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Vitamin B3 - Niacin
Niacin is an essential B-vitamin for many functions in our body
Essential for avoiding dementia, pellegra, keeping joint healthy, growth hormone (hGH) stimulation, HMG Coenzyme A in the mevalonate pathway, responsible for producing cholesterol, vitamin D3 and Squalene,
Niacin, also known as vitamin B3, is a water-soluble vitamin which prevents the deficiency disease pellagra. It is an organic compound with the molecular formula C6H5NO2. It is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide, nicotinamide ("niacinamide"), where the carboxyl group has been replaced by an amide group (CONH2), as well as more complex amides and a variety of esters. The terms niacin, nicotinamide, and vitamin B3 are often used interchangeably to refer to any one of this family of molecules, since they have a common biochemical activity.
Niacin is converted to nicotinamide and then to NAD and NADP in vivo. Although the two are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects of niacin, which occur as side-effects of niacin's conversion. Thus nicotinamide does not reduce cholesterol or cause flushing, although nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults. Niacin is a precursor to NADH, NAD, NAD+, NADP and NADPH, which play essential metabolic roles in living cells. DNA repair, and the production of steroid hormones in the adrenal gland.
Niacin is one of five vitamins associated with a pandemic deficiency disease: these are niacin (pellagra), vitamin C (scurvy), thiamin (beriberi), vitamin D (rickets), and vitamin A (no common name, but one of the most common symptomatic deficiences worldwide).
Dietary niacin and the risk of incident Alzheimer’s disease and of cognitive decline
M C Morris1,2,3, D A Evans1,2,4, J L Bienias1,2, P A Scherr5, C C Tangney6, L E Hebert1,2, D A Bennett1,4,7, R S Wilson1,4,7,8, N Aggarwal1,4,7Rush Institute for Healthy Aging, 1645 W. Jackson, Ste. 675, Chicago, IL 60612; martha_c_morris@rush.edu
Background: Dementia can be caused by severe niacin insufficiency, but it is unknown whether variation in intake of niacin in the usual diet is linked to neurodegenerative decline. We examined whether dietary intake of niacin was associated with incident Alzheimer’s disease (AD) and cognitive decline in a large, prospective study.
Methods: This study was conducted in 1993–2002 in a geographically defined Chicago community of 6158 residents aged 65 years and older. Nutrient intake was determined by food frequency questionnaire. Four cognitive tests were administered to all study participants at 3 year intervals in a 6 year follow up. A total of 3718 participants had dietary data and at least two cognitive assessments for analyses of cognitive change over a median 5.5 years. Clinical evaluations were performed on a stratified random sample of 815 participants initially unaffected by AD, and 131 participants were diagnosed with 4 year incident AD by standardised criteria.
Results: Energy adjusted niacin intake had a protective effect on development of AD and cognitive decline. In a logistic regression model, relative risks (95% confidence intervals) for incident AD from lowest to highest quintiles of total niacin intake were: 1.0 (referent) 0.3 (0.1 to 0.6), 0.3 (0.1 to 0.7), 0.6 (0.3 to 1.3), and 0.3 (0.1 to 0.7) adjusted for age, sex, race, education, and ApoE e4 status. Niacin intake from foods was also inversely associated with AD (p for linear trend = 0.002 in the adjusted model). In an adjusted random effects model, higher food intake of niacin was associated with a slower annual rate of cognitive decline, by 0.019 standardised units (SU) per natural log increase in intake (mg) (p = 0.05). Stronger associations were observed in analyses that excluded participants with a history of cardiovascular disease (ß = 0.028 SU/year; p = 0.008), those with low baseline cognitive scores (ß = 0.023 SU/year; p = 0.02), or those with fewer than 12 years’ education (ß = 0.035 SU/year; p = 0.002)
Conclusion: Dietary niacin may protect against AD and age related cognitive decline.
Abbreviations: AD, Alzheimer’s disease; CHAP, Chicago Health and Aging Project; FFQ, food frequency questionnaire; MMSE, Mini Mental State Examination; RDA, recommended dietary allowance/recommended daily amount
Keywords: niacin; Alzheimer’s disease; dementia; cognitive function; epidemiological study; aged; population-based study
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