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Transcript
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
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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.
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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
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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)
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