Okay all, this will be the last this morning, but I hope it helps
Long post, but I can get you the site link...
http://204.147.80.67/~brecovery/Not_...Your_Mind.html
It's Not All In Your Mind
Alcoholism runs in families. Even before researchers showed how and why some people are predisposed to becoming alcoholic, simple observation showed that when one or both parents are alcoholic, the children are at risk. Until recently, researchers couldn't be sure whether this familial link was hereditary or environmental or both. Do people drink because they "learned to" at home or do they drink because they are genetically programmed to become alcoholic? While the environmental influence certainly can't be discounted, new evidence strongly suggests that heredity plays a much stronger role in alcoholism than was once thought.
What Twins Can Tell Us
Much of the new evidence comes from comparisons of identical and fraternal twins. Since identical twins develop from a single fertilized egg that divides after conception, both have the exact same genetic makeup and can be expected to be alike in most respects. For example, identical twins are always the same sex, always have the same hair and eye color, and usually reach the same adult height and weight. Studies of identical twins separated at birth and raised in different families have produced compelling evidence of the power of their genetic bond. In addition to their strikingly similar physical development, the twins have remarkably similar tastes, preferences, and interests.
Fraternal twins develop from two different eggs fertilized by two different sperm. Fraternal twins are no more closely related than siblings born separately.
If environment were the sole cause of alcoholism, the rate of alcoholism among twins raised in drinking families should be the same regardless of whether they are identical or fraternal. But if a genetic predisposition were responsible, the rate of alcoholism would be similar for both identical twins, who have exactly the same genes. Studies have shown that when one identical twin is alcoholic, the other is four times more likely to be alcoholic than when one fraternal twin is alcoholic, indicating that genetics play a part in alcoholism.
There have been many other studies aimed at showing whether nature or nurture is to blame for alcoholism. One of the first (Donald Goodwin, 1978) compared 133 sons of alcoholics adopted and raised by nonalcoholic parents to a similar group of adoptees with no genetic history of alcoholism. The sons of alcoholics were three times more likely to become alcoholic than the sons of nonalcoholic parents. A larger study in Sweden (C.R. Cloringer, M. Bohman, and S. Sigvardsson, 1981) followed 3,000 adoptees separated from their biological parents at an early age and raised by non-relatives. The risk of these children becoming alcoholic was two and a half times higher when one biological parent was alcoholic.
Researchers have also studied what happens to the children of nonalcoholics who are adopted into households where one parent is alcoholic. They have found no evidence that being raised by an alcoholic parent predisposes a child to alcoholism.
Under the Microscope
Research indicates that some hereditary abnormality of body or brain chemistry must be passed from generation to generation to account for the fact that alcoholism runs in families. The search for such an abnormality has yielded a number of valuable clues. The first was the discovery of certain unusual brain-wave patterns among alcoholics and their non-drinking children. P-300 brain waves, which influence memory, were absent or weaker than normal among the alcoholic families studied. (Not coincidentally, memory lapses are common complaints among alcoholics.)
Researchers discovered that alcoholics are much more likely than nonalcoholics to have a certain gene affecting receptor sites for dopamine, a central-nervous-system neurotransmitter that facilitates communication between nerve cells and is associated with pleasure seeking behavior. Researchers theorize that the newly discovered gene alters dopamine receptor sites in the brain. Receptor sites can be thought of as locks that can be opened only by the correct chemical key-in this case, dopamine. Exactly how the new gene predisposes a person to alcoholism isn't yet known, but the fact that it was found in 77 percent of the alcoholics studied and was absent in 72 percent of nonalcoholics suggests that it underlies some types of alcoholism.
More Chemical Clues
Discoveries about the way alcohol is processed in the body have provided further evidence of a genetic link. For example, Harvard scientist (L. Tunglai et al 1977) recently came upon a previously unknown liver enzyme responsible for metabolizing alcohol. This enzyme, alcohol dehydrogenase II (II ADH), can process or oxidize alcohol up to 40 percent more efficiently than the liver enzymes most of us have. People who have this enzyme and most of us do not- have an inborn ability to drink very large amounts of alcohol without becoming intoxicated. These are the folks who can drink many of us under the table without getting the least bit tipsy and/or feeling hung over the next morning.
Researchers have also discovered that the absence of a crucial liver enzyme accounts for the fact that very few Orientals become alcoholics. In fact, many Asians get sick whenever they drink. Their pulses race and they feel dizzy and nauseated. The explanation for this peculiar reaction is the fact that many Orientals have only one liver enzyme that processes alcohol, rather than the two found in people from other parts of the world. About half the Oriental population is missing this second crucial enzyme.
Alcoholics and nonalcoholics process alcohol differently. When alcohol reaches the liver, it is changed into acetaldehyde, a harmful byproduct of alcohol metabolism that can damage liver cells. Normally the liver rapidly transforms the harmful acetaldehyde into a neutral substance called acetic acid or acetate. The acetic acid is then converted into carbon dioxide and water. We expel the carbon dioxide through respiration and the water through urination.
Until recently, it was believed that the liver always handles alcohol in the same way. But new research shows that a different scenario occurs among certain alcoholics and children of alcoholics with no drinking experience (Figure 2). Their livers change alcohol into acetaldehyde at twice the normal rate, while the subsequent conversion of acetaldehyde into acetic acid is abnormally slow and takes twice as long as usual. The accumulation of acetaldehyde damages liver cells, which become abnormally large as they strive to get rid of the accumulated acetaldehyde. This damage affects the liver's ability to absorb and utilize the nutrients needed for good health. To make matters worse, excess acetaldehyde escapes the liver and travels through the bloodstream to the heart, where it can be very damaging (it interferes with the protein synthesis of the heart muscle). It also reaches the brain, where it blocks proper neurotransmitter action in creating normal feelings, behavior, and memory. The unused natural neurotransmitters begin to build up and combine with the acetaldehyde to form potent psychoactive compounds called tetrahydroisoquinolines (THIQs), which are remarkably similar to opiates. THIQs fit in the same receptor sites in the brain as natural pain-killing chemicals called endorphins and such narcotics as morphine and heroin.
The Chemistry of Addiction
Two decades ago, Texas researcher Virginia Davis noticed during autopsies of skid row alcoholics that their brains contained an opiate that she first mistook for heroin.. This was puzzling because these indigents did not have the money needed to support such an expensive drug habit. The heroin-like substance turned out to be THIQs that have been manufactured inside their brains when acetaldehyde from the breakdown of alcohol had combined with natural neurotransmitters. Davis's data support the concept of alcoholism as a true addiction stemming from specific biochemical events leading to the formation of an addictive substance similar to opiates such as heroin.
We now know that in heavy drinkers, THIQs displace endorphins and bind with the opiate receptors in the brain. In doing so, they signal the brain to stop producing endorphins, As the natural endorphin supply declines, more and more alcohol is needed to produce more THIQs to replace the natural endorphins and bind with opiate receptors to create feelings of well-being.
At the University of Texas, researcher Kenneth Blum, M.D., found that restoring these natural endorphins and neurotransmitters destroyed or depleted by alcohol will reduce cravings for alcohol and restore normal moods.
Some pertinent findings emerged from a study of the reactions to alcohol among two groups of college students. One group was composed of students who had a family history of alcoholism; those in the second group had no alcoholism in their backgrounds. After four drinks, the students from alcoholic families produced much higher levels of acetaldehyde, and they could perform a variety of mental and physical tests better under the influence of four drinks than when they had not been drinking. The students with no family history of alcoholism reported feeling moderately intoxicated and showed impaired physical dexterity, reflexes, and mental ability after four drinks.
Allergic/Addicted: Same Diagnosis, Different Chemistry
Not all alcoholics fit neatly into the pattern described above. Some may actually be allergic to alcohol. This theory has been advanced by Theron Randolph, M.D., the father of clinical ecology, a new field of medicine that contends that allergies to foods and environmental chemicals cause a number of physical conditions. Randolph has shown that addictions to food and alcohol can produce alternating highs and lows. The highs are feelings of well-being that occur when the body is supplied with the addictive substance; the lows are withdrawal symptoms. In his work with members of Alcoholics Anonymous, Randolph discovered that many were allergic/addicted to the sugars, grapes, and grains from which alcohol is made. He demonstrated that these people begin to crave alcohol when exposed to the underlying component to which they are addicted. In addition to Randolph's work, a study of 422 alcoholics by an Illinois researcher, Herbert Karolus, M.D., showed that most were allergic to wheat or rye, the grain bases of many distilled liquors.
An allergic response can affect any organ in the body. The skin may react with hives, the intestinal tract with diarrhea, the brain with migraine headaches or altered moods and behavior. Alcohol can wreak havoc on the brain chemistry of allergic/addicted individuals. Their first drinking experience is always unpleasant. Their bodies send a clear message of alcohol intolerance by making them feel ill. Unfortunately, many people try to overcome this and "learn to drink." With repeated doses of alcohol, their bodies have no choice but to adapt. Allergist William Philpott, M.D., describes this adaptation as an allergic/addicted response to alcohol. The pattern begins with a high when alcohol is ingested. One of the ways the body reacts to substances to which it is allergic is by producing its own addictive narcotics, the opioid endorphins, which create a feeling of euphoria. Once the pleasurable endorphin effect, the high, wears off, the withdrawal phase occurs. This is often manifested by emotional symptoms: depression, confusion, and anxiety. The only way to overcome these feelings is with another dose of the addictive substance.
In the early stages of this type of alcoholism, drinking provides only a gentle lift. The equally subtle letdown that comes later is usually not associated with the pleasure of drinking. But in time the period of pleasure becomes shorter, while the withdrawal symptoms become more intense.
Given this pattern, it is easy to understand why the allergic drinker returns to alcohol in an effort to avoid the pain of withdrawal, Unlike the II ADH/THIQ alcoholic, who can tolerate large amounts of alcohol with minimal behavioral changes and mild or no hangovers, the allergic/addicted alcoholic tends to be a binge drinker who loses control easily. People with this kind of chemistry typically get hangovers. They also have a tendency, when drinking, toward altered personality: sudden anger, depression, or abusiveness caused by the allergic response of their brains and central nervous systems.
Environmental Culprits
Clinical ecologists have also found that exposure to such toxic chemicals as gasoline, cleaning solvents, and formaldehyde can cause alcoholic cravings in sensitive individuals. If they inhale fumes from these chemicals on a daily basis, the same allergic/addicted adaptive mechanism described above can occur. These people can become mildly intoxicated as a result of breathing the fumes from such chemicals. They often find that they can maintain the high and ward off the letdown by heading for the bar at the end of the workday.
Take the case of Janet, a single parent, who cleaned offices at night. She sought our help for her intense depression. Janet had recently joined AA and was no longer drinking, but she still craved alcohol and battled suicidal thoughts. Driving home from work early one morning, she had to fight a powerful compulsion to steer her car over a bridge or into a tree.
Janet's work exposed her daily to fumes from a number of cleaning solvents. We sent her for tests to determine if the chemicals she was inhaling at work played any role in her depression and craving for alcohol When tested for sensitivity to ethanol (alcohol), she first felt high, almost intoxicated, then became withdrawn, and finally burst into tears and cried uncontrollably. Ethanol in any form (alcohol, cleaning fluids, gasoline, perfume) was the root of Janet's problem. After she found a job that no longer exposed her to ethanol fumes, she recovered quickly. Both her cravings and her depression vanished.
Common environmental chemicals not only set the stage for alcoholism, they can also precipitate relapse, as they have in many alcoholics whose AA peers unfairly labeled them 'weak" or "not working their program." In such people, uncontrollable cravings for alcohol can be turned on by provocative testing in clinical-ecology laboratories. Once activated, these cravings are powerful enough to overcome the strongest defenses against alcohol. Their effect on the brain robs sensitive individuals of the ability to make responsible decisions.
A Family Affair: Essential Fatty Acids
More chemical clues to the nature of alcoholism come from research focusing on alcoholics with at least one grandparent who was Welsh, Irish, Scottish, Scandinavian, or Native American. Typically, these alcoholics have a history of depression going back to childhood and close relatives who suffered from depression or schizophrenia. Some may have relatives who committed suicide. There also may be a family history of eczema, cystic fibrosis, premenstrual syndrome, diabetes, irritable bowel syndrome, or benign breast disease.
The common denominator here is a genetic abnormality in the way the body handles certain essential fatty acids (EFAs) derived from foods. Normally, these EFAs are converted in the brain to various metabolites such as prostaglandin E1 (PGE1), which plays a vital role in the prevention of depression, convulsions, and hyperexcitability. When the EFA conversion process is defective, brain levels of prostaglandin E1 are lower than normal, which results in depression.
In affected individuals, alcohol acts as a double-edged sword. It activates the PGE1 within the brain, which immediately lifts depression and creates feelings of well-being. Because the brain cannot make new PGE1 efficiently, its meager supply of PGE1 is gradually depleted. Over time, the ability of alcohol to lift depression slowly diminishes.
Several years ago, researchers hit upon a solution to this problem. They discovered that a natural substance, oil of evening primrose, contains large amounts of gamma-linolenic acid (GLA), which can help the brain convert EFAs to PGE1.
The results are quite dramatic. In a recent study in Scotland, researcher David Horrobin, M.D., matched two groups of alcoholics whose EFA levels were 50 percent below normal. The first group got EFA replacement, the second, a placebo. Marked differences between the two groups emerged in the withdrawal stage. The group that got EFA replacement had far fewer symptoms, while the placebo group displayed the full range of withdrawal symptoms associated with prostaglandin deficiency: tremors, irritability, tension, hyperexcitability, and convulsions.
At the outset of the study, members of both groups had some degree of alcohol-related liver damage. Three months later, the researchers found that liver function among the EFA replacement group was almost normal. There was no significant improvement among the placebo group.
A year later, the placebo group was still deficient in the natural ability to convert essential fatty acids into PGE1. What's more, only 28 percent of this group had remained sober; the rest had resumed drinking. Results were dramatically better among the EFA replacement group: 83 percent remained sober and depression free.
Long post, but I can get you the site link...
http://204.147.80.67/~brecovery/Not_...Your_Mind.html
It's Not All In Your Mind
Alcoholism runs in families. Even before researchers showed how and why some people are predisposed to becoming alcoholic, simple observation showed that when one or both parents are alcoholic, the children are at risk. Until recently, researchers couldn't be sure whether this familial link was hereditary or environmental or both. Do people drink because they "learned to" at home or do they drink because they are genetically programmed to become alcoholic? While the environmental influence certainly can't be discounted, new evidence strongly suggests that heredity plays a much stronger role in alcoholism than was once thought.
What Twins Can Tell Us
Much of the new evidence comes from comparisons of identical and fraternal twins. Since identical twins develop from a single fertilized egg that divides after conception, both have the exact same genetic makeup and can be expected to be alike in most respects. For example, identical twins are always the same sex, always have the same hair and eye color, and usually reach the same adult height and weight. Studies of identical twins separated at birth and raised in different families have produced compelling evidence of the power of their genetic bond. In addition to their strikingly similar physical development, the twins have remarkably similar tastes, preferences, and interests.
Fraternal twins develop from two different eggs fertilized by two different sperm. Fraternal twins are no more closely related than siblings born separately.
If environment were the sole cause of alcoholism, the rate of alcoholism among twins raised in drinking families should be the same regardless of whether they are identical or fraternal. But if a genetic predisposition were responsible, the rate of alcoholism would be similar for both identical twins, who have exactly the same genes. Studies have shown that when one identical twin is alcoholic, the other is four times more likely to be alcoholic than when one fraternal twin is alcoholic, indicating that genetics play a part in alcoholism.
There have been many other studies aimed at showing whether nature or nurture is to blame for alcoholism. One of the first (Donald Goodwin, 1978) compared 133 sons of alcoholics adopted and raised by nonalcoholic parents to a similar group of adoptees with no genetic history of alcoholism. The sons of alcoholics were three times more likely to become alcoholic than the sons of nonalcoholic parents. A larger study in Sweden (C.R. Cloringer, M. Bohman, and S. Sigvardsson, 1981) followed 3,000 adoptees separated from their biological parents at an early age and raised by non-relatives. The risk of these children becoming alcoholic was two and a half times higher when one biological parent was alcoholic.
Researchers have also studied what happens to the children of nonalcoholics who are adopted into households where one parent is alcoholic. They have found no evidence that being raised by an alcoholic parent predisposes a child to alcoholism.
Under the Microscope
Research indicates that some hereditary abnormality of body or brain chemistry must be passed from generation to generation to account for the fact that alcoholism runs in families. The search for such an abnormality has yielded a number of valuable clues. The first was the discovery of certain unusual brain-wave patterns among alcoholics and their non-drinking children. P-300 brain waves, which influence memory, were absent or weaker than normal among the alcoholic families studied. (Not coincidentally, memory lapses are common complaints among alcoholics.)
Researchers discovered that alcoholics are much more likely than nonalcoholics to have a certain gene affecting receptor sites for dopamine, a central-nervous-system neurotransmitter that facilitates communication between nerve cells and is associated with pleasure seeking behavior. Researchers theorize that the newly discovered gene alters dopamine receptor sites in the brain. Receptor sites can be thought of as locks that can be opened only by the correct chemical key-in this case, dopamine. Exactly how the new gene predisposes a person to alcoholism isn't yet known, but the fact that it was found in 77 percent of the alcoholics studied and was absent in 72 percent of nonalcoholics suggests that it underlies some types of alcoholism.
More Chemical Clues
Discoveries about the way alcohol is processed in the body have provided further evidence of a genetic link. For example, Harvard scientist (L. Tunglai et al 1977) recently came upon a previously unknown liver enzyme responsible for metabolizing alcohol. This enzyme, alcohol dehydrogenase II (II ADH), can process or oxidize alcohol up to 40 percent more efficiently than the liver enzymes most of us have. People who have this enzyme and most of us do not- have an inborn ability to drink very large amounts of alcohol without becoming intoxicated. These are the folks who can drink many of us under the table without getting the least bit tipsy and/or feeling hung over the next morning.
Researchers have also discovered that the absence of a crucial liver enzyme accounts for the fact that very few Orientals become alcoholics. In fact, many Asians get sick whenever they drink. Their pulses race and they feel dizzy and nauseated. The explanation for this peculiar reaction is the fact that many Orientals have only one liver enzyme that processes alcohol, rather than the two found in people from other parts of the world. About half the Oriental population is missing this second crucial enzyme.
Alcoholics and nonalcoholics process alcohol differently. When alcohol reaches the liver, it is changed into acetaldehyde, a harmful byproduct of alcohol metabolism that can damage liver cells. Normally the liver rapidly transforms the harmful acetaldehyde into a neutral substance called acetic acid or acetate. The acetic acid is then converted into carbon dioxide and water. We expel the carbon dioxide through respiration and the water through urination.
Until recently, it was believed that the liver always handles alcohol in the same way. But new research shows that a different scenario occurs among certain alcoholics and children of alcoholics with no drinking experience (Figure 2). Their livers change alcohol into acetaldehyde at twice the normal rate, while the subsequent conversion of acetaldehyde into acetic acid is abnormally slow and takes twice as long as usual. The accumulation of acetaldehyde damages liver cells, which become abnormally large as they strive to get rid of the accumulated acetaldehyde. This damage affects the liver's ability to absorb and utilize the nutrients needed for good health. To make matters worse, excess acetaldehyde escapes the liver and travels through the bloodstream to the heart, where it can be very damaging (it interferes with the protein synthesis of the heart muscle). It also reaches the brain, where it blocks proper neurotransmitter action in creating normal feelings, behavior, and memory. The unused natural neurotransmitters begin to build up and combine with the acetaldehyde to form potent psychoactive compounds called tetrahydroisoquinolines (THIQs), which are remarkably similar to opiates. THIQs fit in the same receptor sites in the brain as natural pain-killing chemicals called endorphins and such narcotics as morphine and heroin.
The Chemistry of Addiction
Two decades ago, Texas researcher Virginia Davis noticed during autopsies of skid row alcoholics that their brains contained an opiate that she first mistook for heroin.. This was puzzling because these indigents did not have the money needed to support such an expensive drug habit. The heroin-like substance turned out to be THIQs that have been manufactured inside their brains when acetaldehyde from the breakdown of alcohol had combined with natural neurotransmitters. Davis's data support the concept of alcoholism as a true addiction stemming from specific biochemical events leading to the formation of an addictive substance similar to opiates such as heroin.
We now know that in heavy drinkers, THIQs displace endorphins and bind with the opiate receptors in the brain. In doing so, they signal the brain to stop producing endorphins, As the natural endorphin supply declines, more and more alcohol is needed to produce more THIQs to replace the natural endorphins and bind with opiate receptors to create feelings of well-being.
At the University of Texas, researcher Kenneth Blum, M.D., found that restoring these natural endorphins and neurotransmitters destroyed or depleted by alcohol will reduce cravings for alcohol and restore normal moods.
Some pertinent findings emerged from a study of the reactions to alcohol among two groups of college students. One group was composed of students who had a family history of alcoholism; those in the second group had no alcoholism in their backgrounds. After four drinks, the students from alcoholic families produced much higher levels of acetaldehyde, and they could perform a variety of mental and physical tests better under the influence of four drinks than when they had not been drinking. The students with no family history of alcoholism reported feeling moderately intoxicated and showed impaired physical dexterity, reflexes, and mental ability after four drinks.
Allergic/Addicted: Same Diagnosis, Different Chemistry
Not all alcoholics fit neatly into the pattern described above. Some may actually be allergic to alcohol. This theory has been advanced by Theron Randolph, M.D., the father of clinical ecology, a new field of medicine that contends that allergies to foods and environmental chemicals cause a number of physical conditions. Randolph has shown that addictions to food and alcohol can produce alternating highs and lows. The highs are feelings of well-being that occur when the body is supplied with the addictive substance; the lows are withdrawal symptoms. In his work with members of Alcoholics Anonymous, Randolph discovered that many were allergic/addicted to the sugars, grapes, and grains from which alcohol is made. He demonstrated that these people begin to crave alcohol when exposed to the underlying component to which they are addicted. In addition to Randolph's work, a study of 422 alcoholics by an Illinois researcher, Herbert Karolus, M.D., showed that most were allergic to wheat or rye, the grain bases of many distilled liquors.
An allergic response can affect any organ in the body. The skin may react with hives, the intestinal tract with diarrhea, the brain with migraine headaches or altered moods and behavior. Alcohol can wreak havoc on the brain chemistry of allergic/addicted individuals. Their first drinking experience is always unpleasant. Their bodies send a clear message of alcohol intolerance by making them feel ill. Unfortunately, many people try to overcome this and "learn to drink." With repeated doses of alcohol, their bodies have no choice but to adapt. Allergist William Philpott, M.D., describes this adaptation as an allergic/addicted response to alcohol. The pattern begins with a high when alcohol is ingested. One of the ways the body reacts to substances to which it is allergic is by producing its own addictive narcotics, the opioid endorphins, which create a feeling of euphoria. Once the pleasurable endorphin effect, the high, wears off, the withdrawal phase occurs. This is often manifested by emotional symptoms: depression, confusion, and anxiety. The only way to overcome these feelings is with another dose of the addictive substance.
In the early stages of this type of alcoholism, drinking provides only a gentle lift. The equally subtle letdown that comes later is usually not associated with the pleasure of drinking. But in time the period of pleasure becomes shorter, while the withdrawal symptoms become more intense.
Given this pattern, it is easy to understand why the allergic drinker returns to alcohol in an effort to avoid the pain of withdrawal, Unlike the II ADH/THIQ alcoholic, who can tolerate large amounts of alcohol with minimal behavioral changes and mild or no hangovers, the allergic/addicted alcoholic tends to be a binge drinker who loses control easily. People with this kind of chemistry typically get hangovers. They also have a tendency, when drinking, toward altered personality: sudden anger, depression, or abusiveness caused by the allergic response of their brains and central nervous systems.
Environmental Culprits
Clinical ecologists have also found that exposure to such toxic chemicals as gasoline, cleaning solvents, and formaldehyde can cause alcoholic cravings in sensitive individuals. If they inhale fumes from these chemicals on a daily basis, the same allergic/addicted adaptive mechanism described above can occur. These people can become mildly intoxicated as a result of breathing the fumes from such chemicals. They often find that they can maintain the high and ward off the letdown by heading for the bar at the end of the workday.
Take the case of Janet, a single parent, who cleaned offices at night. She sought our help for her intense depression. Janet had recently joined AA and was no longer drinking, but she still craved alcohol and battled suicidal thoughts. Driving home from work early one morning, she had to fight a powerful compulsion to steer her car over a bridge or into a tree.
Janet's work exposed her daily to fumes from a number of cleaning solvents. We sent her for tests to determine if the chemicals she was inhaling at work played any role in her depression and craving for alcohol When tested for sensitivity to ethanol (alcohol), she first felt high, almost intoxicated, then became withdrawn, and finally burst into tears and cried uncontrollably. Ethanol in any form (alcohol, cleaning fluids, gasoline, perfume) was the root of Janet's problem. After she found a job that no longer exposed her to ethanol fumes, she recovered quickly. Both her cravings and her depression vanished.
Common environmental chemicals not only set the stage for alcoholism, they can also precipitate relapse, as they have in many alcoholics whose AA peers unfairly labeled them 'weak" or "not working their program." In such people, uncontrollable cravings for alcohol can be turned on by provocative testing in clinical-ecology laboratories. Once activated, these cravings are powerful enough to overcome the strongest defenses against alcohol. Their effect on the brain robs sensitive individuals of the ability to make responsible decisions.
A Family Affair: Essential Fatty Acids
More chemical clues to the nature of alcoholism come from research focusing on alcoholics with at least one grandparent who was Welsh, Irish, Scottish, Scandinavian, or Native American. Typically, these alcoholics have a history of depression going back to childhood and close relatives who suffered from depression or schizophrenia. Some may have relatives who committed suicide. There also may be a family history of eczema, cystic fibrosis, premenstrual syndrome, diabetes, irritable bowel syndrome, or benign breast disease.
The common denominator here is a genetic abnormality in the way the body handles certain essential fatty acids (EFAs) derived from foods. Normally, these EFAs are converted in the brain to various metabolites such as prostaglandin E1 (PGE1), which plays a vital role in the prevention of depression, convulsions, and hyperexcitability. When the EFA conversion process is defective, brain levels of prostaglandin E1 are lower than normal, which results in depression.
In affected individuals, alcohol acts as a double-edged sword. It activates the PGE1 within the brain, which immediately lifts depression and creates feelings of well-being. Because the brain cannot make new PGE1 efficiently, its meager supply of PGE1 is gradually depleted. Over time, the ability of alcohol to lift depression slowly diminishes.
Several years ago, researchers hit upon a solution to this problem. They discovered that a natural substance, oil of evening primrose, contains large amounts of gamma-linolenic acid (GLA), which can help the brain convert EFAs to PGE1.
The results are quite dramatic. In a recent study in Scotland, researcher David Horrobin, M.D., matched two groups of alcoholics whose EFA levels were 50 percent below normal. The first group got EFA replacement, the second, a placebo. Marked differences between the two groups emerged in the withdrawal stage. The group that got EFA replacement had far fewer symptoms, while the placebo group displayed the full range of withdrawal symptoms associated with prostaglandin deficiency: tremors, irritability, tension, hyperexcitability, and convulsions.
At the outset of the study, members of both groups had some degree of alcohol-related liver damage. Three months later, the researchers found that liver function among the EFA replacement group was almost normal. There was no significant improvement among the placebo group.
A year later, the placebo group was still deficient in the natural ability to convert essential fatty acids into PGE1. What's more, only 28 percent of this group had remained sober; the rest had resumed drinking. Results were dramatically better among the EFA replacement group: 83 percent remained sober and depression free.
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