Orthomolecular Psychiatry Online
Welcome to Orthomolecular Psychiatry Online. This is an informational site dedicated to providing information about the field of orthomolecular medicine. Orthomolecular medicine uses substances the body naturally produces (vitamins, amino acids, fatty acids, minerals) to treat patients with mood and behavioural disorders.
Work has been shown to prove that the brain is dependent on nutrition. Without nutrients, the brain cannot function at its optimal level. Therefore, when the brain is not nourished, mood and affect are often compromised. This leads to a chain reaction, often resulting in diagnoses including:
-schizophrenia
-manic depresion
-anxiety disorders
-depressive episodes
-and more
The word orthomolecular is derived from the greek word “ortho”. Orthomolecular was first coined by Linus Pauling. The term “orthomolecular” implies the “right” amount in the right “molecular environment”. Individuals often vary from one another, in terms of their vitamin and mineral requirements. This field acknowledges the concept of biochemical individuality, and the need to discover one’s own unique biochemistry in order to treat someone with an illness.
Patients who are seeking natural alternatives to psychiatric medication turn to orthomolecular medicine.
This site provides readers with background information including information about:
-What orthomolecular medicine is, and how it is applicable to treating mood disorders
-Nutrient summaries, including the role these nutrients play in brain function
-Common conditions associated with mental disorders, and common biotypes associated with mental disorders
-The history of the research that has been done in the orthomolecular medicine field
-Resources for those seeking to learn more about this field and how to get in touch with other professionals
Treating Epilepsy with Natural Supplements-An Individualized Approach
Is there an evolutionary purpose to mental illness?
Environmental Risk Factors for Brain Tumors
The four-year Reflex study, co-ordinated by the German research group Verum, studied the effects of radiation on animal and human cells in a laboratory.
They found that, after being exposed to electromagnetic fields, the cells showed a significant increase in DNA damage which could not always be repaired by the cell.
The study, which has not been published in a journal, also reported other harmful effects on cells.
The radiation used in the study was at Specific Absorption Rate (SAR) levels of between 0.3 and 2 watts per kilogram.
The SAR is the rate at which the body absorbs emissions from the phone handset.
Most phones emit radio signals at SAR levels of between 0.5 and 1 W/kg.
Mobile phones cannot be sold to unless they fall within the SAR of 2 watts per kg.
Solvents are substances that are capable of dissolving or dispersing one or more other substances. Organic solvents are carbon-based solvents (i.e., they contain carbon in their molecular structure). Millions of U.S. workers are exposed to organic solvents that are used in such products as paints, varnishes, lacquers, adhesives, glues, and degreasing/cleaning agents, and in the production of dyes, polymers, plastics, textiles, printing inks, agricultural products, and pharmaceuticals.
Many organic solvents are recognized by NIOSH as carcinogens (e.g., benzene, carbon tetrachloride, trichloroethylene), reproductive hazards (e.g., 2-ethoxyethanol, 2-methoxyethanol, methyl chloride), and neurotoxins (e.g., n-hexane, tetrachloroethylene, toluene). Many different classes of chemicals can be used as organic solvents, including aliphatic hydrocarbons, aromatic hydrocarbons, amines, esters, ethers, ketones, and nitrated or chlorinated hydrocarbons.
Compound | Industrial Uses |
---|---|
Acetone | Cleaning solvent |
Acrylamide | Mining and tunneling, adhesives, waste treatment, ore processing |
Benzene | Fuel, detergents, paint removers, manufacture of other solvents |
Carbon disulfide | Viscose rayon, explosives, paints, preservatives, textiles, rubber cement, varnishes, electroplating |
Ethylene oxide (ETO) | Instrument sterilization |
N- hexane | Glues and vegetable extraction, components of naphtha, lacquers, metal cleaning compounds |
Hydrogen sulfide | Sulfur chemical manufacturing, by-product of petroleum processing, decay of organic matter |
Methane | Industrial settings |
Methyl mercaptan | Odorant in natural gas and fuels |
Methyl-N- butyl ketone | Many industrial uses |
Methylene chloride (dichloromethane) | Solvent, refrigerant, propellant |
Organochlorine | Insecticides |
Organophosphates | Insecticides |
PCE | Dry cleaning, degreaser, textile industry |
Styrene | Fiberglass component, ship building |
Toluene | Paint, fuel oil, cleaning agents, lacquers, paints and paint thinners |
1,1,1-Trichloroethane (methyl chloroform) | Degreaser and propellant |
TCE | Cleaning agent, paint component, decaffeination, rubber solvents, varnish |
Vinyl chloride | Intermediate for polyvinylchloride resins for plastics, floor coverings, upholstery, appliances, packaging |
Xylene | Paint, lacquers, varnishes, inks, dyes, adhesives, cements, fixative for pathologic specimens |
Cancer and Adrenochrome
The steps to create adrenochrome are described as follows in What Really Causes Schizophrenia:
The oxidation of adrenaline to adrenachrome occurs in 2 steps. Initially, adrenaline loses one electron to form oxidized adrenaline, a highly reactive molecule. In the presence of nicotinamide adenine dinucleotide, which is created in both oxidized(NAD) and reduced(NADH) forms in niacin, oxidized adrenaline recpatures one electron to reform adrenaline. If NAD and NADH are in short supply, however, oxidized adrenaline loses another electron and is converted to adrenochrome. This reaction is not reversible. Adrenochrome, therefore, cannot be converted back to adrenaline.
Abram Hoffer describes in his paper on the adrenochrome hypothesis the conditions needed to form adrenochrome:
All the conditions re-quired for the oxidation of adrenalin to adrenochrome in vivo are present. These are: (1) the substrate – noradrenalin, adrenalin; (2) the enzymes and metallic oxidizers which convert adrenalin to adrenochrome, or accelerate its auto-oxi-dation. Auto-oxidation does not require an enzyme. The oxidation of adrenalin to adrenochrome in water is an example. It requires oxygen and is accelerated by traces of metal such as copper ions. We have dis-cussed the theoretical argument for the formation of adrenochrome in several previous reports (Hoffer, 1981, 1983, 1985; Hoffer and Osmond, 1967).
http://www.orthomoleculartherapy.net/library/jom/1999/articles/1999-v14n01-p049.shtml
The most complete (and only placebo controlled) study was carried out by Grof et al (1963) on 15 subjects (10 normal and 5 neurotic or psychopathic patients). They used adrenochrome prepared in 2 different laboratories…
During the psychotic reactions the following symptoms were reported:
Thought disorder(8)
Bizarre ideation(1)
Derealization(5)
Depersonalization(1)
Body image disturbances(2)
Tactile hallucinations (2)
Auditory hallucinations(1)
Visual hallucinations (0)
Minor visual illusions (3)
Euphoria (5)
Complete loss of insight(2)
Taken from:
http://www.fpgrahamco.com/pdfs/4_2_147.pdf
Rarely, mutations are detrimental to health. If the mutation is so severe that the person dies before procreation, the muation dies with them and is not passed into the next human generation. These are "negative" mutations. A mutation that severely impairs the body’s defense system against bacterial infection, for instace would fall into this category.
Even less common are mutations that give the recepient an advantage over other people. Sometimes the advantage improves the ability to survive a potentially deadly illness. The affected individual can then pass his/her genes to the next generation more efficiently than other people because they are more likely to reach reproductive age. This increases the chance that the modified gene will survive into the first generation (that of the children) and from there move into the following generation (that of the grandchildren). This is a "positive" mutation.
The mental symptoms of schizophrenia that arose are simply a by-product of what happened when we tried to balance our bodies from shooting too much adrenalin. Some adrenalin is fine within certain limits, but constantly raising adrenalin levels as a result of constant exposure to carcinogens is dangerous to our body-we need to get rid of it somehow. The adaptation was to oxidize it into adrenochrome. The thing to remember is that adrenalin circulates throughout the whole body. When it is oxidized to adrenochrome, it should be protecting the body when leucocytes(white immune cells) utilize adrenochrome to attack cancer cells that may be arising throughout various parts of the body-liver, kidneys, stomach lining.
Exerpts from Botanical Inhibitors of Amine Oxidase: Relevance to Cancer Therapy from the Journal of Orthomolecular Medicine describes the mechanisms of adrenochrome’s action to prevent cancer cells from multiplying:
This part of the article describes the chain reaction that gets set off starting with a physiological response to stress, then adrenaline production, and finally, adrenocrhome production.
The autonomic nervous system controls physiological responses to stress. Its chemical mediators on the sympathetic side are the catecholamines, dopamine, noradrenalin and adrenalin particularly the last two. Dr. Cannon’s original description of the flight or fight mechanism is still valid. In response to an emergency or a perceived emergency there is a major shock to the autonomic nervous system, releasing a large amount of adrenalin.
The autonomic nervous system controls physiological responses to stress. Its chemical mediators on the sympathetic side are the catecholamines, dopamine, noradrenalin and adrenalin particularly the last two. Dr. Cannon’s original description of the flight or fight mechanism is still valid. In response to an emergency or a perceived emergency there is a major shock to the autonomic nervous system, releasing a large amount of adrenalin.
However, adrenalin is very toxic and it elevates blood pressure. The body must remove it as quickly as possible. To do so it has developed two main pathways for converting adrenaline to other substances. One pathway leads to adrenochrome, which does not elevate blood pressure. The second pathway leads to non indolic derivatives and is controlled by several enzymes called amine oxidases. Thus, a highly reactive compound which elevates pressure is replaced by other compounds that do not have this property.
As the article states, adrenochrome is shown in studies to be antimitotic. It limits cell division:
But adrenochrome (and the other chrome indoles from noradrenalin and from dopamine) have other properties. Adrenochrome is a known mitotic poison,
i.e. it decreases the rate of cell division. In heart muscle and in leukocyte about 80% of the adrenalin is converted into adrenochrome. It is a highly reactive compound with a short half life in the body where it is quickly converted into adrenolutin (3,5,6 tri hydroxy N-methyl indole) which is also toxic, and to 5,6 dihydroxy N-methyl indole which is not. These substances circulate in the body.
Rat studies were done with these rodents undergoing stress. Now, under stress, mammals produce adrenaline. Through experiments, they found that adrenaline itself had no antimitotic effect on the epidermis of the rodents. However, inside it had an antimitotic effect-inferring that adrenaline was oxidized to adrenochrome. In comparison, adrenochrome exerted its anitmitotic effects both in vitro(inside the rodent’s body) and in vivo(outside-in the epidermis).
In 1967 Hoffer and Osmond wrote, “Adrenochrome markedly inhibits mitotic rate of cells, probably by interfering in the glucolytic cycles Bullough found that when mice were stressed by overcrowding, the adrenal medulla increased in size 80%. At the same time the epidermal mitotic rate fell 60%. In vitro adrenaline had no antimitotic effect on epidermis but when it was injected it did. In contrast adrenochrome was antimitotic both in vitro and in vivo. Bullough suggested that during stress the increased quantity of adrenaline was converted into adrenochrome which produced the antimitosis.
This is the hypothesis which will be elaborated, i.e that too little adrenochrome will increase incidence of cancer while too much will decrease the incidence of cancer. Small amounts of adrenalin are produced all the time even when asleep, but during the day and when exposed to stress, the amount is increased. The continually
fluctuating level of adrenalin will ensure a constant production of adrenochrome and its conversion to adrenolutin and other indoles. We suggest that this is one of the mechanisms the body uses to deal with excess mitotis. The leukocytes probably destroy abnormal cells by releasing adrenochrome which has the properties of a free radical and will destroy the cell. It is recognized that pro oxidants are needed to destroy cancer cells. Adrenochrome may be the best and safest natural prooxidant in the body. This hypothesis suggests a number of testable subhypotheses. We will elaborate on one only.
http://www.orthomolecular.org/library/jom/1996/articles/1996-v11n02-p083.shtml
Adrenochrome is very powerful, but when it crosses the blood brain barrier and enters the brain, the effects it exerts is incidental, and not intended by mother nature. Sometimes evolutionary traits that develop comes with trade-offs. You have a powerful chemical like adrenochrome that can attack cancer cells, and yet acts as a neurotoxin when it crosses the blood brain barrier, so the result is perceptual distortion. Unfortunately, this side effect is merely a byproduct, since adrenalin receptors are present in the brain.
Science daily included an article titled Why People with Schizophrenia have Lower Cancer Rates: New Clues. The article talks reveals elucidating evidence that schizophrenics utilize genes to help them fight cancer even though they share the same genes as cancer genes. How this process occurs is described below:
Researchers at the National Institute for Mental Health (NIMH) emphasize that many of the genes associated with schizophrenia are the same as the genes associated with cancer, but that the cells that have these genes use them in opposite ways in the two disorders. While cancer results from changes in the genes that cause cells to go into metabolic overdrive and multiply rapidly, those same genes cause cells in schizophrenia to slow to a crawl.
Dr. Amanda Law of the University of Oxford, who heads one of the teams working at the NIMH, explored specific genetic pathways that cells use to make basic decisions about their development and their fate.
"This is about basic decision making by cells–whether to multiply, move or change their basic architecture," says Dr. Law. "Cancer and schizophrenia may be strange bedfellows that have similarities at the molecular level. The differences lie in how cells respond to external stimuli: in cancer the molecular system functions to speed up the cell and in schizophrenia the system is altered in such a way that causes the cell to slow down." Law adds that selective targeting of these pathways may be a potential target in developing treatments for schizophrenia.
"It’s very curious that a brain disorder associated with very complicated human behavior has at a genetic and cellular level a striking overlap with cancer, a very non-behavior related disorder. Understanding these pathways might provide us with some new strategies for thinking about cancer," said Dr. Weinberger.
Dr. Weinberger added that future research involves using this information to search for therapeutic insights that can reverse these processes, with implications not only for treatment of schizophrenia, but also maybe for cancer as well.
http://www.sciencedaily.com/releases/2007/12/071208092440.htm
The speculation of treaments based off of the current research actually took a practical turn when a new cancer drug was developed and is currently being tested.
93. Matrix Pharmaceutical, Inc. (2000). Matrix Updates Interim Phase II
Results for IntraDose in Primary Liver Cancer.
http://archive.maillist.com/hbv_research/msg01155.html
.
Doctor’s Guide. Personal Edition, Stein, J. (2001). DG Dispatch – WCM:
Intratumal IntraDose (Cisplatin/Epinephrine) Shows Promise in
Metastatic Malignant Melanoma.
http://www.pslgroup.com/dg/1f3ed2.htm
.
Final Thoughts:
Onset of Psychosis in Young Adults
Schizophrenia is a disorder afflicting 1 in every 100 people, roughly, in North America. It is characterized by the following characteristics according to the current DSM IV:
- Characteristic symptoms: Two or more of the following, each present for much of the time during a one-month period (or less, if symptoms remitted with treatment).
- Delusions
- Hallucinations
- Disorganized speech, which is a manifestation of formal thought disorder
- Grossly disorganized behavior (e.g. dressing inappropriately, crying frequently) or catatonic behavior
- Negative symptoms—affective flattening (lack or decline in emotional response), alogia (lack or decline in speech), or avolition (lack or decline in motivation)
- If the delusions are judged to be bizarre, or hallucinations consist of hearing one voice participating in a running commentary of the patient’s actions or of hearing two or more voices conversing with each other, only that symptom is required above. The speech disorganization criterion is only met if it is severe enough to substantially impair communication.
- Social/occupational dysfunction: For a significant portion of the time since the onset of the disturbance, one or more major areas of functioning such as work, interpersonal relations, or self-care, are markedly below the level achieved prior to the onset.
- Duration: Continuous signs of the disturbance persist for at least six months. This six-month period must include at least one month of symptoms (or less, if symptoms remitted with treatment).
Schizophrenia is actually a label slapped on to a variety of symptoms that are also present with psychosis. The diagnosis is further divided into subtypes according to the DSM IV
- Paranoid type: Where delusions and hallucinations are present but thought disorder, disorganized behavior, and affective flattening are absent. (DSM code 295.3/ICD code F20.0)
- Disorganized type: Named hebephrenic schizophrenia in the ICD. Where thought disorder and flat affect are present together. (DSM code 295.1/ICD code F20.1)
- Catatonic type: The subject may be almost immobile or exhibit agitated, purposeless movement. Symptoms can include catatonic stupor and waxy flexibility. (DSM code 295.2/ICD code F20.2)
- Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met. (DSM code 295.9/ICD code F20.3)
- Residual type: Where positive symptoms are present at a low intensity only. (DSM code 295.6/ICD code F20.5)
The ICD-10 defines two additional subtypes.
- Post-schizophrenic depression: A depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present. (ICD code F20.4)
- Simple schizophrenia: Insidious and progressive development of prominent negative symptoms with no history of psychotic episodes. (ICD code F20.6)
The course and prognosis of schizohprenia varies from person to person. There is also evidence that schizophrenia does have a genetic basis to it, but however, the severity of psychotic symptoms can change due to other factors-namely, environmental, nutritional.
Someone is usually diagnosed with schizophrenia when they have a psychotic episode. However, as many studies indicate, this person is already showing some syndromes that are prodromal long before their first psychotic episode. As eva edelman describes in her book, natural healing for schizophrenia and other mental disorders, the onset and symtoms include:
early symptoms-personality changes, alterations in sleep patterns, depression, mania, fear.
One might readily assume that the man is sullen, the child is spirited and will learn to read in his own good time, and the teenager is heartbroken. The symptoms are insidious; they often develop slowly. Most people don’t notice, or can’t recognize them for what they are. What is happening biochemically in their bodies, according to orthomolecular psychiatry, is probably a sign of undernourished neurons, insufficient brain enzymes, allergic susceptiblity, or an overload of a heavy metal or toxin. These imbalances are what give rise to behavioural and mood abnormalities.
Given time, the individual may be so out of reach that the early omens are unmistakable-in retrospect. At this piont the patient is usually brought in for medical care and diagnosed as schizophrenic.
But what exactly tips schizophrenics over the edge and leads them to lose insight? It can be common for some people to experience dysperceptions as a child or young teen and be fully aware of their sensory experiences. There are momentary lapses of judgment when objects appear distorted to their eyes, they hear voices that aren’t there, they smell flavours for a minute, but then they snap back to reality. The dysperceptions gradually become more pronounced and more frequent, and then finally there is a point when one finally loses the awareness their dysperceptions are not real and they become hospitalized when the ones around them observe them act and behave in strange ways and become alarmed. That is the classic diagnosis of the onset of schizophrenia, but in reality, schizophrenia is a developmental disorder of the brain that wreaks havoc slowly and steadily from an early age with signs such as fear, mania, depression that goes unnoticed by others and is well hidden until the final breaking point. A common well known fact is that the frequency of a first psychotic episode appears in 75% of schizophrenics between the ages of 16-25. Why is that the case? I’m going to attempt to answer this question
There is a dysfunction in prefrontal cortex development during adolescence that gradually starts the ball rolling and acts as a trigger for the first psychotic episode.
The brain runs its course in development from birth to adulthood, with vast changes that occur. Neurons make synapses with each other and then a pruning process also occurs. Along with that, myelination(wrapping of myelin sheath around the axons to conduct messages faster) also occurs. There are bursts of development within different brain regions corresponding to each stage of development. The last stages of brain development occur during late adolescence to early adulthood and are characterized by the myelination of the dorsolateral prefrontal cortex.
The development of the dorsolateral frontal cortex during this stage in life requires the trace metal copper to maintain the myelin sheath. Myelin sheath constitutes the white matter of the brain and its function is wrap itself around axons to conduct neural impulses quicker. Therefore, the frontal cortex, which is under construction during this point, should be faster and speedier when it finishes developing.
However, in schizophrenics, they have underactive activity in the dorsolateral prefrontal cortex as shown through PET scans, which is an indication that messages aren’t traveling as efficiently as they could be.
An indication of underactivity is thin myelin sheath. There is evidence that the myelin sheath is less dense in schizophrenics:
http://linkinghub.elsevier.com/retrieve/pii/S0920996403001816
"Our previous electron microscopic study of the prefrontal cortex (PFC) demonstrated ultrastructural signs of apoptosis and necrosis of oligodendroglial cells in schizophrenia (SCH) and bipolar disorder (BPD). "
"The data suggest that lowered density of oligodendroglial cells(myelin sheath) that occurs in schizophrenia and mood disorders could contribute to the atrophy of neurones that has been described in the prefrontal cortex of subjects with severe mental illness. "
http://www.sciencedaily.com/releases/2007/04/070423185615.htm
"We show that causing a defect in white matter is sufficient to cause biochemical and behavioral changes resembling those seen in neuropsychiatric disorders," says Corfas, the study’s senior author. "I think this will provide a new way of thinking about the causes of, and possibly, therapies for schizophrenia."
"The idea of schizophrenia arising from white-matter defects may also help explain the timing of its emergence, Corfas notes. Recent evidence suggests that myelination of the prefrontal cortex (a brain area that has been implicated in schizophrenia) occurs not only during infancy and toddlerhood, but also during late adolescence or early adulthood — just when schizophrenia strikes. "
The dorsolateral prefrontal cortex governs functions such as judgment and logic. Delusions are a crucial part of psychosis, so disruption in the prefrontal cortex alludes to the decline of rational judgment and reasoning. As described by Wikipedia:
DL-PFC serves as the highest cortical area responsible for motor planning, organization, and regulation. It plays an important role in the integration of sensory and mnemonic information and the regulation of intellectual function and action.
Dorsolateral prefrontal cortex plays an executive function by making "sense" of incoming sensory information. Now, we know that when this process is disrupted, making sense out of voices and hallucinations and evaluating them becomes distorted.
This is also inferred through the fact that underactive dorsolateral prefrontal cortex is apparent in parallel delusional states in normal human subjects in PET scans. Interestingly enough, a state of psychosis is often referred to as dreaming wide awake. There are similarities in metabolic activity that underlies both REM sleep and psychosis. Underactive dorsolateral prefrontal cortex activity is apparent in REM sleep, providing clues as to the underlining mechanisms giving rise to the ablation of logic and the rise of delusional and irrational thinking as found in dreaming and psychosis.
As I mentioned before, it is copper that is the important nutrient for maintaining myelin sheath during brain development. However, there is one caveat. Although copper maintains myelin sheath formation, it also contributes to myelin sheath destruction as well through free radical formation. Instead of copper doing its normal job of building myelin sheath in normal brain development, it instead acts in an opposite direction by destroying it gradually instead-a process that occurs in persons with a genetic predisposition to schizophrenia. I will explain how copper contributes to free radical formation . But first off, a little description of copper. Copper is a trace metal with the highest concentrations in the liver and the brain. The highest concentrations of copper are especially pronounced in developing tissues. It is explained in Neurobiology of the Trace Elements: Trace element neurobiology and deficiences that copper concentrations within the brain vary across brain regions. There is a trend for brain copper concentrations to increase with age. This could correspond with the needed resources of copper containing enzymes to fuel normal brain development. For many of the brain regions in humans, adult levels have been reached by 11 years. However, myelination still occurs after age 11, hence, the recruitment of copper into cuproenzymes within the dorsolateral prefrontal cortex.
Copper functions as a co-factor in enzymes called cuproenzymes, that help speed up important chemical reactions in the body. The protein carrier ceruloplasmin transports copper to the enzymes needed to catalyze biochemical reactions:
As mentioned in the Bulletin of Clinical Psychopharmacology:
Ceruloplasmin is a protein in the human serum that is synthesized by hepatocytes, but extrahepatic gene expression in the brain, lung, spleen, and testis has also been reported. Ceruloplasmin contains approximately 95% of serum copper and it carries copper from liver to numerous tissues. Ceruloplasmin level refects largely the copper concentration of the serum.
Copper in the bloodstream of the human body can also circulate as ionic copper as well, meaning that it’s a charged metal without anything attached to it. Ionic copper is very reactive, as metals are inherently very reactive. When copper enters into the brain, it either floats around and eventually reacts with another molecule, either incorporating itself into the copper containing enzymes, or participates in other chemical reactions that produces free radicals. Free radicals are highly reactive molecules with at least one unpaired electron. They latch onto nearby molecules, oxidizing them. Oxidation is defined as the interaction between oxygen molecules and all the different substances they may contact, from metal to living tissue. Technically, however, with the discovery of electrons, oxidation came to be more precisely defined as the loss of at least one electron when two or more substances interact. When a molecule loses an electron, it becomes unstable, and will participate in reactions with other substances to capture electrons in order to make it stable again. Oxidation changes the nature of nearby molecules. The result of accumulated, extensive oxidation in the human body, can result in biological damage, such as disruption of DNA patterns, organ malfunction, immune disorders, heart disease, cancer, and aging.
Now, it is presumed that the concentration of copper in its ionic form will be in the brain as well as the curproenzymes essential for brain function. Most schizophrenics have high levels of ceruloplasmin, reflecting high levels of copper in general. When copper levels become too high, they become toxic and encourage the production of free radicals. Compared to other subjects without a predisposition to schizophrenia, they have disproportionately more copper levels in general at each stage of nervous system development during the lifespan. Schizophrenics produce too many free radicals in comparison with non-schizophrenics. A genetic basis could be behind this, and it can possibly manifest as copper metabolism deficiences.
A study conducted by Osman Virit et al, showed higher levels of ceruloplasmin in schizophrenic patients. The abstract follows:
In the present study, we aimed to investigate the association between plasma ceruloplasmin level and schizophrenia in Turkish patients. Methods: 60 patients (36 women and 24 men, mean of age 31.93±9.37 years, range 19-55) that were diagnosed as schizophrenia according to DSM-IV were included for this study at the Psychotic Disorders Unit, Department of Psychiatry, Faculty of Medicine, Gaziantep University, Gaziantep, Turkey. The control group consisted of 40 healthy subjects in similar age and gender (23 women, 17 men). Venous blood samples were collected from the left forearm into heparinized tubes. The blood samples were centrifuged and the plasma was removed. Erel’s ceruloplasmin measurement method that is based on the enzymatic oxidation of ferrous ions to ferric ions was used. SPSS Windows program 13.0 was applied for statistical analysis. Results: Plasma ceruloplasmin levels of schizophrenic patients were significantly higher than the healthy controls (p<0.001)
http://www.psikofarmakoloji.org/pdf/18_4_6.pdf
It should also be noted that there are other disorders and health conditions that present with psychotic symptoms, caused by faulty copper metabolism as well. In Wilson’s disease, the liver does not excrete excess copper into the bile as it normally does, resulting in accumulation of copper in the liver and liver damage. The symptoms include include tremors, difficulty speaking and swallowing, drooling, incoordination, involuntary jerky movements (chorea), personality changes, and even psychosis (such as schizophrenia or manic-depressive illness). Patients with liver problems tend to come to medical attention earlier, generally as children or teenagers, than those with neurological and psychiatric symptoms, who tend to be in their twenties or older. (http://gut.bmj.com/cgi/content/full/56/1/115)
Post partum psychosis is due to rapidly changing hormones just after birth. Copper and ceruloplasmin are elevated due to the increased estrogen. Copper is more than twice what it was before pregnancy. Psychotic breaks tend to cocur within 2 weeks after a first birth, in women between the ages 22 and 28, and are more frequent after a male baby. Even if untreated, however, copper gradually returns to normal over several months, with an accompanying remission of the psychosis. (Journal of Applied Nutrition, 27(2)"Copper, zinc, manganese, b3 and b6 in the schizophrenias")
The common thread amongst all these conditions( schizohprenia, wilson’s disease, and post partum psychosis), is the common onset periods-young adulthood. This implies dorsolateral prefrontal cortex dysfunction during adolescence and myelin deterioration must play a role in the common periods of onset.
Furthermore, copper is also important in forming another free radical classified as a hallucinogen. Copper also catalyzes the formation of a hallucinogen called adrenochrome by oxidizing adrenalin. Adrenalin loses an electron to become oxidized adrenalin. It furthermore, in the presence of copper, loses another electron to form adrenochrome. Evidently, adrenochrome was first discovered decades ago. It was hypothesized by Abram Hoffer in the 50s to be a hallucinogen that caused schizophrenic symptoms. In an interview with an online jouranlist, he described the relationship between adrenalin and adrenochrome:
"Adrenalin can become an indole when it oxidizes into adrenochrome. We proved that adrenochrome was active. It’s a hallucinogen, but not a nice one. With adrenochrome, you always get a bad, horrible reaction.
Now under stress, humans start pouring out adrenaline. Adrenalin is very dangerous. Normally we get rid of it by doing something-muscles use it up. The body also uses antioxidants like vitamin C, E, and glutathione. If these mechanisms fail, there’s one final fail-safe mechanism: copper and iron in the body change the adrenaline to adrenochrome. But that creates a huge overload of adrenochrome. "
Another similarity between PET scans of schizophrenics and subjects in REM sleep is an overactivated limbic system. This runs parallel to adrenochrome’s function in the schizophrenic brain, as adrenochrome is thought to especially activate parts of the limbic system and give rise to perceptual distorations and emotional sensations. After all, adrenochrome acts as a hallucinogen.
To wrap up what was just stated, these 2 component processes, demyelination and adrenochrome formation, which are cascaded by copper,influence the high likelihood of a first psychotic episode. Insight is destroyed through demyelination of the dorsolateral prefrontal cortex, and perceptual distortions result when excess adrenochrome activates the limbic system.
What follows now are just some ideas I’m throwing around and linking together to explain why teens and young adults are so vulnerable to psychosis if they have a genetic predisposition to schizophrenia. They are just brief points to note about the above mentioned factors that play a role in adolescent psychosis. For our purposes I will be examining schizophrenia within the context of psychosis. Let’s examine the following ideas in the following order to come to a conclusion.
-Defining psychosis
-Discussing the development of the dorsolateral prefrontal cortex during adolescence
-linking brain states in psychosis with brain states during REM sleep
-Examing the role of copper during myelination of the prefrontal cortex and the formation of adrenochrome
-Examining how adrenochrome is formed
What is Psychosis?
-defining what psychosis is. As defined in wikipedia, psychosis is:
Psychosis (from the Greek ψυχή "psyche", for mind or soul, and -οσις "-osis", for abnormal condition), with adjective psychotic, literally means abnormal condition of the mind, and is a generic psychiatric term for a mental state often described as involving a "loss of contact with reality". People suffering from psychosis are said to be psychotic.
People experiencing psychosis may report hallucinations or delusional beliefs, and may exhibit personality changes and disorganized thinking. This may be accompanied by unusual or bizarre behavior, as well as difficulty with social interaction and impairment in carrying out the activities of daily living.
A lot of the times, psychosis is also embedded within an emotional context. So one’s delusions are always derived from fear and paranoia, e.g fear that the devil is out to get you, everyone is talking behind your back, etc.
Myelination of the Dorsolateral Prefrontal Cortex
As described in an excerpt from an article below below, myelination in normal development increases in the dorsolateral prefrontal cortex during adolescence.
Two studies have identified differences between adolescent and adult brains. One study conducted by Dr. Arthur Toga of the Laboratory of Neuro Imaging located at UCLA demonstrates that children and adolescents from ages 12 to 16 have less myelination in the frontal lobes of the brain (2). The frontal lobes, located at the front of the cranium, have been identified as the area of the brain that dictates rational behavior and reasoned weighing of consequences (4). Myelin is composed of neural cells that form insolating lipid layers around nerve processes. Myelinated processes can more effectively conduct electrical signals from one neuron to another. The presence of more myelin in adult frontal lobes implies that more neural processes are connecting neurons together. If connections between neurons in adolescent frontal lobes are not as abundant, adolescents may not be as capable of using their frontal lobes Decreased myelination may mean that neurons in the frontal lobes of children and teenagers are not as interconnected and not as capable of communicating via passing signals as the neurons of adult frontal lobes, resulting in decreased ability to make reasoned decisions
http://serendip.brynmawr.edu/bb/neuro/neuro04/web1/epowell.html
However, myelination is suppressed in the dorsolateral prefrontal cortex because there is some factor that is suppressing the genetic expression of myelination. (probably the presence of free radicals) Biology Psychiatry reported evidence of down-regulated genes in post-mortem analysis of schizophrenics in this area of the brain:.
In addition, DNA microarray analysis of post mortem tissue from the dorsolateral prefrontal cortex demonstrated that six genes whose expression is enriched in myelin-forming oligodendrocytes were down-regulated in the schizophrenic compared to control subjects
This hypomyelination is indicative of poor development in the dorsolateral prefrontal cortex, and as a result, the functions this area of the brain is responsible for becomes far less efficient at tasks such as reasoning and rational integration of emotional information. The less developed the myelination, the more severe the deficits are.
Dreaming Wide Awake
-There are similarites in PET scans between schizophrenics and normal subjects during REM sleep states. The striking similarities occur in the areas of the prefrontal cortex and limbic system.
It’s interesting, but dreams during REM sleep are characterized by very emotional narratives and illogical and irrational concepts we accept as logical-much like a schizophrenic experience. There are hallucinations too. There is underactive dorsolateral prefrontal cortex activity in schizophrenia. The same type of underactive activity in the dorsolateral prefrontal cortex is evident when normal subjects are in REM sleep.
Linden in the Accidental Mind describes how deactivation of the dorsolateral prefrontal cortex gives rise to our acceptance of bizarre situations in our REM dreams:
portions of the prefrontal cortex, in particular the dorsolateral prefrontal cortex, are deactivated in REM sleep. This is a crucial part of the brain for executive functions (judgment, logic, planning) and working memory. It’s deactivation may help explain the illogical character of dreams and the dreamer’s acceptance of bizarre and improbable circumstances and plotlines. In this sense, it is wroth mentioning that deactivation of this region is a hallmark of hallucinating schizophrenics.
Another feature of the brain in REM sleep is strong activation of regions subserving emotion. In particular, the amygdala and anterior cingulate are strongly activated and these regions appear to play a role in fear, anxiety, and the emotional aspects of pain as well as responses to fearful and painful stimuli. This may underlie the prevalence of fear, anxiety, and aggression in the emotional tone of narrative dreams. Interestingly, abnormal activity in the limbic system including the amygdala has been evidenced in schizophrenics.
In a study done by Human Neurobiology in 1982, stimulation of parts of the limbic system produced pronounced sensations and hallucinations:
Direct electrical stimulation of any limbic sector may evoke a visceral sensation or an emotion, usually fear or anxiety. Vivid formed dream- or memory-like hallucinations, or intense feelings of familiarity, may be evoked from the hippocampal formation and amygdala. Conversely, amnesia may result from stimulation-induced bilateral disruption of the same region. Cingulate gyrus stimulation near the supplementary motor cortex may evoke partially adaptive movement sequences, or may interfere with the performance of movements. In general, those phenomena are not due to epileptic pathology, nor to gross spread of activation. The particular response evoked is not related to the precise electrode location, but rather to the patient’s psychological traits and concerns. Thus, there is no direct relationship between specific mental contents and the activation of particular limbic neurons. Limbic stimulation appears to produce deep mental alterations whose manifestation at the surface of awareness, or in specific movements, is defined by the ongoing context.
The dorsolateral prefronal cortex serves as the highest cortical area responsible for motor planning, organization, and regulation. It plays an important role in the integration of sensory and mnemonic information and the regulation of intellectual function and action. However, it is not exclusively responsible for the executive functions. All complex mental activity require the additional cortical and subcortical circuits that the dorsolateral prefrontal cortex is connected with.
As described in mind, brain, and schizophrenia, the frontal lobe has circuits that connect to the limbic system.The frontal cortex of the brain responsible for integrating sensory information it receives from other subcortical structures poorly organizes sensory information and makes poor judgments about them. Schizophrenics form delusions as a result of the incoming sensory information they are bombarded with. They don’t know how to correctly judge the sensory stimulation they come across, and when the frontal lobes receive information from the limbic system, it cannot distinguish reality from non-reality.
A large prefrontal ccortex allows anticipation and planning but has to be integrated with older structures in the brain designed to respond to affective cues. Many investigators have pointed to the imbalance between these 2 parts of brain in schizophrenia over the years. When activity in the limbic inputs through the nucleus accumbens overwhelms the input through the dorsal striatum, critical information about self-monitoring could be lost to conscious appraisal, leading to positive symptoms. The observation that the entire limbic system becomes hyperactive on the PET during hallucinations is compatible with this suggestion."
So far, we’ve pinpointed the 2 major neural correlates that contribute to heightened emotions, hallucinations, and delusional thinking in the brain (dorsolateral prefrontal cortex and limbic system). Let’s delinneate a possible chemical mechanism in schizophrenia that imitates the metabolic activity found in REM dream states. copper catalyzes free radicals that lead to both demyelination of the dorsolateral prefrontal cortex and creation of limbic pathways for adrenochrome to travel and disrupt.
What’s Copper Got to do With it?
Copper is a double edged sword, participating in functions that are both beneficial and detrimental to a developing nervous system. As mentioned before in my introduction, copper concentrations increase within the dorsolateral prefrontal cortex area during development, because copper concentrations are especially pronounced in developing tissues. With that said, the fact that schizophrenics have too much ionic copper floating around, its going to form free radical, causing damage to the myelin sheath. It will also form more adrenochrome.
The copper containing enzymes critical to brain function include superoxide dismutase, dopamine-B-monooxygenase, and cytochrome c oxidase. superoxide dismutase acts as an antioxidant. Dopamine-B-monoxygenase is responsible for catalyzing the formation of the neurotransmitter norepinephrine from dopamine. Cytochrome c oxidase is the copper containing enzyme responsible for maintaining the myelin sheath. As described in The Eye and Nutrition, cytochrome c oxidase is vital in myelin synthesis:
Copper is most frequently present in biologic systems as Cu2+, including at least 3 types of bound Cu2+ which are formed in copper-containing enzymes. Copper is required for formation or maintenance of myelin, comprosed primarily of phosphoipids. Cytochrome-oxidase activity is related to phospholipd synthesis. Thus, copper deficiency may lead to poor development of myelin, necrosis of nerve tissue, and neonatal ataxia.
As mentioned previously, copper potentially participates in reactions that form free radicals that damage nervous system tissues. When copper manifests itself in detrimental reactions it is because the presence of oxygen reacts with copper.
Environmental Health Perspectives sums up the pro-oxidant and antioxidant properties of copper:
The ability of copper to cycle between stable oxidized Cu2+ and unstable reduced Cu+ states is used by cuproenzymes involved in redox reactions (e.g., Cu/Zn superoxide dismutase and cytochrome oxidase). However, the Cu2+ <-> Cu+ transitions can in certain circumstances also result in the generation of reactive oxygen species (e.g., superoxide radical and hydroxyl radical), which, if not detoxified efficiently, can damage susceptible cellular components.
Although Cu2+ is an essential element for life and the function of numerous enzymes is basic to neurobiology, free or incorrectly bound Cu2+ can also catalyze generation of the most damaging radicals, such as hydroxyl radical, giving a chemical modification of the protein, alternations in protein structure and solubility, and oxidative damage to surrounding tissue.
http://www.ehponline.org/members/2002/suppl-5/869-870kowalik-jankowska/kowalik-jankowska-full.html
Free radicals can deteriorate the myelin sheath, as they destroy the structure of molecules by stealing electrons from other stable molecules in myelin. An experiment done by The Journal of Neurochemistry titled Effect of Reactive Oxygen Species on Myelin Membrane Proteins demonstrated myelin deterioration from the brainstems of adult rats when they were incubated in the presence of copper ions and hydrogen peroxide(the result of the reaction being free radical formation). The abstract of this study is described below:
Fresh myelin, isolated from brainstems of adult rats, was incubated in the presence of Cu2+ and H2O2. Electrophoretic analysis of the reisolated myelin membrane revealed a gradual loss of the protein moiety from the characteristic pattern and an increase in aggregated material appearing at the origin of the gel. The aggregation of proteins was time-dependent and was concomitant with the accumulation of lipid peroxidation products reactive with thiobarbituric acid. Furthermore, during the course of incubation, there was a gradual decrease in the amount of recovered light myelin and a quantitatively similar increase in heavier myelin subfractions. The aggregation of proteins seems not to be directly related to the buoyant densities of myelin fragments. The peroxidative damage to the myelin proteins may be an important contributor to pathochemistry of myelin sheath, in particular, and in general it implies the susceptibility of the protein moiety of cell membranes to oxygen-induced deterioration.
http://www3.interscience.wiley.com/journal/119508461/abstract?CRETRY=1&SRETRY=0
Ionic copper is also an oxidizing agent in reactions with adrenalin. It creates another important free radical, adrenochrome.
How is Adrenochrome Formed?
It was shown through experiments in the 50s and 60s that adrenochrome was a hallucinogen that provoked psychotic symptoms. What is the exact pathway that leads to psychosis?
psychosis occurs when:
undernourished neurons
insufficient brain enzymes
allergic susceptibilities
overload of a heavy metal or toxins…
create pathways in the body that, through various chemical reactions, lead to the end result of adrenalin becoming oxidized. When the person with a vulnerability to schizophrenia first comes across some type of stressor during adolescence or young adulthood, it induces them to produce more adrenalin. The stressor can be emotional stress, cerebral allergies, heavy metal toxicity, etc.
Adrenalin is also known as epinephrine and functions as a neurotransmitter in the brain. Neurotransmitters follow pathways in the brain, and adrenalin neurotransmitters traverse parts of the limbic system and extend to the cortex, including the frontal lobes. It is classified as a catecholamine, and the name of the pathway system it travels is called the noradrenergic system. Here is a diagram illustrating the routes adrenaline travels:
The steps to create adrenochrome are described as follows in What Really Causes Schizophrenia:
The oxidation of adrenaline to adrenachrome occurs in 2 steps. Initially, adrenaline loses one electron to form oxidized adrenaline, a highly reactive molecule. In the presence of nicotinamide adenine dinucleotide, which is created in both oxidized(NAD) and reduced(NADH) forms in niacin, oxidized adrenaline recpatures one electron to reform adrenaline. If NAD and NADH are in short supply, however, oxidized adrenaline loses another electron and is converted to adrenochrome. This reaction is not reversible. Adrenochrome, therefore, cannot be converted back to adrenaline.
Abram Hoffer describes in his paper on the adrenochrome hypothesis the conditions needed to form adrenochrome:
All the conditions re-quired for the oxidation of adrenalin to adrenochrome in vivo are present. These are: (1) the substrate – noradrenalin, adrenalin; (2) the enzymes and metallic oxidizers which convert adrenalin to adrenochrome, or accelerate its auto-oxi-dation. Auto-oxidation does not require an enzyme. The oxidation of adrenalin to adrenochrome in water is an example. It requires oxygen and is accelerated by traces of metal such as copper ions. We have dis-cussed the theoretical argument for the formation of adrenochrome in several previous reports (Hoffer, 1981, 1983, 1985; Hoffer and Osmond, 1967).
http://www.orthomoleculartherapy.net/library/jom/1999/articles/1999-v14n01-p049.shtml
Hoffer also asserts that adrenochrome acts as a hallucinogen and is produced endogenously
Adrenochrome is a member of a class of chemicals known as aminochromes, each one derived by the oxidation of its precursor amine. Thus, 1-dihydroxy pheny-lalanine (L-dopa) is oxidized to dopachrome; tyrosine to a series of coloured indoles; no-radrenalin to noradrenochrome and adren-alin to adrenochrome. The chemistry of these oxidation reactions is very complex for these compounds are very reactive. They are formed via free radicals and rapidly break down to several classes of trihydroxy and dihydroxy N methyl indoles. Adrenolutin is the best known example of trihydroxy N methyl indole, and leukoadrenochrome is the best known of the dihydroxy N methyl indoles. Both are derived from adreno-chrome. Adrenolutin is coloured yellow and is toxic, as is adrenochrome. It is psychoto-mimetic. Leukoadrenochrome is colourless and non-toxic. On the contrary, even in small doses given sublingually, it has anti-tension and anti-anxiety properties. Adrenolutin is more stable than adreno-chrome.
http://www.orthomoleculartherapy.net/library/jom/1999/articles/1999-v14n01-p049.shtml
Furthermore, experiments done by Hoffer et al isolated samples of adrenochrome and ingested these substances themselves:
Adrenochrome causes more perceptual changes but they are rarely as pronounced as those caused by LSD or mescalin. Its effect may last a long time. It produced a two-week paranoid depression in one of us (A.H.) and a one-week paranoid depressive reaction with visual illusions in a distinguished colleague of ours.
http://www.orthomoleculartherapy.net/library/jom/1999/articles/1999-v14n01-p049.shtml
In the Paper, the Adrenochrome Hypothesis of Schizophrenia Revisited, Smythies tells us the studies that were done when adrenochrome was taken in by subjects. Here is an excerpt from the paper where he describes the results of a double blind study conducted with adrenochrome administration:
The most complete (and only placebo controlled) study was carried out by Grof et al (1963) on 15 subjects (10 normal and 5 neurotic or psychopathic patients). They used adrenochrome prepared in 2 different laboratories…
During the psychotic reactions the following symptoms were reported:
Thought disorder(8)
Bizarre ideation(1)
Derealization(5)
Depersonalization(1)
Body image disturbances(2)
Tactile hallucinations (2)
Auditory hallucinations(1)
Visual hallucinations (0)
Minor visual illusions (3)
Euphoria (5)
Complete loss of insight(2)
Taken from:
http://www.fpgrahamco.com/pdfs/4_2_147.pdf
As mentioned in The Adrenochrome Hypothesis Revisited, there is evidence that adrenochrome appears within specfic sites of the brain:
The recent evidence that adrenochrome may occur in strategic areas of the brain related to anxiety and to basic limbic system suggests that further research in this area is indicated
http://www.fpgrahamco.com/pdfs/4_2_147.pdf
Conclusions and Final Thoughts
What does all the information I provided tell us? well, presumably genetic markers encode copper to migrate near the dorsolateral prefrontal cortex during frontal cortex development during adolescence. The onset of a first psychotic episode occurs between the ages of 16-25 for 75% of schizophrenics. Why is psychosis so rare in childhood? The explanation for this could lie in the fact that copper content circulating within dorsolateral prefrontal cortex myelin sheath hasn’t reached it’s threshold yet in terms of development.
Remember: In the brain, copper is either attached to an enzyme such as cytochrome c oxidase, or freely circulates as ionic copper. Ionic copper is biounavailable to participate in critical brain functions, so it instead acts as an oxidizing agent for the formation of free radicals. Copper concentrations increase during adolescence, potentiating the chances that more adrenochrome will form in the presence of excess adrenalin, as well potentiating the chance of more incursions on myelin sheath through free radical formation
So to sum up, the first psychotic episode in a schizophrenic ultimately is a result of the accumulation of frequent free radical attacks on the frontal lobe during the stage of development when the frontal lobe should be myelinating. There is more free ionic copper then cytochrome c oxidase created to maintain the myelin sheath. Adrenochrome’s deleterious effects have been shown through hyperactive limbic metabolic activity in PET scans of schizophrenics. Schizophrenic states mimic dreaming states during REM sleep, giving rise to the phrase, "dreaming wide awake".
Orthomolecular Psychiatry
Let’s talk about psychotropic drugs.
What I hate is that the public is misinformed. How many people do you know who don’t know what else to do except go on psychotropic medication to treat their depression and anxiety or other mental illness? It the conventional thing to do.They think depression or anxiety is their only noticeable problem. That isn’t the case a lot of the times.
Mental disorders are a SYMPTOM of several factors that give rise to behavioral and emotional disturbances
Cerebral allergies
Vitamin B3 and B6 dependencies
Vitamin deficiencies such as scurvy or pellagra
Essential fatty acid deficiencies
Mineral deficiencies, such as zinc
Toxic reactions to lead or to drugs
LSD and similar hallucinogens
Infections such as rheumatic fever, syphilis, and many others.
Eva Edelman mentions in her book Natural Healing for Schizophrenia: And Other Common Mental Disorders only 20-25% of Americans have allergies, yet 85% of depressed patients have allergies—a four-fold difference, and very statistically significant. What does this say about the link between our body and our minds?Histamine may also contribute to anxiety and ADD. symptoms of depression, mania, hallucinations could be masquerading as zinc deficincies or a vitamin b12 deficiency. Signs of anxiety, depression, hallucinations are a SIGN-a sign that the delicate balance of the body is being disturbed-and you must fix the cause, not the symptom.
If you treat the root cause, you will succeed further than masking the symptoms with pharmaceutical drugs. For instance, if your plant is sick, do you pour gasoline on it? No. You check for toxicities and other imbalances. Is it getting enough sunlight? What have you been feeding it? Etc. You see, this same approach is applied in orthomolecular psychiatry. An orthomolecular psychiatrist will use diagnostic tools (blood tests, urine tests, hair and mineral tests) to determine toxicities and nutrient deficiencies, and then feed your body what it needs in order to get well again. Not inject you with synthetic medication-that is, basically tantamount to pouring gasoline on your plant-a last stop gap measure in order to put the fire out.
Orthomolecular psychiatry has existed for decades, it encompasses the basic principle of treating patients with substances that the body naturally produces. This is a viable alternative for those who are dealing with mental illness. This includes vitamins, amino acids, fatty acis-nutraceuticals that don’t give patients awful side effects. These are substances that the body utilizes as its building blocks to build the neurotransmitters. It is an instinctive reaction for our human bodies to react negatively to synthentic psychotropic medications. Antyhing that is foreign is considered an attack on the body, so an adverse reaction follows. Natural substances on the other hand, are recognizable and do far less harm than pharmaceutical medications. This approach to treatment is more safe, and an alternative that is promising to those who just don’t want to deal with the side effects of taking a pharmaceutical.
Pharmaceutical drugs are like dams that try to prevent the river from overlowing onto the land, but orthomolecular psychiatry’s tenet is to calm the overflowing river by attacking the root cause-nutrient metabolism deficiencies. And everyone’s different as to the causes of their mental disorders. Luckily, in this day and age, you can get diagnostic tests through bloodwork and hair and mineral tests to see what you’re deficient in. Once you fix that and treat it by adding it with nutrients the body usually recognizes and synthesizes, the increased pressure from the overflowing water will subside. Then the stop gap measure of dams won’t be needed anymore.
According to Orthomolecular Medicine Online, these are the 15 principles that identify the spirit of orthomolecular medicine:
Here is a list of 15 principles that identify the spirit" of Orthormolecular Medicine:
1. Orthomolecules come first in medical diagnosis and treatment. Knowledge of the safe and effective use of nutrients, enzymes, hormones, antigens, antibodies and other naturally occurring molecules is essential to assure a reasonable standard of care in medical practice.
2. Orthomolecules have a low risk of toxicity. Pharmacological drugs always carry a higher risk and are therefore second choice if there is an orthomolecular alternative treatment.
3. Laboratory tests are not always accurate and blood tests do not necessarily reflect nutrient levels within specific organs or tissues, particularly not within the nervous system. Therapeutic trial and dose titration is often the most practical test.
4. Biochemical individuality is a central precept of Orthomolecular Medicine. Hence, the search for optimal nutrient doses is a practical issue. Megadoses, larger than normal doses of nutrients, are often effective but this can only be determined by therapeutic trial. Dose titration is indicated in otherwise unresponsive cases.
5. The Recommended Daily Allowance (RDA) of the United States Food and Nutrition Board are intended for normal, healthy people. By definition, sick patients are not normal or healthy and not likely to be adequately served by the RDA.
6. Environmental pollution of air, water and food is common. Diagnostic search for toxic pollutants is justified and a high "index of suspicion" is mandatory in every case.
7. Optimal health is a lifetime challenge. Biochemical needs change and our Orthomolecular prescriptions need to change based upon follow-up, repeated testing and therapeutic trials to permit fine-tuning of each prescription and to provide a degree of health never before possible.
8. Nutrient related disorders are always treatable and deficiencies are usually curable. To ignore their existence is tantamount to malpractice.
9. Don’t let medical defeatism prevent a therapeutic trial. Hereditary and so-called ‘locatable disorders are often responsive to Orthomolecular treatment.
10. When a treatment is known to be safe and possibly effective, as is the case in much 0 Orthomolecular therapy, a therapeutic trial is mandated.
11. Patient reports are usually reliable, The patient must listen to his body, The physician must listen to his patient.
12. To deny the patient information and access to Orthomolecular treatment is to deny the patient informed consent for any other treatment.
13. Inform the patient about his condition; provide access to all technical information and reports; respect the right of freedom of choice in medicine.
14. Inspire the patient to realize that Health is not merely the absence of disease but the positive attainment of optimal function and well-being.
15. Hope is therapeutic and orthomolecular therapies always are valuable as a source of Hope. This is ethical so long as there is no misrepresentation or deception.
Here’s a youtube video that describes the basic gist of orthomolecular psychiatry in 7 minutes:
The history can be traced back to the work of Abram Hoffer and Linus Pauling. In a nutshell, Abram Hoffer, a biochemist with a pHD, is credited with his research with treating schizophrenic patients with nutritional therapies, megadoses of niacin was discovered to help alleviate the symptoms. He realized that nutritional therapies that were adjunct to antipsychotics helped patients recover a lot quicker. Some patients eventually got off their medication and relied on megavitamin therapy alone, while others were able to at least lower their antipsychotic dosages substantially. With a passion to see mentally ill thrive without the cruches of psychotropic medications, he opened up his own private practice and has been treating thousands of patients successfully for over 50 years. His research further sprouted into other areas of mental illness. Abram Hoffer is equated with being the pioneer of this field, being the first of its kind to use nutritional therapy to help heal patients.
Here is the link to his extensive published work:
http://www.doctoryourself.com/biblio_hoffer.html
He’s also written books such as Putting it All Together: the New Orthomolecular Medicine, Orthomolecular Treatment for Schizophrenia, Healing Children’s Attention and Behavior Disorders, among others.
I’ve read success stories about orthomolecular psychiatry. Some famous advocates of Orthomolecular psychiatry include celebrity Margot Kidder, a Candian celebrity who credits orthomolecular psychiatry for helping her overcome her bipolar disorder.
http://www.doctoryourself.com/lois.html
She was also featured in the documentary called Masks of Madness filmed by the Canadian Schizophrenia Foundation which discusses orthomolecular treatment. Doctors such as Hoffer as well as other schizophrenic sufferers provide commentary and insight into their conditions as well as nutritional interventions and vitamin therapy.
William J Walsh, PhD in chemical engineering began working with prison inmates in Stateville Penitentiary in Joliet, IL. This lead him to initiate research into the link between biochemical patterns and behavioral disorders. That research formed the basis of the diagnostic and treatment protocols being used at the Pfeiffer Treatment Center in Naperville, IL. The non-profit Center has provided individualized nutrient therapy to more than 14,000 patients with behavior disorders, attention-deficit hyperactivity disorder (ADHD), learning problems, autism, depression, and schizophrenia. He has written an article titled "biochemical treatment of mental illness and behavior disorders" discussing the limitations of medication therapy.
Taken from http://www.hriptc.org/BioTreatment.html:
Any medication aimed at a specific neurotransmitter will inevitably alter some of the dozens of other neurotransmitters. The net result is likely to be changes in behavior or other side effects. We should not expect that a powerful psychiatric medication will have effectiveness without some unwanted alteration of brain function. Moreover, schizophrenia, bipolar depression, and other mental disorders are not single illnesses but a diverse collection of disorders, each with different biochemistry. Thus any single drug may have strikingly different outcomes for different patients.
The development of new psychiatric drugs will not conquer mental illness, but will instead place additional weapons in the arsenal of the practitioner. Since mental illnesses are diverse and individual patients are biochemically unique, a larger number of candidate drugs will increase the likelihood of finding a beneficial medication (or combination of medications). Thus in future times, psychiatric patients will probably have medications with improved effectiveness and fewer side effects. However, it is likely that these patients will still suffer from residual mental illness and experience side effects.
The ultimate remedy for mental illness may not be a collection of drug medications aimed at adjusting neurotransmitters. Advances in molecular biology and brain chemistry will eventually identify the basic causes and mechanisms of chemical imbalances, which may lead to more direct (and more natural) methods of adjusting neurotransmitters.
Walsh goes on further to discuss biochemical treatment:
The brain is a chemical factory that constantly produces neurotransmitters throughout our lives. The raw materials are amino acids, vitamins, minerals, and other nutrients. The step-by-step processes by which the body produces the major neurotransmitters have been known for years.
Sufficient nutrients to produce neurotransmitters can usually be obtained from a well-balanced diet involving the major food groups. However, many persons have absorption or metabolic disorders which result in severe nutrient imbalances that adversely affect brain functioning. For example, animal studies (Dakshinamurti, et.al.) have shown that a diet low in vitamin B-6 can result in reduced serotonin levels in the brain. This is not surprising since B-6 is a vital cofactor required for natural synthesis of serotonin.
It would be a simple matter if all nutrient imbalances were deficiencies, since a multiple vitamin/mineral supplement would then have efficacy. Unfortunately, most imbalances involve overloads of certain nutrients, and multiple vitamin/mineral supplements can make these persons worse. For example, elevated copper has been associated with paranoia (Pfeiffer and Iliev), and high folate levels have been observed in obsessive-compulsive schizophrenics (Pfeiffer, et.al.).
Biochemical treatment is a modality in which nutrient levels in blood, urine, and tissues are balanced to improve physical and mental functioning. The procedure involves extensive chemical analysis of blood, urine, and tissues to define the patient’s biochemistry. Treatment requires supplements of specific amino acids, vitamins, and minerals which need to be supplied with rifle-shot precision. Biochemical treatment can be effective only for persons with significant biochemical imbalances. This new therapy has been applied primarily to victims of schizophrenia, depression, and behavior disorders.
Walsh founded the Pfieffer Treatment Centre, with Carl Pfieffer, pHD, specializes in an orthomolecular approach to treating illnesses. Patients undergo bloodwork, hair and mineral analysis, and urine tests to discover their unique biochemstry and possible metabolic nutrient imbalances. The homepage to their site describes the treatment center in a nutshell:
Pfeiffer Treatment Center (PTC) is a not-for-profit, medical outpatient facility specializing in the treatment of symptoms from biochemical imbalances. PTC’s dedicated medical team treats children, teens, and adults with symptoms of behavioral and learning disorders (including ADD/ADHD), autism spectrum disorders, depression (including postpartum depression), bipolar disorder, schizophrenia, anxiety, post traumatic stress syndrome and Alzheimer’s disease. PTC takes a unique, integrative approach to identify and treat the root metabolic causes of these symptoms with a multi-disciplinary clinical team involving physicians, nurses, dietitians, pharmacists and other clinical specialists.
Everyone has a unique, individualized biochemistry that causes their deficiencies and hence symptoms of anxiety, bipolar disorder, depression, etc. Psychotropic drugs only mask the symptoms, they don’t hint at the root cause.
According to the site nutritional-healing.com, mental disorders can be categorized into certain major biochemical subtypes. Of course, persons presented with a mental illness can have overlap, but it is generally agreed upon that these persons fall into one of these categories:iLow Histamine (histapenia), High Histamine(histadelia), Pyroluria, and High Copper levels-all of which trigger mental symptoms(click on links to learn more about these subtypes).
For instance, according to Dr. Walsh, through blood and urine tests, Carl Pfieffer discovered 90% of the schizophrenic patients he’s treated fall under 3 categories: they either have histapenia, histadelia, or pyroluria.
Pfeiffer studied more than 20,000 patients with schizophrenia and reported 90% of them fell into one of these three categories. He developed individualized nutrient treatments for each of these conditions and reported good treatment effectiveness across each group.
(Taken from http://www.hriptc.org/BioTreatment.html: )
In terms of behavioral disorders, Carl Pfieffer classified them into 4 types:
In the late 1970’s, Dr. Walsh and co-workers developed a biochemical classification system for behavior disorders based on trace-metal concentrations. Based on chemical analysis data from hundreds of violent criminals and behavior-disordered children, behavior disorders were divided into four distinct types.
Type A individuals are characterized by an elevated copper/zinc ratio, along with elevated lead and cadmium and low sodium and potassium levels. They exhibit episodic rages which may be quite violent, and usually exhibit remorse after they have calmed down. Patrick Sherrill who killed 17 co-workers in an Oklahoma post office was found to have a severe Type A imbalance. Many school children who are Type A individuals may have mild, moderate, or severe versions of this chemical imbalance.
Type B individuals are characterized by low copper/zinc ratios, along with elevated sodium, potassium, lead and cadmium. Most exhibit behavior disorders by age 2, and are often described as oppositional, defiant, pathological liars, remorseless, and cruel. The incidence of the Type B imbalance appears to be less than 0.5% in the general population, but between 20-75% in maximum-security prisons in Illinois, California, and Ohio. In studies of ex-convicts and violent children, Dr. Pfeiffer found these individuals to exhibit elevated blood histamine, low blood spermine, elevated kryptopyrroles in urine, and zinc deficiency. Notable examples of persons with a severe Type B imbalance include James Huberty (McDonalds massacre), serial killer Henry Lee Lucas, and Charles Manson.
Type C individuals are low in most nutrients and Dr. Pfeiffer identified their primary imbalance to be malabsorption. The majority are slender, non-violent, impulsive persons who underachieve in school and in the workplace.
Type D persons were found by Dr. Pfeiffer to exhibit glucose-control problems. These individuals are often non-violent underachievers who complain of irritability, fatigue, and sugar cravings.
The Health Research Institute (parent organization of the Pfeiffer Treatment Center) has accumulated a data base of chemistry levels for more than 6,500 behavior-disordered children, 800 violent criminals, and 26 serial killers and mass murderers. We have found that about 90% of these persons fit into one of the A/B/C/D categories.
In the early 1980’s, Dr. Pfeiffer developed individualized biochemical treatments for each of these behavior syndromes. Under this system, patients are screened and treated for trace-metal imbalances, histamine disorders, pyroluria, malabsorption, glucose disorders, and other biochemical imbalances. Nearly 7,000 behavior-disordered persons have been treated at the Pfeiffer Treatment Center using this system. In four separate outcome studies involving a total of 1,400 patients, a majority of the families reported major improvements in behavior control after biochemical treatment. These studies indicated good treatment effectiveness for most patients below the age of 14.
(Taken from http://www.hriptc.org/BioTreatment.html: )
Certain supplements willl help restore the balance in the body and alleviate the mental symptoms resulting from imbalanced histamine levels and mineral and vitamin deficiencies. For instance, individuals with high copper levels have depressed levels of the mineral zinc. They also display high levels of elevated norepineprhine and epineprhine-hormones that are released by the adrenal glands in fight-or-flight stressful situations. Elevated norepinephrine and epinephrine ultimately does the body harm and creates pervasive mood problems if found in excess levels in the brain. The laboratory test to to show this is roughly a serum copper over 140 mcg/dL and low ceruloplasmin. And beneficial supplements that will help decrease the amount of copper accumulated in one’s body are zinc, manganese, vitamin D, and B6.
According to orthomolecular psychiatry, these dosages of supplements are going to be larger than what you’d usually find in your food, because perhaps there exists a genetic tendency towards losing some of these vitamins and minerals. Especially if you suffer from disorders that have a highly genetic component linked to it, and you’ve been a long time sufferer. The key is to find the optimum amount. It really is as simple as finding out what vitamins, fatty acids, amino acids that you need. Substances your body recognizes. The main building blocks and essential nutrients the body machine must need, and is seriously deprived of, in order to function well again. Then you can pick them up at the local supplement shop.
Here are some success stories I’ve come across in terms of treatment of pyroluria with megadoses of vitamins:
a mother describes her treatment for her son diagnosed with ADHD in this forum:
http://www.dr-bob.org/babble/alter/20050510/msgs/498689.html
And orthomolecular treament could stand to benefit those 1/5 North Americans who suffer from a mental illness at one time. The main solution to our problem is letting this alternative practice that does encompass the concept of holistic healing and inject it into the consciousness of the lay population. It’s time to find some real, safe solutions-and this orthomolecular approach may be it.