-linoleoylethanolamine which inhibit anadamide’s breakdown in the brain. These “endocannabinoids” are thought to be active in regulating dopamine release in the PR pathway of the mesolimbic system, and have been shown to increase extracellular dopamine concentrations. It makes a good headline, but sceptics claim that even if they got past the stomach acid, you would need to consume pounds of chocolate to derive any noticeable effect from them. Interestingly, anecdotal reports state that mixing raw cocoa with emulsifying agents (like those found in milk or lecithin, commonly added to commercial chocolate) is better at extracting these cannabinoids into the body and renders chocolate “psychoactive”. We are on much surer ground with chocolate’s family of methylxanthine alkaloids, however, which lift the “sleepiness-inducing” adenosine “brake” on the addicts sluggish dopamine system. Although the psychostimulant effects of the trace amounts of caffeine and the cardiac and respiratory tonic effects of theophylline can be discounted, addicts may well be drawn to the mood-brightening effects of the last in this series of methylxanthines; theobromine. Meaning literally “food of the gods” (from the Greek theo “God” and brosi “food”), theobromine, despite having only one tenth the stimulant effect of caffeine, is the primary psychoactive constituent of co- coa (1.5 –3.0% by weight), giving it its bitter taste and is the most likely candidate for its popular mood-altering effects. Chocolate may be considered an all-round panacea with its smorgasbord of psychoactives because whereas the opiate user or alcoholic might snack on it for its narcotic anadamide and casomorphin content, and the stimulant user for its high level of its psychoactive amines and xanthines, both drug and alcohol users will be irresistibly drawn to the dopamine-raising effect of chocolate’s added sugar. Interestingly, the most widely preferred chocolate among the general population is not unsweetened dark chocolate with its higher drug cocktail, but sweetened milk chocolate suggesting that the majority of us may in fact be craving its addictive psychoactive sugars, fats and narcotic casomorphins more than anything else. All of this forces us to reconsider how fragile the food-drug distinction actually is. TYRAMINE AND THE USER Stimulant users will often make a bee-line for foods rich in L-tyramine during the “comedown” phase once the drug’s effects have worn off. Not to be confused with its parent amino acid and DA-precursor Ltyrosine, tyramine is produced by the decarboxylation of L-tyrosine during the fermentation and decay of protein. It is found in particularly high concentrations in smoked, pickled, aged, or marinated meats (beef, poultry, fish) and fermented foods like most cheeses, yeast products, alcoholic beverages, sour cream, yoghurt, shrimp paste, soy sauce, teriyaki sauce, tofu, miso soup, and sauerkraut. It is also found in naturally high quantities in cocoa, avocados, bananas, aubergine (eggplant), figs, plums, raspberries, fava beans, green pod beans and nuts. Although, like phenethylamine, tyramine is extensively metabolized by gut MAO enzymes, it retains some of its ability to release stored monoamines like “Alcohol affects dopamine and its breakdown products noradrenaline and adrenaline in the brain, people in and so weakly mimic the effect of stronger different ways, stimulants like amphetamine and cocaine on the pleasure-reward pathway of the depending on mesolimbic system. Recently, neuroscientheir biotype.” tists discovered that tyramine binds to a class of trace amine receptors responsible for mediating the effects of amphetaminelike substances. It seems to explain why stimulant users will often find themselves bingeing on tyramine-rich foods like cheeseburgers, chocolate, alcohol and indulging cravings for Marmite or Vegemite on toast to recapture some of the euphoria of the “night before” and postpone the after-effects of comedown. Recent studies have also shown that tyramine might enhance the brain’s response to repeated doses of drugs like cocaine over time. Genetically modified Drosophila melangaster flies, which do not possess the enzyme tyrosine-decarboxylase, cannot synthesise tyramine and for this reason remain sedated despite repeated doses of cocaine. This abnormality is reversed if tyramine is given which suggests that it may have a facilitatory role in sensitising the mesolimbic system to stimulants. Also because of its blood pressure raising effects, tyramine-rich foods can have some nasty side effects like headaches, insomnia, palpitations and hypertension. Moreover, because it is normally de-activated by MAO enzymes in the gut wall, which inactivate dietary amines that would otherwise produce unwanted effects, tyramine-rich foods can produce a sudden and dangerous rise in blood pressure, throbbing headache (sometimes called the “Cheese reaction” after the toxic effects of tyramine in aged cheeses), and even intracranial haemorrhage if taken with certain MAO-inhibitor antidepressant drugs. HETEROCYCLIC AMINES AND THE USER Users may also crave chargrilled meats like chicken, steaks and burgers because they are high in psychoactive heterocyclic amines. These are addictive substances similar to tyramine, but instead of being the product of decay, are formed in the cooking process when proteins react with carbohydrates or creatine (in red meat) and nitrate (from meat preservative or accompanying vegetables). Generally when the aldehyde functional group of simple sugars and carbohydrates react with cyclic amino acids like phenylalanine, tyrosine, tyramine and tryptophan found in animal protein, psychoactive morphine-like compounds called isoquinolines and anxiety-forming substances called betacarbolines are the result. Whilst the isoquinalines act as “false transmitters” by depleting the brain of its own neurotransmitters and binding to narcotic receptor sites in the brain, beta-carbolines inhibit transport of tryptophan and block “tranquillising” benzodiazepine and 5-HT receptors. Cooked foods rich in these heterocyclic amines may offer a mild temporary high but they may be followed by symptoms of dysphoria like irritability, discomfort and anxiety when endogenous neurotransmitters are unavailable to resume their function. Some foods like red meat SureScreen Diagnostics Ltd www.surescreen.com 3 contain a good source of both protein and creatine which when cooked give rise to another family of addictive heterocyclic amines called imidazoquinolines and imidaziquioxalines. Other prepared foods high in heterocyclic amines include fish, poultry, flavour enhancers, bouillon protein concentrates and some fermented foods like beer and soy sauce. MONO SODIUM GLUTAMATE (MSG) AND THE USER Stimulant users will also be drawn to fast food meals because of their monosodium glutamate (MSG) content. Often hidden in processed foods under aliases like “hydrolysed vegetable protein”, “E621”, “textured vegetable protein”, “yeast extract”, “sodium caseinate” and “natural flavouring”, MSG is a flavour enhancer with known psychoactive, addictive and neurotoxic properties. It is used in savoury foods, snacks, soups, sauces, meat products and Chinese restaurant cooking especially, and has a similar uplifting effect to tyramine when not taken to excess. Some stimulant lovers even report consuming raw MSG for a “buzz”, though we wouldn’t recommend it. MSG is essentially the sodium salt of glutamate, which is the main excitatory amino acid in the central nervous system with over half of all nerve cells releasing it. MSG is involved in arousal, learning and memory formation and like stimulant drugs, determines the brain’s overall level of excitation. Stimulant addicts love MSG-rich foods because drugs like cocaine and amphetamine tend to overtax the adrenal gland leading to low stress hormone output and raised free copper levels in the blood. Copper is normally bound to the protein ceruloplasmin in a form the body can use, but unbound (biounavailable) copper depletes the brain of 5-HT, DA and GABA which aggravates stimulant comedown symptoms. MSG temporarily binds and transports this toxic copper out of the blood of stimulant users providing a temporary relief from “brainfog”. Before it is even digested MSG tricks “savoury” taste receptors on the tongue called umami into thinking one is consuming a meal of nutritious food and this stimulates appetite. Once it gets into one’s system, MSG triggers massive pancreatic insulin secretion which removes sugar from the bloodstream too quickly leaving one feeling hypoglycaemic and hungry an hour later with the urge to eat more. Also as insulin rises encouraging tryptophan uptake in the brain, these glutamates interrupt its conversion to 5-HT in the appetite centre of the hypothalamus, preventing the generation of feelings of satiety after eating, which intensifies appetite and the desire to eat more MSG-rich foods. Over time the body will stop responding to all this insulin (as it does in Type II diabetics), leaving sugar hanging around in the blood stream where it is converted into fat, and this promotes obesity. It would appear that the food industry are well aware of this and have been routinely using MSG in their scientific research as a control-substance in animal obesity experiments for decades. A cursory internet search for MSG on Medscape will bring back some revealing studies shedding light on the problem of America’s expanding waistlines. Excess MSG is thought to be converted into the tranquillising neurotransmitter GABA which may paradoxically calm those users who are too “wired”. Another drawback with MSG is that it may also increase the addictiveness of other drugs by sensitising the “neuroadaptive” N-methyl D-asparate (NMDA) receptor in the brain; responsible for linking memories of drug taking experiences with the pleasure-reward response. Bingeing on MSG-rich junk food to get through the “comedown” experience of stimulant abuse might inadvertently be teaching the brain to become more addicted to that particular drug. For instance, when experimental mice are bred without the metabotropic (the slow, long-term firing) glutamate receptor mGLuR5 they turn their noses up at cocaine even though their dopamine systems respond normally. The animals literally don’t remember the rewarding effects of cocaine. This indicates a possible drug-reinforcement role for MSG in enhancing memories and learning related to behaviours necessary for “stimulant seeking” in drug users. MSG is also an excitotoxin (in excess it triggers cells to kill themselves) linked to a long list of health problems from the well known “Chinese restaurant syndrome” and other CNS disorders like ADD, Autism, Alzheimer’s, depression, epilepsy, insomnia migraine and panic disorder to bodily diseases like asthma, diabetes, hypertension, hypothyroidism, obesity and stroke. So whilst it may perk up a dopamine-deficient brain and clear the brainfog associated with stimulant “comedown”, MSG seems to create more problems than it solves. CURRY AND THE USER One quarter of UK adults eat a curry once a week, and up to half eat one once a fortnight, which makes this dish more popular than the British classic, fish and chips. We all know how popular a curry is after a few drinks at the pub, but few of us will know precisely why. Neuroscientists tell us that hot curry stimulates pain cell receptors in the mouth to release the neurotransmitter ‘Substance P’ and this tricks the brain into releasing painkilling and mood-elevating beta-endorphins which makes the burning taste sensation paradoxically enjoyable. Researchers at Nottingham Trent University have discovered that the taste stimulation associated with eating curry creates excitement and stimulates adrenaline output to raise the heart rate by 3-7 beats per minute. Apparently just anticipating eating a curry is equally effective. Indian curries also tend to contain a lot of spinach leaves which, as previously mentioned, contains the opiate-like rubiscolins 5 and 6 and which can trigger cravings in the susceptible. But what is perhaps more interesting is that the ground poppy seeds (often found on whole on granary breads) added to Indian curries contain high levels of morphine-n-oxide, a powerful psychoactive and addictive narcotic agent, which actually prolongs and intensifies the pleasurable effect of alcohol. Alcohol does not have an “ethanol receptor” per se in the brain but rather exerts its pro-dopamine effects by interacting with the same opioid (painkiller) receptors as morphine and other narcotic drugs instead. Clinical studies have shown that alcoholics lose interest in ethanol when given the opiate antagonist drug naloxone, because it blocks the rewarding effects of alcohol, leaving the drinker unpleasantly sedated. Because both drugs use the same receptors to reward their users, it makes sense that drinkers (especially addicted THIQ biotype drinkers and those with dopamine-depleted brains) will make a beeline for the Indian curry house at the end of the night to maintain the feeling alcohol gives them. Incidentally the vomiting centre in the brainstem contains high concentrations of the neuropeptide substance P, as well as neurotransmitters such as choline, histamine, dopamine, serotonin, and opioids. Their activation stimulates the vomiting reflex. Recent studies have found that type 1 diabetes could be linked to insufficient substance P, and injecting substance P into the pancreas of diabetic mice produced an overnight cure(3). CONCLUSIONS The food chain is a potential cornucopia for the addicted person. Whilst some food cravings are harmless and may actually be beneficial, others are potentially hazardous to health and counterproductive to abstinence. Most addicted people tend to eat foods that make them feel better temporarily rather than those that are good for them long term. Successful recovery from drug and alcohol addiction then, will depend on identifying the food cravings that follow particular patterns of substance misuse, and using this data to steer through the pitfalls of the 21st century western diet. Where necessary this will involve implementing dietary restriction of offending psychoactive substances and the use of foodstuffs rich in beneficial amino acids, fats, vitamins and minerals to replenish depleted neurotransmitters and restore proper brain function. For them, a carefully chosen, wholesome well prepared diet may truly be the best medicine. In the next bulletin we will explore the vitamin, mineral and nutrient deficiencies that affect drug and alcohol users, and how addiction might be helped with natural supplementation. Bulletin 11 is based on commissioned research undertaken for SureScreen. References can be obtained by contacting [email protected] If you have any comments or observations to make on this or other Bulletins in this series we would be delighted to hear them. Here are your comments so far about ‘Best Practice’ Bulletins. REFERENCES (1) The McCarrison Society Newsletter 42.2 Summer 2008 (2) www.mybodylanguage.co.uk (3) New Scientist 15 Dec 2006 Next issue - Mood Food and Addiction (2) SureScreen Diagnostics Ltd is a family owned business and one of Europe’s leaders in diagnostic testing, including drugs, pregnancy, disease and lifestyle tests, with a passion to keep the British innovative spirit alive with the latest diagnostic developments. SureScreen is very often first in the market place with the latest tests. Choose SureScreen's extensive range of products for best quality, competitive price and fast delivery. Every product comes from SureScreen's dedicated team of experts with the aim of exceeding your highest expectations. Back Issues: Issue 1 - How drugs of abuse are handled by the body Issue 2 - Drug retention times and cut-off levels Issue 3 - Alcohol Issue 4 - Oral Fluid, Urine and Hair testing Issue 5 - Definitive Guide to Urine Best Practice Technical Bulletins are prepared by SureScreen and represent a definitive guide on all aspects of drugs, alcohol and health. © 2008 SureScreen Diagnostics Ltd. SureScreen Diagnostics Ltd www.surescreen.com Issue 6 - Definitive Guide to Oral Fluid Issue 7 - Definitive Guide to Hair Testing Issue 8 - Electronic Curfew Monitoring Issue 9 - Addiction Issue 10 - Testing solid drugs To request an electronic copy, simply email us at [email protected] with the issue number(s) you require. SureScreen Diagnostics Ltd, 1 Prime Parkway, Derby. DE1 3QB. U.K. Tel: 0044 (0)1332 365318 Fax: 0044 (0)1332 292230 Web: www.surescreen.com Email: [email protected] 4