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.”
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