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Any sudden change in normal bowel habits should be careful investigated.

Vitamin D deficiency is the cause of common obesity. Foss YJ. Med Hypotheses. 2009 Mar;72(3):314-21. Epub 2008 Dec 2. PMID: 19054627 doi:10.1016/j.mehy.2008.10.005 Common obesity and the metabolic syndrome may therefore result from an anomalous adaptive winter response. The stimulus for the winter response is proposed to be a fall in vitamin D. The synthesis of vitamin D is dependent upon the absorption of radiation in the ultraviolet-B range of sunlight. At ground level at mid-latitudes, UV-B radiation falls in the autumn and becomes negligible in winter. It has previously been proposed that vitamin D evolved in primitive organisms as a UV-B sensitive photoreceptor with the function of signaling changes in sunlight intensity. It is here proposed that a fall in vitamin D in the form of circulating calcidiol is the stimulus for the winter response, which consists of an accumulation of fat mass (obesity) and the induction of a winter metabolism (the metabolic syndrome). Vitamin D deficiency can account for the secular trends in the prevalence of obesity and for individual differences in its onset and severity. It may be possible to reverse the increasing prevalence of obesity by improving vitamin D status.

Are omega-3 fatty acids options for prevention and treatment of cognitive decline and dementia? Cederholm T, Palmblad J. Curr Opin Clin Nutr Metab Care. 2009 Dec 16. [Epub ahead of print] PMID: 20019606 PURPOSE OF REVIEW: To report recent data on the potential role of omega-3 fatty acids (n-3 FA) found in oily fish, especially docosahexaenoic acid (DHA), to prevent and treat cognitive decline and Alzheimer's disease. RECENT FINDINGS: Observational studies still provide conflicting results, in which the majority indicate beneficial effects on cognition, both when assessed as a continuous variable or as incident dementia, mainly Alzheimer's disease. Experimental studies have demonstrated potentially ameliorating effects of eicosapentaenoic acid (EPA) and DHA on amyloid fragment formation, signal transduction including upregulation of the apolipoprotein receptor SorLA, as well as on angiogenesis. The role of EPA and DHA metabolites on Alzheimer's disease pathology is under investigation. Recently, three randomized intervention studies, with duration up to 6 months have been reported. In contrast to a small study from Taiwan, no positive overall effects were reported from the Swedish OmegAD Study or from a Dutch study, although post hoc analyses indicate that selected individuals with mild forms of Alzheimer's disease or cognitive decline may respond to treatment. SUMMARY: No firm conclusions can be drawn. Based on epidemiological data, fish including oily fish could be advised as part of a balanced diet for public health purpose, although the evidence for better cognition is only fairly consistent. It is unlikely that n-3 FA will emerge as a treatment option in general for improving cognitive function in patients with Alzheimer's disease. n-3 FA, especially DHA, may turn out as an adjuvant therapy in selected cases. Further long-term intervention studies on individuals with mild cognitive reductions are awaite"

"Apigenin is described as a nonmutagenic bioflavonoid which is presented in leafy plants and vegetables (e.g., parsley, artichoke, basil, celery) and has significant chemopreventive activity against UV-radiation. Current research trials indicate that it may reduce DNA oxidative damage; inhibit the growth of human leukemia cells and induced these cells to differentiate; inhibit cancer cell signal transduction and induce apoptosis; act as an anti-inflammatory; and as an anti-spasmodic or spasmolytic. "

Vitamin D and calcium insufficiency-related chronic diseases: molecular and cellular pathophysiology. Peterlik M, Cross HS. Eur J Clin Nutr. 2009 Dec;63(12):1377-86. Epub 2009 Sep 2. PMID: 19724293 doi:10.1038/ejcn.2009.105 A compromised vitamin D status, characterized by low 25-hydroxyvitamin D (25-(OH)D) serum levels, and a nutritional calcium deficit are widely encountered in European and North American countries, independent of age or gender. Both conditions are linked to the pathogenesis of many degenerative, malignant, inflammatory and metabolic diseases. Studies on tissue-specific expression and activity of vitamin D metabolizing enzymes, 25-(OH)D-1alpha-hydroxylase and 25-(OH)D-24-hydroxylase, and of the extracellular calcium-sensing receptor (CaR) have led to the understanding of how, in non-renal tissues and cellular systems, locally produced 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and extracellular Ca2+ act jointly as key regulators of cellular proliferation, differentiation and function. Impairment of cooperative signalling from the 1,25-(OH)2D3-activated vitamin D receptor (VDR) and from the CaR in vitamin D and calcium insufficiency causes cellular dysfunction in many organs and biological systems, and, therefore, increases the risk of diseases, particularly of osteoporosis, colorectal and breast cancer, inflammatory bowel disease, insulin-dependent diabetes mellitus type I, metabolic syndrome, diabetes mellitus type II, hypertension and cardiovascular disease. Understanding the underlying molecular and cellular processes provides a rationale for advocating adequate intake of vitamin D and calcium in all populations, thereby preventing many chronic diseases worldwide.

"(NaturalNews) New research published in The Journal of the Federation of American Societies for Experimental Biology (FASEB) has found that the "Western" diet, typically high in sugar and fat, may be responsible for activating genes that signal the body to become fatter. According to scientists, the body's response to high amounts of energy-dense food is to activate the kappa opioid receptor which triggers increased fat storage. Researchers arrived at this conclusion by conducting an experiment on two groups of mice. One group had its kappa opioid receptors genetically deactivated while the other remained intact. Both groups were fed diets high in fat and sugar for 16 weeks. At the end of 16 weeks, the group with the deactivated receptor remained lean while the control group gained significant weight. Besides limiting their bodies' ability to store energy-dense food in their fat stores, the mice whose receptors had been deactivated were noted to also have a limited ability to assimilate and store nutrients from the foods they ingested. Traci Ann Czyzyk-Morgan, one of the study's researchers, indicated that the findings prove the hypothesis long held by many in the scientific community that the kappa opioid receptor may be responsible for causing widespread obesity in Western countries. She and others continue to encourage people to avoid diets high in fat and sugar. "

"Butyric acid (from Greek βούτυρος = butter), also known under the systematic name butanoic acid, is a carboxylic acid with the structural formula CH3CH2CH2-COOH. Salts and esters of butyric acid are known as butyrates or butanoates. Butyric acid is found in rancid butter, parmesan cheese, vomit, and body odor and has an unpleasant smell and acrid taste, with a sweetish aftertaste (similar to ether). It can be detected by mammals with good scent detection abilities (such as dogs) at 10 ppb, whereas humans can detect it in concentrations above 10 ppm. Butanoate is produced as end-product of a fermentation process solely performed by obligate anaerobic bacteria. Fermented Kombucha "tea" includes butyric acid as a result of the fermentation. This fermentation pathway was discovered by Louis Pasteur in 1861. The role of butyrate changes depending on its role in cancer or normal cells. This is known as the "butyrate paradox". Butyrate inhibits colonic tumor cells but promotes healthy colonic epithelial cells.[1], but the signaling mechanism is not well understood.[2]. A review suggested that the chemopreventive benefits of butanoate depend in part on amount, time of exposure with respect to the tumorigenic process, and the type of fat in the diet.[5] Low carbohydrate diets like the Atkins diet are known to reduce the amount of butanoate produced in the colon

Berberine suppresses in vitro migration and invasion of human SCC-4 tongue squamous cancer cells through the inhibitions of FAK, IKK, NF-kappaB, u-PA and MMP-2 and -9. Ho YT, Yang JS, Li TC, Lin JJ, Lin JG, Lai KC, Ma CY, Wood WG, Chung JG. Cancer Lett. 2009 Jul 8;279(2):155-62. Epub 2009 Feb 28. PMID: 19251361 doi:10.1016/j.canlet.2009.01.033 There is increasing evidence that urokinase-type plasminogen activator (u-PA) and matrix metalloproteinases (MMPs) play an important role in cancer metastasis and angiogenesis. Inhibition of u-PA and MMPs could suppress migration and invasion of cancer cells. Berberine, one of the main constituents of the plant Rhizoma coptidis, is a type of isoquinoline alkaloid, reported to have anti-cancer effects in different human cancer cell lines. There is however, no available information on effects of berberine on migration and invasion of human tongue cancer cells. Here, we report that berberine inhibited migration and invasion of human SCC-4 tongue squamous carcinoma cells. This action was mediated by the p-JNK, p-ERK, p-p38, IκK and NF-κB signaling pathways resulting in inhibition of MMP-2 and -9 in human SCC-4 tongue squamous carcinoma cells. Our Western blowing analysis also showed that berberine inhibited the levels of urokinase-plasminogen activator (u-PA). These results suggest that berberine down-regulates u-PA, MMP-2 and -9 expressions in SCC-4 cells through the FAK, IKK and NF-κB mediated pathways and a novel function of berberine is to inhibit the invasive capacity of malignant cells.

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Ever had cravings... also known as the munchies? Your body keeps sending hunger signals so you then keep eating as you feel hungry. Many of you satisfy those cravings with unhealthy foods like sweets or bad carbs. This can not only pile on the weight, but also give you little to no nutritional value making you feel sluggish. Most if not all cravings can be traced back to a nutritional deficiency. By eating a healthy diet most cravings will stop over time...

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Serve your food from smaller plates and bowls. A three ounce serving on a 12-inch plate looks small, but the same serving on a 10-inch plate looks larger. 2. Sleep at least 7 hours a erferes with these signals. 3. Walk, Jog, Bike or Run Whichever exercise(s) you choose, exercise smart instead of hard.

WEST LAFAYETTE, Ind. - Researchers have uncovered new evidence suggesting factors other than genes could cause obesity, finding that genetically identical cells store widely differing amounts of fat depending on subtle variations in how cells process insulin. Learning the precise mechanism responsible for fat storage in cells could lead to methods for controlling obesity. "Insights from our study also will be important for understanding the precise roles of insulin in obesity or Type II diabetes, and to the design of effective intervention strategies," said Ji-Xin Cheng, an assistant professor in Purdue University's Weldon School of Biomedical Engineering and Department of Chemistry. Findings indicate that the faster a cell processes insulin, the more fat it stores.

A Role of DNA-PK for the Metabolic Gene Regulation in Response to Insulin Roger H.F. Wong, Inhwan Chang, Carolyn S.S. Hudak, Suzanne Hyun, Hiu-Yee Kwan, Hei Sook Sul Cell 20 March, 2009 Volume 136, Issue 6, p1056 doi:10.1016/j.cell.2008.12.040    

Researchers at the University of California, Berkeley, have identified a gene that plays a critical regulatory role in the process of converting dietary carbohydrates to fat. In a new study, they disabled this gene in mice, which consequently had lower levels of body fat than their normal counterparts, despite being fed the equivalent of an all-you-can-eat pasta buffet. The authors of the study, to be published in the March 20 issue of the journal Cell, say the gene, called DNA-PK, could potentially play a role in the prevention of obesity related to the over-consumption of high-carbohydrate foods, such as pasta, rice, soda and sugary snacks..