The word “alcoholism” does not describe a disease but rather it’s a behavior. Behavior is self-determined by choice.  Choice, then, is the cure for alcoholism and any other form of drug abuse.  In fact, personal choice is the only method by which people stop alcohol and drug abuse.

“Men at some time are masters of their fates: The fault, dear Brutus, is not in our stars, but in ourselves, that we are underlings.” ~ Julius Caesar Act I, Scene II

For at least the last 500 years man has tried to blame unwanted behavior on anything and everything but himself: as in, “If there is a disease for overindulging in alcohol or other drug, then I am not really responsible for my drinking and drugging behavior.”

I am not alone in the assertion that alcoholism and drug additions are not diseases. So, let’s set aside the hysteria and look at this from a common sense point of view.

In science, nothing exists that has no proof of existence.  That which has no proof, but is thought to exist, exists as a matter of conjecture and faith, not science.  In the case of disease, meaning “a condition that results in medically significant symptoms in a human,” there exists no credible evidence supporting the notion that regular excessive use of any substance is a disease.  This conclusion is based on the normally accepted understanding of the word “disease.”

Diseases are determined and described by the scientific method.   If, indeed, the excessive consumption of alcohol is a disease there must exist some scientific study that determined it to be a disease.  Such a study would describe a specific and predictable set of symptoms that would involuntarily manifested in the sufferer.  No such study exists.

Consider the facts surrounding the disease theory, and its development, which provides evidence that the “disease of alcoholism,” indeed alcoholism itself, is merely folklore and not established by way of the scientific method.

When adding “alcoholism” to the Diagnostic and Statistical Manual of Mental Disorders in 1956 the American Psychiatric Association was, for the most part, relying on the work conducted by Dr. E.M. Jellinek at Yale University during the  the 1940’s.  Subsequently, Jellinek’s study was determined to be flawed according to Yale University. At the request of Yale University, Jellinek retracted all of his conclusions, stopping just short of admitting that his research was fraudulent.  Later, Jellinek was found to be a fraud:  The schools where he claimed to have earned his degrees had no record of him receiving any. The point here is not to malign Jellinek or Yale, but to merely provide an historical account with respect to the origin of “alcoholism, the disease.”

It is important to understand that the disease theory is just that – a theory. Additionally, it is important to understand that this theory is only accepted as fact by the treatment industry here in the United States. The rest of the world considers the disease theory for alcoholism unsubstantiated. In his book Why We Should Reject The Disease Concept of Alcoholism, Herbert Fingarette, Ph.D., makes the following observations:

“…In the United States, but not in other countries such as Great Britain (Robertson and Heather, 1982), the standard answer is to call the behavior a disease – ‘alcoholism’ – whose key symptom is a pattern of uncontrollable drinking. This myth, now widely advertised and widely accepted, is neither helpfully compassionate nor scientifically valid. It promotes false beliefs and inappropriate attitudes, as well as harmful, wasteful, and ineffective social policies.”

The myth is embodied in the following four scientifically baseless propositions:

1. Heavy problem drinkers show a single distinctive pattern of ever greater alcohol use leading to ever greater bodily, mental, and social deterioration.
2. The condition once it appears persists involuntarily: the craving is irresistible and the drinking is uncontrollable once it has begun.
3. Medical expertise is needed to understand and relieve the condition (“cure the disease”) or at least ameliorate its symptoms.
4. Alcoholics are no more responsible legally or morally for their drinking and its consequences than epileptics are responsible for the consequences of their movements during seizures.

The idea that alcoholism is a disease has always been a political and moral notion with no scientific basis. It was first promoted in the United States around 1800 as a speculation based on erroneous physiological theory (Levine, 1978), and later became a theme of the temperance movement (Gusfield, 1963). It was revived in the 1930s by the founders of Alcoholics Anonymous (AA), who derived their views from an amalgam of religious ideas, personal experiences and observations, and the unsubstantiated theories of a contemporary physician (Robinson, David, 1979)

Another observation is offered by Jeffery Schaler, Ph.D.  in June of 1995:

“Extensive research supports the idea that addiction is a voluntary process, a behavior that is better explained by individual psychological and environmental factors, than physiology and the chemical properties of drugs.”

In another article authored by Dr. Phil Stringer entitled Disease, Victimization, and Personal Responsibility, he raises the question:

“How many people who never decide to drink would ‘catch’ the ‘disease’ of alcoholism?”

The obvious answer is none. In the traditional meaning of the word “disease,” a chosen behavior does not define a disease because one can just as reasonably choose not to drink or use drugs. The disease theory simply provides the person with a drug or alcohol problem an easy out from taking responsibility for themselves, their behavior, and the problems they cause.

There are hundreds of researchers who have looked carefully at the alcoholism disease theory. Most have rejected the notion that alcoholism is a disease. The only studies that support the disease theory are those conducted by organizations and individuals who have a vested interest in the over consumption of alcohol or other drugs being a disease (e.g. Alcoholics Anonymous, NIAAA and NCADD). The studies that have touted alcoholism as a disease are researchers who derive a living, in one way or another, from the treatment industry. These are hardly sources that can be trusted.

Finally, consider the paradoxical nature of the disease theory: the theory contends that once the disease is in place (diagnosed), the alcoholic has lost the power of choosing not to drink or the drug addict to not use drugs. But, how can that be true when millions of “diagnosed” alcoholics have stopped drinking and never return to problem drinking and drug addicts have stopped using drugs? If, indeed, they lost their power to choose to not use alcohol or other drugs, how did these millions of people with drug and alcohol problems stop drinking or drugging? Are we to believe that counselors and other professionals can make the choice for their patients because their patients have “lost their personal power of choice?” Or perhaps Alcoholics Anonymous and other 12-step programs provide some “magic” that gives members their choice back, but only “one day at a time.” Or maybe we are to believe that there is some universal power (choice power) that is channeled only through licensed counselors and other would-be professionals.

When common sense prevails, often the right answer is what we have known all along: The fault, dear Brutus …is in ourselves. Alcoholism and drug addiction is not disease. There is not now, nor has there ever been, any scientific evidence of such a nonsensical assertion.

I want to be clear: I am in no way asserting that physical addiction to a substance does not exist. It is a fact that the human body does become accustomed to, and even learn to relay on, unhealthy and even poisonous substances. The human body is extremely adaptable, even to extremely adverse conditions. The result of physical drug addiction can be observed as the withdrawal symptoms seen when drugs or alcohol stop being introduced to body: it is caused by the body trying to again learn, or adapt, to regulating body functions without the interference of the substance. However, once the sustenance has been cleansed from the body, only the psychological effects remain. Just as drug use is a learned behavior, overcoming the habitual and destructive thought processes associated with  drug use are skills that can be acquired, practiced, and eventually mastered. It is not a lifetime disability; it’s a choice.

Don’t be fooled by the propaganda that attempts to make you believe you are helpless and have a lifetime incurable disease. You can choose to learn how to be well, and stay well for the rest of your life. While it can be difficult, and take time to learn to how to overcome unhealthy habits and thought processes, it is possible.

By Shari Roan
Originally published by The Los Angeles Times, January 6, 2010

Only people with severe depression benefit from antidepressants, says research published in the Journal of the American Medical Assn. Others do better with non-medical approaches.

Antidepressant medications probably provide little or no benefit to people with mild or moderate depression, a new study has found. Rather, the mere act of seeing a doctor, discussing symptoms and learning about depression probably triggers the improvements many patients experience while on medication.

Only people with very severe depression receive additional benefits from drugs, said the senior author of the study, Robert J. DeRubeis, a University of Pennsylvania psychology professor. The research was released online Tuesday and will be published today in the Journal of the American Medical Assn.

Hundreds of studies have attested to the benefits of antidepressants over placebos, DeRubeis said. But many studies involve only participants with severe depression. Confusion arises, he said, “because there is a tendency to generalize the findings to mean that all depressed people benefit from medications.”

The current analysis attempted to quantify how much of antidepressants’ benefit is attributable to chemical effects on the brain and how much can be explained by other factors, such as visiting a doctor, taking action to feel better or merely the passage of time.

Researchers reviewed six randomized, placebo-controlled studies with a total of 718 patients who took either an antidepressant or placebo. The patients were adults with levels of depression ranging from mild to very severe based on the Hamilton Depression Rating Scale, a questionnaire widely used in depression research. The studies did not exclude patients who were likely to have a strong response to a placebo. Researchers then compared the patients’ depression scores at the beginning of treatment with those after at least six weeks of treatment.

The study found that the magnitude of the drugs’ benefit increased with the baseline level of depression. The effect of treatment was similar in people with mild, moderate and severe symptoms, regardless of whether they took an antidepressant or placebo. Only the people who rated very severe on the depression scale at the start of the study showed measurable improvements on antidepressants.

“There is no doubt that there are tremendous benefits from antidepressants, as our study showed,” DeRubeis said. “But this study helps us resolve, to some degree, the question of how much benefit people can expect from the medicines themselves when symptoms are not severe.”

Other research has also found that antidepressants are most effective for severe symptoms, said Dr. Philip Wang, deputy director of the National Institute of Mental Health. Though it could be that antidepressants don’t work well for mild to moderate depression, it’s also possible that people enrolled in antidepressant studies have robust placebo responses that mask some of the impact of the medication.

A severely depressed person who would probably benefit from antidepressants might have symptoms such as frequent weeping, feelings of guilt and sadness, thoughts that life is not worth living, problems sleeping, fatigue and withdrawal from normal activities, DeRubeis said.

Better antidepressants are needed for people with mild to moderate depression, Wang said, as is research on how to diagnose depression with tools, such as biomarkers, that could help personalize treatment.

Of the six studies in the current analysis, three involved selective serotonin reuptake inhibitors, or SSRIs, the most commonly used antidepressants, and three involved an older class of medications called tricyclics. Both classes are thought to be equally effective, although SSRIs are associated with fewer side effects.

One exception to the study findings, DeRubeis said, was people with dysthymia, or chronic, low-level depression. The analysis assessed severity of symptoms, not chronically, he said. Other studies have established that people with chronic depression, no matter how severe, tend to respond well to antidepressants while other treatment may be ineffective.

Study Finds Medication of Little Help to Patients with Mild to Moderate Depression

by Jon Hamilton
Originally published by www.npr.org July 1, 2009

Three new genetic studies are providing some tantalizing hints about what causes schizophrenia.

The studies, published in the journal Nature, identify sections of our genetic code in which small changes can affect a person’s risk for developing the disorder.

The studies found such changes in stretches of code involved in brain development, memory and the immune system.

The findings are important because schizophrenia has been so hard to study, says Kari Stefansson, CEO of the Icelandic company deCODE Genetics and an author of one of the studies. One reason is that schizophrenia doesn’t occur in animals.

“It’s a disease of thoughts and emotions,” Stefansson says, “the two functions of the brain that define us as a species and define us as individuals.”

Scientists have tried for decades to find differences between the brains of typical people and those with schizophrenia, but without much success. So Stefansson and a consortium of researchers from around the world decided to look for subtle differences in the genes of thousands of people. Some had schizophrenia; some didn’t.

One place the studies found a clue about what might be going wrong in the brains of people with schizophrenia was in a gene responsible for a protein called neurogranin, which can affect memory and thought.

“The neurogranin pathway could be one of the biochemical pathways that lead to this disturbance of thought,” Stefansson says.

But he says a more provocative finding is a genetic hot spot in a stretch of code that affects the immune system.

“It raises the question that somehow the tendency to develop schizophrenia may have something to do with infections of mothers during pregnancy.”

The idea is that some families carry a genetic variation that affects the way the immune system responds to infection, Stefansson says. If a mother gets the flu while she’s pregnant, this immune response may affect her child’s brain.

It’s also possible that the immune system is involved in schizophrenia in some other way, says Dr. Tom Insel, director of the National Institute of Mental Health, which helped fund the new studies.

He says the stretch of genetic code affecting immunity is pretty mysterious.

“In some ways it’s a little bit like the Bermuda Triangle of the human genome,” he says. “It’s an area with tremendous amounts of variability. And it’s an area where we often find variation that’s associated with many different disorders: diabetes, rheumatoid arthritis, Crohn’s disease.”

In those diseases, the immune system attacks the body’s own cells, a process that could also affect the brain. Researchers have suspected the immune system before, Insel says. Now, they’ll probably take a harder look.

Insel says he’s particularly intrigued by the finding that some genetic variations linked to schizophrenia are also linked to depression and bipolar disorder.

“It suggests, potentially, that when we’re talking about the genetic factors that contribute, what we’re really thinking about are genetic factors that contribute to how a brain gets built,” he says.

That would mean problems in the brain start very early in life, even though the symptoms of schizophrenia may not appear for decades.

One thing the genetic studies clearly show is just how many different systems in the brain may contribute to schizophrenia, says Harvard’s Dr. Pamela Sklar, an author of one of the studies.

“That’s a hopeful finding because the implication is that there may be more places to intervene,” she says, “if we understand the biology.”

Schizophrenia May Be Linked To Immune System