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How to prevent the damaging effects of smoking,alcohol consumption, and air pollution
Sources of Acetaldehyde
Ethanol (more commonly known as alcohol) is the chemical contained in beer, wine, liquor and
liqueurs that gets people drunk. These beverages serve as carriers to get ethanol into the
drinker’s brain, promoting some degree of intoxication. Once in the body, alcohol is broken down
into carbon dioxide and water. However, this process takes time and occurs in several steps.
The first step occurs primarily in the liver, although other organs such as the brain and kidney
can also perform this stage of alcohol detoxification to a slight extent. An enzyme called "alcohol
dehydrogenase" converts alcohol into AH. Then another enzyme "aldehyde dehydrogenase"
must break the AH down into acetate. Acetate can then serve as a fuel in cellular energy
production. (Acetate is a form of acetic acid, the acid that makes vinegar sour.)
However, the conversion of AH to acetate does not always occur quickly or smoothly and therein
lies the problem. Research over the last several decades has shown that alcoholics tend to
rapidly convert alcohol to AH, but then convert AH to acetate very slowly, thus giving AH a
chance to work its mischief in the body.1 And depending on a person’s genetics, nutritional
status, and exposure to other chemicals such as formaldehyde, which also utilize aldehyde
dehydrogenase for their detoxification, even non-alcoholics may have difficulty rapidly
detoxifying AH.
The second major route of AH into the brain is through its production by a yeast called Candida
albicans. Candida is known to occur in the intestinal tract of virtually all humans to some degree.
When present only in small amounts, being kept in check by a healthy immune system and the
so-called "friendly flora," such as Acidophilus and Bifidus bacteria, Candida is relatively
harmless. Yet due to the modern overuse of antibiotics, birth control pills, and
cortisoneI/rednisone drug therapy, as well as excessive stress (which naturally produces excess
cortisone in the body), sugar consumption and malnutrition, millions of Americans now suffer
from an excessive growth of Candida in their intestines the so-called "yeast syndrome."2
Candida lives by fermenting sugars to produce energy. Unfortunately for the humans who harbor
large colonies of Candida in their gut, the waste by-product of this sugar fermentation by
Candida is AH.3 Biochemical research has shown that this AH may combine with red blood
cells, proteins, enzymes, and other substances present in the gut or gut lining, and thus travel
through the bloodstream to reach more distant parts of the body such as the brain.3 Research
has also shown that AH can then detach from the red blood cells or proteins it traveled with
through the bloodstream, thus enabling AH to damage cells far from the site of its intestinal
production by Candida.3
For those suffering from the yeast syndrome, the ingestion of beer, wine, and liqueurs provides a
double-barreled dose of AH. Not only is the alcohol in these beverages turned into AH, but the
malt and grain in beer and the sugar in wine and liqueurs provide excellent fuel for Candida to
produce the energy it needs to live.2 More AH is the inevitable by-product of the yeast’s sugar
fermentation.
When oil, gasoline, diesel fuel, and natural gas are burned, ending up in the air, AH is
produced.4 Thus, another major route of entry into the body for AH is through inhaling air laden
with vehicle and factory exhaust. People who spend hours commuting in dense freeway traffic,
professional drivers such as truck and taxi drivers in urban areas, and even those who live or
work in heavily trafficked areas or near freeways or major streets are especially at risk for
inhaling small but significant chronic levels of AH.
AH is also produced through the burning of tobacco.7 Thus, heavy cigarette smokers are also at
risk of inhaling AH through the inhaled smoke. And while the amounts of AH inhaled through
auto exhaust and cigarette smoke may be small compared to that from alcohol, research shows
that low-dose chronic AH exposure may still be sufficient to gradually damage proteins, enzymes
and other cellular structures in the brain and other organs.21
How Acetaldehyde Damages the Brain
Acetaldehyde alters red blood cell structure. It has been known since 1941 that AH easily
combines with red blood cell membrane proteins to convert the red blood cells into a "time-
release capsule" for AH, releasing the AH in the body far from the site where it attached to the
red blood cell.3 As this happens, however, the membrane covering the red blood cell becomes
stiffer.21 Yet in order to travel through the capillaries, which are the smallest blood vessels and
which feed the trillions of individual cells, the red blood cell must be able to fold or deform. The
average red blood cell diameter is 7 microns; yet a typical capillary is only 2 microns in diameter.
Red blood cells stiffened through chronic AH exposure will have difficulty deforming sufficiently
to pass through capillaries. Consequently, red blood cell-carried oxygen to many cells is
reduced.3 (Our brains require 20% of all the oxygen we breathe!) In addition, the work of K.K.
Tsuboi and colleagues has shown that AH forms stable combinations with hemoglobin in red
blood cells. This reduces the ability of red blood cells to accept, hold, and transport oxygen
through the bloodstream, which is their primary function.5
Acetaldehyde decreases the ability of the protein tubulin to assemble into microtubules.6
Microtubules are long, thin, tube-like structures that serve several functions in the brain cell.
They help provide structural support to the nerve cell, somewhat like girders in a bridge or a
building, keeping the nerve cell and the dendrites semi-rigid. Dendrites are the feathery-looking
extensions from the main body of the nerve cell which connect nerve cells to each other, with
some neurons connecting through dendrites to as many as 100,000 other neurons. Microtubules
also serve to transport nutrients and biochemical raw materials manufactured in the cell body to
the dendrites. When this raw material transport is compromised, the dendrites will gradually
atrophy and die off. Two classic examples of brain pathology involving degeneration of the
dendrites in humans are chronic alcoholic brain damage and Alzheimer’s disease.
Acetaldehyde induces a deficiency of vitamin B1. Thiamin, or Vitamin B1, is so critical to brain
and nerve function it is often called the "nerve vitamin." AH has a very strong tendency to
combine with B1, as the work of Herbert Sprince, M.D. (discussed below) has shown.7
Unfortunately, in detoxifying AH through combination with it, B1 is destroyed. Moderately severe
BI deficiency in humans leads to a group of symptoms called Wernicke-Korsakoff syndrome.9
This syndrome is characterized by mental confusion, poor memory, poor neuromuscular
coordination, and visual disturbances. Its primary accepted cause is chronic alcoholism. B1 is
also necessary for the production of ATP bioenergy in all body cells including the brain, and the
brain must produce and use 20% of the body’s energy total, even while asleep. Vitamin B1 is
also essential for production of acetylcholine. Acetylcholine is one of the brain’s major
neurotransmitters, facilitating optimal memory, mental focus and concentration, and learning.
Alzheimer’s disease represents a rather extreme case of memory loss and impaired
concentration due to destruction of acetylcholine-using brain cells. In a classic experiment
reported in 1942, R.R. Willams and colleages found that even mild B1 deficiency in humans
continued over a long period of time (the experiment ran six months) products symptoms including
apathy, confusion, emotional instability, irritability, depression, feelings of impending doom,
fatgue, insomnia, and headaches 8 all symptoms of less-than-optimal brain function.
Below is a range of possible nutrients levels that may offer pprotection to those suffering
from chronic AH toxicity. (divide into 2-3 doses, take with meals)
Acetaldehyde induces deficiencies of niacin and NAD. Niacin (Vitamin B3) is present in the
human body primarily in its coenzyme form, NAD.1 NAD is involved in the majority of steps in
which sugar and fat are burned for energy in all cells.10 NAD is normally the most plentiful
vitamin coenzyme in the human brain. NAD is important as a catalyst in the production of many
key, brain neurotransmitters, such as serotonin. Neurotransmitters are the biochemicals that
allow nerve cells to communicate with each other. NAD is also the coenzyme that activates
alcohol dehydrogenase and aldehyde dehydrogenase, the enzymes that break down alcohol
and AH.11 Zinc is also required along with NAD to activate these two enzymes.12
Since the need for NAD in all cells is great, yet the supply is limited, NAD is normally recycled
continually during cellular energy production. Yet, when NAD helps detoxify AH, this recycling of
NAD is blocked, and an altered form of NAD called "NADH" accumulates, impairing cellular
biochemistry in many ways.1, 21 Thus, chronic AH exposure may produce a mild, functional,
niacin/NAD deficiency, even in a person consuming a so-called "balanced diet" which meets
RDA levels of niacin intake.
Extreme niacin deficiency produces the classic nutritional disease Pellegra with dramatic
symptoms, both physical and mental. Since niacin is needed in large amounts for optimal brain
function, a mild niacin deficiency tends to produce mostly psychological symptoms. These
symptoms may include feeling fearful, apprehensive, suspicious, and worrying excessively with
a gloomy, downcast, angry and depressed outlook. Headaches, insomnia, depression, agitation,
and inability to concentrate may also occur.13 This profile certainly applies to many chronic
alcoholics and Candida patients, who obviously suffer from long-term, mild AH exposure.
Acetaldehyde reduces Acetyl Coenzyme A and impairs cellular energy production. Pantothenic
Acid (Vitamin B5) is one of the most critical vitamins for normal brain function. The active form of
B5 is Coenzyme A. Coenzyme A in turn is combined with acetate in all cells to form Acetyl
Coenzyme A. Acetyl Coenzyme A is perhaps the most pivotal single biochemical in all cellular
biochemistry; both sugar and fat must be transformed into Acetyl Coenzyme A to power the
Krebs’ cycle which produces 90% of all the energy used by every cell in the body, including brain
cells.11 Unfortunately, for Acetyl Coenzyme A, however, AH has a strong affinity to combine with
Acetyl Coenzyme A. The work of biochemist H.P. Ammon has shown that AH suppresses the
activity of Acetyl Coenzyme A in a dose-dependent fashion. He has also demonstrated that the
energy-producing activity of cells falls in parallel with the declining levels of Acetyl Coenzyme A
as the concentration of AH increases.1 The brain use. 20% of all body energy for normal
function. Acetyl Coenzyme A is also necessary for the production of acetylcholine, the memory,
learning and concentration neurotransmitter. 14
Acetaldehyde induces a deficiency of Pyridoxal-5-Phosphate (P5P). P5P is the major coenzyme
necessary to form virtually all major brain neurotransmitters.10 It is involved in all transamination
reactions, whereby cells may convert many different amino acids into each other to satisfy their
ever-shifting amino acid needs.10 P5P is necessary to convert essential fatty acids into their
final use forms, as well as to turn linoleic acid into the key, nerve cell-regulating biochemical,
Prostaglandin E1.15 P5P helps regulate magnesium entry into cells,16 and the level of
excitability of nerve cells is strongly dependent upon their magnesium level. P5P is also
necessary to convert vitamin B3, niacin/niacinamide, into the active coenzyme form, NAD.17
Unfortunately for P5P (and we humans who are so dependent on it), AH is known to strongly
combine with the protein portion of P5P enzymes in a way that displaces the P5P portion of the
molecule. This subjects P5P to an increased rate of destruction and results in abnormally low
blood and tissue levels of this coenzyme.1,18
Acetaldehyde unfavorably influences prostaglandin metabolism. Delta-6-Desaturase is the
enzyme that converts the common fatty acid linoleic acid into gamma linolenic acid, which is
totally absent from any typical diet. Gamma linolenic acid in turn is the only raw material that can
be converted into prostaglandin El. Prostaglandin El is a key regulatory biochemical for both
nerve cells and the immune system. It also serves to regulate the production of the pro-
inflammatory prostaglandin E2. Prostaglandin El prevents excessive production of
prostaglandin E2 from the dietary fatty acid, arachidonic acid, which is plentiful in meat, poultry
and dairy products. Researchers in prostaglandin biochemistry have discovered, however, that
AH is a powerful deactivator of Delta-6-Desaturase.15 AH thus tends to suppress gamma
linolenic acid production, which in turn suppresses prostaglandin El production. Low
prostaglandin El production "takes the brakes off" production of prostaglandin E2 and a related
compound, TXB2, increasing their levels far above normal. The published research of David
Horrobin, M.D.,15 and psychiatrist Julian Lieb,l9 has shown high levels of prostaglandin E2 and
TXB2, coupled with low levels of prostaglandin El,to be a major causal factor in some forms of
depression.
Acetaldehyde promotes addiction to toxic substances. Perhaps one of the most surprising ways
AH may alter normal brain function is due to its tendency to combine in the brain with two key
neurotransmitters, dopamine and serotonin.20 When AH and dopamine combine, they form a
condensation product called salsolinol. When AH combines with serotonin, another product
called beta-carboline is formed. Salsolinol and beta-carboline are two of a group of inter-related
and interconvertible compounds called tetrahydro-isoquinolines.20 The various tetrahydro-
isoquinolines which both animal and human research have shown to occur at high levels in the
brains, spinal fluids, and urine of chronic alcoholics are closely related in structure, function, and
addictive power to opiates!20 Successfully detoxifying alcoholics have been shown to excrete
especially high levels of these opiate-like chemicals in their urine.20 Thus, these AH-generated,
opiate-like biochemicals may at least partly explain why alcoholics are so addicted to alcohol,
cigarette smokers to cigarettes, and Candida-sufferers to sugar, since all three of these
conditions promote chronic excessive body AH levels.20 And, like opiates, these
tetrahydroisoquinoline biochemicals would tend to promote lethargy, mental cloudiness and
fogginess, depression, apathy, inability to concentrate, etc. These, of course, are symptoms
common to both alcoholism and Candidiasis, the two conditions which would tend to generate
the highest chronic AH levels in the body.20
The difficulties discussed above that are caused by chronic AH toxicity should indicate to the
reader that AH has a significant ability to compromise brain function. A partial summary of AH’s
damaging effects on brain function includes the following:
Impaired memory
Herbert Sprince, M.D. and his colleagues published many articles in the 1970’s detailing the
results of their experiments which used various nutrients to protect rats from AH poisoning.
Sprince fed a control group of rats an amount of AH sufficient to kill 90% of the control group in
72 hours. The experimental group of rats given the same amount of AH were also given various
nutrients, either singly or in combination, that might detoxify the AH. After 72 hours, the death
rate for rats given large oral doses of Vitamin C was only 27% (vs 90% in controls), 20% for rats
given the sulfur amino acid L-cysteine, 10% for rats receiving Vitamin BI, and an amazing 0%
for rats protected by N-acetyl cysteine or lipoic acid. A lower dose combination of C, B1 and
either L-Cysteine or N-acetyl cysteine also gave near 0% death rates!7 But, the nutrient doses
Sprince administered were rather gigantic compared to RDA levels of nutrients, being equivalent
to multi-gram doses for humans. Fortunately, however, most people are not subjected to such
high levels of AH, so lower doses of these nutrients would doubtless provide significant AH-
detoxifying power when used on a long-term basis.
John Cleary, M.D. has published papers summarizing many doctors’ and researchers’
successful use of niacin (Vitamin B3) and zinc in alcohol and AH detoxification.1 Since the
enzymes that break down alcohol and AH are both B311 and zinc-activated,12 this provides an
obvious rationale for their protective use in chronic alcohol/AH toxicity situations. Finally,
because chronic high tissue levels of AH impair the normal process of recycling the active form
of B3 (NAD) for continual re-use,1 it is obvious why normal dietary levels of B3 might be
insufficient to provide optimal brain B3 levels in chronic AH toxicity situations.
References:
References:
1. Cleary, J.P. The NAD Deficiency Diseases. J Orthomolecular Med, 1986,1:164-74.
Special Notice: The statements contained in this article have not been evaluated
by the U.S. Food & Drug Administration (FDA).
The products discussed are not intended to diagnose, treat, cure, or prevent
any disease.
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