Some people with schizophrenia may simply have B3 deficiency

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Some People With Schizophrenia May Simply Have a Vitamin Deficiency

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The idea behind the hypothesis occurred to Esme Fuller-Thomson, professor at the University of Toronto’s Factor-Inwentash Faculty of Social Work (FIFSW) after learning about recent research conducted in South India. This study newly identified a link between schizophrenia and a variant of the gene NAPRT1, which lowers the body’s ability to use niacin, or Vitamin B3, which naturally occurs in meat, poultry, fish, and eggs.

“When I read this study a light bulb went on in my head,” says Fuller-Thomson, who published the hypothesis in the journal Schizophrenia Research this month with doctoral student, Rukshan Mehta. “This seems to be the missing link that explains all these medical mysteries.”

The researchers speculate that there is a critical interaction between an expectant mother’s prenatal niacin deficiency due to malnourishment and the NAPRT1 variant that impedes the fetus’ ability to use niacin. This interaction between the gene and the prenatal environment may predispose the offspring to develop a psychotic disorder.

Several studies indicate that the offspring of mothers who experience famine in their first trimester of pregnancy have double the chance of developing schizophrenia. Most researchers assume nutrient deficiency must be playing a role, but the particular nutrient has yet to be identified. Fuller Thomson now speculates that niacin may be the key nutrient involved.

Note that there is also a connection with the ketogenic diet.

Since NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels (preventing also oxidative stress of cells)
and NAD is also a precursor to SIRT6 which is also critical in DNA repair (thus longevity!)

See also


NAPRT1 (Nicotinate phosphoribosyltransferase) is essential for increasing cellular NAD levels and, thus, to prevent oxidative stress of cells. NAPRT1 converts Nicotinic acid (NA; niacin) to NA mononucleotide (NaMN), which is then converted to NA adenine dinucleotide (NaAD), and finally to nicotinamide adenine dinucleotide (NAD)

Ketogenic diet slows progression of 5 neuro degenerative diseases

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Source reference paper:

Letter to the editor/
Could a gene-environment interaction between NAPRT1 risk allele and pre-natal niacin deficiency explain 4 medical mysteries of schizophrenia research?/
Esme Fuller-Thomson, Rukshan Mehta; Schizophrenia Research
Available online 12 December 2019

Connection between immune system, microbiome and psychiatric disorders

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"He Got Schizophrenia. He Got Cancer. And Then He Got Cured." by Moises Velasquez-Manoff, NYT, Sept. 29, 2018

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...A year later, the man’s condition worsened. He developed fatigue, fever and shortness of breath, and it turned out he had a cancer of the blood called acute myeloid leukemia. He’d need a bone-marrow transplant to survive. After the procedure came the miracle. The man’s delusions and paranoia almost completely disappeared. His schizophrenia seemingly vanished.

Years later, “he is completely off all medication and shows no psychiatric symptoms,” Dr. Miyaoka told me in an email. Somehow the transplant cured the man’s schizophrenia.

A bone-marrow transplant essentially reboots the immune system. Chemotherapy kills off your old white blood cells, and new ones sprout from the donor’s transplanted blood stem cells. It’s unwise to extrapolate too much from a single case study, and it’s possible it was the drugs the man took as part of the transplant procedure that helped him. But his recovery suggests that his immune system was somehow driving his psychiatric symptoms.

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In the late 19th century, physicians noticed that when infections tore through psychiatric wards, the resulting fevers seemed to cause an improvement in some mentally ill and even catatonic patients.

Inspired by these observations, the Austrian physician Julius Wagner-Jauregg developed a method of deliberate infection of psychiatric patients with malaria to induce fever. Some of his patients died from the treatment, but many others recovered. He won a Nobel Prize in 1927.

One much more recent case study relates how a woman’s psychotic symptoms — she had schizoaffective disorder, which combines symptoms of schizophrenia and a mood disorder such as depression — were gone after a severe infection with high fever.

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Indeed, in the past 15 years or so, a new field has emerged called autoimmune neurology. Some two dozen autoimmune diseases of the brain and nervous system have been described. The best known is probably anti-NMDA-receptor encephalitis, made famous by Susannah Cahalan’s memoir “Brain on Fire.” These disorders can resemble bipolar disorder, epilepsy, even dementia — and that’s often how they’re diagnosed initially. But when promptly treated with powerful immune-suppressing therapies, what looks like dementia often reverses. Psychosis evaporates. Epilepsy stops. Patients who just a decade ago might have been institutionalized, or even died, get better and go home.

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Dr. Robert Yolken, a professor of developmental neurovirology at Johns Hopkins, estimates that about a third of schizophrenia patients show some evidence of immune disturbance. “The role of immune activation in serious psychiatric disorders is probably the most interesting new thing to know about these disorders,” he told me.

Studies on the role of genes in schizophrenia also suggest immune involvement, a finding that, for Dr. Yolken, helps to resolve an old puzzle. People with schizophrenia tend not to have many children. So how have the genes that increase the risk of schizophrenia, assuming they exist, persisted in populations over time? One possibility is that we retain genes that might increase the risk of schizophrenia because those genes helped humans fight off pathogens in the past. Some psychiatric illness may be an inadvertent consequence, in part, of having an aggressive immune system.

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Another case study from the Netherlands highlights this still-mysterious relationship. In this study, on which Dr. Yolken is a co-author, a man with leukemia received a bone-marrow transplant from a schizophrenic brother. He beat the cancer but developed schizophrenia. Once he had the same immune system, he developed similar psychiatric symptoms.

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And there may be other, softer interventions. A decade ago, Dr. Miyaoka accidentally discovered one. He treated two schizophrenia patients who were both institutionalized, and practically catatonic, with minocycline, an old antibiotic usually used for acne. Both completely normalized on the antibiotic. When Dr. Miyaoka stopped it, their psychosis returned. So he prescribed the patients a low dose on a continuing basis and discharged them.

Minocycline has since been studied by others. Larger trials suggest that it’s an effective add-on treatment for schizophrenia. Some have argued that it works because it tamps down inflammation in the brain. But it’s also possible that it affects the microbiome — the community of microbes in the human body — and thus changes how the immune system works.

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The study is preliminary, but it suggests that targeting immune function may improve mental health outcomes and that tinkering with the microbiome might be a practical, cost-effective way to do this.

Schizophrenia put into remission on keto diet

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Chronic Schizophrenia Put Into Remission Without Medication/New research suggests ketogenic diet may play a role in treating schizophrenia.
by Chris Palmer, M.D., Apr 06, 2019

Quotes

An 82 year old woman with chronic paranoid schizophrenia since age 17

The first patient documented in the Schizophrenia Research article is a woman who spent nearly her whole life suffering chronic, treatment-resistant schizophrenia. For more than 50 years, she endured paranoia, disorganized speech, visual and auditory hallucinations. By the time she was 70, she was suicidal and had been hospitalized repeatedly for psychosis or suicide attempts. She had been treated with over ten different antipsychotic and mood stabilizing medications, including regular antipsychotic injections. None of them helped her symptoms. She was unable to care for herself and had a court-appointed guardian and home health services.

At the age of 70, weighing 330 pounds, she went to a medical weight loss clinic and was started on a ketogenic diet. Within two weeks of starting the diet, she reported a noticeable reduction not only in her weight but also her psychotic symptoms. Within several months, she started to feel so much better that she was able to stop taking her psychiatric medications while remaining on the diet. Over time, her mood stabilized, and her hallucinations and paranoia remitted completely. She was no longer suicidal. Her case was first reported in 2009.

Today, 12 years later, she has lost a total of 150 pounds and remains on the ketogenic diet. She takes no medications and remains symptom-free. She was able to regain her independence, no longer requiring the guardian and the home health care team. When I recently spoke with her, she recalled her decades of suffering and hopelessness, and said that since starting the diet, she has had a "new life," and is happy to be alive.

A 39 year old woman with schizophrenia for 20 years

The second patient described in the article is a thirty-nine year old woman who suffered from depression, anxiety, anorexia nervosa, hallucinations and paranoia since her teens. As patients sometimes do, she concealed her psychotic symptoms when she was initially treated for depression and anorexia. When she finally reported her psychotic symptoms later in her twenties, she was diagnosed with schizophrenia. For the next ten years, she was treated with 7 different antipsychotic medications—including clozapine (called the “gold standard antipsychotic medication”) - along with antidepressants and anti-anxiety medications. Nevertheless, she continued to have symptoms.

She was having chronic gastrointestinal problems, so she saw a doctor who recommended the ketogenic diet. Noticing some improvement of her symptoms and being frustrated with all of her psychiatric medications, she unwisely stopped taking all 14 of her medications “cold turkey.” This sent her into severe psychosis requiring an extended hospitalization. In the hospital, she was re-medicated with Haldol-decanoate (an injectable medication which had not worked for her previously) and she continued the ketogenic diet. Within a month on both Haldol and the ketogenic diet, she reported complete remission of her psychotic symptoms for the first time since she was 14. Over the following year, she slowly tapered off Haldol, and remained free of psychotic symptoms. Of note, she lost 70 pounds from the diet, which exacerbated her anorexia. She has since regained 30 of those pounds and maintains a healthy weight today. 5 years after starting the ketogenic diet, she is off all antipsychotic medications, remains on the diet, and is free of all psychotic symptoms. She has since finished graduate school and now works full time.

Interestingly, these aren’t the first reports of the ketogenic diet for schizophrenia
While inspiring, these two case reports join a growing body of evidence supporting the use of the ketogenic diet in the treatment of schizophrenia.

Schizophrenia in 1965

In 1965, ten women hospitalized with schizophrenia who were already receiving medications and electroconvulsive therapy (ECT or “shock therapy”) were also placed on the ketogenic diet for a month. The researchers reported that their symptoms improved after two weeks on the diet, but then returned back to their baseline level of symptoms after the diet was stopped.

Schizoaffective disorder in 2017

In 2017, I reported two other cases of schizoaffective disorder improving significantly on the ketogenic diet. Schizoaffective disorder is a diagnosis that includes both a mix of schizophrenia and a mood disorder, often bipolar disorder. One man and one woman, both in their 30’s, had suffered treatment-resistant schizoaffective disorder for years. On the diet, their symptoms were greatly improved, and they both lost significant amounts of weight. Off the diet, their symptoms returned.

Schizophrenia in Ecuador

In 2018, two Ecuadorian twins, one male and one female, diagnosed with schizophrenia since the ages of 14 and 18 were started on a 6-week trial of the ketogenic diet. This study had a psychiatrist rate each twin’s symptoms while being unaware of their diet status. Interestingly, only when the patients were compliant with the diet did their symptoms improve. They also both lost weight. When they stopped the diet at the end of the study, their symptoms returned to their baseline level.

Stan's comments: - who were the medical criminals who stopped their patients' treatment as the article described, in spite of the clear improvement and despite of no viable alternatives? Why there was no information published and made available over the years, to other patients suffering from this debilitating disease, and their families? It is very symptomatic of a very serious disease rotting the medical system from within, in all countries. What have the government departments in charge of public health policies done to make that treatment available? Why did the judicial system refrain from punishing the people involved in maintaining this information hidden or even actively discouraging it by denigrating all ketogenic diets, all high fat low carbohydrate diets publicly and in the media? Who were the people, and who financed those who campaigned in the media smearing Drs. Yudkin, Atkins, Bernstein and others and why did public prosecutors and politicians allowed that to continue?

More connections between metabolic disorder and psychiatric/neurological conditions:

"Impaired insulin signaling in unaffected siblings and patients with first episode psychosis", by Virginie-Anne Chouinard et al., Mol Psychiatry. 2018 Mar 9


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Patients with psychotic disorders are at high risk for type 2 diabetes mellitus, and there is increasing evidence that patients display glucose metabolism abnormalities before significant antipsychotic medication exposure. In the present study, we examined insulin action by quantifying insulin sensitivity in first episode psychosis (FEP) patients and unaffected siblings, compared to healthy individuals, using a physiological-based model and comprehensive assessment battery. Twenty-two unaffected siblings, 18 FEP patients and 15 healthy unrelated controls were evaluated using a 2-hour oral glucose tolerance test (OGTT), with 7 samples of plasma glucose and serum insulin concentration measurements. Insulin sensitivity was quantified using the oral minimal model method. Lipid, leptin, free fatty acids and inflammatory marker levels were also measured. Anthropometric, nutrient and activity assessments were conducted; total body composition and fat distribution were determined using whole-body dual energy x-ray absorptiometry. Insulin sensitivity significantly differed among groups (F=6.01, P=0.004), with patients and siblings showing lower insulin sensitivity, compared to controls (P=0.006, and P=0.002, respectively).

Comment: Comparison between people diagnosed with psychiatric disorder and their sibling who were not diagnosed and therefore not affected by psychiatric drugs, showed the common underlying metabolic disorder involving insulin insensitivity and high risk of developing diabetes type 2.

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Update 11/04/2019 Another interesting paper on this subject. A different angle:

"Psychosis and Symbiosis: Microbiome and Schizophrenia. Fascinating new research links the gut and brain in sickness and health.", by Emily Deans M.D., Posted Mar 31, 2019

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Those mice that received the transplants from schizophrenic patients had higher levels of glutamine in the serum and hippocampus, decreased glutamate in the hippocampus, and increased GABA in the hippocampus. These difference were localized to areas of the brain particularly rich in glutamate and its metabolites (i.e., the outer shell of the brain and the hippocampus). This means that a transplant of a different microbiome led to different GABA-glutamate-glutamine neurotransmission in mouse brains. Corresponding human brain areas are related to memory, neuron repair, and executive functioning, all significantly impacted in schizophrenia.

In addition, the schizophrenia microbiome recipient mice had different behaviors than the healthy control mice, with exaggerated startle response and increased activity.

Vit D in childhood and diabetes T1 or schizophrenia - almost total protection!

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Fatty fish, such as salmon etc, are natural sources of vitamin D. (source - Wikipedia)

How often do we see a statistical risk reduction of some disease 8-times (relative risk reduction RR=0.12) or by a factor of 12 (RR=0.08)?   One cannot be 100% sure based on the outcome of just two studies but I am tempted to entertain an idea of the TOTAL PROTECTION, with the residual incidents possibly explained by non-conformance or observational errors.

Intake of vitamin D and risk of type 1 diabetes: a birth-cohort study.

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Vitamin D supplementation was associated with a decreased frequency of type 1 diabetes when adjusted for neonatal, anthropometric, and social characteristics (rate ratio [RR] for regular vs no supplementation 0.12, 95% CI 0.03-0.51, and irregular vs no supplementation 0.16, 0.04-0.74. Children who regularly took the recommended dose of vitamin D (2000 IU daily) had a RR of 0.22 (0.05-0.89) compared with those who regularly received less than the recommended amount. Children suspected of having rickets during the first year of life had a RR of 3.0 (1.0-9.0) compared with those without such a suspicion.

Vitamin D supplementation during the first year of life and risk of schizophrenia: a Finnish birth cohort study.

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RESULTS: In males, the use of either irregular or regular vitamin D supplements was associated with a reduced risk of schizophrenia (Risk ratio (RR)=0.08, 95% CI 0.01-0.95; RR=0.12, 95% CI 0.02-0.90, respectively) compared with no supplementation. In males, the use of at least 2000 IU of vitamin D was associated with a reduced risk of schizophrenia (RR=0.23, 95% CI 0.06-0.95) compared to those on lower doses. There were no significant associations between either the frequency or dose of vitamin D supplements and (a) schizophrenia in females, nor with (b) nonpsychotic disorder or psychotic disorders other than schizophrenia in either males or females.

CONCLUSION: Vitamin D supplementation during the first year of life is associated with a reduced risk of schizophrenia in males. Preventing hypovitaminosis D during early life may reduce the incidence of schizophrenia.

Update (6/9/2010):

Another paper on the subject (thanks Neonomide):

Relation of schizophrenia prevalence to latitude, climate, fish consumption, infant mortality, and skin color: a role for prenatal vitamin d deficiency and infections?

A review article by J.J. Cannell MD of "The Vitamin D Council":

The Vitamin D Newsletter August 2009, Vitamin D and Schizophrenia

More update (18/09/2010)

Paper: Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature

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C.D. is a 70 year-old Caucasian female with a diagnosis of schizophrenia since the age of seventeen. Her diagnosis was based on paranoia, disorganized speech, and hallucinations. She reported both auditory and visual hallucinations,... she has had these hallucinations on almost a daily basis since the age of seven. ...has also been hospitalized at least five times over the last six years for suicide attempts and increased psychotic symptoms.

... Over the course of 12 months, C.D. has continued the low-carbohydrate, ketogenic diet and has had no recurrence of her auditory or visual hallucinations. She has also continued to lose weight (body weight 131.4 kilograms) and experience improvements in her energy level.

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