Some people with schizophrenia may simply have B3 deficiency

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Some People With Schizophrenia May Simply Have a Vitamin Deficiency

Quote:

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

Ketogenic diet slows progression of 5 neuro degenerative diseases

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SCIENCE SUPPORTS THE ANTI-AGING AND ANTI-DEGENERATIVE PROPERTIES OF KETOGENIC DIETS!

Slowing down of neuro-degenerative disease by ketogenic diet was claimed in the recent paper:
Nourishing the Aging Brain, By Morten Scheibye-Knudsen,  The Scientist, March 2015

( in pdf format )


Quotes (see here ):

ALS:
Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

ALZHEIMER’S DISEASE:
Normal or lowered basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

PARKINSON’S DISEASE:
Increased basal metabolism
Caloric restriction slows progression
Ketogenic diet slows progression

HUNTINGTON’S DISEASE:
Increased basal metabolism
Caloric restriction may slow progression
Ketogenic diet slows progression

COCKAYNE SYNDROME [accelerated aging disease]:
Increased basal metabolism
Caloric restriction exacerbates progression
Ketogenic diet slows progression

[added on 6/03/2015, from the same source]

And the low carbohydrate (or low glucose) nutrition appears to contribute to longevity by increasing the SIRT6 activity (*), according to this paper, from the same issue of The Scientist magazine:

Wrangling Retrotransposons, by Michael Van Meter, Andrei Seluanov, and Vera Gorbunova | March 1, 2015

Quote

Perhaps the best evidence for the retrotransposon’s role in aging comes from the link between the activity of a longevity gene, SIRT6, and the repression of L1 in somatic tissues. SIRT6 encodes an enzyme critical to the forestallment of aging: it maintains telomere length, promotes DNA repair, regulates metabolism, opposes tumorigenesis, and attenuates inflammation—all processes associated with the prevention of age-related decline. Mice lacking SIRT6 suffer from a severe premature aging syndrome, while mice that overexpress SIRT6 enjoy extended life spans.

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One explanation for this failure may relate to SIRT6’s critical role in DNA repair. Several studies have indicated that SIRT6 helps catalyze repair of the damage at numerous types of DNA lesions, including single- and double-strand breaks. A characteristic feature of aging cells is an increase in the amount of DNA damage.

...

While overexpression of SIRT6 may not be tractable in a therapeutic context, SIRT6 activity can be increased by caloric restriction, reducing glucose consumption, or increasing NAD+ bioavailability (**) - interventions that have already shown promise in increasing longevity in animal models. (Such interventions are also showing promise in slowing the progress of some age-related neurodegenerative disorders.

Notes:

*) Underexpression or removal of SIRT6 gene is linked to accelerated aging disease, while overexpression of SIRT6 has been shown to extend the lifespan, in mice studies, see Wiki.

**) Niacin is one of the precursors of NAD+, another one is tryptophan.

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