Rich sources of niacin include lean meat, fish, legumes, nuts, dairy products, enriched grains and cereals, and coffee and tea.
The researchers base their findings on almost 4000 people aged 65 and older, who had no Alzheimer's disease. These participants completed a dietary questionnaire and were checked for any signs of decreasing mental agility (cognitive decline) three and six years after the start of the study.
At three years, a random sample of 815 people, who had not initially had Alzheimer's disease, were checked for clinical changes and their dietary niacin intake assessed by means of food frequency questionnaires.
Among this smaller group, 131 people were diagnosed with Alzheimer's disease. After adjusting the results for age, gender, race, educational levels, and the ApoE gene - all important risk factors for the disease - those with the lowest food intake of niacin (an average of 12.6 mg/day) were 80% more likely to be diagnosed with Alzheimer's disease than those with the highest intake (22.4 mg/day).
An analysis of the larger group showed that the rate of cognitive decline among those with the highest niacin intake was almost half (44%) that of those with the lowest intake.
Niacin has been prescribed to older people to prevent confusional states, and severe deficiency causes pellagra, a condition characterised by dementia, diarrhoea, and dermatitis, but its role in Alzheimer's disease has not been thoroughly explored, say the authors.
Previous research has indicated that niacin has an important role in DNA synthesis and repair, neural cell signalling, and acts as a potent antioxidant in brain cells, they say.
Click here to view the paper in full: press.psprings/jnnp/july/1093_jn25858.pdf
According to Dr. Luo, the gene expression patterns of benign adjacent tissue were significantly overlapped with those of prostate cancer and distinctly different than the disease-free tissue. Furthermore, the adjacent tissue was so genetically altered that it resembled a cancer field effect, undergoing genetic changes similar to prostate cancer, even though it was morphologically benign tissue.
"It appears that genetic alterations in the prostate occur in parts of the gland that otherwise look benign," said Joel Nelson, M.D., professor and chairman, department of urology, University of Pittsburgh and co-author of the study. "We have long suspected a so-called field change in the prostate gland containing cancer, meaning some alteration has occurred throughout the prostate tissue. This study lends support for such a hypothesis."
The researchers also created a gene model using GeneSpringTM software to predict the aggressiveness of the disease and found that the expression profile model was more than 80 percent accurate in predicting the aggressiveness of the disease.
"Since only a fraction of prostate cancers are metastatic, identifying variables that predict the behavior of a prostate cancer tumor based on gene expression patterns should prove important in clinical management of the disease," said Dr. Luo. "The results of this study are a first step in that direction."
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