Showing posts with label Vitamin B. Show all posts
Showing posts with label Vitamin B. Show all posts

Vitamin B3 modulates mitochondrial vulnerability and prevents glaucoma in aged mice | Science

"Glaucoma is the most common cause of age-related blindness in the United States. There is currently no cure, and once vision is lost, the condition is irreversible. Williams et al. now report that vitamin B3 (also known as niacin) prevents eye degeneration in glaucoma-prone mice (see the Perspective by Crowston and Trounce). Supplementing the diets of young mice with vitamin B3 averted early signs of glaucoma. Vitamin B3 also halted further glaucoma development in aged mice that already showed signs of the disease. Thus, healthy intake of vitamin B3 may protect eyesight."



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B vitamins could delay dementia

 "Despite spending billions of dollars on research and development, drug companies have been unable to come up with effective treatments for dementia and Alzheimer's Disease (AD). Now, A. David Smith at the University of Oxford and his colleagues have discovered that, in some patients experiencing mild cognitive impairment (MCI), a cocktail of high-dose B vitamins could prevent gray matter loss associated with progression to AD. The study appears in the Proceedings of the National Academy of Sciences."


Antigenic Vitamins -- Ferrarelli 5 (253): ec307 -- Science Signaling

The gut microbiota and immune surveillance are important for gastrointestinal (GI) function and health. Mucosal-associated invariant T (MAIT) cells are an abundant population of innate-like T cells associated with GI mucosa and activated by a diverse range of bacteria and yeast strains. The T cell antigen receptor (TCR) of MAIT recognizes antigens bound to MR1, an MHC class I-like–related molecule, which folds into a stable complex with β2 microglobulin (β2m). Noticing that MR1β2m yields were enhanced in RPMI medium, which contains vitamins isolated from bacteria and plants, Kjer-Nielsen et al. identified 6-formyl pterin (6-FP), a photodegradation product of folic acid (vitamin B9) as a molecule in RPMI medium that promoted the formation of MR1β2m. Crystallographic analysis revealed that the antigen-binding cleft of the MR1β2m complex is structurally distinct from the peptide- and lipid-binding antigen-presenting MHC-I and -II molecules HLA-A2 and CD1d. Despite increasing the abundance of MR1 at the cell surface in lymphoid CR1 cells, 6-FP failed to activate either primary MAIT cells or Jurkat cells transduced with a MAIT TCR, whereas supernatant from Salmonella typhimurium cultures activated both cell types. Using supernatant from S. typhimurium cultures grown in M9 minimal medium to exclude competing vitamin complex ligands, they identified derivatives of riboflavin (vitamin B2) that both bound MR1 and activated MAIT cells but not other types of T cells. Although similar to 6-FP, these compounds contain an extra ribityl moiety that may permit direct contact with the MAIT TCR. Notably, these riboflavin metabolites are produced by biosynthetic pathways present only in bacteria and yeast strains that activate MAIT cells. Thus, microbially produced vitamins are recognized as antigens, enabling the immune system to respond to microbial infection in the gut.

Lack of nutrients and metabolic syndrome linked to different subtypes of depression

A low intake of folate and vitamin B12 increases the risk of melancholic depressive symptoms, according to a study among nearly 3,000 middle-aged and elderly Finnish subjects. On the other hand, non-melancholic depressive symptoms are associated with an increased risk for the metabolic syndrome. Based on these new observations, melancholic and non-melancholic depression may be separate depressive subtypes with different etiologies in terms of proinflammation and diet. The study was the first to look at these depressive sub-types separately.

Read more at: http://medicalxpress.com/news/2012-11-lack-nutrients-metabolic-syndrome-linked.html#jCp

How the body uses vitamin B to recognize bacterial infection

Humans are unable to make vitamin B and obtain it mostly from diet. Because bacteria can synthesise vitamin B, our immune system uses this as a point of difference to recognise infection

Read more at: http://medicalxpress.com/news/2012-10-body-vitamin-bacterial-infection.html#jCp

News: Vitamin B12 deficiency: tracking the genetic causes

Vitamin B12 is essential to human health. However, some people have inherited conditions that leave them unable to process vitamin B12. As a result they are prone to serious health problems, including developmental delay, psychosis, stroke and dementia. An international research team recently discovered a new genetic disease related to vitamin B12 deficiency by identifying a gene that is vital to the transport of vitamin into the cells of the body. This discovery will help doctors better diagnose this rare genetic disorder and open the door to new treatments. The findings are published in the journal Nature Genetics.

Vitamin and mineral intakes in adults with mood disorders

OBJECTIVE: The purpose of this study was to investigate the nutrient intakes of people with mood disorders. Method: A cross-sectional survey using 3-day food records was carried out in 97 adults with bipolar or major depressive disorder to compare nutrient intakes with Dietary Reference Intakes and British Columbia Nutrition Survey (BCNS) data. Blood levels of selected nutrients were compared to reference ranges. Bivariate and multivariate analyses examined the effects of sociodemographic and clinical variables on nutrient intakes. Results: The average age of respondents was 46 (±13) years; most were women (n = 69) who had less than a university degree (n = 60) and whose incomes were in the government-defined lower range (n = 39). Compared with the BCNS, a larger proportion of the sample was below the estimated average requirement for thiamin (26% vs 8%), riboflavin (21% vs 4%), folate (64% vs 27%), phosphorous (12% vs 1%), and zinc (39% vs 15%; all P < 0.0001), as well as vitamin B(6) (25% vs 16%) and vitamin B(12) (27% vs 8%; both P < 0.05). Combined intakes of food and supplements helped reduce the prevalence of inadequacy; however, with supplementation, the proportion of participants exceeding the tolerable upper intake levels for niacin, vitamin B(6), folate, vitamin C, calcium, magnesium, iron, and zinc ranged from 1%-8%. Income, relationship status, age, gender, and caloric intake were associated with intakes of many nutrients. Types of medications were associated with nutrient intakes, as lower intakes of thiamin and phosphorous (P < 0.05) were found with antidepressant use, higher calcium and iron intakes (P < 0.05) were associated with antianxiety medication use, and magnesium intakes were increased with mood stabilizers (regression coefficient = 52.61, P < 0.05, 95% confidence interval = 0.74 to 104.48). Conclusions: Adults with mood disorders are at risk for many nutrient inadequacies, as well as occasional excesses; social, demographic, and clinical factors may affect their nutrient intakes.
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Women Who Start Prenatal Vitamins Early Are Less Likely To Have Children With Autism

The effects were attributed to folic acid, the synthetic form of folate aka vitamin B9, and the other B vitamins which may protect against deficits in early foetal brain development.

Risk factors: Autism risk factors :  Kegg pathways of autism genes 
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Induction of Alzheimer's-like changes in brain of mice expressing mutant APP fed excess methionine.

Homocysteine levels are a risk factor in Alzheimer's disease, (see database) and this study showed that manipulation of homocysteine levels in APP transgenic mice modified beta-amyloid deposition and also has effects on brain cholesterol levels. Homocysteine and methionine metabolism regulate B vitamin synthesis . B vitamins may have beneficial effects in Alzheimer's disease and ageing (see posts).


See also Kegg pathways for homocysteine, methionine and Vitamin B6 metabolism
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