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ScienceDaily (Feb. 10, 2009) - Eating a Mediterranean diet appears to be associated with less risk of mild cognitive impairment-a stage between normal aging and dementia-or of transitioning from mild cognitive impairment into Alzheimer's disease, according to a report in the February issue of Archives of Neurology, one of the JAMA/Archives journals

Association of vitamin D deficiency with cognitive impairment in older women. Cross-sectional study. Annweiler C, Schott AM, Allali G, Bridenbaugh SA, Kressig RW, Allain P, Herrmann FR, Beauchet O. Neurology. 2009 Sep 30. [Epub ahead of print] PMID: 19794127 doi:10.1212/WNL.0b013e3181beecd3 Conclusions: 25-Hydroxyvitamin D deficiency was associated with cognitive impairment in this cohort of community-dwelling older women.

NEW YORK (Reuters Health) - New research suggests that low vitamin D levels in the body are associated with thinking or "cognitive" impairments in older men, but whether vitamin D supplements can help is not yet known. In the study, an investigation of European men, subjects with low levels of vitamin D scored worse on a standard test of cognitive ability than did their peers with normal levels, Dr. David M. Lee, from the University of Manchester, UK, and co-researchers found. Although, the authors emphasize, the difference in scores was not that great.

Endothelial-Vasoprotective Effects of High-Density Lipoprotein Are Impaired in Patients With Type 2 Diabetes Mellitus but Are Improved After Extended-Release Niacin Therapy. Sorrentino SA, Besler C, Rohrer L, Meyer M, Heinrich K, Bahlmann FH, Mueller M, Horváth T, Doerries C, Heinemann M, Flemmer S, Markowski A, Manes C, Bahr MJ, Haller H, von Eckardstein A, Drexler H, Landmesser U. Circulation. 2009 Dec 21. [Epub ahead of print] PMID: 20026785 doi: 10.1161/CIRCULATIONAHA.108.836346 Conclusions-HDL from patients with type 2 diabetes mellitus and metabolic syndrome has substantially impaired endothelial-protective effects compared with HDL from healthy subjects. ER niacin therapy not only increases HDL plasma levels but markedly improves endothelial-protective functions of HDL in these patients, which is potentially more important.

Supplementation with trans10cis12-conjugated linoleic acid induces hyperproinsulinaemia in obese men: close association with impaired insulin sensitivity. Risérus U, Vessby B, Arner P, Zethelius B. Diabetologia. 2004 Jun;47(6):1016-9. Epub 2004 May 28. PMID: 15168020 DOI: 10.1007/s00125-004-1421-8 Conclusions/interpretation In obese men, t10c12CLA induces hyperproinsulinaemia that is related to impaired insulin sensitivity, independently of changes in insulin concentrations. These results are of clinical interest, as hyperproinsulinaemia predicts diabetes and cardiovascular disease. The use of weight-loss supplements containing this fatty acid is worrying.

Conjugated linoleic acid impairs endothelial function. Taylor JS, Williams SR, Rhys R, James P, Frenneaux MP. Arterioscler Thromb Vasc Biol. 2006 Feb;26(2):307-12. Epub 2005 Dec 8. PMID: 16339498 CONCLUSIONS: A CLA isomeric mixture had at most modest effects on adiposity and worsened endothelial function. On the basis of these results, the use of the isomeric mixture of CLA as an aid to weight loss cannot be recommended

Serum 25-Hydroxyvitamin D Concentration and Cognitive Impairment.\nLlewellyn DJ, Langa K, Lang I.\nJ Geriatr Psychiatry Neurol. 2009 Feb 4. [Epub ahead of print]\nPMID: 19073839 \ndoi:10.1177/0891988708327888\n

"Dec. 29, 2009 - The hot-selling herbal supplement ginkgo biloba doesn't slow age-related mental decline, a six-year clinical study shows. The study has already shown that ginkgo does not prevent dementia or Alzheimer's disease in the elderly. Now study leader Steven T. DeKosky, MD, and colleagues have sifted through the data to look for some sign that ginkgo might slow mental decline in healthy, aging individuals -- or, perhaps, in those already showing the first signs of cognitive impairment. No such sign was found. "Compared with placebo, the use of Ginkgo biloba, 120 mg twice daily, did not result in less cognitive decline in older adults with normal cognition or with mild cognitive impairment," the researchers conclude."

Fish oil-fed mice have impaired resistance to influenza infection. Schwerbrock NM, Karlsson EA, Shi Q, Sheridan PA, Beck MA. J Nutr. 2009 Aug;139(8):1588-94. Epub 2009 Jun 23. PMID: 19549756 doi:10.3945/jn.109.108027 These results suggest that the antiinflammatory properties of fish oil feeding can alter the immune response to influenza infection, resulting in increased morbidity and mortality.

"Hypovitaminosis D is a deficiency of Vitamin D. It can result from: inadequate intake coupled with inadequate sunlight exposure (in particular sunlight with adequate ultra violet B rays), disorders that limit its absorption, conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders, or, rarely, by a number of hereditary disorders.[1] Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and contributes to osteoporosis.[1] Osteomalacia may also occur rarely as a side-effect of phenytoin use Hypovitaminosis D is typically diagnosed by measuring the concentration in blood of the compound 25-hydroxyvitamin D (calcidiol), which is a precursor to the active form 1,25-dihydroxyvitamin D (calcitriol).[6] One recent review has proposed the following four categories for hypovitaminosis D:[7] * Insufficient 50-100 nmol/L (20-40 ng/mL) * Mild 25-50 nmol/L (10-20 ng/mL) * Moderate 12.5-25.0 nmol/L (5-10 ng/mL) * Severe < 12.5 nmol/L (< 5 ng/mL) Note that 1.0 nmol/L = 0.4 ng/mL for this compound.[8] Other authors have suggested that a 25-hydroxyvitamin D level of 75-80 nmol/L (30-32 ng/mL) may be sufficient

PLYMOUTH medical researchers have discovered a link between lack of the 'sunshine vitamin' and the onset of dementia.\n\nTeams from the city's Peninsula Medical School and the universities of Cambridge and Michigan have for the first time found a relationship between lower Vitamin D levels and cognitive impairment in older people.\n\nThe results of their large-scale study are to be published in the Journal of Geriatric Psychology and Neurology.

Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression. Li Y, Liu L, Tollefsbol TO. FASEB J. 2009 Dec 17. [Epub ahead of print] PMID: 20019239 doi: 10.1096/fj.09-149328 Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction. However, the precise molecular mechanisms leading to different responses to glucose restriction between normal and cancer cells are not fully understood. We analyzed normal WI-38 and immortalized WI-38/S fetal lung fibroblasts and found that glucose restriction resulted in growth inhibition and apoptosis in WI-38/S cells, whereas it induced lifespan extension in WI-38 cells. Moreover, in WI-38/S cells glucose restriction decreased expression of hTERT (human telomerase reverse transcriptase) and increased expression of p16(INK4a). Opposite effects were found in the gene expression of hTERT and p16 in WI-38 cells in response to glucose restriction. The altered gene expression was partly due to glucose restriction-induced DNA methylation changes and chromatin remodeling of the hTERT and p16 promoters in normal and immortalized WI-38 cells. Furthermore, glucose restriction resulted in altered hTERT and p16 expression in response to epigenetic regulators in WI-38 rather than WI-38/S cells, suggesting that energy stress-induced differential epigenetic regulation may lead to different cellular fates in normal and precancerous cells. Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.

"One of the surprises over the past year has been all the research regarding Vitamin D and brain health. Give that many people are spending less time outdoors and more time in front of their computers, we all should be concerned, as Vitamin D comes in part from our exposure to the sun. Low Vitamin D levels have been associated with pain, depression, MS, cancer and now perhaps even dementia. Here are the results of a new study that should cause all of us to pay attention. I frequently check the Vitamin D levels in my patients and frrequently see that they are below the optimal level. Get your levels checked if you have any of these concerns. A new large-scale senior population study has found that a lack of vitamin D in the elderly could be linked to cognitive impairment. The study, conducted on almost 2,000 adults over the age of 65, is the first of its scale to identify this relationship, and prompted researchers to suggest vitamin D supplementation as a possible means of reducing the risk of dementia. "

March 6, 2009 -- Social drinking seems to impair older people more than their younger drinking buddies. Also, older people are less likely to realize how the alcohol is affecting them, according to a new study.

Supplementation with cholecalciferol does not improve glycaemic control in diabetic subjects with normal serum 25-hydroxyvitamin D levels. Jorde R, Figenschau Y. Eur J Nutr. 2009 Apr 16. [Epub ahead of print] PMID: 19370371 10.1007/s00394-009-0020-3 Conclusions We were not able to demonstrate that vitamin D supplementation had a significant effect on glucose metabolism in subjects with type 2 diabetes but without vitamin D deficiency. Further studies are needed in larger groups of subjects with type 2 diabetes or impaired glucose tolerance, who also exhibit low serum 25-hydroxyvitamin D levels.

Simultaneously Blocking Glycolysis and Fat Metabolism Can the use of DCA and a fatty acid metabolism blocker together force more cancer cells into using aerobic metabolism? Tim McGough used green tea extract, which contains EGCG, in his fantastic response. DCA works by reactivating mitochondria and shifts metabolism from glycolysis to glucose oxidation. Hopefully the cancer cell will then undergo apoptosis. However, cancer cells have an alternate energy source: fat metabolism. This page explores to possibility of blocking fat metabolism to help force the cell into apoptosis. Oral squamous cell carcinoma is a cancer that does not respond well to DCA. This study, Head and Neck Cancer Cell Lines Are Resistant to Mitochondrial-Depolarization-Induced Apoptosis states: "Results: ΔΨm in head and neck cell lines started to show slight loss of ΔΨm, while HL-60 showed significant loss of ΔΨm after 30 min of treatment. All cell lines demonstrated complete mitochondrial depolarization within 24 h, however, only the control cell line HL-60 underwent apoptosis. In addition, HNSCC cell lines did not demonstrate cytoplasmic cytochrome c release despite significant mitochondrial membrane depolarization, while HL-60 cell initiated apoptosis and cytochcrome c release after 24 h of treatment. Conclusions: Head and neck cancer cell lines exhibit defects in mitochondrial-membrane-depolarization-induced apoptosis as well as impaired release of cytochrome c despite significant mitochondrial membrane depolarization. Proximal defects in the mitochondrial apoptosis pathway are a feature of HNSCC.(head and neck squamous cell carcinoma)" Note that although the cell lines were depolarized, apoptosis did not occur. So I checked to see if fatty acid metabolism is used by squamous cell carcinoma.

The human brain has high energy and nutrient needs. Changes in energy or nutrient intake can alter both brain chemistry and the functioning of nerves in the brain. Intake of energy and several different nutrients affect levels of chemicals in the brain called neurotransmitters. Neurotransmitters transmit nerve impulses from one nerve cell to another, and they influence mood, sleep patterns, and thinking. Deficiencies or excesses of certain vitamins or minerals can damage nerves in the brain, causing changes in memory, limiting problem-solving ability, and impairing brain function.

A new study in animals demonstrates that a diet rich in coconut oil protects against 'insulin resistance' (an impaired ability of cells to respond to insulin) in muscle and fat. The diet also avoids the accumulation of body fat caused by other high fat diets of similar calorie content. Together these findings are important because obesity and insulin resistance are major factors leading to the development of Type 2 diabetes. "

"Quality of HDL differs in diabetics but improves with niacin therapy December 22, 2009 | Michael O'Riordan Hannover, Germany - A small study published this week hints that the effects of HDL cholesterol differ in healthy patients from those with diabetes mellitus [1]. HDL cholesterol in individuals with diabetes has impaired endothelial protective functions compared with the HDL from healthy subjects, although treatment with extended-release niacin can improve these endothelial protective effects, according to researchers. Publishing their findings online December 21, 2009 in Circulation, lead investigator Dr Sajoscha Sorrentino (Hannover Medical School, Germany) and colleagues write that because recent HDL-raising intervention studies have yielded mixed results, "circulating HDL-cholesterol levels alone likely do not represent an adequate measure of therapeutic efficacy, and indexes of HDL functionality are urgently needed for assessment of the potential of HDL-targeted therapies to exert vasoprotective effects." Speaking with heartwire, senior investigator Dr Ulf Landmesser (University of Zürich, Switzerland), said the results have implications for clinical research. "We have to understand that we can't look only at the HDL levels in the plasma, but we need to look at the quality," he said. "The quality of the HDL is not the same in different patients. This is very important for targeting HDL as a treatment. Second, niacin therapy is a promising way not only to raise HDL but also to improve the quality; it is a good treatment option, especially if the larger outcomes data are positive.""