B-complex
Hart en vaatziekten
Er is een duidelijke relatie tussen een te lage foliumzuur en B6 bloedwaarde en een verhoogde homocysteine en daarmee een verhoogd risico op een hart en vaatziekte. Andere onderzoeken bevestigen deze visie.Als homocysteine niet voldoende wordt omgezet in methionine doordat het remethylatie proces niet goed verloopt is er vaak een tekort aan foliumzuur. Als het overtollige homocysteine niet voldoende door de lever via het transsulfuratie pad wordt omgezet in cysteine is er ook sprake van een tekort aan B6 en B12.
- Lowering blood homocysteine with folic acid-based supplements: meta-analysis of randomised trials
In conclusion, typically in Western populations, daily supplementation with both 0.5-5 mg folic acid and about 0.5 mg vitamin B12 would be expected to reduce blood homocysteine concentrations by about a quarter to a third (for example, from about 12 micromol/L to 8-9 micromol/L). Large scale randomised trials of such regimens in high risk populations are now needed to determine whether lowering blood homocysteine concentration reduces the risk of vascular disease. - Group B vitamins as new variables related to the cardiovascular risk
The nutritional status and plasma concentrations of some group B vitamins, namely vitamin B6, vitamin B12 and folic acid, have recently emerged as inverse correlates of cardiovascular risk, and several experimental and clinical studies, these latter mostly retrospective and case-control studies, indicate a defect of such vitamins as capable of promoting the progression of atherosclerosis. - Folate and vitamin B6 from diet and supplements in relation to risk of coronary heart disease among women
These results suggest that intake of folate and vitamin B6 above the current recommended dietary allowance may be important in the primary prevention of CHD among women. - Homocysteine metabolism and risk of myocardial infarction: relation with vitamins B6, B12, and folate
These data provide further evidence that plasma homocyst(e)ine is an independent risk factor for myocardial infarction. In this population, folate was the most important determinant of plasma homocyst(e)ine, even in subjects with apparently adequate nutritional status of this vitamin.
B-complex
Kanker
- DNA damage from micronutrient deficiencies is likely to be a major cause of cancer
A deficiency of any of the micronutrients: folic acid, Vitamin B12, Vitamin B6, niacin, Vitamin C, Vitamin E, iron, or zinc, mimics radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. For example, the percentage of the US population that has a low intake (<50% of the RDA) for each of these eight micronutrients ranges from 2 to >20%. A level of folate deficiency causing chromosome breaks was present in approximately 10% of the US population, and in a much higher percentage of the poor. Folate deficiency causes extensive incorporation of uracil into human DNA (4 million/cell), leading to chromosomal breaks. This mechanism is the likely cause of the increased colon cancer risk associated with low folate intake. Some evidence, and mechanistic considerations, suggest that Vitamin B12 (14% US elderly) and B6 (10% of US) deficiencies also cause high uracil and chromosome breaks. Micronutrient deficiency may explain, in good part, why the quarter of the population that eats the fewest fruits and vegetables (five portions a day is advised) has about double the cancer rate for most types of cancer when compared to the quarter with the highest intake. For example, 80% of American children and adolescents and 68% of adults do not eat five portions a day. Common micronutrient deficiencies are likely to damage DNA by the same mechanism as radiation and many chemicals, appear to be orders of magnitude more important, and should be compared for perspective. Remedying micronutrient deficiencies should lead to a major improvement in health and an increase in longevity at low cost. - Micronutrients prevent cancer and delay aging
Approximately 40 micronutrients are required in the human diet. Deficiency of vitamins B12, folic acid, B6, niacin, C, or E, or iron, or zinc, appears to mimic radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. The percentage of the US population that has a low intake (< 50% of the RDA) for each of these eight micronutrients ranges from 2% to > or = 20%; half of the population may be deficient in at least one of these micronutrients. Folate deficiency occurs in approximately 10% of the US population, and in a much higher percentage of the poor. Folate deficiency causes extensive incorporation of uracil into human DNA (4 million/cell), leading to chromosomal breaks. This mechanism is the likely cause of the increased cancer risk, and perhaps the cognitive defects associated with low folate intake. Some evidence, and mechanistic considerations, suggest that vitamin B12 and B6 deficiencies also cause high uracil and chromosome breaks. Micronutrient deficiency may explain, in good part, why the quarter of the population that eats the fewest fruits and vegetables (five portions a day is advised) has approximately double the cancer rate for most types of cancer when compared to the quarter with the highest intake. Eighty percent of American children and adolescents and 68% of adults do not eat five portions a day. Common micronutrient deficiencies are likely to damage DNA by the same mechanism as radiation and many chemicals, appear to be orders of magnitude more important, and should be compared for perspective. Remedying micronutrient deficiencies is likely to lead to a major improvement in health and an increase in longevity at low cost. Aging appears to be due, in good part, to the oxidants produced by mitochondria as by-products of normal metabolism. In old rats mitochondrial membrane potential, cardiolipin levels, respiratory control ratio, and overall cellular O2 consumption are lower than in young rats, and the level of oxidants (per unit O2) is higher. The level of mutagenic aldehydes from lipid peroxidation is also increased. Ambulatory activity declines markedly in old rats. Feeding old rats the normal mitochondrial metabolites acetyl carnitine and lipoic acid for a few weeks, restores mitochondrial function, lowers oxidants to the level of a young rat, and increases ambulatory activity. Thus, these two metabolites can be considered necessary for health in old age and are therefore conditional micronutrients. This restoration suggests a plausible mechanism: with age-increased oxidative damage to proteins and lipid membranes causes a deformation of structure of key enzymes, with a consequent lessening of affinity (Km) for the enzyme substrate; an increased level of the substrate restores the velocity of the reaction, and thus restores function. - Vitamins B6 and B12 and folate status in an adult Mediterranean population
In men, intakes were below two-thirds of the RDA in 10.8, 2.9 and 22.6% for B(6), B(12) and folate, respectively. The corresponding figures in women were 16.7, 5.1 and 23.5% for vitamins B(6), B(12) and folate. Age, place of residence and educational level, alcohol use and smoking were also associated with differences in the intake of these nutrients.
Maagdarmstoornissen: Candida infectie - Prikkelbaredarmsyndroom - Crohn - Colitus Ulcerosa - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Bloeduiker stabilisatie - Neuropathie - Retinopathie - Nefropathie - Hart- en vaatziekten: Cardiomyopathie en Hartfalen - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose) - Spataderen - Levensverlenging: 100 jaren jong - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Bot en gewrichtsaandoeningen: - Artrose - Artritis - Osteoporose - Fibromyalgie: - Fibromyalgie - Urinewegaandoeningen: - Prostaatklachten - Blaasontsteking - Vrouwenklachten: Menopauze - Premenstrueelsyndroom - Overgewicht: - Overgewicht - SLIM - Oogaandoeningen: Staar - Slecht zien Andere artikelen: - HPU - Astma - Multiple Sclerose - Psoriasis - Depressie