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In Search of the Holy Grail:

Natural Treatment of Schizophrenia

Introduction

Schizophrenia is a profoundly debilitating mental disorder. Victims often suffer from hallucinations, delusions of grandeur and/or paranoia, and disorganized thought and speech patterns. It knows no class, ethnic, or racial boundaries. Brilliant young scholars have had their lives destroyed. People from every walk of life have been reduced to living in padlocked wards for their self-protection. Even in the mildest of cases, the hallucinations and delusions interfere with cognitive abilities.

Most psychological and neurological researchers believe that the root cause of schizophrenia is a set of genetically caused malfunctions in neurotransmitter chemistry, and that people with schizophrenia are therefore just unfortunate victims of bad genes. The focus of treatment protocols has been the development of psychopharmacology – the synthetic creation of medicines that manipulate such factors as neurotransmitter production, storage, release, and reception.

People with schizophrenia are treated today primarily with powerful tranquilizers, mood stabilizers, and anti-psychotic drugs that tinker with neurotransmission. All of the drugs have serious side effects on brain functioning and body metabolism, some of them potentially deadly. Most of them require even more drugs to compensate for their side effects. Some of them are psychologically or physically addictive.

The usual explanation given for the affliction and its treatment lacks completeness. Most medical and psychological literature contains no analysis of the underlying neurobiology that caused the problem. The research that has revealed the cause came from a different source: people studying the chemistry of the membrane surrounding the nerve cells in our brain (neurons). About twenty-five years ago, a few researchers in the US and Canada hypothesized that the root cause of schizophrenia was a metabolic disturbance in cell membrane chemistry. Their research has expanded into a framework in which the many different causative factors in psychoses, as well as the action of the best anti-psychotic drugs, can be explained. This framework also provides the basis for research into and clinical trials of safe, natural, effective remedies that have no side effects.

This research has opened the possibility of finding a root cause and possible effective natural treatment for schizophrenia.

What is Schizophrenia?

Schizophrenia is the word that we use to describe a number of conditions in which the victim loses contact with reality. These are commonly defined as psychoses. "The hallmark of the schizophrenias is thus a more or less sharp break with the world in which most less disturbed people live, a world that is rooted in a basic consensus about what is true and real in our shared experience" (Carson, 2002, p. 396).

It is a profoundly debilitating affliction, affecting about 1 percent of the U.S. population in any given year. It accounts for 40 percent of admissions to mental hospitals and 50 percent of mental health bed occupancy. It is not a new affliction; in ancient writings people who likely had schizophrenia are described as being possessed by demons and evil spirits. During the Middle Ages "exorcism became a treatment of choice" in Europe (Carson, 2002, p. 15).

The classic symptoms are disruption of thought, perception, and behavior on every level. Thoughts become disorganized and appear to be totally random, and are often overwhelmed by delusions, or false beliefs, such as the notion that one owns a franchise to sell copies of the Bill of Rights and could potentially become wealthy by selling copies of it. Verbal communication is incoherent and disorganized. Sentences appear to be put together from unconnected phrases. "The guy across the street has the sky blue" would be a typical example. Perceptions are distorted and, according to reports by people with the affliction, overwhelming; it is as if the selectivity of the brain has been shut off.

Emotional responses and affect appear inappropriate or bizarre. Many people with schizophrenia experience hallucinations – false perceptions – such as voices and images that only they can hear and see. Some experience extreme paranoia, seeing the world and the people around them as evil and a personal threat to them. They often have a confused sense of self, often completely delusional, thinking that they are God, Jesus Christ, or someone tied intimately to universal powers.

Volition – that is, the coordination of thought leading to action – is impaired; some people with schizophrenia cannot even take care of their personal hygiene. Patients may retreat into an inner world, and become unable to interact with the outside world at all. Finally, many people with schizophrenia "look crazy." There are disturbances in motor function and muscle control that appear to be bound up with the emotional aspects of the affliction, such as peculiar or bizarre facial expressions. These symptoms and signs are separated by psychologists into "positive symptoms" – such as hallucinations, delusions, bizarre behavior, and disorganized thought – and "negative symptoms," which include withdrawal, absence of emotion, and loss of speech (Carson 2002).

In my own experience working with people with schizophrenia, I have found that it is an incredibly frustrating affliction to deal with. For, unlike the panic and mood disorders and those caused by trauma, people with schizophrenia appear to be suffering from an organic and permanent brain disorder, rather than a situational or emotionally based illness. Traditional therapy can be useful, but it must be intensive. Given the nature of the medical and human service support systems in place today, this is not usually a viable option. While some cases of schizophrenia have cycles of illness and remission, most cases do not and remissions are rare.

It is almost impossible for people with untreated schizophrenia to function in society or even to take care of themselves physically. The anti-psychotic drugs, even the best ones such as Clozapine, are only partially successful in resolving the disorder, and the side effects are absolutely dreadful. In the case of Clozapine, they are potentially life-threatening, as will be explained below. Many patients are on multiple drugs, each with their own side effects and interactions. These drugs sometimes allow people to pursue their lives, but although the symptoms are more manageable, they are most often still there, along with horrible drug side effects. Thus the pursuit of meaningful career goals is often thwarted.

From modern MRI scanning we now know that some people with schizophrenia have larger than average brain ventricles – the "holes in your head" that contain the cerebral spinal fluid, which is the primary mechanism for nutrient and waste transport in the brain. In addition, there may be enlarged "sulci" – the fissures on the surface of the brain. This ventricle and sulci enlargement is generally thought to be a sign of brain atrophy or degeneration (Carson 2002).

Finding a Cause

There have been a number of possible explanations of the cause of schizophrenia. These range from genetic models to those that attribute the disease to social environment.

Diathesis-stress model

One of the more useful concepts in psychology is the "diathesis-stress model" of mental disorders, which hypothesizes that many psychological disorders are brought about by genetic or early childhood factors (diathesis) followed by stresses later in life (Carson, 2002, p. 37). Following this line of reasoning, researchers of origins of schizophrenia have been looking long and hard for evidence of genetic predisposition for the affliction, but have been only partially successful. There are strong correlations, especially if both parents have schizophrenia. But without knowledge of the actual biological cause, this research quickly reaches a dead-end: "Thus, evidence of a shared family trait, while persuasive, remains incomplete because of the difficulty of figuring out where genetic influences end and environmental influences begin" (Carson, 2002, p. 412).

Neurodevelopmental explanations

As modern medical study of schizophrenia and the possible causes of the physical abnormalities progressed, several researchers began looking into the possibility that it was a neurodevelopmental affliction, that is, that it progressed over time, perhaps even starting before birth. In several studies, researchers found a correlation between schizophrenia and maternal influenza in the second trimester of pregnancy. It was discovered that more people with schizophrenia were born during winter months than during warmer seasons, suggesting another possible connection to maternal illness.

In another quite startling study, the early home movies of people who later developed schizophrenia were compared by trained observers with those of healthy people. (This was a "blind" study: the observers were not informed of the children’s outcomes). The children who later developed schizophrenia showed less emotionality in their expressions, had poorer motor skills, and also had a higher rate of peculiar movements. Thus there were signs that these children’s brains had been profoundly compromised in some way during gestation or very early infancy. (Carson 2002).

Blaming the victim and circular reasoning

For psychologists and psychiatrists it appears that the root cause of schizophrenia remains a mystery. Some psychology textbooks refer to its cause as "elusive" (Hockenbury, 2003, p. 612), or "unclear" (Carson, 2002, p. 411), or, quoting Winston Churchill, "a riddle wrapped in a mystery inside an enigma" (Coon, 2004, p. 610). Unfortunately, these textbooks (and researchers) do not leave it at that. Their proposed causative factors, besides the genetic factors discussed above, include poverty, problematic families and upbringing. These shed little light on the affliction while further stigmatizing its victims. In addition, it should be noted that having a disturbed individual in a household itself causes family problems. This seems to be a confusion of cause and effect.

Some research into the brain chemistry of people with schizophrenia have found that one of the neurotransmitter chemicals, called dopamine, appears to be overactive. This symptom has been turned into one of the proposed possible "causes," now referred to the "dopamine hypothesis" (Hockenbury, 2004, p. 610). This is a classic scientific mistake referred to as circular reasoning, in this case turning a symptom into a cause. A good analogy might be blaming a train wreck on two moving trains being in the same place at the same time, rather than a failing brake, broken rail, burnt-out semaphore lamp, or human error.

Outside the U.S., however, an unusual group of researchers in cell membrane chemistry were hot on the trail to a real answer to this mystery.

The Cell Membrane (Phospholipid) Hypothesis

About twenty-eight years ago, a few researchers in brain cell membrane chemistry began to report new findings on the root causes of schizophrenia. In 1977, David Horrobin, who at that time was at the Clinical Research Institute and the University in Montreal, wrote what appears to have been the first short peer-reviewed paper on the connection between schizophrenia and the cell membrane, published in the British Medical Journal The Lancet. He hypothesized a root cause of schizophrenia having to do with defects in cell membrane chemistry, specifically a deficiency in chemicals called prostaglandins that are manufactured from essential fatty acids (Horrobin 1977, p 936).

Four years later Donald Rudin from the Eastern Pennsylvania Psychiatric Institute wrote a major journal article in Biological Psychiatry, in which he expanded upon this idea. He hypothesized that the major neuroses and psychoses were an "Omega-3 Essential Fatty Acid Deficiency Syndrome," a profound metabolic disturbance involving the creation of prostaglandins, that caused these mental illnesses as well as a physical skin disorder: pellagra (Rudin, 1981, p. 837). Rudin gave testimony of fairly dramatic results merely using flaxseed oil ("linseed oil") for twelve patients with serious mental disorders.

By the early 1990s, a network of researchers working on the cell membrane hypothesis had formed, and in 1996 these researchers were able to present their work in a peer-reviewed journal devoted to human lipid chemistry (Prostaglandins, Leukotrienes, and Essential Fatty Acids) that had been established by Horrobin. Since then, their work has begun to appear in prominent psychological journals (such as Schizophrenia Research and Archives of General Psychiatry), and the interest in lipid research has increased dramatically. But it has not yet entered the mainstream of psychiatric treatment.

An explanation of the phospholipid hypothesis

Every cell in living tissue is surrounded by a permeable membrane to enable nutrients to enter the cell and to enable waste products to leave. In the brain, a part of this cell membrane, sometimes referred to as the neural membrane, makes up the connection point, called the synapse, between neurons (Klein, 2000). The membrane is composed of a collection of phospholipids (complex molecules containing phosphorus and essential fatty acids) as well as special proteins, receptors, and a number of other structures that allow nutrients, hormones, and neurotransmitters to enter the cell and waste products to leave (Marieb, 2004, p. 49). Our bodies need a collection of fats, called essential fatty acids, in order to build and maintain this cell membrane, as well as to properly create the packets of neurotransmitters that are sent from one neuron to another in the brain (Haag, 2003).

Essential fatty acids (EFAs) are called "essential" because they cannot be created by the body. The most important of these are alpha linoleic acid (ALA), linoleic acid (LA), arachadonic acid (AA), docosahexanoic acid (DHA), and eicosapentanoic acid (EPA). We must consume them in order to stay healthy. The human body is capable of creating the latter three fatty acids (AA, DHA, and EPA), from the former two, but this transformation mechanism is weak in infants and in old age. Furthermore, the ratio of ALA to LA is important in maintaining a proper balance of EFAs in the cell membranes. The primary source of LA in Western diets is cooking oils such as corn and safflower oil. ALA comes from cereals such as flaxseed. The primary direct source of AA is meat, and the direct source of DHA and EPA is fish. For infants, the source of all EFAs is mother’s milk.

Three essential fatty acids - EPA, DHA and AA - are the most important for healthy neural membranes. These membranes serve as a reservoirs of these fatty acids, and exchange two of them – DHA and AA – on a regular basis for neurotransmission and other cell functions. To enable this pattern of fatty acid exchange, the body produces certain chemicals called phospholipases, which remove fatty acids from the membrane, and enzymes that attach them again. As the fatty acids are used up, they must be replaced from the foods we eat (Horrobin 1998).

If this exchange mechanism is not functioning properly, or there is a dietary deficiency in these essential fatty acids, and the neural membrane is weakened, the neuron and neurotransmission will be weakened as well. If, for some reason, the membrane of every neuron (or nerve cell) in the brain began to deteriorate as a result of depletion of its essential fatty acid building blocks, one could well imagine that neuron function throughout the brain would deteriorate as well.

If this happened, neurotransmission would likely become random, irregular, distorted, and asynchronous. Thought patterns and images from the past, images and sounds from TV and movies, and images from dreams might suddenly arise and present themselves as current thought. Coordination of thought patterns and their presentation as speech would become impossible. Eventually, there would be neuron death and anatomical changes that would be visible by means of various diagnostic procedures. These are precisely the diagnoses of schizophrenia (Carson, 2002).

Recent findings

The network of cell membrane researchers, discussed above, correlated anomalies among people with schizophrenia and possible explanations relating to phospholipid breakdown (Horrobin, 1998; Yao, 1996; Mahadik, 1996; Hudson, 1996; Bates, 1996):

People with schizophrenia have a surplus of Phospholipase A2 (PLA2) circulating in their bloodstream. This chemical splits essential fatty acids from the cell membrane.

There are reduced levels of DHA and AA in the red blood cell membranes of people with schizophrenia.

People with schizophrenia often show a reduced maximum response to light. This response is dependent on the availability of DHA in the retina.

People with schizophrenia often have increased pain tolerance, indicating a defect in the neural membrane.

People with schizophrenia appear to have a defect in the mechanism that binds essential fatty acids to the neural membrane.

Two genetic abnormalities relating to the excessive production of Phospholipase A2 have been found in people with schizophrenia.

The kinds of brain abnormalities found in people with schizophrenia are consistent with a defective response to high fever caused by severe colds or influenza during gestation. Some people with schizophrenia were exposed to hyperthermia (fever) and viral infection (primarily influenza) during gestation and/or hypoxia (lack of oxygen) at birth.

The increased ventricular size in brains of some people with schizophrenia, which is indicative of loss of brain matter, is consistent with brain atrophy, or neuron death, caused by EFA depletion and/or oxidative stress.

The behavioral and neuromotor function abnormalities in childhood that are predictors of schizophrenia and are consistent with the brain dysfunction that would be caused by EFA depletion.

Schizophrenia is highly correlated with poor health, it increases with stress and old age, and it is more common among men than women. These correlations are consistent with EFA deficiency. David Horrobin wrote in 1998: "The rate of synthesis and of incorporation of these EFAs into phospholipids is reduced by viral infections, male sex, stress and old age…"(Horrobin, 1998)

In summary, schizophrenia can result from one or more genetic metabolic abnormalities and/or events during gestation and childbirth that are then accentuated by poor nutrition, in particular a deficiency in certain essential fatty acids in the diet common in the United States.

Schizophrenia and oxidative stress

There is now also strong evidence that depletion or failure of the body’s antioxidant system is correlated with schizophrenia. This comes from several lines of research. First, studies have found that people with schizophrenia have measurable amounts of pentane – the hydrocarbon molecule most identified with gasoline – in their breath. This chemical is produced by oxidative damage of the omega-6 fatty acids (Peet 1996). Second, there is evidence that there is depletion of the body’s primary antioxidant enzyme, glutathione, which is correlated with increased size of the brain ventricles – a sign of brain tissue destruction – common in schizophrenia (Buckman, 1987, reported by Peet, 1996).

Schizophrenia, influenza and heat stress

There is some evidence that there is a correlation between maternal influenza during gestation and the development of schizophrenia in the affected offspring (Carson, 2002). Bates et al. (1996) have hypothesized that the genetic defect in lipid metabolism correlated with schizophrenia, and the resultant compromised phospholipid membrane system in the developing fetus, set the stage for an abnormal heat shock response. Such an abnormal response, which leads to a deficiency of protective heat shock proteins, would lead to the anatomical abnormalities commonly found in the brains of people with schizophrenia.

Evidence for the Hypothesis

A hypothesis such as this, which appears to be very different from the current view of the origins of schizophrenia and its pharmacological treatment, demands clinical evidence.

Clinical studies of people with schizophrenia and trials using various EFAs to treat schizophrenia, both as a sole agent and as an adjunct to pharmacological treatments, have been moderately to extremely successful in reducing or eliminating the positive and negative symptoms of schizophrenia. In one case, a man with long-term stable schizophrenia experienced complete remission of all positive and negative symptoms by simple administration of EPA. The most recent research has revealed that supplemental EPA inhibits excess PLA2, identified as the central cause of lipoprotein breakdown and resultant schizophrenia (Puri 1998).

Additionally, the most effective psychopharmacological treatment for schizophrenia, Clozapine, is a "prostaglandin E analog." More simply stated, this drug, whose anti-psychotic properties have never been adequately explained using classical neurotransmission theories, inhibits the action of Phospholipidase A2 and thereby increases the availability of AA and DHA to the neural membrane (Horrobin 1996). This may not be totally coincidental; Clozapine was developed by the pharmaceutical company Novartis shortly after publication of David Horrobin’s first paper in 1977, in which he suggested that schizophrenia was a prostaglandin E deficiency disease.

The clinical studies

Since Horrobin’s first publication of the phospholipid hypothesis, there have been several small but significant clinical studies of natural treatment protocols. Some of these were analytical studies, which sought to obtain information about a set of patients with schizophrenia. Others were clinical tests of various amounts and mixtures of essential fatty acids added to the diet. These clinical tests demonstrated the effect of EFAs in reducing or eliminating the characteristics of schizophrenia in the research subjects.

An analytical study done by Peet et al. (1996) was designed primarily to confirm the phospholipid hypothesis. Twenty-three drug-treated schizophrenic patients were measured for essential fatty acid content in their red blood cell membranes. Depletions were evident for linoleic acid (LA), arachidonic acid (AA), eicosapentanoic acid (EPA) and docosahexanoic acid (DHA), with the most significant depletion reported for AA and DHA.

The first clinical trial was done even before the mechanism of EFA destruction was known. In this study, Donald Rudin administered daily doses of flaxseed oil (then called linseed oil), in increasing amounts, to five patients with schizophrenia, three patients with major depression, and four patients with agoraphobia (Rudin, 1981). Three of the five people with schizophrenia reported improvement that was fairly dramatic. These were people with "remitting schizophrenia," that is, those people for whom schizophrenic symptoms cycled from mild symptoms or none at all to severe symptoms. They reported (and were observed to have) very long, sustained periods of remission.

Four other studies used specific amounts of eicopentaenoic acid (EPA). One by Mellor et al. (1996) involved giving twenty chronic hospitalized schizophrenic patients a daily dose of ten grams of a supplement called MaxEPA. After six weeks their mean schizophrenic symptom rating (called PANSS) had decreased from 78.9 to 65.6, which is a significant drop. The amount of omega-3 fatty acids in the patients’ blood correlated directly with the improvement of their symptoms. Even more significantly, a measure of tardive dyskenesia, a dreadful side effect of many anti-psychotic drugs, had dropped from 20.2 to 12.3.

A randomized, double-blind, placebo-controlled study by Emsley et al. (2002) used a fixed amount of EPA to confirm its efficacy. Forty patients with schizophrenia with ages varying from eighteen to fifty-five took part in this twelve-week study. They were assessed for symptoms using PANSS at the beginning of the study and at three, six, nine, and twelve weeks, and assigned to receive three grams of EPA per day or a placebo, in addition to their usual anti-psychotic medications. The patients taking EPA showed a significant reduction of negative and positive symptoms of schizophrenia, as well as symptoms of tardive dyskenesia.

Peet and Horrobin (2002) conducted a study to determine the most effective amount of EPA to use for schizophrenia. They studied 115 patients, all taking various anti-psychotic medications. Patients were given placebo or one, two, or four grams of EPA per day in addition to their regular medications. There were significant improvements reported for patients taking two grams per day, and a positive relationship found between these improvements and the concentration of arachadonic acid in their blood. The researchers hypothesized that larger doses of EPA overload the cellular membranes and compete with AA and DHA, which are needed for neurotransmission.

There is also a dramatic case study of a thirty-one-year-old man with chronic, unremitting schizophrenia since his teen years, and who had taken only one dose of an anti-psychotic medication several years before this study (Puri et al., 1998, 2000). He was given two grams of EPA per day, and he experienced visible and sustained improvement, which was clinically evaluated as remission, of both his positive and negative symptoms of schizophrenia. Prior to this trial, it was also determined, by means of high-resolution 3D cerebral MRI scans, that his brain was undergoing cerebral atrophy. Follow-up scans revealed that this atrophy had been reversed.

The relative value of EPA versus DHA (docosahexaenoic acid) was demonstrated by a pair of studies (reported by Peet et al., 2001). In the first study, forty five schizophrenic patients were administered either EPA or DHA for three months, to determine the most efficacious EFA to use. In the second study, using placebo controls, EPA was used alone, without anti-psychotic drugs, except where the symptoms made it essential. Patients taking EPA had "significantly lower scores on the PANSS rating scale [used to measure the symptoms of schizophrenia] by the end of the study."

All of this research indicates that schizophrenia is highly correlated with depletion of essential fatty acids. The clinical trials and the case study further demonstrate that supplementation with EFAs significantly reduces the symptoms of this disorder.

Discussion

What is dramatic about the phospholipid hypothesis is that it explains, quite simply, all of the features, symptoms, progression, and epidemiological data known about schizophrenia. It takes into consideration and neatly explains the defective neurotransmission models that were previously proposed as "causative" but had unknown corresponding biological bases, as well as the neurodevelopmental stresses that are highly correlated with schizophrenia.

The phospholipid hypothesis holds out the promise of prevention of schizophrenia in the future, as well as safe, natural treatment of schizophrenia, and, by analogy, bipolar disorder and other mental disorders such obsessive-compulsive disorder (OCD), attention deficit disorder (ADD), and attention deficit hyperactivity disorder (ADHD), since aberrations or severe deficiency in EFAs could cause a wide range of abnormal, compromised neurotransmission. There is strong evidence, already published, that unipolar depression – the most common psychological disorder – responds to treatment with EFA supplementation (Stoll 2001).

For prevention, a simple blood test could be provided for expectant parents to test for low essential fatty acids in blood cells, the hallmark of elevated phospholipase PLA2 that these researchers found be the root cause of schizophrenia. Expectant mothers could be provided with sufficient ascorbate (vitamin C) to prevent oxidative stress and reduce the chances of causing the heat shock reaction mentioned earlier. Finally, newborns could be tested with the same red blood cell test, and provided with supplemental essential fatty acids to allow their brains to develop normally and avoid schizophrenia.

Current medical treatments for schizophrenia, as mentioned earlier in this paper, are deficient and dangerous. The most successful medication, called Clozapine, has terrible side effects and it is horrifically dangerous. It reportedly causes impotence, weight gain, and slowing of peristalsis, and often requires daily laxatives to prevent intestinal blockage. According to its official side-effect literature, Clozapine causes depletion of the essential mineral selenium, and compromises immunity. Any sudden increase in dosage, including a patient forgetting to take the drug for several days and then starting again, can cause seizures or coma. It can spontaneously cause sudden, rapid depletion of white blood cell count and resultant death. Patients taking Clozapine must have their white blood cell count monitored every two weeks before being allowed to continue taking the drug.

And even this drug is not completely effective. In my own experience, Clozapine is often used in concert with the standard anti-psychotic drugs, such as Haldol, and some of the newer, atypical ones, such as Risperdal. Additionally, people with schizophrenia often have co-occurring disorders such as depression, for which even more drugs are prescribed. Each of these carries its own side effects and extreme risks of drug interactions, such as serotonin syndrome, a potentially deadly interaction between SSRI anti-depressants and other drugs (Ener 2003, Karki 2003).

One of the side effects of the standard anti-psychotic medications, commonly called "neuroleptic" drugs, is so common and so serious that it has itself become a named affliction: tardive dyskinesia, or TD. It is "a persistent and often irreversible syndrome characterized by abnormal movements, including lingual and orofacial dyskinesia, grimacing, tics, choreic movements of the limbs or trunk, and athetosis and dystonia." (Retrosin 1996).

TD is so common that the Massachusetts Department of Mental Health, for instance, requires that psychiatrists report whether TD has been noted at each patient visit. According to some statistics, its prevalence is "on the order of 10-15% in young populations, 12-25% in more chronic patients, and 25-40% in very chronic patients…TD is a social handicap that leads to social isolation and compromises dignity and quality of life. They are less likely to be accepted into rehabilitation programs, and they are less likely to be employable…" (Retrosin 1996).

Thus a natural treatment for schizophrenia, even one that could substantially reduce a patient’s dependence on anti-psychotic medications, is greatly needed. The clinical studies cited above indicate that use of supplemental essential fatty acids – particularly EPA supplementation – appears to alleviate the EFA imbalance and improve the symptoms of schizophrenia.

Retrosin’s finding regarding oxidative stress caused by anti-psychotic medications and the successful use of antioxidants to alleviate it indicates that an antioxidant supplementation regimen should be used as an adjunct to EFAs.

Current thinking vs. the phospholipid hypothesis

I believe that it is merely wishful thinking to imagine that the entire psychiatric establishment in the United States is going to readily accept the idea that a few capfuls of pharmaceutical-grade fish oil are going to take the place of the anti-psychotic medicines that are prescribed for schizophrenia today. The biochemistry involved in the phospholipid hypothesis is outside of the worldview of most doctors who treat patients with psychotic disorders; the last time they ever studied the nature of the cell membrane was in their Anatomy and Physiology in college. These doctors – as dedicated as they are to helping their clients – are stuck in the pharmaceutical paradigm. Their approach is defined by the search for the correct amounts of various drugs for each individual, and looking to the pharmaceutical industry for the next "miracle drug." This paradigm is bolstered by mountains of industry-funded research reports, advertising, and sales representatives. There are few, if any, truly independent clinics or universities without any kind of pharmaceutical company connection.

Even if the psychiatric profession understood the science, the very structure of psychiatric care is focused around drug administration. Many major psychiatric hospitals now have Clozapine testing labs, where patients come every two weeks to have their blood monitored for white blood cell counts and Clozapine levels. Reductions of funding during the last thirty years has meant that patients spend only a few minutes with their psychiatrists every three months, just enough time for the psychiatrists to figure out whether the drugs are working to bring the worst symptoms under control.

Adverse outcomes: nutritional status and health

Schizophrenia is so debilitating, even when compensated by drugs, that many people who have it fall into poverty because it interferes with their cognitive and reasoning abilities and especially their social skills. Often homeless or on poverty’s edge, many turn to alcohol or drugs. Compounding the problem is that many people with schizophrenia follow a diet that is deficient in nutrients, high in saturated fats and sugars, and low in essentially fatty acids, a diet associated with worse long-term outcomes (Peet 2004). These findings make it clear that closer monitoring of dietary health would be needed if even people with schizophrenia were to begin long-term therapy with EFAs.

Conclusions

David Horrobin began an entirely new and innovative research direction in the study of schizophrenia – the malfunctioning of the cell membrane in neurons. In order to publish his own research and the work of an expanding network of research physicians intent on developing this new line of study, he apparently needed to establish a new peer-reviewed journal: Prostaglandins, Leukotrienes, and Essential Fatty Acids. Given the historical context, that virtually all psychological research was focused on the role of neurotransmitters in abnormal psychology and the creation of drugs to manipulate them, this is not surprising.

I believe that Horrobin and his colleagues have found the Holy Grail of psychology – an integrative root cause explanation for schizophrenia that takes into consideration all of the manifestations of this horrible syndrome that has wrecked so many people’s lives through the ages. The clinical and case studies have provided ample evidence. The phospholipid hypothesis provides insights into safe, natural treatment protocols that have been tested with some success. It identifies the specific genetic predisposition and the biological/environmental stressors that lead to the progression of the syndrome, thus providing some possible strategies for prevention and very early treatment.

But influencing the medical system so that the phospholipid hypothesis is accepted and acted upon is a daunting challenge. David Horrobin’s breathtaking and extensive article in Schizophrenia Research appeared in 1998, but there is little evidence that this knowledge is making its way into mainstream medicine yet. Psychology textbooks that I reviewed, some written as recently as 2004, have no mention of it at all, and quick scans using google and PubMed, the National Library of Medicine’s public access website, result mostly in pointers to the original work done by Horrobin and his colleagues.

There are many medical truths in recent history that have not entered into mainstream thinking simply because there is so much investment (money, facilities, resources, and personnel) in the current paradigms. More than ten years ago, for instance, two research scientists, Matthias Rath and Linus Pauling, identified the true root cause of cardiovascular disease (Pauling, 1991) They proposed a treatment – now clinically proven – that reverse this affliction without drugs, stents, or bypass surgery. Their work provides a simple nutritional regimen that would eradicate the affliction worldwide. It would also eradicate a $200 billion dollar per year industry along with the entire profession of cardiology. Needless to say it is still virtually unknown among health professionals.

Fortunately there are well-placed researchers and clinicians who understand and accept the phospholipid hypothesis and are making it part of their daily practice. For instance, Andrew Stoll, who is the director of the psychopharmacology clinic at McLean Hospital in Belmont, Massachusetts is using EFAs in his clinical research. He also wrote a popular book, The Omega-3 Connection, which has an entire chapter devoted to the Horrobin’s phospholipid hypothesis of schizophrenia. When he spoke at the recent Defeat Autism Now conference held in Quincy, Massachusetts, he showed a slide indicating that the interest in EFA research has increased dramatically just in the last two years.

David Horrobin unfortunately passed away last year, before his hypothesis and the treatment protocols he and his colleagues developed had the opportunity to become accepted theory and practice. Let us hope that their research has not been in vain.

References:

Bates P, Hawkins A, Mahadik S, McGrath J. Heat stress lipids and schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2): 101-107

Carson RC, Butcher, JN, Mineka S. Fundamentals of Abnormal Psychology. Boston. Allyn and Bacon. 2002.

Coon D. Introduction to Psychology: Gateways to Mind and Behavior. Belmont, California. Wadsworth/Thomson Learning. 2004.

Emsley R, Myburgh C, Oosthuizen P, Van Rensburg S. Randomized, placebo-controlled study of ethyl-eicosapentaenoic acid as supplemental treatment in schizophrenia. American Journal of Psychiatry 2002; 159(9):1596-1597.

Ener RA, Meglathery SB, Van Decker WA, Gallagher RM. Serotonin syndrome and other serotonergic disorders. Pain Medicine 2003; 4(1):63-74

Gattaz WF, Brunner J. Phospholipase A₂ and the hypofrontality hypothesis of schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):109-113.

Haag M. Essential fatty acids and the brain. The Canadian Journal of Psychiatry 2003 (April). From the website of the Canadian Psychiatric Association, http://www.cpa-apc.org.

Hockenbury, D, Hockenbury S. Psychology. Third Edition. New York, N.Y. Worth Publishers. 2003.

Horrobin, DF. Schizophrenia as a prostaglandin deficiency disease. The Lancet 1977 (April 30): 936-937.

Horrobin DF. Schizophrenia as a membrane lipid disorder which is expressed throughout the body. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2):3-7.

Horrobin DF. The membrane phospholipid hypothesis as the biochemical basis for the neurodevelopmental concept of schizophrenia. Schizophrenia Research 1998; 30:193-208.

Hudson CJ, Lin A, Horrobin DF. Phospholipases: in search of a genetic base of schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):119-122.

Karki S, Masood G. Combination Risperidone and SSRI-Induced Serotonin Syndrome, Annals of Pharmacotherapy 2003; 37:388-391.

Klein SB. Biological Psychology. Upper Saddle River, NJ. Prentice-Hall. 2000.

Marieb EN. Human Anatomy & Physiology, Sixth Edition. San Francisco. Pearson Benjamin Cummings. 2004.

Mellor J, Laugharne J, Peet M. Omega-3 Fatty Acid Supplementation in Schizophrenic Patients. Human Psychopharmacology 1996; 11:39-46

Peet M. Essential fatty acids: theoretical aspects and treatment implications for schizophrenia and depression. Advances in Psychiatric Treatment 2002;8:223-229.

Peet M. Eicosapentaenoic acid in the treatment of schizophrenia and depression: rationale and preliminary double-blind clinical trial results. Prostaglandins, Leukotrienes and Essential Fatty Acids 2003;69(6):477-85.

Peet M. Nutrition and schizophrenia: beyond omega-3 fatty acids. Prostaglandins, Leukotrienes and Essential Fatty Acids 2004; 70(4):417-22.

Peet M, Brind J, Ramchand CN, Shah S, Vankar GK. Two double-blind placebo-controlled pilot studies of eicosapentaenoic acid in the treatment of schizophrenia. Schizophrenia Research 2001; 49(3):243-51.

Peet M, Horrobin, DF. A dose-ranging exploratory study of the effects of ethyl-eicosapentaenoate in patients with persistent schizophrenic symptoms. Journal of Psychiatric Research 2002; 36(1):7-18.

Peet M, Laugharne JDE, Mellor J, Ramchand CN. Essential fatty acid deficiency in erythrocyte membranes from chronic schizophrenic patients, and the clinical effects of dietary supplementation. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):71-75.

Puri B, Richardson A, Horrobin DF, et al. Eicosapentaenoic acid treatment in schizophrenia associated with symptom remission, normalization of blood fatty acids, reduced neuronal membrane phospholipid turnover and structural brain changes. International Journal of Clinical Practice 2000; 54:57-63.

Puri BK, Steiner R, Richardson A. Sustained remission of positive and negative symptoms of schizophrenia following treatment with eicosapentaenoic acid. Archive of General Psychiatry 1998; 55(2):188-189.

Retrosen J, Adler L, Lohr J, Edson R, Lavori P. Antioxidant treatment of tardive dyskinesia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55(1&2):77-81.

Rudin DO. The major psychoses and neuroses as Omega-e essential fatty acid deficiency syndrome: substrate pellagra. Biological Psychiatry 1981; 16(9):837-850.

Stoll AL. The Omega-3 Connection. New York: Fireside, 2001.

Vaddadi K. Dyskinesias and their treatment with essential fatty acids: a review. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):89-94.

Williamson PC, Brauer M, Leonard S, Thompson T, Drost D. ³¹P magnetic resonance spectroscopy studies in schizophrenia. Prostaglandins, Leukotrienes and Essential Fatty Acids 1996; 55 (1&2):115-118.

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