Schizophrenia is a chronic, disabling brain disease. People with schizophrenia experience altered realities, including hallucinations, hearing voices, delusions, and confused or paranoid thoughts. Speech and behavior of people with schizophrenia can be very disorganized, which can be disturbing or confusing to those around them. During acute periods, people with schizophrenia experience a loss of energy, sense of humor, and interest in living. It affects one million Americans each year, and 1 percent of us will have it during our lifetime. It’s one of the top 10 worldwide causes of disability. It can be progressive or episodic. Schizophrenia has an autoimmune component, which may be a result of the disease itself. A large number of studies find correlation between prenatal and postnatal infections, including flu, herpes, polio, German measles, toxoplasmosis, and respiratory infections, and increased incidence of schizophrenia.
Medication is useful for many people with schizophrenia, but some are not greatly helped by it. Fortunately there are other therapies.
This is definitely an illness where a complete approach must be taken to get the best results. An entire field of nutritional medicine, called orthomolecular medicine (named by Linus Pauling), is based on treatment of schizophrenia and other mental illnesses, although its original definition was broader. Specific testing of amino acids, food sensitivities, fatty acids, heavy metals, and gut health will reveal information relevant to each person. Often, studies of schizophrenia using nutritional models have been disappointing because all patients are lumped into one group. When groups are broken into subtypes or patients are treated individually, improvements are seen.
Deficiencies in vitamin C, niacin, and folic acid have been found in people with schizophrenia.
Abram Hoffer, M.D., and Humphry Osmond, M.D., were pioneers in the field. Their protocols are based around use of niacin at 3,000 mg daily (vitamin B3), vitamin C at 3,000 mg daily, and loving care. Niacin therapy works best when used early after the diagnosis. Be patient: it can take months before it begins to work. Niacin causes a skin flush brought on by the release of prostaglandins in the skin; in people who don’t flush, it probably indicates a fatty acid deficiency. A niacin challenge offers a simple way to test for this group of people. Loving care expedites the healing process.
Carl Pfeiffer, M.D., Ph.D., found that some people with schizophrenia had faulty metabolism of specific B-complex vitamins. He once stated, “For every drug that yields a beneficial result, there is a nutrient that can produce the same effect.”
Fatty acid metabolism is faulty in people with schizophrenia, and schizophrenics have shown altered fatty acid panels. Levels of arachidonic acid and the omega-3 fatty acids EPA and DHA are often low. Schizophrenics are found to have high levels of interleukin-2, an inflammatory substance known to have the potential to cause symptoms similar to schizophrenia. Fish oils can help reduce levels of interleukin-2 and cytokines. Doing a fatty acid test would make sense.
People with schizophrenia have an increased need for antioxidant nutrients. Other antioxidants have also been found to be deficient. Poor free radical protection can damage fat-dependent membranes, the nervous system, and the brain. Testing for specific antioxidants would be advised.
The incidence of gluten intolerance in people with schizophrenia is higher than average. It’s speculated that where the two meet is having a leaky gut and being undernourished. Review studies indicate that between 2.6 and 4.2 percent of people with schizophrenia also have celiac disease. It has been estimated that 10 percent of people with schizophrenia will improve on a gluten-free trial. The earliest reports were published by Lauretta Bender, M.D., in 1953, who noticed an increase of celiac disease in children diagnosed with schizophrenia when 4 out of 37 boys admitted that year for schizophrenia also had celiac disease.
F. C. Dohan noted less schizophrenia during World War II in five countries when wheat was scarce, while in the United States both wheat consumption and schizophrenia increased. Dohan also used anthropological data from the South Pacific islands to show that as wheat, barley, beer, and rice consumption increased, so did schizophrenia. He subsequently compared two groups of schizophrenic males. Forty-seven were assigned a grain-free diet; 55 ate a high-grain diet. Sixty-two percent of those on the gluten-free diet were released to a non-locked ward within seven days, compared to 36 percent on a high-gluten diet. Wheat sensitivity can stimulate the production of chemicals in the brain that resemble opiates and cause hallucinations and behavior disturbances.
M. M. Singh and S. R. Kay studied 14 people with schizophrenia who were in a locked research ward. They followed a gluten-free diet for six weeks and were rated on 33 psychopathology measures and 6 social measures of social avoidance and participation. Treatment was blinded from the people who did the outcome measurements. There was significant improvement on 30 of 39 measures.
It appears that for the most part, people with schizophrenia and gluten intolerance have different genetics than people with celiac disease. In 2010, Diana Samaroo and colleagues found that people with schizophrenia did not have elevated tissue transglutaminase antibodies or HLA-DQ2 or HLA-DQ8 genotypes (95 percent of people with celiac have these genotypes), and most did not have high levels of deaminated gliaden. Nonetheless, they found high levels of antigliaden antibodies, indicating gluten sensitivity.
Although gluten intolerance and celiac disease are not present in all people with schizophrenia, it is important to screen for it.
Checking for additional food allergies and sensitivities can be useful. Elevated IgA antibodies to the dairy proteins beta-lactoglobulin and casein have been reported. Casein can have opioid-like effects in the brains of people with schizophrenia and autism. There are four specific types of casein in milk, and 13 genetic variations of beta-casein. It is believed that the A1 variant leads to the type of bioactive peptide beta-casomorphin 7 (BCM-7). High levels of BCM-7 have been found in the urine of people with schizophrenia and autism. This peptide crosses the intestinal mucosa, gets absorbed into the blood, and passes through the blood-brain barrier, causing an opioid-like response.
Other classic food offenders in schizophrenia include dairy products, food additives, and chocolate, although nearly any food can cause problems.
In 2009 Bryan D. Kraft and Eric C. Westman reported on a schizophrenic woman whose auditory hallucinations resolved on a ketogenic diet. A ketogenic diet is a very low-carbohydrate diet, such as the Atkins Diet. The woman’s hallucinations resolved by day 19 of the diet and remained so over the next 12 months, even though she had a couple of lapses during the winter holidays. Dohan and colleagues previously have noted an association between schizophrenia and consumption of grains. Others have noted an association specifically with gluten-containing grains. Still others have noted an increased incidence of psychotic episodes immediately after eating a carbohydrate load.
People with schizophrenia have an increased risk of developing stomach and duodenal ulcers. Others have found that when there is an ulcer, H. pylori–associated gastritis, or motor disorders of the upper GI, schizophrenic episodes are less severe.
Celiac testing
Food allergy testing—IgE and IgG, plus IgM and IgA if possible
Nutrient testing
Essential fatty acid testing
Urinary amino acid testing
Genetic testing for methylenetetrahydrofolate reductase gene (MTHFR)
Homocysteine testing
Schizophrenia is a complex illness. Digestive issues do not play a role in all people with schizophrenia, but for the subset of those whom it does affect, resolving these issues can be life changing.
Rule out celiac disease and food sensitivities. Do blood testing for food allergies and sensitivities. Try an elimination diet.
Look for nutritional deficiencies. Checking for specific nutrients and supplementing will give the best results because each person’s needs will be different. Beginning with a good multivitamin and mineral supplement can help but probably won’t fill in the gaps if there are severe deficiencies in specific nutrients.
Take niacin. Abram Hoffer, M.D., long used niacin therapy for schizophrenia. It is believed that there is faulty niacin metabolism in this condition, because people with schizophrenia often do not experience the intense flushing that usually occurs with niacin ingestion. Take up to 3,000 mg daily.
Increase intake of 5-hydroxytryptophan (5-HTP). In 14 patients tested, dietary restriction of tryptophan worsened their symptoms. Tryptophan can easily be converted to niacin, which may be one reason why it is of benefit. Tryptophan is also a precursor to serotonin, which affects mood, behavior, sleep, and carbohydrate cravings. At a recent conference Bill Walsh, Ph.D., medical director at Great Plains Laboratory, expressed concern about possible negative effects of tryptophan and recommended using only 5-HTP. To err on the side of caution, I am recommending 5-HTP. Take 300 to 600 mg 5-HTP.
Increase consumption of good fats. Schizophrenics often have low omega-3 fatty acid levels, low arachidonic acid levels, and low levels of polyunsaturated fatty acids. Benefit would be found by increasing good fats in the diet from sources such as nuts, seeds, whole grains, unprocessed vegetable oils, and cold-water fish, including salmon, halibut, tuna, mackerel, sardines, or herring. Twenty hospitalized patients were given 10 grams of fish oil daily. There were significant improvements in psychological symptoms, behavior, and tardive dyskinesia (uncontrollable movements) after six weeks. Another study used a smaller dose: 180 mg EPA, 120 mg DHA, plus 400 IU vitamin E and 500 mg vitamin C twice daily. There was improvement in lab testing and also in schizophrenic symptoms.
Try serine. Research indicates that high-dose glycine is beneficial for schizophrenia. Concern has been posted as to the possible long-term neurological effects of high-glycine supplementation, however. The mechanism of the response was believed to be the effect on the receptor sites for NMDA, a neurotransmitter. NMDA function is low in people with schizophrenia. Newer research on serine, by Toru Nishikawa, shows that the positive effects of enhancing NMDA function can be achieved by taking serine, without the risks of high-dose glycine. Dosage in one study was 0.8 grams of serine per kilogram of body weight daily. It would be advisable to do a urine amino acid test before using this type of therapy. Work with a physician.
Check your MTHFR gene and homocysteine levels. Homocysteine levels are often high in people who have schizophrenia. There are many studies looking at genetic variations in the MTHFR gene in people with schizophrenia. These studies have mixed results. Nonetheless, if you do have a genetic variation of this gene, you are less able to utilize folic acid from food and supplements. People with this genetic variation (MTHFR gene 677 C>T) benefit from supplements that have preformed folic acid, called methyltetrahydrofolate. People who have this genetic variation and schizophrenia are more likely to develop metabolic syndrome.
Take magnesium. Magnesium deficiency can produce depression, agitation, confusion, and disorientation. In one study, 20 schizophrenic patients were evaluated for serum magnesium levels. Twenty-five percent were found to be magnesium deficient. Serum magnesium is not a sensitive test of magnesium deficiency, so if red blood cell magnesium had been analyzed, the results would probably have been much higher. Half of the magnesium-deficient patients were exhibiting psychotic behavior, including hallucinations. In drug-treated schizophrenics, magnesium levels have been found to be consistently low. Supplementing with magnesium does not always show improvement in symptoms. Magnesium injections or use of choline citrate may be necessary at first to “prime the pump.” Because so many enzymes are dependent on magnesium, a deficiency could affect other nutrients, including vitamins B1, B6, E, and C and minerals such as zinc, copper, and selenium.