It's Not All In Your Mind
Excerpts from 7 Weeks to Sobriety, by Joan Mathews Larson
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.
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.
Is There an Alcoholic Personality?
One of the most persistent myths about alcoholism is that it stems from some sort of personality disorder. Dr. George Vaillant, an eminent Harvard psychiatrist, has spent forty years trying to determine if there is any truth to this popular conception. His team of psychologists and sociologists has studied more than 650 young men in hopes of finding traits that predict alcoholism. In a 1984 report on his long-term study, Vaillant concluded that there is no evidence to support the belief that personality disorders predispose a person to alcoholism:
Future alcoholics do NOT appear different from future asymptomatic drinkers in terms of premorbid psychological stability. It is the heavy use of alcohol that causes personality alternations.
Even sociopathic behavior is almost always a consequence, not a cause of alcohol abuse.
Just as light passing through water confounds our perceptions, the illness of alcoholism profoundly distorts the individual's personality.
For a better understanding of Dr. Vaillant's conclusions, let's take a look at one of his subjects, James O'Neill, chosen for the study at age nineteen. This case study is taken from Dr. Vaillant's book The Natural History of Alcoholism.
Vaillant's study group was composed of college sophomores chosen on the basis of their psychological health. At the time, in the forties, the dean's office rated O'Neill's stability as "A" and ranked him in the top third of the study group. The project psychiatrist described O'Neill's parents as "reliable, consistent, obsessive and devoted." O'Neill's relationship with his mother was rated among the best in the study. In 1950, six months after his mother died, O'Neill still felt the loss deeply.
When he was twenty-one, O'Neill married his high school girl-friend, whom he had been in love with since age sixteen. Six years later the marriage still seemed solid.
O'Neill had begun drinking heavily in 1948, and by 1950 he had begun drinking in the morning. He admitted that between 1952 and 1955 he had written his Ph.D. dissertation while continuously intoxicated and had regularly sold books from the university library in order to support his drinking. By 1955, his alcoholism was campus gossip; by 1957, O'Neill recognized that his pattern of drinking, sexual infidelity, gambling, and unrepaid borrowing suggested a psychopathic personality. In discussions with a psychologist in the 1960s, O'Neill voiced no sorrow about his mother's death and could not even remember when she had died. Later, a psychiatrist observed that O'Neill "felt quite hostile and anxious about the fact that he was an army brat and never had a normal childhood, and his parents were always very cold toward him. He harbored many feelings of hostility toward his wife."
In 1970, when he was fifty-two, O'Neill stopped drinking and joined AA. Two years later he described himself to a project psychiatrist as "a classic psychopath totally incapable of commitment to any man alive. I'm hyperemotional. In AA, I'm known as Dr. Anti-Serenity."
What happened to this promising, psychologically stable young man?
There is no doubt that his brain no longer served him normally. His thinking had become negative. He felt isolated and hyperactive. A reasonable explanation for his personality changes is that heavy alcohol use gradually disrupted his normal brain function by blocking or destroying the natural chemicals that maintain emotional stability. This kind of chemical disruption cannot be talked away by therapy.
Your Alcoholic Brain: The Malfunctioning Computer
Recent discoveries about the workings of the brain have shed important new light on the role a wide variety of natural chemicals play in maintaining normal thought patterns, feelings, self-awareness, memory, and perception. There is also an enormous body of research to show that alcohol diminishes or destroys many of the substances the brain must use to create and regulate our emotions. The human mind cannot operate in a vacuum. It depends on the molecular functioning of the brain to maintain mental processes and emotional health.
For the parents, husbands, wives, and friends of an alcoholic, there is some comfort in knowing that the personality changes they have observed are a result of alterations in normal brain chemistry caused by heavy drinking. It is no more logical to blame the alcoholic for altered behavior than to demand accountability from someone with Alzheimer's disease. They don't choose to behave as they do. They are ill, victims of chemical changes they cannot control.
My search for an explanation for my son's suicide finally ended when I came to understand how alcohol had affected his brain, altered his personality, and turned him into a suicidal depressed young man.
But this understanding gave rise to more questions. What could be done to prevent similar tragedies? Is there no way to undo the damage alcohol causes?
As I pondered these questions, I began to wonder about the value of the conventional approach to the treatment of alcoholism. For all the spiritual resources provided by AA and the psychological insights available in counseling and group therapy, no attempts were being made to undo the damaging effects of alcohol on the delicate chemical balance that keeps the brain and central nervous system functioning normally. Why weren't we trying to fix what alcohol had broken?
Was I overlooking something? Surely others had asked the same questions that nagged at me. George Vaillant had brilliantly and conclusively demonstrated that the alcoholic's unstable behavior is a consequence, not a cause, of alcoholism and that personality changes stem from the physical damage done by this disease. Was there no treatment to repair that damage?
Back to the Drawing Board
In 1896 Sigmund Freud predicted that "the future may teach us to exercise a direct influence by means of chemical substances upon the amounts of energy and their distribution in the apparatus of the mind." By 1927 he had become "firmly convinced that one day all these mental disturbances we are trying to understand will be treated by means of hormones or similar substances."
Today, we see how right he was. We now have drugs to treat depression, the schizophrenias, and obsessive-compulsive disorder. And lying unused in libraries everywhere are reports on studies of the destructive effect of alcohol on the mind and body through its power to inhibit access to key amino acids, vitamins, minerals, trace elements, enzymes, hormones, and essential fatty acids-the natural chemicals that support life and sustain sanity.
My question was whether it would be possible to restore depleted or damaged natural chemicals. If it was, I theorized, recovery from alcoholism might be more successful than it was with current treatment.
Nobel Prize laureate Linus Pauling coined the word "orthomolecular" to describe the process of "establishing the right molecules in the body by varying the concentrations of substances normally present and required for optimum health." Could orthomolecular treatment be the answer I sought? At the time I had been working as a chemical-dependency counselor for five years and was weary of seeing people discharged when they were still depressed and ill. My peers didn't see what I was getting at. Small wonder, their training hadn't included the study of the physical basis of psychological problems.
But the clients understood. They were painfully aware that therapy had failed to eliminate their cravings, anxiety, insomnia, depression, and mental confusion. I finally decided to test my theories to see what would happen by combining biochemical repair with traditional treatment for alcoholism. In January 1981, I established the Health Recovery Center as a pilot program offering physical detoxification and biochemical repair along with counseling and participation in Alcoholics Anonymous.
We focused on the internal symptoms as well as the obvious external calamities that brought our clients to treatment. We knew they could put their calamities behind them, but it would take more than talk to relieve the agony emanating from their chemically disrupted brains.
Our biochemical repair program is built around two premises
1.Addressing the substances that must be kept out of the alcoholic's body (including alcohol and other drugs, such as nicotine, caffeine, and refined sugars)
2.Addressing the substances that must be restored to the brain and body (chemicals depleted by alcohol.)
We begin with a physical exam and laboratory testing to identify where damage has occurred. Clients are also screened for vulnerability to substances that can cause cravings for alcohol
At the outset we explain why it's so important that clients avoid caffeine, nicotine, and refined sugars in addition to alcohol. We were amazed at how much coffee our clients had been drinking; some were up to forty cups a day. Caffeine is a drug. Although it recently received a clean bill of health for those concerned about heart disease and cancer, it can complicate or retard recovery from alcohol. Caffeine pumps a lot of adrenaline into the bloodstream. This temporarily provides energy-the morning lift so many people get from their first cup of coffee. Adrenaline also dumps stored glycogen (sugar) into the bloodstream, which triggers an outpouring of insulin. This caffeine-triggered rush of sugar and insulin is no help for alcoholics attempting to stabilize their glucose metabolism.
Foods containing refined sugars are also off-limits because they intensify hypoglycemic symptoms (often described as "dry-drunk" behaviors).
Smoking and using snuff or chewing tobacco is bad for everyone, but many alcoholics already have a lower than normal resistance to disease and do not need any more health hazards than they have already accumulated.
Few treatment programs require clients to avoid these substances on the theory that patients should not have to give up anything more than alcohol. It is a sympathetic attitude we don't think our clients can afford.
From the start, our treatment results were dramatic. Even clients who had failed to recover repeatedly in the past did very well. After two years, we knew we were on the right track. Most clients recovered both their sobriety and their health. The time had come to collect scientific data to confirm (or disprove) what we thought was happening. The research became the basis of my Ph.D. dissertation. I collected data on one hundred alcoholic clients chosen at random. Each was followed for up to three and a half years after treatment. Briefly, this is what I found:
Ninety-eight percent had either an alcoholic parent or close relative. (The other two were adopted, so their genetic heritage was unknown.)
There were ninety-eight previous treatment experiences among the one hundred patients (some had been treated more than once; others, not at all). Of those previously treated, more than half had relapsed by the third month following their last treatment
After one year, only 24 percent had remained sober.
Of the one hundred clients, eighty-eight had abnormal glucose metabolism (hypoglycemia or diabetes).