Natural Treatment of Schizophrenia

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In Search of the Holy Grail:Natural Treatment of SchizophreniaIntroduction

 

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 schizophrenia 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

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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

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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

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