August 25, 2004

• SuperSize Blog

  My readers know that a brief blog from me is a rare exception to the
  general rule.  Be warned:  this one may turn out to be longer
  than most.  I realized last night as I was talking to Greyfox and
  he said I absolutely must blog about that morning’s events here at
  home, that if I continue as I had been, blogging each day the events of
  the day or the weekend, etc., just past, I would never catch up. 
  In an effort to catch up, I intend to cover in this entry both
  yesterday and at least the first part of today, particularly some
  comments received on yesterday’s blog about the past weekend.  One
  comment in particular stimulated in me a desire and intention to cover
  in depth the subject of addiction, something I’ve previously dealt with
  only superficially here.

  Before I get into that past stuff, I want to deal with here and now –
  a sitrep.  The long drive, busy weekend and deficient sleep left
  me in sorry shape on Sunday, Monday and Tuesday.  Today, at least
  I can walk straight and my vision is clearing up.  If anyone wants
  to commisserate with me or offer me well-meant suggestions on how they
  deal with fatigue, please spare me unless you yourself have ME/CFIDS
  (myalgic encephalomyelopathy / chronic fatigue immunodysfunction
  syndrome) or have a degree and a specialty in a related field. 
  Perhaps my physiological fatigue is a contributing factor, and perhaps
  not — but anyhow, I’m simply sick of hearing about what a bunch of
  normal healthy people do to deal with their normal healthy fatigue and
  aches and pains.  Believe me, I have my own coping mechanisms and
  have learned through decades of experience what works and what does
  not.  We with this disease exhibit many paradoxical reactions to
  such simple things as exercise, massage or steam baths, etc.  Just
  spare me, okay?

  Rude Awakening
  or, the cat’s catch-and-release program

  About 4:30 yesterday morning, I awoke to some sounds I later identified
  as an excited Koji doing his kangaroo impression.  He frequently
  stands on his hind legs like a bear, to see farther.  When he gets
  excited, such as yesterday when Doug took his leash and head collar off
  the hook in preparation for his walk, he stands on those back legs and
  hops, apparently just because he can’t contain his eagerness. 
  It’s amusing to see and can be challenging to deal with when one is
  trying to get him into that head harness, but it’s nothing unusual.

  There’s nothing unusual about Doug walking the dog or doing anything
  else at 4 AM, either.  He cannot properly be called a day person
  or a night person.  He is not bound by an ordinary person’s
  diurnal patterns.  His internal clock runs on a longer cycle than
  most.  Each day he rises and falls asleep a few hours later than
  the day before, by our 24-hour clock.  To be able to guess at what
  hours he might or might not be awake, one needs to know where he is in
  his own idiosyncratic cycle.  Even then, it’s unpredictable
  because he sometimes finds it inconvenient to go to sleep at all and
  stays up for 36 hours or more, completely throwing the cycle out of
  sync.

  The thing that was unusual, that led me to exclaim, “What the fuck!?!”
  and get both Doug’s attention and the dog’s, was the rodent running
  across my pillow and through my hair.  As I watched the little
  brown body squeeze down between the book shelf and the wall behind my
  bed, I responded to Doug’s query about my exclamation.  He then
  told me that Granny Mousebreath (see where our Catriarch gets her
  name?) had brought in some live prey and turned it loose.  Then he
  harnessed Koji and they went out.

  Soon after that I heard the familiar sound of Granny, “talking with her
  mouth full.”  She came through the hallway from the bathroom,
  where she had entered through an open window.  The whole way, she
  was calling, announcing her entrance, with another live vole or
  lemming, or something, in her mouth.  I’m not more specific about
  the species of her prey because the little things move so fast and get
  under cover as quickly as they can.  From the size and color of
  the one that scampered through my hair, I’d guess it to be a
  lemming.  The one I saw her carry in was smaller and darker,
  probably a vole or shrew.

  It lay still when she dropped it and I breathed a sigh of relief: 
  one less live rodent in the house.  But it was only stunned or
  playing dead.  When she patted it with a paw, it leapt up and
  scurried under the couch.  All day yesterday the evidence of my
  own ears and the sight of Koji sniffing around in various parts of the
  room revealed where those two rodents and/or others of their kind had
  gotten to.

  This bringing in of live prey is something the cats don’t do all the
  time.  That behavior is usually confined to the end of
  summer.  There may be some other reason for it, such as a
  superabundance of prey at this time, but I suppose it is because the
  cats know that soon the window will be closed for winter, many of the
  rodents will have burrowed out of reach, and so they are now stocking
  their own private hunting preserve.  

  Occasionally, Granny has brought in a live bird, but that does not work
  out so well for her.  The birds don’t run for cover.  They
  fly at the windows until I capture and release them.  I suppose,
  if the birds were not so frantic, and so stupid about slamming their
  little feathery bodies into solid glass, I’d be more tolerant and
  Granny’s winter prey would be more interesting and diverse.  But
  that is not the way things are.

  If this year follows the patterns set in previous years, by November or
  December the household rodent population will be extinct.  They
  can’t remain in hiding, but must come out searching for food, silly
  things.  They play right into the cats’ claws and jaws.  I
  don’t make life easy for them, as I did the first winter I found a nest
  of shrews resting on the shoulders of some things hanging in my
  closet.  That time, I placed a jar lid full of grains and seeds on
  the floor of the closet for mama shrew and her cute babies.  That
  was before I had a cat, before I’d gotten more than enough of the wild
  rodents’ shredding clothing and bedding and gnawing through packages in
  the pantry.  Now, if they are foolish enough to come in here out
  of the cold, or not fast enough to avoid becoming Granny’s captive
  stock, then they are fair game.

  Okay, that’s the Lite Blog for today.  Next comes the real meat of
  the matter, my treatise on addiction replete with quotes from various
  authoritative sources.  Since little of it is my own work (except
  for the introduction, selection and editing), I think I’m not overly
  immodest to suggest that it’s worth reading, even if that means you
  must do it in more than one installment.

  Oh, and it’s not just for dope fiends, either.  This information
  applies equally well or even better to the “moderate” drinker or user,
  or one who is addicted to sex, gambling, soap operas or the internet.

  Trite Sayings and
  Bogus Philosophy
  
  versus
  
  Biochemistry and
  Observable Phenomena

  I have long suspected that dingus5
  sprinkles his comments here with worn out platitudes and silly ideas
  just to bait me and see how I react.  If I am mistaken about that,
  so be it.  I won’t apologize.  It simply does not seem
  appropriate to apologize to someone for overestimating his
  intelligence.  If he truly believes such facile, puerile crap,
  then my opinion of him is the least of his problems.

  The ancient Greeks preached, “moderation in all things.”  It is
  reasonable to infer from such preaching that they were well experienced
  in the hazards of immoderate behavior.  To Greeks of the
  Pythagorean school, temperance, moderation, or the “mean” between two
  extremes — the reconciliation of opposites — was believed to create
  harmony.  That’s a pretty theory, I will admit.  When it
  comes to practical reality, however, time and again in the centuries since the
  Golden Age of Greece the theory has failed to prove itself valid.

  I would challenge anyone to preach moderation at an AA or NA
  meeting.  Experienced drunks and dope fiends know that path won’t
  work for them.  In the quest for moderate drug use, many have
  died.  In AA’s “Big Book” one essay lists the ways one might try
  to moderate his drinking with strategems such as drinking only at
  home, drinking only beer, only after five, etc.  Whenever that
  list is read at a Big Book meeting, it is greeted with the rueful
  laughter of those who have tried some of those things themselves.

  Among the routine readings at the start of each of our NA meetings is
  this:  “The only way to keep from returning to active addiction is
  not to take that first drug. If you are like us you know that one is
  too many and a thousand never enough. We put great emphasis on this,
  for we know that when we use drugs in any form, or substitute one drug
  for another, we release our addiction all over again.”

  David F. Horrobin has explained why alcoholics cannot moderate their
  drinking.  I have extracted here some portions of Chapter 11 of
  Mary Greeley’s book, Alcoholism as an Allergy:

  Prostaglandins (PGs) are powerful chemicals found in every cell of the
  body.  They appear to be key controlling factors which regulate
  the way every organ works.  There are at least 20 of them, each
  with a specific function.  They are being constantly produced just
  when needed and then are instantly destroyed so their effects are not
  too prolonged.  

  PGs come in three families, all formed from relatively stable chemicals
  called essential fatty acids (EFAs).  EFAs are like vitamins, they
  cannot be made in the body and must be provided regularly in
  food.  Every body cell has an EFA store and when PGs are needed,
  EFAs are brought out of storage…. rapidly converted to PGs which
  briefly exert their effects and then are destroyed….  

  PGE1 is formed from an EFA known as dihomo gamma linolenic acid
  (DGLA).  PGE1 can open blood vessels which have gone into spasm,
  reducing the amount of damage due to a heart attack, and possibly even
  prevent heart attacks.  PGE1 can also lower high blood pressure,
  and reduce cholesterol production in the body.  PGE1 can stimulate
  a poorly functioning immune system, block inflammation and control
  arthritis.  PGE1 has dramatic effects on the Central Nervous
  System and behavior.  PGE1 added to cancer cells in the laboratory
  can make them function like normal cells.

  
  EFAs, DGLA, cLA and GLA
  
  
  The Pump and the Alcohol Converter

  Limited amounts of DGLA, the EFA from which PGE1 is made, is found in
  most cells of the body and PGE1 is produced from it by two main steps:

  1)  The DGLA has to be removed from storage in a free form, and,

  2)  The free DGLA has to be converted into PGE1….”

  Following published research by Dr. Joe Abdulla of Guy’s Hospital,
  London, on the formation of PGE1 by platelets taken from patients with
  various forms of mental illness, Dr. Horrobin (noting similarities
  between mania and early stages of alcohol intoxication) studied the
  effects of alcohol on platelets.  Independently, Dr. John Rotrosen
  of NYU’s Dept. of Psychiatry and the Veteran’s Administration Center,
  did almost the same experiments.  Both experimenters concluded
  that, “alcohol at concentrations relevant to human drinking has a
  potent effect on PGE1.”

  Many of the effects of alcohol and almost all of the good ones are due
  to the increase of PGE1 formation and this can explain the behavioral
  effects of alcohol.  PGE1 has profound effects on behavior, and
  behavioral changes in animals can be blocked by preventing the alcohol
  action on PGE1.

  Facial flushing produced by alcohol has a similar effect as produced by
  PGE1.  This effect can be blocked by drugs which block PGE1
  formation.  The desirable effects of alcohol in reducing the risk
  of death to diseases of the heart and circulation are similar to
  PGE1.  Alcohol may possibly lower the risk of infections, as
  witnessed by travelers to the tropics, and by the traditional remedy of
  a hot alcoholic drink for flus or colds.  PGE1 is able to
  stimulate weakened immune systems, and to help them resist
  infections.  It is certainly not beyond the bounds of possiblity
  that alcohol, like vitamin C, which acts much the same way, could have
  a protective effect.

  With so many good actions to PGE1′s credit, how is it possible that
  something which increases the production of the prostaglandin could
  have so many bad effects?  Surely, it would seem taking more of a
  good thing should be even better, but this is not true.  For one
  thing, DGLA stores within cells are limited.  Stimulation of PGE1
  formation by alcohol cannot go on forever.  Eventually the stores
  become depleted and even if alcohol is still present, PGE1 levels will
  fall catastrophically, far below normal….

  …alcohol, beyond depleting DGLA stores, has another effect which
  compounds the damage.  There is very little DGLA in foods. 
  The exception is human milk.  Therefore, we have to make DGLA in
  our bodies from another nutrient, cis-Linoleic Acid (cLA) which is
  particularly in vegetable oils.  Most of our PGE1 is ultimately
  formed from cLA in the diet.  The cLA must first be converted to a
  substance called Gamma Linoleic Acid (GLA) itself….

  Alcohol temporarily increases PGE1 formation by stimulating its
  production from DGLA, but in the process DGLA stores are
  depleted.  In a normal person, such stores could be rapidly made
  up from the cLA in the diet.  But the person who drinks too much
  alcohol cannot do this because the conversion of cLA to GLA is blocked
  so that paradoxically, chronic overconsumption of alcohol leads to a
  chronic deficiency of PGE1.  This lack of PGE1 may then lead to an
  increased risk of heart attacks and stroke, to high blood pressure,
  reduced ability to cope with infections, to brain and nerve
  deterioration and liver damage.

  How much is “too much” varies from person to person.  Variables in
  genetic makeup and diet, as well as such factors as exposure to other
  toxins, make such an assessment unpredictable.  People starting
  out with low levels of PGE1 are most likely to quickly become
  alcoholics, but alcohol’s blocking of conversion of cLA to GLA will, at
  some point, begin to lower anyone’s PGE1 levels.

  
  A perfectly normal person readily able to cope with alcohol and not
  depressed before or after drinking, may become alcoholic.  His
  PGE1 levels in the absence of alcohol are normal, but gradually
  repeated drinking depletes his DGLA and simultaneously prevents its
  replenishment from cLA.  The resting level of PGE1 drops, a
  depression develops in the absence of alcohol and increasing amounts
  are required to get the PGE1 level up to normal.  Before he knows
  what he is doing, the social drinker is drifting into alcoholism. 
  He is drinking more and more of a substance which transiently and with
  increasing difficulty brings PGE1 up, but at the same time
  progressively destroys the body’s ability to make PGE1. [emphasis added]

  Dr. Horrobin’s recommended treatment for alcoholism is
  twofold:  first reducing the cravings, and then avoiding or
  reversing the damage
  from the lack of PGE1.  He does not address a way to reduce
  cravings.  Many doctors do it with toxic drugs such as
  antidepressants.  We do it with orthomolecular supplements of
  amino acids, vitamins and minerals.  We also follow Dr.
  Horrobin’s recommendation for increasing PGE1:  evening primrose
  oil for GLA, with cofactors B6, B3, pyridoxine, niacin, zinc, magnesium,
  and vitamin C.

  With other drugs besides alcohol, other prostaglandins are
  involved.  However, in any addiction, even those to activities and
  processes as opposed to substances, there are similar biochemical
  cycles:  the addiction stimulates some beneficial effect while
  at the same time depleting the chemistry involved in making that
  happen.  Here is the way nutramed.com describes some common food
  addictions:

  We notice similar patterns of addictive behavior with food, alcohol and
  drugs. Alcoholics and drug abusers frequently have atrocious dietary
  habits. So many of them grew up dysphoric with bad chemicals in their
  food and environment. These addicts often report they first felt well
  when they had their first drink or injected the initial dose of heroin.
  Opiates, like other molecules, are effective but temporary remedies for
  dysfunctional body-mind states. The drive to maintain an opiate level
  is less to “get high” and more to feel “normal” and mostly to avoid the
  terrible experience of withdrawal.

  The digestion of food proteins may produce substances having opiate or
  narcotic properties. There are also a large number of regulatory
  peptides feeding back to brain control centers to form the brain-gut
  axis. A stop signal to the brain when enough food is eaten would be
  important for appetite control and may be defective in compulsive
  eaters.

  
  Exorphins

  Pieces of milk and wheat proteins (peptides) can act like the body’s
  own narcotics, the endorphins, and were described by Zioudro, Streaty
  and Klee as “exorphins” in 1979. Other food proteins, such as gluten,
  results in the production of substances having opiate- (narcotic) like
  activity. These substances have been termed “exorphins.” Hydrolyzed
  wheat gluten, for example, was found to prolong intestinal transit time
  and this effect was reversed by concomitant administration of naloxone,
  a narcotic-blocking drug. Digests of milk proteins also are opioid
  peptides. The brain effects of exorphins may contribute to the mental
  disturbances and appetite disorders which routinely accompany
  food-related illness. The possibility that exorphins are addictive in
  some people is a fascinating lead which needs further exploration.

  Another mechanism, similar to dependency on food-derived neuroactive
  peptides such as exorphins, would be a dependency on gastrointestinal
  peptides, released from the bowel during digestion. Deficiencies in the
  bowel production of regulatory addictive peptides, such as endorphins,
  would likely be associated with cravings and compulsions to increase
  food ingestion. There are a large number of gut-regulatory peptides
  feeding back to brain control centers to form the brain-gut axis. The
  information flow between the gut and brain is likely critical in
  regulating feeding behaviors.

  Eugenio Paroli reviewed the peptide research, especially the link
  between food and schizophrenia. He suggested: “The discovery that
  opioid peptides are released by the digestion of certain food has
  followed a line of research that assumes pathogenic connections between
  schizophrenic psychosis and diet.”

  Milk and wheat proteins have been studied and shown to yield active
  peptides. These substances may be numerous in the digestive tract after
  a meal and several effects could occur in sequence. The absorption of
  larger peptides may be irregular, with variation in symptom production
  after meals, making the interpretation of milk and wheat disease
  difficult. Other foods are likely to yield similar peptides.

  From our basic understanding of protein digestion, we should predict
  that there will be regular traffic of peptide information passing from
  food digests into the body. Ingestion of normal food may result in
  information-molecules streaming into our bloodstream from stomach or
  small intestine with all the impact of narcotic drugs! A “Gluten
  Stimulatory Peptide” is also described with narcotic (opiate)
  antagonist properties. It has been suggested that gluten hydrolysates,
  digests of wheat protein, have mixed opiate agonist-antagonist activity
  and, like two drugs with mixed narcotic activating and blocking actions
  (nalorphine and cyclazocine), produce dysphoria and even psychotic
  symptoms. Loukas and colleagues have derived the structure of cow’s
  milk-derived exorphins: Opioid activities and structures of
  casein-derived exorphins. These two peptides carry information by
  finding and binding to brain receptors which ordinarily respond to
  endorphins. The message is go to sleep, feel bad, but go back for more.

      Arg-Tyr-Leu-Gly-Tyr-Leu-Glu (exorphin, digested from alpha casein)

      Tyr-Pro-Phe-Pro-Gly (exorphin, digested from beta casein)

  
  Chocolate

  Chocolate is an interesting psychoactive food. Chocolate and romance
  have been inseparable. Chocolate artistry is one of the truly admirable
  pursuits in food preparation. If nature had been more kindly disposed
  to us, chocolate confections would be an authentic pleasure, free of
  any penalty. Chocolate begins as the cacao bean of South American
  origin. The botanical name, Cacao Theobroma, means “food of the Gods”.
  One of the medically useful methylxanthine drugs, theobromine, is found
  in chocolate as well as coffee and tea. Theobromine is related to
  caffeine and is useful as a treatment of asthma.

  The cacao tree produces melon-sized pods full of beans. The pod is
  split and the beans removed and fermented until they turn the
  characteristic deep brown color. Dried beans are then roasted and
  processed by grinding and heating. The powdered fraction is the water
  soluble cocoa powder. The bean fat is separated as cocoa butter.
  Chocolate candies are all based on some combination of cocoa powder,
  cocoa butter, milk, sugar, and diverse other ingredients. Drugs in the
  cocoa powder make chocolate addicting. Chocolate enthusiasts often
  admit they are addicts and find it difficult to resist cravings and
  binge with unpleasant consequences. Chocolate confections are complex
  mixtures of milk, sugars, nuts, flavors, including cinnamon and other
  spices; they present drug and allergenic effects simultaneously. Post
  chocolate symptoms include anxiety, migraine headaches, abdominal pain,
  joint pain, mental agitation and depression. Chocolate addiction is
  more socially acceptable than it is healthy. Some chocolate eaters
  become quite ill and quite obese.

  Women often report chocolate cravings in the premenstrual week.
  Chocolate also serves as a surrogate for companionship or affection.
  The addictive molecules in chocolate include caffeine and another
  speed-like drug, phenyethylamine (PEA). PEA is related to our own
  catecholamine neurotransmitters and their amino acid precursors,
  tyrosine and phenylalanine. PEA has arousal properties similar to
  catecholamines and may be one of the pleasure substances in the brain.
  PEA has been called the “love drug”. Most PEA absorbed from the bowel
  is destroyed in the blood or liver by the enzyme MAO-B.

  
  Coffee and Tea

  Coffee makes us speedy, irritable, sleepless, and often causes
  heartburn or ulcers. The removal of caffeine is supposed to reduce some
  of these undesirable effects. Coffee is an addicting beverage. If you
  consume more than 2 cups per day, you are likely to experience
  unpleasant withdrawal if you stop. The minimal suffering includes a
  headache, irritability, and fatigue. The popular idea that the bad
  effects of coffee are caused by one chemical, caffeine, is misleading.
  The 500 or so other chemicals in coffee include aromatic or phenolic
  chemicals and many are probably neurotoxic; other chemicals are
  allergenic. Coffee is also a crop with high pesticide residues. Coffee
  is definitely allergenic and makes some people obviously sick.
  Chlorogenic acid is one of the allergens which coffee shares with
  oranges.

  Black Tea and coffee have much in common, although they different plant
  products from different geographic zones. Tea contains caffeine and
  other members of the drug family, methylxanthines. Tea also contains
  tannin, a good tanning agent. The caffeine dose in a cup of coffee
  ranges from 100 to 160 mg. A cup of tea has 20-60 mg per cup and 12
  ounces of regular Coca Cola has 45 mg of caffeine. The symptom complex
  produced by tea parallels coffee, although overall, tea is milder and
  better tolerated. Green teas are the mildest of the caffeine drinks and
  have beneficial phytochemicals which make their use more attractive.

  Daily coffee ingestion induces a 24 hour cyclic disturbance with
  morning arousal, irritability, difficulty concentrating, subtle levels
  of disorganization, clumsiness, and forgetfulness. As the day
  progresses, 3 or more cups later, a heavy fatigue sets in by mid to
  late afternoon. Further coffee doses may rouse one a bit, but then
  further collapse is inevitable by evening. Irritability may evolve into
  disproportionate or inappropriate angry outbursts, pleasure-loss,
  absence of good-feelings, or empathy anesthesia.

   It is likely that the subtle pyschopathology of moderate to heavy
  coffee consumption contributes to the production of unnecessary
  conflict and dysphoria. The subtle cognitive and memory deficits which
  appear after coffee intake should alarm employers who expect their
  employees to think, remember, or carry out skilled, coordinated acts.
  It may be that coffee facilitates dull, routine, rote tasks where
  thinking, skill and initiative are unimportant.

  Under the circumstances, knowing what I know of addiction from
  firsthand experience and the shared experiences of other addicts, as
  well as from biochemical research, I would never recommend even
  moderate consumption of addictive poisons.  I have noticed that
  most if not all of the people who do recommend such moderate
  consumption have an axe to grind, usually the defense of their own
  addiction, which they are reluctant to relinquish.  It saddens me
  that many of those I witness doing such defending are educated and
  aware addicts who go way out of their way to avoid illicit drugs but
  will not consider what the legal drugs they’ve substituted are doing to
  their biochemistry and their health.  Far too many of them and of
  other Americans are morbidly obese from their addictions to
  foods.  Thus they make of their abstinence and recovery a
  difficult white-knuckle experience, filled with temptations and
  cravings.  There are many far
  healthier and longer-lasting ways to stimulate the production of
  beneficial biochemicals
  such as PGE1 and the pleasure neurotransmitters such as dopamine.

  “The only way to keep from returning to active addiction is not to take
  that first drug.”
   

  • 7:10 pm
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