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:

-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


July 21, 2011 at 11:39 pm Leave a comment

Treating Epilepsy with Natural Supplements-An Individualized Approach

Epilepsy is an umbrella term for a variety of things. The cause, onset, the symptoms, the comorbid medical conditions, and severity range from person to person. Causes include oxygen deprivation, brain tumor, brain injury, heavy metal toxicity, metabolic/endocrine disease, stroke. You can develop epilepsy at any age. The symptoms vary depending on which parts of the brain tissue are vulnerable to seizure activity. You can experience visual distortions, abnormal motor movements, intense fear, etc. The comorbid medical conditions can involve diagnosis of psychiatric problems such as schizophrenia, panic disorder, and metabolic problems food allergies, gastrointestinal disturbances, etc.
Which is why epilepsy is really just a simplified term to explain a large group of things. This is why I am going to highlight the fact that treating epilepsy involves an individualized approach suited to the unique personal needs of an individual. Unfortunately, the fact that epilepsy requires such a personalized treatment program usually requires a lot of effort into researching the existing circumstances relating to the epileptic as well as extensive medical testing to find out underlying metabolic tendencies and the resultant vitamin, mineral, and amino acid deficiences which accompany seizure activity.
The field of orthomolecular medicine is suited to treating medical disorders. The word orthomolecular means same molecules. It advocates treating individuals with medical conditions with substances the body naturally produces. Amino acids, vitamins, minerals, and fatty acids. Orthomolecular medicine also acknowledges the concept of "biochemical individuality". What is biochemical individuality? It implies the acknowledgement that individuals vary from each other to a wide extent biochemically. It was the biochemist Roger Williams, author of  such books as You are Extraordinary, who pioneered reserach into biochemical individuality. He pointed out that people are born with a great variety of shapes, sizes, functions, and strengths of various organs. For instance, Williams finds that a range of 2000% in vitamin requiresments from one healthy person to another is not uncommon, and the need for individual vitamins can vary by 4000%. We also  have tremendously different levels of enzymes-the catalysts to speed up chemical reactions in our bodies. (Natural healing for schizophrenia and other disorders, Eva Edelman). And for people with epilepsy, a lot of the times, they do have certain vitamin, mineral, fatty acid, amino acid deficiencies when compared to the baseline population of healthy individuals who do not have epilepsy.  
The field of orthomolecular medicine can help treat epilepsy. This is a safe alternative to pharmaceuticals, which are recognized by the body as foreign invaders a lot of the times, whereas with natural nutritional supplements, the body is absorbing chemicals the body naturally produces. The reported deaths from vitamin supplements has been drastically lower than the reported deaths from pharmaceutical drugs. As alternative health advocates take on the quote from Hippocrates, "first do no harm", orthomolecular medicine fits in with the criteria of helping individuals treat their medical problems without doing substantial harm to the body as a trade off. The science has sped up and nowadays, when you walk into a natural supplement store, you will find a whole host of isolated vitamins, amino acids, minerals, and fatty acids which you can buy over the counter.
Before I begin explaining more about the concept of biochemical individuality in orthomolecular medicine, I will first point out what the common denominator in Epilepsy is, because obviously epilepsy does share some basic, generalized commonalities. The watered down, simplified explanation for epilepsy is seizures.
The brain is an organ that controls various functions. These functions are localized to different compartmentalized areas. Different lobes control different functions.The basic constituent of brain tissue are neurons, the individual brain cells in our brain tissue(we have billions of them). Neurons send messages to one another via neurotransmitters. It is these messages that fire that contribute to brain activity, and as a result, control commands from the brain to perform specific functions: i.e motor movements, visual tasks, etc.
There are billions of connections between neurons in the brain through synapses. Synapses contain different neurotransmitters, which are the chemical messengers of the brain. To send one message from neuron to neuron, neurotransmitters act as chemical messengers which bridge the gap between adjacent neurons. Neurotransmitters create 2 categories of effect: excitation or inhibition. Inhibitory neurotransmitters tell a neuron not to fire, whereas excitatory neurotransmitters code a neuron to fire. The complex, orderly interconnected of cells and chemicals enables us to complete a number of tasks simultaneously. As Patricia A. Murphy describes, "for example, when I ride the bicycle, the nerve cells in my occipital lobe(the part of the brain that controls vision) discharge as I focus on stop signs, cars, etc, while nerve cells in the parts of the brian that control movement tell my legs to move so I can pedal. Meanwhile, neurons that activate speech, hunger, or urination don’t discharge. As long as the excitation and inhibition processes are maintained, my body remains balanced on the bike."
A seizure begins when groups of neurons within the brain become overstimulated. As the neurons discharge excessively, excitatory neurotransmitters tell neurons to fire and inhibitory neurotransmitters tell them not to. If the inhibitory neurotransmitters are able to keep the discharges contained to one area of teh brain, a person may experience a brief alteration in consciousness, bu if neurons are firing very rapidly and the discharges spread throughout the brain, a tonic-clonic seizure occurs.
The basic message then, in a nutshell, is that a seizure occurs when there is an excess of excitatory neurotransmitters telling neurons to fire, and not enough inhibitory neurotransmitters to counter the overstimulation. The scale and proportion of this leads to the severity of the seizure-from absences in localized areas, to generalized-which affects the whole brain, to status epilepticus.
Excitatory neurotransmitters include:
Glutamic Acid
Inhibitory neurotransmitters include:
GABA(This is a major neurotransmitter-present in 30-50% of brain synapses)(natural healing for schizophrenia, eva edelman)
For those who seek to treat epilepsy using natural supplements, the aim is to promote the production of more inhibitory neurotransmitters in the brain. Preferably GABA, since it is so abundant in the brain. Taurine and Glutamine also eventually can be converted to GABA through chemical reactions(Both are precursors to GABA).
Now how do we produce more GABA? I would say that the most obvious way to control seizures is to take amino acid supplements which are inhibitory neurotransmitters. GABA, Taurine, Glutamine, and Glycine are all available over the counter for purchase in natural supplement stores.
But I have to note that epileptics are not only deficient in inhibitory neurotransmitters. They are deficient in other vitamins, minerals, and fatty acid as well which give rise to lowered production of inhibitory neurotransmitters. Inhibitory neurotransmitters are produced with the help of these vitamins, minerals, and fatty acids-keep that in mind.  
For instance, supporting nutrients needed to create and regulate GABA include:
B6, Manganese, Biotin, Lysine
I will not go through the various chemical steps in the process whereby certain vitamins, amino acids, fatty acids, and minerals which eventually can help promote more GABA and other inhibitory neurotransmitters in the brain, but rather list the most common accompanying deficiencies in epileptics which give rise to a lowering of the proportion of inhibitory neurotransmitters in the brain, and hence, a lowering of the seizure threshold. Research has been done on how these chemicals play their role in lowering the seizure threshold. The list includes:
Vitamin B6
Vitamin C
Vitamin D
Vitamin E
Vitamin deficiences are correlated and probably either caused and/or accompanied by medical conditions, including:
Brain tumor
Celiac disease
Brain allergies
and others
There is no need to go out and buy all these supplements. Not every epileptic will have the same deficiencies. Not every epileptic is is deficient in calcium for instance, this is why testing for levels of these vitamins and minerals is required in order to find out what each person needs.
A lot of people acknowledge the fact natural supplements, specifically, isolated vitamin, mineral, amino acid and fatty acid supplements are beneficial for the treatment of epilepsy. But here is where people run into problems, and I came across this problem myself when I first began researching natural alternative measures to treating epilepsy. I would here and there run into snippets of information about how a particular supplement could help control seizures, but I wouldn’t know what to do with that information. Okay, so there are various supplements that are shown to suppress seizures, but which ones do I take, and at what dosages?
This is where visiting either a naturopath or a practitioner in orthomolecular medicine comes in. They take the time to do extensive testing for vitamin and mineral and amino acid deficiences in each individual. They also test for underlying metabolic conditions which ultimately give rise to these deficiences epileptics. A visit to a naturopath who is familiar with orthomolecular medicine involves an initial 2 hour appointment to take in your medical history and dietary and lifestyle habits.  They will find out:
Metabolic conditions which are correlated with epilepsy( celiac disease, brain allergies, etc)
What are your bad habits? drinking, smoking, etc?
What are you deficient in?(done through testing)
After all these questions are answered, an individualized treatment plan is laid out for the patient tailored to their individual needs.Dosages of supplements must also be tailored to the individual depending on the severity of their deficiencies.
I will provide my personal example of my experience with epilepsy and how I came about with my own treatment plan. I had my first seizure when I was 21. They did an MRI scan and found an abnormal brain mass in my right temporal lobe. They are not sure what it is(a biopsy wasn’t done), the mass could possibly be congenital or a very benign brain tumor. I am getting yearly MRIs to track the size of the abnormal mass to make sure it doesn’t get any bigger. Part of my  epilepsy treatment plan involves raising my seizure threshold by avoiding the mass from getting bigger. Because a bigger, malignant tumor usually implies more severe seizures. I take precautions, in the event that this mass does happen to be a brain tumor, to do certain things which are researched to either help prevent or treat brain tumors. I’ve done my research, and what I found for instance,  was that heavy metals such as mercury, lead, cadmium play a large role in brain tumors. So I can take supplements which help chelate(remove) heavey metals, and avoid foods containing heavy metals(such as large fish). I also have a metabolic disorder called Pyroluria, which is abnormal hemoglobin synthesis. This condition causes someone to become deficient in vitamin B6 and Zinc. I excrete pyrroles which are chemicals which contain B6 and Zinc. The deficiency in B6 causes seizures as well. A test for pyroluria can be done with a urine test.
Therefore, as you can tell, my situation does not apply to every epileptic’s situation. One epileptic may have celiac’s disease-and wheat is a trigger for their seizures, so they must avoid wheat. I don’t have celiacs disease, so I can eat wheat. Not everyone’s seizures are caused by a brain tumor, so they may not need to take the exact same dietary and lifestyle precautions as me.  Epilepsy treatment is never one size fits all. Although the common denominator is lower concentrations of inhibitory neurotransmitters in the brain, there are many pathways to get to that point-remember that. It takes time to finally come up with a personalized treatment plan, but in the end, it will be worth it to know that you are controlling your seizures and tackling any accompanying medical problems which surface with the epilepsy.

December 9, 2009 at 10:57 am 2 comments

Is there an evolutionary purpose to mental illness?

How on earth could hallucinating E.T the alien or having the compelling urge to hang yourself to death,  possibly be of any benefit to one’s survival? These mental traits do not increase your reproductive fitness or chance of survival. In fact, some of it is downright counterintuitive-especially the compelling urge to end your life.  Yet these thoughts are all common occurences in conditions of  schizophrenia and major depression. Schizophrenia and major depression are mental disorders that have a strong heritable component to them, chances are you will develop these conditions if you have a close relative with a mental illness. And these mental illnesses continue to be passed on from generation to generation, scraping by and surviving in the human gene pool. Why?
On the surface, these traits don’t appear to provide any benefit whatsoever evolutionarily speaking. However, I’m going to argue that mental illness does provide an evolutionary purpose-solely due to the fact that mental illness is a byproduct of something else. Mental illness is, evolutionarily speaking, a byproduct of the physical body adapting to some kind of harsh physical environment. It is a side effect. Side effects are not always positive, but if one is still able to pass on their genes to the next generation, then the trait will suffice.
I will start my argument with an example of how a chemical can be advantageous to the body depending on the physical environment a species resides in. Let’s begin by using an example of cholesterol and how it helps the body produce vitamin D. Cholesterol obviously has bad side effects. Obviously cholesterol is deemed as a bad thing these days, it’s a dirty word. Cholesterol increases the chance of heart attacks and strokes by clogging up our arteries. What you probably aren’t aware of is the fact that although cholesterol is looked at in a bad light these days, once upon a time our ancestors thrived in an environment where cholesterol was useful.
Do you have a family history of high cholesterol? The tendency to produce a lot of cholesterol is a genetic tendency that’s passed on from generation to generation. People of African descent have darker skin and are much more likely to have a gene that causes them to produce greater amounts of cholesterol. As humanity evolved, different groups of humans encountered widely different circumstances-from infectious tropical diseases to sudden ice ages to pandemic plagues. The evolutionary pressure that accompanied all these challenges was intense enough to account for the differences we see between populations today. For those of African descent, a genetic trigger called for increased cholesterol in order to maximize production of vitamin D.
Vitamin D is vital in order to produce the skin pigmentation melatonin that helps Africans brave the harsh UV rays of the sun. And this is why they, on average, have higher cholesterol levels than other groups. The genetic tendency to  produce excess cholesterol is a trait that gets passed on from generation to generation because cholesterol was useful in some way. If cholesterol didn’t bring forth any advantages whatsoever, we wouldn’t have people with natural inclinations to produce too much cholesterol. Excess cholesterol doesn’t appear to be beneficial in colder, northern climates, but it was once very beneficial for those near the equator.
We can see how cholesterol exerts negative side effects. Yet despite these negative side effects, the tendency to metabolize excess cholesterol is still able to be passed on. As long as one is able to reproduce, they will pass on their genes. Now, we see cholesterol manifests in physical side effects of hypertension and strokes. There are other chemicals that can manifest itself in severe mental symptoms when they enter the brain. Circulating excess adrenochrome and  histamine function to fight off some type of physical bodily illness in the body very well. However, in the brain, excess adrenochrome and histamine produce hallucinations and suicidal ideation respectively.
Adrenochrome is a chemical that helps ward of cancer and is created in the heart muscle. It also happens to be a hallucinogen that is responsible for perceptual distortations experienced by schizophrenics. Adrenochrome has a multipronged function. It limits cell division by using white blood cells to kill cancer cells throughout various parts of the body. When it enters the brain however, the indole compound creates hallucinations. There is no evolutionary purpose to hallucinating. There is, however, an evolutionary purpose to killing cancer cells, and that’s survival. The adaptive function of adrenochrome is to ward of cancer. The hallucinations are simply the strings attached as a mere consequence, without a functional purpose evolutionary speaking, yet hallucinations from adrenchrome are necessary by products.
Schizophrenics have a genetic tendency to produce above average levels of adrenochrome. This metabolic tendency is passed on from generation to generation, as a child’s chances of inheriting the genes for schizophrenia is 50% when a parent has schizophrenia. Schizophrenia is a modern conception that has arisen alongside industrialization and levels of circulating carcinogens in the environment. The rates have intensified over the centuries, and continues to increase. Something tells us that schizophrenia must have some adaptive advantage-otherwise the genes for schizophrenia, or in other words, excess adrenochrome production, would just fie off if this was just some mutation. Mother nature must have a purpose for adrenochrome. And this purpose is to ward off the evils of cancer. Mother nature’s cure for cancer is evidently the cause of schizophrenic hallucinations. Also, as it has been noted by researchers, schizophrenics and their close relatives have the lowest rates of cancer.
Adrenochrome is a derivative of adrenalin. Adrenalin, as you may be familiar with, is a chemical that is involved in fight or flight reactions in the sympathetic nervous system. It gets the body prepared to fight or flee in dangerous situations. Adrenalin in excess amounts however, is dangerous to the body. Since the advent of industrialization, we have come across numerous stressors that shoot adrenalin through the roof. This will do the body harm. If adrenalin, however, is oxidized into adrenochrome, it affords the body a protective effect because adrenochrome is antimitotic-it limits cell division. This was apparent in rat studies that showed adrenochrome limiting cell division in vivo. Adrenalin receptors are apparent in places that are responsible for smooth muscle contraction, encompassing the kidney, gastrointestinal tract, and various other parts of the body. Adrenochrome, being a direct oxidation derivative of adrenalin, therefore shows up in the same pathways as adrenalin pathways. Adreonchrome should be limiting cell division in various parts of the body.
One thing that must be noted is that adrenalin is present in the brain-there are receptors for adrenalin. Following the same logic then, adrenochrome, which follows the same pathways as adrenalin, is also present in the brain. In the brain, adrenalin is a neurotransmitter that follows the adrenergic pathway. This pathway cuts across various parts of the brain-limbic system and through to the frontal lobe as part of a circuit. Therefore, adrenochrome also travels to the limbic system and can reach all the way to the frontal lobes. Here’s the thing about adrenochrome-it has a chemical structure that is similar to hallucinogens such as mescaline and LSD. There is a ring structure called an indole in adrenochrome, LSD, and mescaline. By virtue of having the same "indole", the chemical reactions that result are pretty much the same-perceptual distortion. Hallucinogenic compounds that disrupt the limbic system and reach the frontal lobes disrupt the normal processing of the brain.
So in essence, adrenochrome has a multipronged function. It limits cell division by using white blood cells to kill cancer cells through various parts of the body. When it enters the brain however, the indole compound creates hallucinations. Again, as I stated before, there is no evolutionary purpose to hallucinating. The adaptive function of adrenochrome is to ward of cancer.
Another chemical that has its roots in fighting bodily illnesses, yet just so happens to provide mental symptoms manifesting into mental illness, is histamine. Excess levels of histamine is associated with suicidal ideation. The genetic tendency to produce excess histamine is inherited. Histamine is a chemical that is released in allergic reactions. Why do we need so much histamine? Well, once upon a time our ancestors once braved environments filled with parasites. Histamine is a chemical that triggers an immune response in the body to fight parasites and other infections.
Now, histamine is a chemical that triggers an immune response in the body. There are various parts of the body with histamine receptors. There are several different types of histamine receptors that respond to histamine. These include bone marrow and white blood cells, smooth muscle and central nervous system tissue, parietal cells. You may associate histamine reactions with allergic reactions such sneezing, runny nose, coughing, since this is what happens when histamine production is triggered in the body.
But what you aren’t so familiar with is the fact that there are also histamine receptors in the brain. These receptors are found abundantly in the hypothalamus, a lower order structure of the brain that is responsible for sleeping, eating, temperature regulation, and sexual arousal. Individuals who produce too much histamine, termed histadelics, constantly stimulate the hypothalamic area because histamine receptors also happen to be present there. This is why such mental symptoms of histadelia-hypersexuality, insomnia, are present.
Another well known association is histamine and suicidal ideation. When allergy season rolls around, suicide rates go up. Why do excess levels of histamine trigger suicidal thoughts? Because histamine also works in the brain to inhibit important neurotransmitters such as serotonin, the "feel good" chemical of the brain. Lack of serotonin in the hypothalamic area (the hypothalamic pituitary axis)  has been evidenced in brain autopsies of sucessful suicides. This is why there are antidepressants that function by trying to limit re-uptake of serotonin, and products such as 5-htp and tryptophan that are used to trigger serotonin production.     
There is no functional purpose to suicidal ideation in evolutionary terms, but there is an evolutionary purpose to histamine production-it protects the body from parasites and increases a human’s chance of survival. Histamine just so happens to be present in the hypothalamic area, and disrupts the normal neurotransmission of important neurotransmitters that promote feelings of well-being.
By virtue of having receptors in the brain that are sensitive to adrenochrome and histamine, any excess amount will cause a disturbance. When the body must produce extra adrenochrome and extra histamine elsewhere in the body, you cannot expect some of that extra histamine or adrenochrome not to somehow leak into the brain. The doors are open for the possibility, because the pre-existing condition is met with pathways in the brain that welcome histamine and adrenochrome. This is just how it is when human ancestors were adapting. In order to survive in the immediate future, some consequences may have to ensue as a rseult.
Heart disease and strokes are not functionally adaptive. Yet cholesterol is. My point is that hallucinations and suicidal ideation in and of themselves are not functionally adaptive, adrenochrome and histamine are. Harsh UV rays, carcinogens, and parasitic environments fostered and promoted the survival of individuals who metabolize cholesterol, adrenochrome, and histamine to excess. And when our bodies produce a chemical-it leaves us with a whole host of physical as well as mental side effects. These are just trade offs that we have to deal with. Evolution isn’t perfect.

May 18, 2009 at 9:53 am 1 comment

Environmental Risk Factors for Brain Tumors

Of course, genetics also plays a huge role in this, but I will simply focus on environmental stressors for the time being. Simply put, the environmental risk factors for brain tumors are:
toxins that can cross the blood brain barrier easily: These are classified as neurotoxins
substances that severely compromise the blood brain barrier
Here is a run down of a list of things you might want to avoid if you don’t want a brain tumor. By no means is this list exhaustive, but these are the most common culprits that easily cross the blood brain barrier and do severe damage to the blood brain barrier:
Radiation Sources
Cell Phones?
Well, I’m sure the #1 thing you hear these days about cell phones is that, depending on the sources, they are either or aren’t a risk factor for brain tumors. Sometimes these studies are funded by cell phone companies themselves, so you can’t really trust them. I am going to make some commonsense arguments here. As it is widely known, radiation causes mutations in cell division. This is indisputable. Whether one will get bran tumors or not is widely dependent on many factors, including time spent chatting on the phone, age, genetics. You are probably at most risk if you are: a child, talk at least 1 hour on the phone everyday, and have a compromised immune system. However, don’t rule out the fact that radiation from cell phones can’t penetrate the blood brain barrier-because it can if you hold up your cell phone right up against your head. Afterwards, this leaves the blood brain barrier open for other lipid soluble neurotoxins to either seep in, or further allows more radiation to mutate brain cells. The take home message nonetheless is this:  you should heed the infromation that radiation can compromise the blood brain barrier, and create mutations.
Here is an exerpt from article from  BBC news titled mobile phones alter human DNA

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.

Damage was also seen in the next generation of cells. Mutated cells are seen as a possible cause of cancer.

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.

The studies on cell phone use are mixed I believe, because the variables used-demographic age range, time span of cell phone use studied, frequency vary from study to study. Cell phone use was introduced in the 90s, so it is a fairly new device. Benign brain tumors take about a decade or more to develop until patients discover they’ve been harboring one. Those susceptible cell phone users who do end up getting a brain tumor are most likely to get a type of brain tumor called an acoustic neuroma, which is a benign inner ear tumor(this shouldn’t come as a surprise)-on the side which you held your cell phone up against your head all those years(this shoulsn’t come as a surprise either).
When looking at correlational studies involving cell phone use and incidence of brain tumors, pay attention to the frequency of use(is it 15 min/day, 1 hour/day), the demographic age range of the correspondents (susceptible young children, or 25 year olds), and the time span this correlational study covers(do they track down their cell phone use for 3 years, 10 years). 
Nuclear Power Plants
Those at a high risk of getting a brain tumor includes personnel in nuclear power plants. It is a very dangerous industry to work in.
Organic Solvents
Organic solvents are liquids used to dissolve or to reduce the viscosity of a particular organic substance. On exposure to air, many organic solvents become gaseous, making inhalation probable. There is no blood brain barrier through the nasal passages, remember that. Substances, especially odourous substances, can pass through the nose into the brain easily through this route due to lack of blood brain barrier protection.
Millions come into contact with organic solvents in occupational settings. There is a higher incidence of brain tumors in those whose occupation involves frequent contact with organic solvents, i.e those in the rubber making industry, automobile industry, farming industries. Organic solvents easily get into the brain through the nasal passages. When odorant molecules pass through the nose, messages are sent directly to the brain. The smell of such chemicals as polyvinyl chloride or cleaning agents is quite strong, and if one is exposed to these agents frequently enough, it’s possible for a tumor to develop inside the brain, since the nose is a surefire way to circumvent penetration of the blood brain barrier. This explains why, for instance, there is this new trend of snorting vodka through the nose, since only one shotglass is enough to produce the brain signals needed in order to feel the effects of alcohol.
Despite this, organic solvents by their nature, should easily cross the blood brain barrier even without using the nasal route. Organic solvents are also readily absorbed through the skin. The brain is particularly vulnerable, since it is 50% lipid(dry weight) as compared with 6-20% in other organs. Moreover, fat soluble comopounds (such as these solvents) are more readily admitted across the blood brain barrier, and usually must cross the blood brain barrier in order to be made water soluble before they can be eliminated.
As defined by the National institute for occupational health and safety,

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.

Here is a list of organic solvents, and their industrial uses

Industrial Uses


Cleaning solvent


Mining and tunneling, adhesives, waste treatment, ore processing


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


Industrial settings

Methyl mercaptan

Odorant in natural gas and fuels

Methyl-N- butyl ketone

Many industrial uses

Methylene chloride (dichloromethane)

Solvent, refrigerant, propellant






Dry cleaning, degreaser, textile industry


Fiberglass component, ship building


Paint, fuel oil, cleaning agents, lacquers, paints and paint thinners

1,1,1-Trichloroethane (methyl chloroform)

Degreaser and propellant


Cleaning agent, paint component, decaffeination, rubber solvents, varnish

Vinyl chloride

Intermediate for polyvinylchloride resins for plastics, floor coverings, upholstery, appliances, packaging


Paint, lacquers, varnishes, inks, dyes, adhesives, cements, fixative for pathologic specimens

 Heavy Metals
Heavy metals can cross the blood brain barrier. They include mercury, lead, cadmium. Mercury especially steals the spotlight as a neurotoxin. You can find mercury in metal amalgam fillings, which consists of 50% mercury, 35%j silver, up to 3% copper, 13% tin, and up to 1% zinc. Fish is also a source of mercury, with larger fish containing higher amounts of methyl mercury. Sources of lead include automobile exhaust, house paint(especialy older or exterior paint), lead solder (often present in water coolers, water tanks, tin cans used for food, and electrical devices), battery terminals and casings. Industrial expsoure to lead includes ammunition, pipes, solder, cables, lead shielding, pigments, some chemicals and processed metals. Drinking water is the most common source of ingested lead. Lead can leach from lead solder, leaded brass or bronze pipes, etc. To minimize intake, drink water drawn from the cold water faucet only, and have it run cold. Cadmium may be found in black rubber, pesticides, fungicides, certain dental prosthetics, dust, certain paint pigments, ceramics, polyvinyl plastics. Exposure can occur in manufacturing cadmium alloys, fungicides, jewelry, nickel-cadmium batteries, and lead. Also in process engraving, soldering, copper refining, rustproofing tools and marine hardware, polymetallic ore smelting.
There was a case whereby the town of Cameron, Missouri had experienced a strange phenomenon of clusters of benign brain tumors a few years back. Investigation ensued to find the culpirt of these brain tumor clusters, since brain tumors in general, are very rare amongst the general population. Authorities examined the drinking water, a common source for all residents, and found high levels of lead:
Read the story about clusters of brain tumors in Cameron here: http://www.digitaljournal.com/article/270160
Artificial Sweeteners
Artificial sweeteners include such brands as Splenda and Aspartame. They were introduced into the market during the 1980s and marketed as an alternative to sugar. You can find such artificial sweeteners in products ranging from yogurts, diet soda, energy drinks, and sugar free chewing gum. Artificial sweeteners are actually worse than sugar itself. For instance, Dr. Wurtman wrote a book called Dietary Phenylalanine and Brain Function. Phenylalanine is 50% of aspartame and Wurtman contends that as an isolate it is neurotoxic and goes directly in the brain. Aspartame breaks down into diketopiperazine(DKP)-a known brain tumor agent. The three toxic ingredients of Aspartame are methanol (wood alcohol), and phenylalanine and aspartic acid; both the latter are amino acid isolates.(Source: http://www.wnho.net/aspartame_brain_damage.htm). In the documentary, Sweet Misery: A Poisoned World, epidemiological studies have shown a spike in malignant brain tumors since the introduction of aspartame into the market in the 1980s, despite all other cancers in other parts of the body remaining the same.
The reason why artificial sweeteners affect the brain especially is because the brain uses up 20% of the body’s glucose resources. It runs on glucose. Sugar, and sugar-like substances such as aspartame can easily cross the blood brain barrier and acts as excitotoxins by stimulating nerve cells to such an extent that they die. Therefore, it makes sense that neurological disorders and brain tumors are common with overconsumption of artificial sweeteners since the brain loves this sugar substitute.

April 17, 2009 at 10:31 am Leave a comment

Cancer and Adrenochrome

As I highlighted earlier, adrenochrome is essentially oxidized adrenalin. Adrenalin is part of the sympathetic nervous system, so the pathway it travels begins with the adrenal glands (where adrenalin is released), and then travels and circulates throughout the bloodstream of the body and also enters the brain. It is released during flight-or-fight situations, and there are numerous ways to increase adrenalin production. Inside the brain, there are receptors that are sensitive to oxidized adrenalin (aka adrenochrome), and as a result, brain wave changes are exerted as well as electrical disturbances. When the limbic system becomes overaroused by adrenochrome, psychosis occurs. This is the underlying premise behind the chemical involved in hallucinations in schizophrenia The steps and conditions to create adrenochrome are described as follows:

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).


Schizohprenics produce abnormal amounts of adrenochrome, which gives rise to hallucinations. Adrenochrome was discoverd in the 50s, and was determined to be a hallucinogen derived from adrenalin and exerts perceptual distortions when taken in high enough amounts. 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)



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:


Now here’s the thing: some people speculate that adrenochrome is actually a protective factor in schizophrenics that helps them stave off cancer for as long as possible. As described by orthomolecular psychiatrist Abram Hoffer:
"Schizophrenics have excellent genes. I wish I had them. They hardly ever get cancer. Adrenochrome kills cancer cells; I think the gene is nature’s answer to the cancer pandemic. On the psychological side, they’re brilliant: artists, scientists, poets, philosophers. "


Could schizophrenia, or well, rather, adrenochrome specifically, be an adaptation to the millions of industrial carcinogens we inhale and ingest on a daily basis that are contributing to soaring cancer rates? It’s interesting because schizophrenia was extremely rare until the advent of industrialization. Adrenochrome production is speculated to be a marker of an auto-immune response the body makes in response to allergens, which we have been bombarded with since industrialization. When we have an allergic response, more adrenalin is produced.
I’ve always speculated that adrenochrome must have some kind of adaptive mechanisms to it. if it didn’t, why would schizophrenia continue to be passed on from generation to generation? An illness that shows up can confer evolutionary advantages-depending on the environment. Also, the possibility of schizophrenia being a mere genetic mutation is dismissed, as the frequency of schizophrenia (1 in every 100) must be too high to be maintained by genetic mutation alone. Furthemore, schizophrenia is a result of inheriting both allelles (from father and mother) in homozygous form. When this occurs, mental illness appears. However, only inheriting one allelle confers advantage, and this advantage is resistance to disease (cancer).  As described by Foster,

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.

If the schizophrenia trait did not provide some counterbalancing advantage, the number of those suffering from the associated mental illness would decline very rapidly to a much lower level that could be maintained by mutation alone. If true, this means that the high prevalence of the gene(s) partly responsible for schizophrenia can only occur because this trait confers both unfavourable and favourable properties. WHen 2 selective forces oppose one another in this way, the frequency of the 2 genes stabilize, in what is known as a balanced polymorphism. What this would mean in this case is that inheriting the schizophrenia trait in its heterozygrous form does not lead to schizophrenia and also carries with it some selective advantage, such as resistance to another disease. Conversely, those inheriting the schizohprenia trait in homozygous form would very likely become mentally ill. This type of trade-off situation occurs with the "sickling" trait which in its heterozygrous form gives considerable protection against malaria but in its homozygrous form causes deadly sickle cell anemia.
Foster mentions sickle cell anemia, but there are plenty of other diseases which we inherit from our parents’ genes that also confer evolutionary adaptation to some situation. Maolem Sharom espouses this in his book, Survival of the Fittest: A Medical Maverick Discovers Why We Need Disease: She explains why we need sickness by taking us through examples of disorders that have genetic traits which help us survive harsh conditions. Dr. Sharon Moalem demonstrates how conditions that are considered unhealthy (such as hemochromatosis, diabetes, and high cholesterol), or even deadly in extreme cases, might actually put their carriers at an advantage in combating other life-threatening illnesses. For example, he explains that hemochromatosis, a disease that, if left untreated, will kill you, may have actually been a defense against the deadliest pandemic in history–the bubonic plague during the 14th century. It turns out that this genetic mutation, which continues to be passed down through generations, actually helped spare many lives at one point.
Schizophrenia is just another example of how our bodies have changed metabolism in order to cope. However, obviously the disorder comes with disadvantages as the trait that defends cancer appears in homozygous form, but that’s just a result of the genetics of reproduction when one happens to inherit both of the same genes from their parents. Schizophrenia, just like a natural genetic inclination towards diabetes, high cholesterol, and hemochromatosis, is a result of  homozygous traits of a certain genes which helped us at some point in history to rough it out in extreme environmental conditions that threatened our health.

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.


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.

Nonetheless, the psychiatric symptoms that manifest in this disorder could be more appropriately labeled as some sort of auto-immune response that starts attacking the brain.  Auto-immune can be summed up as what happens when our immune system goes into overdrive and starts attacking our own body tissues and can’t discern between foreign invaders and normal healthy cells. Adrenochrome destroys brain cells, as evidenced by structural changes in the schizophrenic brain, including enlarged ventricles and demyelination. And of course, ur human bodies have developed allergic reactions to the environmental triggers we face with industrialization, including: rapid sugar consumption, increased noise, thousands of man-made chemicals, etc. all leading to increased adrenalin production. Here’s some links to some evidence that auto-immune tendencies are markedly more pronounced in schizophrenics:
As I mentioned earlier, the rise of schizophrenia shows a sharp positive correlation with industrialization. Schizophrenia is being coined as the invisible pandemic. Foster states the correlation between industrialization and schizophrenia:
Prior to the Industrial Revolution, traditional baseline prevalence seems to have been roughly one case per 2,000 people. This figure began to change at the end of the 16th century as prevalence started to rise with industrialization. As a result, in England, Ireland, Canada, and the US increased at least 7-fold between the mid-18th and mid-20th centuries. In all of these countries, schizophrenia is most common in urban areas.
What are the environmental changes that induce us to produce adrenalin, and in turn, produce adrenochrome?
-quality and quantity of our food supply: imported and processed foods
-Man-made chemicals
-Increased consumption of sugar
-increased noise
-quicker pace of life leading to higher stress levels
Industrialization has changed the human environment in numerous ways, several of which significantly promote the production of adrenaline and/or its oxidation to adrenochrome and its derivatives. Over the past 200 years, for example, the quantity and quaity of the food supply has altered dramatically. A wide diversity of both imported and processed foods are now available, increasing the probability that any individual may be exposed to something in diet to which he or she is allergic. Similarly, the amount of sugar being consumed, and therefore, the chance of developing hypoglycemia has greatly increased, so stimulating adrenaline production in the average citizen who is now quite likely to be diabetic and obese. Beyond this, soils, air, and water are polluted by over 32,000 chemicals that are in widespread commercial use. These substances again increase the probability of allergic reactions and consequently, the oxidation of adrenaline to adrenochrome. In the past 200 years, industrialized societies have become increasingly noisy. Both animal studies and research with human subjects adversely affected by traffic noise have shown that noise significantly affects catecholamine levels, stimulating the adrenal glands to release both noradrenaline and adrenaline.
There is evidence that adrenochrome is plausibly our body’s reaction to fighting cancer. That adrenochrome might mitigate the rapid speed of cancer comes from several pieces of evidence. For one, schizophrenics smoke their asses off, but the recorded incidence of lung cancer among schizophrenics is extremely low. What’s more, it’s been speculated that schizophrenics share genes that are common with cancer genes. The difference is that these genes work in opposing directions in schizophrenia and cancer. Cells with cancer genes will proliferate and multiply abberently, whereas those cells in schizophrenics with the same genes will cause cells to slow to a halt. There’s also been a new product called IntraDose, used as chemotherapy to fight tumors. Intradose contains cisplantin (an oxidant) and adrenaline. It’s been tested and shows promise as a cancer fighting treatment. Further information on these pieces of evidence follows:
Low Incidence of Lung Cancer
Schizophrenics are typically heavy smokers, but very rarely do they develop lung cancer. There is a chapter in the book What Really Causes Schizophrenia called Medical Anomalies, and there is a section in this chapter that mentions the disproportionate amount of schizophrenics who smoke:
Schizohprenics typically are heavy smokers, but very rarely do they develop lung cancer. Together with Abram Hoffer, I have argued that this medical anomaly may eventually provide new treatments for both disorders. About 33% of Americans smoke, but this figure rises to 90% amongst US schizophrenics. Similarly, in Ireland about 49% of males and 36% of females smoke, compared to 92% of chronic male and 82% of chronic female schizophrenics. Indeed, every available study confirms that schizohrenics are much more likely to smoke than are the general population.
Why do schizophrenics gravitate towards smoking? As described by Foster,
If the adrenochrome theory is correct, many schizphrenics may be deficient in brain adrenaline because too much of it is oxidized to adrenochrome. Animal tests have shown that nicotine increases adrenaline turnover in the hypothalamus, especially the median eminence. This nicotine-adrenaline relationship seems to have a therapeutic role in many neuropsychiatric disorders including depression, Tourett’s syndrome, and schizophrenia. It seems likely, therefore, that, in the short term, elevated nicotine from tobacco helps alleviate the adverse impacts of low brain adrenaline experienced because of its excessive oxidation to adrenochrome. This is why so many schizohrenics smoke as a form of self-medication.
Yet, the incidence of lung cancer is incredibly rare given the high proportion of schizophrenics who smoke:
It follows that lung cancer must be rampant amongst schizophrenics. Strangely it is not. Indeed, the available evidence suggests it is rare. In 1979, Rice claimed that there had never been a recorded case of bronchogenic carcinoma in a hospitalized chronic schizophrenic, despite that group’s abnormally  high tobacco use. Craig and Lin also documented a depressed incidence of lung cancer in chronic schizohrenic smokers. Probably, the most comprehensive study of the occurence of cancer amongst schizohrenics was conducted by Gulbinate and colleagues. They also established very low relative risks of lung cancer, during the period 1957 to 1980, amongst Dutch male (rr=0.38) and female (rr=0.33) schizophrenics. Similarly, in Canada, Hoffer has treated some 4,000 schizophrenics since 1952. There have been only 5 cases of cancer amongst them; lymphoma, thyroid cancer, and 3 examples of breast cancer. In every case, the patient responded well to treatment and is still alive.
Abram Hoffer notes the antagonism between cancer and schizophrenia in, Basic health publications user’s guide to natural therapies for cancer:
Adrenochrome is also toxic to mitosis, the process of cell division, so it appeared plausible that there would be a natural antagonism between cancer and schizophrenia if our hypothesis was correct. Since cancer is the result of uncontrolled cell division, it could not co-exist with adrenocrhome. If a patient  made too much adrenocrhome due to extreme amounts of adrenaline oxidation, he could develop schizophrenia but not cancer, because the adrenocrhome would inhibit cell division.
Furthermore, Hoffer laments on the extremely low rates of cancer among schizophrenic patients AND relatives
I have not seen one schizophrenic patient die from cancer. This clear antagonism between cancer and schizohrenia applies, but not to the same degree, to first order relatives of the patient.
Here is what I found, Foster and Hoffer (2004)
Patients with cancer-N=114:
Number of relatives-785
relatives with schizohprenia-3
Relatives with cancer-89
Patients with schizophrenia-N=95
Number of relatives-437
Relatives with schizophrenia-29
Relatives with cancer-26
Foster further hints at the possibility that it’s the biochemistry of schizophrenia that provides the protective factor in cancer, rather than antipsychotics:
All the available evidence then suggests that schizophrenics are very heavy smokers who, nevertheless, die far les frequently of lung cancer than the general public. This low lung cancer incidence has been recorded amongst the patients of both conventional and unconventional physicians over a long time period. It appears very likely, therefore, that it cannot be due to treatment but must be related to the biochemistry of the mental illness itself.
Same Genes as Cancer Genes?

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.

We found that many of the same genes are involved in schizophrenia as in cancer, but in a yin and yang way. This will provide critical insight into the molecular structure of schizophrenia," said lead researcher and ACNP member Dr. Daniel Weinberger of NIMH. Some of the genes showing this yin-yang effect include NRG1, AKT1, PIK3, COMT, PRODH and ErbB4. While these genes can’t be used to predict exactly who will develop these diseases, Dr. Weinberger says they can be used to help determine risk.

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.


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.

Intraose contains ingredients that combine to form adrenochrome. It is a combination of ciplatin and drenaline. Cisplatin is a very powerful oxidant which will almost certainly convert any adrenaline to adrenochrome when the 2 are inected together into a tumour mass. As described in What Really Causes Schizophrenia,
A new product called IntraDose, which contains cisplatin and epinephrine, is being tested as a treatment for liver cancer, cancer of the head and neck and breast, and malignant melanoma. In all of these types of cancer the treatment is sowing great promise.
 In liver cancer, for example, 38 patients were treated with IntraDose and 55(21) percent of these responded to the drug. In nine of the cases the tumor disappeared, while in the other 12 there was a reduction in viable tumour mass of more than 50%.

93. Matrix Pharmaceutical, Inc. (2000). Matrix Updates Interim Phase II

Results for IntraDose in Primary Liver Cancer.




Excellent responses were also achieved in malignant melanoma patients and those with head and neck cancers and breast cancer.

Doctor’s Guide. Personal Edition, Stein, J. (2001). DG Dispatch – WCM:

Intratumal IntraDose (Cisplatin/Epinephrine) Shows Promise in

Metastatic Malignant Melanoma.




Final Thoughts:

The effect that industrialization has on our bodies cannot be understated. Along with other illnesses, schizophrenia is a response to drastic changes in an environment urban dwellers live in. The problem we encounter is the auto-immune response that destroys brain tissue.
New evidence suggests that cancer genes and schizophrenic genes are shared, yet they work in totally opposite fashion when expressed as cell division. Whereas cancer cells are rapidly dividing, these cells that contain these genes shrivel up.
And as far as adrenochrome being the miracle drug, well, nothing is ever a miracle drug because cancer is so complex and there are many other factors that come into play when it comes to battling cancer. THERE IS NO MAGIC BULLET. Despite all this, as the studies show, adrenochrome can possibly be utilized to treat cancer in the near future-provided psychotic reactions don’t escalate in patients. There is always the possibility that adrenochrome will cross the blood brain barrier and that would be the adverse reaction of an adrenochrome drug.
As described in Why Schizophrenics Smoke but Have a Lower incidence of lung cancer: implications for the treatment of both disorders,
Elevated adrenochrome is double-edged sword. On the one hand it appears to protect against cancer, while on the other it promotes psychosis. This suggests that the treatment of schizophrenia requires the prescription of natural methyl acceptors such as niacin (vitamin B3) and ubiquinones (coenzyme Q10) to reduce adrenochrome production. While conversely, the successful treatment of many cancers may ultimately require the prescription of substances that cause abnormally high adrenochrome levels and temporary psychosis.

March 25, 2009 at 1:20 pm Leave a comment

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:

  1. 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).
    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.
  2. 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.
  3. 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:


"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. "


"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 ceruloplasminreflecting 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-schizophrenicsA 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)


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


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.


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.


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).


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.


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.


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)



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:


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


Specficially, adrenocrhome follows the adrenergic pathway, which also cuts across the limbic system as well. Adrenochrome’s effect on the limbic system is essentially similar to the effects shown when experiments are done with electrical stimulation to parts of the limbic system. In both instances, they give rise to hallucinations. Adrenochrome’s action raises the electrical activity found in neurons sending messages to each other rapidly. On a similar note,a proportion of epileptics sometimes report such symptoms as hallucinations as well, and this is attributed to rapidly firing electrical synaptic transmission. This is most common in epileptics whose focal seizure activity is within the temporolibmic region. Furthermore, a sizeable proportion of schizophrenics have epilepsy too, providing overlap.

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".

March 1, 2009 at 4:50 pm Leave a comment

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:


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.


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:



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.


October 11, 2008 at 1:42 pm 2 comments

Orthomolecular Online

A site dedicated to providing informational resources on the field of orthomolecular treatment of mood and behavioural disorders.

Orthomolecular medicine advocates the use of natural substances found in the body to treat patients with biochemical disorders. The brain is a factory dependent on raw nutrients naturally produced by the body.