by Gwen Olsen
The fact is, not a single study of personality traits in human populations successfully disentangles similarity because of shared family experience and similarity because of genes…The argument confuses the observation [that a condition is running in families] with its explanation (Glenmullen 199).
Consider the evidence that schizophrenia and depression, especially manic depression, tends to run in families. (Mine is a prime example.) This alone is not proof of a genetic cause because poverty also runs in families. However, strong epidemiological evidence also supports the inheritance factor in mental disorders and is substantiated by studies comparing twins and data obtained from studies of adopted children (Valenstein 144-145).
Although no reports to date of the discovery of a gene responsible for manic- depressive disorders or schizophrenia have replicated, most knowledgeable people are convinced there is sufficient evidence to suggest genetic factors play some role in the etiology (origin) of mental disorders. Therefore, it is reasonable to assume people may inherit a predisposition to develop mental disorders. Valenstein uses the term diathesis, which originally comes from pathology. It means there is a constitutional predisposition or tendency toward developing a particular disease, but that predisposition is only realized under specific conditions (Valenstein 145).
In the case of my family, it appeared that stress, genetic predisposition, and learning and social networks had all played a part in determining our vulnerability to depression and bipolar disorder. But I certainly couldn’t help but wonder if the final element that precipitated each diagnosis had not been our exposure to potent, CNS-altering drugs. After all, it does not require a broken brain to respond negatively to drugs. Many psychoactive substances produce profound effects on the brains of people who have nothing wrong with them. Ask anyone who has smoked a joint, snorted a line of cocaine, taken a shot of tequila, or drank a cup of espresso. These drugs pretty much affect everyone—to varying degrees—in the same way (Breggin, Talking Back to Prozac, 37).
Linking Bipolar Illness to an Endocrine Disorder
My last full-time position (before becoming an independent contractor) was as a cardiovascular and diabetes specialist rep with Bristol-Myers Squibb. I was there for the beginning of the cholesterol wars selling Pravachol (pravastatin). I also helped educate America about the silent killer aspect of hypertension with the ace-inhibitors, Capoten (captopril) and Monopril (fosinopril). I witnessed the onslaught of the diabetes epidemic that has now swept the United States while selling Glucophage (metformin). I profited from the ill-fated diabetes drug, Rezulin, that was fast-tracked through the FDA in six months, only to be pulled off the market later because of several deaths that resulted from liver failure.
Interestingly enough, I had heard immediate concerns expressed by specialists in the field about this drug. They were all talking about an editorial that had appeared in the New England Journal of Medicine discussing liver failure. Regardless, Rezulin was a tremendous marketing success. In a bid for the lucrative pre- diabetic market, reps even told doctors it could prevent diabetes. Millions of patients were placed on Rezulin in a matter of months. Warner-Lambert reluctantly announced the removal of Rezulin from the American market in March 2000, almost thirty months after the first reports of liver failure had surfaced. Great Britain had withdrawn it from their market in December 1997. All in all, Rezulin would be suspected in 391 deaths and linked to 400 cases of liver failure. However, in spite of the rocky ride, Rezulin managed to generate $2.1 billion in annual sales before its demise (Strand 67-71).
In my training to sell and compete in these highly competitive markets, I learned a lot about blood sugar, blood pressure, the adrenals, and the role cortisol plays in hormonal regulation. I put this information to use in my own hypothesis about my family mental illness. As I tracked the history of bipolar illness specifically, several things became very clear. One was that there was definitely an endocrine component to this illness because it surfaced in times of peak pituitary activity in our lives, for example, in the teens, postpartum, and perimenopausal years. The cyclic nature of the female hormonal cycle itself mimics the fluctuations of the illness. Mood is closely linked to hormones.
Neurons are very sensitive to their hormonal environment. The hormones produced by stress, particularly cortisol and thyroxin, can be key influences in determining the limbic brain’s (the part of the brain that experiences feeling and controls mood) homeostasis (balance). Any rapid changes in hormone levels require the brain to make immediate adjustments and can result in unstable mood changes while adaptation occurs (Whybrow 212). Chronic arousal of the limbic brain induced by stress can lead to a process called kindling. Stress kindles the activity of neurons, much in the way a fire is kindled. Kindling can be thought of as aberrant, learned activity by the brain and indicates a sensitization to stimulation. In experiments done on animals with cocaine, the kindling was capable of “initiating long-lasting, possibly permanent changes in neuronal excitement” (Whybrow 166). Prolonged or repeated stress through “this kindling mechanism may have the capacity to modify the long-term genetic expression of behavior” (Whybrow 188). Chronic stress can result in a hyperactive cortisol response and cause “anxiety, insomnia, exhaustion, and disruption of function until a vicious feedback cycle develop” (Whybrow 167).
Secondly, our brain’s homoeostasis is further interrupted by the introduction of CNS-altering exogenous chemicals, for example, drugs and alcohol. It produces excess serotonin to compensate for the damaged neurotransmitters. The rise and fall of the chemical levels creates the classic mood swings experienced as manic-depressive episodes. This hypersensitivity to various drugs and substances was an obvious inherited factor that linked our mental symptoms to a possible biologic predisposition.
You cannot separate the effects of chemicals on the body from the brain. When the bloodstream is full of chemicals, they will interfere with brain functioning. Many of the depressive episodes I tracked were a direct result of anesthesia administered with childbirth or for other surgical procedures. (In fact, I recently had a hypomanic reaction when given Versed, a very short-acting benzodiazepine that was used in my anesthesia, and Restoril, another benzodiazepine I was prescribed as a sleep aid following minor cosmetic surgery.) Others’ symptoms were directly related to the administration of antidepressants, stimulants, pain medication, or other mind-altering drugs that were prescribed following some stressful life event such as an accident, divorce, death, or postwar experience. Many of us had experienced repetitive adverse drug reactions throughout our lifetimes.
Nearly everyone who suffered from bipolar symptoms and/or depression in my family had glycemic (blood sugar) issues. Most were hypoglycemic initially. Some became diabetic with time because hypoglycemia is a predisposing factor to developing diabetes. I, myself, had gestational diabetes with my pregnancy, but I would battle with hypoglycemia thereafter. Even the alcoholism in my lineage could be linked to blood sugar issues.
The brain will create cravings for glucose (sugar) when it is in crisis. Blood glucose is the main fuel of the brain and is critical in regulating its activity. If the brain is low or runs out of fuel, brain cells begin to die. As a preservation technique, you can develop cravings for sugary food or alcohol, which is nearly one hundred percent sugar, as a sort of jump-start for the brain. We had all experienced cravings for sugar and/or alcohol.
The first endocrine organ to come into contact with ingested chemicals is the pancreas. The pancreas, under attack from the chemical toxicity, misinterprets the stimuli and produces insulin. The extra insulin in the blood then lowers the blood sugar level excessively, and the brain puts out distress signals to the adrenals to release adrenaline (and cortisol) in order to convert glycogen into glucose and increase blood sugar. We often consume substances like alcohol, caffeine, nicotine, or sugary snacks in order to achieve that equivalent of the adrenaline rush and spike the blood sugar. However, this behavior creates additional problems by dropping blood sugar leve
ls even lower than before, thus perpetuating a vicious cycle. If the progress of disease is not halted by severe dietary and/or lifestyle changes, the pancreas eventually burns out and diabetes is the result.
The list of hypoglycemic symptoms is strikingly similar to bipolar symptoms as well as serotonin toxicity. Taber’s Medical Dictionary lists hypoglycemic symptoms in their order of frequency:
exhaustion, depression, insomnia, anxiety, irritability, headaches, vertigo, sweating, tremor (internal trembling), tachycardia (palpitation of heart), muscle pain and backache, anorexia, crying spells, phobias, difficulty in concentration, numbness, chronic indigestion, mental confusion, cold hands or feet, blurred vision, muscular twitching or abdominal spasms, fainting or blackouts, convulsions, and suicidal tendencies (Tracy 331).
Tempers flair easily in individuals with blood sugar imbalances, and the alcoholics in my family all have a tendency toward violence and explosive temperaments when intoxicated. This has landed many of them in trouble with the law. Most confessed to having blackouts or severe memory loss after drinking excessively. Several reported severe moodiness if they skip meals.
I became convinced this “mental illness” and “alcoholism” that runs in my family has a much larger physiological component than was given credit or consideration by our doctors. Granted, our family history is as stressful and dysfunctional as they come, which would substantiate an experiential or psychological component to our illnesses. But if there was a biochemical imbalance to be blamed for our collective issues of criminality, drug abuse, alcoholism, depression, and other behavioral abnormalities, it did not appear to be a brain defect to me. Instead, it appeared to be an endocrine defect that was passed from generation to generation. After evaluating all the predisposing factors, it was amazing to me that any of us had escaped the sanitarium considering the onslaught of chemicals we are exposed to in our environment and the poor nutrition plaguing our modern culture.
Orthomolecular Psychiatry: Feeding the Brain
It was validating to discover that several researchers had indeed postulated there was a correlation between mental disorders and endocrine deficiencies or blood sugar imbalances. There is substantial documentation that delinquent probationers who are placed on restricted diets to control the intake of processed foods, sugar, caffeine, and other additives and who increase the consumption of fresh fruits and vegetables have remarkable improvements in behavior and attitude.
Similar results have been obtained with schizophrenic and bipolar patients who were previously unresponsive to medication. Food that feeds the brain and allows the rich neuronal environment needed for proper brain transmission and communication has an ameliorating effect on attitude and behavior. If the diet contains the substances needed for proper brain function, it works normally. Behavior is then both rational and constructive. A healthy body means a healthy mind. However, if the brain does not receive the proper nutrients and in addition is struggling to overcome drug toxicity, it will malfunction. Anything from irritability to psychosis can result. This is the foundation of orthomolecular psychiatry, the restoration of the proper molecular balance of the brain. This dietary approach is generally accompanied by vitamin and mineral supplementation and/ or other therapies such as counseling (Reed Stitt 75, 137).
Orthomolecular psychiatry has gotten very little attention in the field. No wonder, it is relatively uncomplicated theoretically. It doesn’t cost a lot of money and require a tremendous amount of technology or specialized staff. It is not profitable at all to industry. Therefore, it has remained a back alley approach basically ignored by the scientific community. The most wonderful thing about the orthomolecular approach is that it is completely safe compared to drug therapy. No one has died or had permanent brain damage from eating healthfully. In addition, many young people whose lives were destined to be wasted away in the correctional system have since become productive, contributing members of society (Reed Stitt 135).
Additionally, in 1999, a study was published in the American Journal of Psychiatry clearly substantiating previous theories about the “disturbance in glucose homeostasis in psychiatric populations.” The study states there was an, “elevated frequency of diabetes mellitus in hospitalized manic-depressive patients” (Cassidy et al).
What Causes Manic Psychosis?
It has been scientifically proven that experience can modify brain anatomy, causing structural and functional changes in the brain. Numerous experiments have shown exposure to stressful situations, for example, can produce long-lasting brain changes. Animals that are stressed continually have a hypersensitive response to amphetamines, even when the drugs are administered months later. Stress can produce changes in the same class of dopamine neurons on which the neuroleptic drugs act. Even when the dopamine neurons that have been removed from the brains of stressed animals are challenged with amphetamines in a petri dish, excessive amounts of dopamine are released. These results indicate that stress can produce prolonged physical changes in dopamine neurons that make them hypersensitive not only to drugs, but also to subsequent stress (Valenstein 127).
It is important to be aware that a number of drugs, both legal and illegal, can induce psychotic symptoms. Among these are steroids, stimulants (for example, ephedra, diet pills, and antidepressants), amphetamines, cocaine, hallucinogens (such as ecstasy, mescaline, peyote, mushrooms, and LSD), hypnotic painkillers and sleep aids (like Halcion, Vicodin, and Oxycontin), marijuana, and PCP. Psychosis has also been reported in rare instances with the antibiotic class known as quinolones. Stephen Fried, an investigative journalist and husband of a “Floxie” (Floxin victim) details his own wife’s life-altering adverse drug reaction to Floxin (ofloxacin) in his sobering book Bitter Pills. Fried’s wife, who took only one dose of this powerful antibiotic for a minor urinary tract infection, now permanently suffers from a drug-induced manic-depressive illness and was told she must take mood stabilizers and antipsychotic drugs for the rest of her life.
Drugs can become neurotoxic when they reach high enough concentrations to penetrate the blood-brain barrier. Drug-induced manic psychosis is a severe psychotic disorder whose symptoms include insomnia, extreme overactivity, racing thoughts, grandiosity, paranoia, exhausting outbursts of energy and suicide (Breggin and Cohen 62). Psychosis can also occur in bipolar disorder, depression, dementia, and post-traumatic stress disorder. This makes the appropriate diagnosis of psychotic symptoms and identification of adverse drug reactions extremely critical to the patient’s treatment and recovery. And, because there is no objective measure to prove or disprove a patient has any psychiatric disorder, this can be a difficult assessment, even for the well-trained psychiatrist (Drummond 35).
Acute psychosis is generally a response to stressful situations or, as I said, can sometimes follow the use of stimulants, psychoactive drugs, or prolonged use of marijuana. It is imperative to immediately discontinue the use of any drug that causes psychotic symptoms. This type of psychosis is known as brief reactive psychosis and generally abates within the time necessary to detoxify the body from the offending chemicals. People normally return to their usual ability to function once their symptoms subside, although permanent brain damage can occur (Drummond 124).
Neuroleptics: A Combination Chemical Strait Jacket and Lobotomy
One medication class used to treat psychosis and schizophrenia is known as neuroleptics or antipsychotics. The term neuroleptic essentially describes what these drugs do, that is, they “clamp down, in the manner of a chemical restraint, on the central nervous system” (Whitaker 208). They can dramatically curb the neurotransmitter activity that underlies motor movement. Neuroleptics alter behavior and thinking by partially shutting down dopamine receptor pathways, in essence, having the effect of a chemical lobotomy. These drugs cause a variety of unpleasant side effects, including weight gain, emotional blunting, fatigue, visual disturbances, constipation, urinary retention, sexual dysfunction, and dry mouth. However, the most alarming side effects associated w
ith these drugs are the muscular side effects such as rigidity, decreased muscle movement, tremor, muscle spasms, and restlessness.
Moreover, neuroleptics can cause permanent neurological damage known as tardive dyskinesia. This is a devastating disorder involving abnormal, involuntary, constant, rhythmical muscle movements, commonly referred to as tics. These movements generally affect the mouth, tongue, hands, fingers, trunk of the body, and toes. Mouth movements can mimic the action of chewing gum, or the tongue may involuntarily dart out of the mouth, also known as fly tongue. Trunk movements may appear as constant rocking back and forth. In severe cases, body parts may lock in bizarre positions.
Women, the elderly, and people with brain injury are more likely to develop tardive dyskinesia. There is no cure for it, but there is a ten to thirty percent chance of developing it if you take an antipsychotic drug for more than one year (Drummond 122).
For political and financial reasons, most of the research in psychiatry has been done on white males. In 1977, the FDA issued guidelines that practically banned “women of child-bearing potential” from early clinical trials (Phase I and Phase II). These trials generally determine a drug’s standard dosage. They also determine the baseline of a drug’s toxicity. So, by law, these studies have only been populated by men (Fried 265). The absence of research in other populations has led the medical and psychiatric professions to make treatment recommendations by extrapolating findings made from these adult white male studies. Consequently, the unique biological makeup of women and other groups is not taken into account, and psychiatric medications (among others) can pose additional risk to these patients (Drummond 34). It is also important to remember that clinical trials done during the approval process for drugs involve healthy subjects or patients that only have the disease being studied. The participants are rarely allowed to be on concomitant drug therapies. This is not the case in the general population and the real world (Strand 109).
