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"ScienceDaily (Dec. 26, 2009) - Going back for a second dessert after your holiday meal might not be the best strategy for living a long, cancer-free life say researchers from the University of Alabama at Birmingham. That's because they've shown exactly how restricted calorie diets -- specifically in the form of restricted glucose -- help human cells live longer. They found that the normal cells lived longer, and many of the precancerous cells died, when given less glucose. Gene activity was also measured under these same conditions. The reduced glucose caused normal cells to have a higher activity of the gene that dictates the level of telomerase, an enzyme that extends their lifespan and lower activity of a gene (p16) that slows their growth. Epigenetic effects (effects not due to gene mutations) were found to be a major cause in changing the activity of these genes as they reacted to decreased glucose levels. "Western science is on the cusp of developing a pharmaceutical fountain of youth" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This study confirms that we are on the path to persuading human cells to let us to live longer, and perhaps cancer-free, lives.""

"I know what you may be thinking: "Fish oil?! I thought fish oil was supposed to be healthy! One day you say we should take it, now you're saying it puts us at risk for Swine Flu?" Well, there is a reasonable answer, but it doesn't come in the form of a simple "fish oil is good" or "fish oil is bad" kind of package. The truth is that eating fish and taking fish oil is very often extremely beneficial for a great number of health conditions. But there is no substance on Earth that is 100% healthy under every conceivable circumstance. Take water, for example. Drinking plenty of pure water is a healthful practice. On the other hand, drinking excessive amounts (water intoxication) can lead to serious bodily damage and even death. The August issue of the Journal of Nutrition reports on a study conducted on two groups of mice fed either a fish oil or corn oil enriched diet. (4) All the mice were infected with the flu virus and were then examined over a two week period. Several interesting observations were made at the conclusion of the trial: * The mice receiving the fish oil exhibited lower levels of lung tissue inflammation. This confirms the known anti-inflammatory activity of omega-3 fatty acids found in fish. * However, these same mice suffered a "40% higher mortality rate", a "70% higher lung viral load" and "a prolonged recovery period following infection". * The researchers also noted a decline in NK (natural killer) cells in the spleens of the mice that were fed fish oil and a decrease in CD8+ T cells. NK cells and cytotoxic T cells are vital players in the body's ability to deal with infections."

Phosphatidylserine (PS) is a phospholipid that is found in all cells, but is most highly concentrated in the walls (membranes) of brain cells, making up about 70% of its nerve tissue mass. There it aids in the storage, release and activity of many vital neurotransmitters and their receptors. Phosphatidylserine also aids in cell-to-cell communication.

Phosphatidylserine (abbreviated Ptd-L-Ser, or PS) is a phospholipid component, usually kept on the inner-leaflet, the cytosolic side, of cell membranes by an enzyme called flippase. When a cell undergoes apoptotic cell death phosphatidylserine is no longer restricted to the cytosolic part of the membrane, but becomes exposed on the surface of the cell. First pilot studies indicate that PS supplementation might be beneficial for children with attention-deficit hyperactivity disorder PS can be found in meat fish, but is most abundant in the brain and in innards such as liver and kidney. Only small amounts of PS can be found in dairy products or in vegetables, with the exception of white beans.

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.

DHA and EPA generally modulated different sets of genes, although a few common effects were noted. In our approach, we used preneoplastic adenoma cells which are a relevant model for target cells of chemoprevention. If verified with real time PCR, these results identify genes and targets for chemoprevention of colon cancer. Modulation of gene expression in eicosapentaenoic acid and docosahexaenoic acid treated human colon adenoma cells. Habermann N, Lund EK, Pool-Zobel BL, Glei M. Genes Nutr. 2009 Mar;4(1):73-6. Epub 2009 Feb 21. PMID: 19234733 doi: 10.1007/s12263-009-0112-y.

It was concluded that omega-3 fatty acid could inhibit the proliferation of pancreatic cancer cell line SW1990 cells and promote their apoptosis. The down-regulation of the cyclin E expression by omega-3 fatty acid might be one of the mechanisms for its anti-tumor effect on pancreatic cancer. Modulatory effects of EPA and DHA on proliferation and apoptosis of pancreatic cancer cells. Zhang W, Long Y, Zhang J, Wang C. J Huazhong Univ Sci Technolog Med Sci. 2007 Oct;27(5):547-50. PMID: 18060632

A recently published study in Nutrition and Cancer (60(5), 643-651) by researchers at Kansai Medical University in Osaka, Japan has shown that AHCC (Active Hexose Correlated Compound) enhances immune function by increasing the number of dendritic cells (DCs). DCs are a key part of the immune system responsible for presenting foreign substances to other immune system cells. The study was conducted in a double-blind randomized fashion where twenty-one healthy subjects received a placebo or AHCC at 3.0 g/day for 4 weeks. Blood samples were obtained and measured at baseline and at 4 weeks. The number of circulating types of DCs was measured which included CD 11c+ DCs (myeloid DC population; DC1) and CD11c- DCs (lymphoid DC population; DC2). Other parameters measured included mixed-leukocyte reaction (MLR), natural killer (NK) cell activity, the proliferative response of T lymphocytes toward mitogen (phytohemagglutinin [PHA]) and cytokine production of interleukin (IL)-2, IL-4, IL-6, IL-10, interferon gamma-gamma, and (alpha)-tumor necrosis factor.

Berberine inhibits human tongue squamous carcinoma cancer tumor growth in a murine xenograft model. Ho YT, Yang JS, Lu CC, Chiang JH, Li TC, Lin JJ, Lai KC, Liao CL, Lin JG, Chung JG. Phytomedicine. 2009 Sep;16(9):887-90. Epub 2009 Mar 20. PMID: 19303753 Our primary studies showed that berberine induced apoptosis in human tongue cancer SCC-4 cells in vitro. But there is no report to show berberine inhibited SCC-4 cancer cells in vivo on a murine xenograft animal model. SCC-4 tumor cells were implanted into mice and groups of mice were treated with vehicle, berberine (10mg/kg of body weight) and doxorubicin (4mg/kg of body weight). The tested agents were injected once per four days intraperitoneally (i.p.), with treatment starting 4 weeks prior to cells inoculation. Treatment with 4mg/kg of doxorubicin or with 10mg/kg of berberine resulted in a reduction in tumor incidence. Tumor size in xenograft mice treated with 10mg/kg berberine was significantly smaller than that in the control group. Our findings indicated that berbeirne inhibits tumor growth in a xenograft animal model. Therefore, berberine may represent a tongue cancer preventive agent and can be used in clinic.

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"While research in lectinology is in its infancy this information is critical to your health and it is important to begin to understand lectins NOW. Read the following report carefully. I'll get specific about how this all applies to you. ALL foods contain lectins. Some are your friends, others neutral, and others may be your enemies. Know your lectins. Avoid your enemies. DEFINITION Protein or glycoprotein substances, usually of plant origin, of non-immunoglobulin nature, capable of specific recognition of and reversible binding to, carbohydrate moieties of complex glycoconjugates without altering the covalent structure of any of the recognized glycosyl ligands. This group includes monovalent lectins (i.e. bacterial and plant toxins). These lectins bind to sugar moieties in cell walls or membranes and thereby change the physiology of the membrane to cause agglutination, mitosis, or other biochemical changes in the cell. (agglutination- clumping; mitosis-multiplication or division of a cell forming two daughter cells) High levels of lectins (specialized proteins) may be found in grains (also known as cereals or pulses), legumes (that is 'beans' including peanuts), dairy and plants in the nightshade family. Many other foods contain lectins but are less well studied and the amounts of lectins present are not thought to be as high or as potentially toxic.!

Differential effects of selenium on benign and malignant prostate epithelial cells: stimulation of LNCaP cell growth by noncytotoxic, low selenite concentrations. Kandaş NO, Randolph C, Bosland MC. Nutr Cancer. 2009;61(2):251-64. PMID: 19235042

A signalling pathway that influences how sensitive cancer cells are to the beneficial effects of dietary restriction is described in this week's Nature. Dietary restriction - eating less calories while maintaining essential vitamins and minerals - can extend lifespan, and reduce cancer incidence and growth. But some types of cancer cell are more sensitive to the anti-growth effects of dietary restriction than others, Nada Kalaany and David Sabatini report. The effect hinges on the activity of the phosphatidylinositol-3-kinase (PI3K) pathway. If the pathway is active, dietary restriction has no effect on cancer cells. However, if the pathway is inactive, tumours are sensitive to dietary restriction.

The combination effects index (CI) analysis confirmed the synergy of clioquinol and clofibrate on inhibiting cancer cell viability. Using inhibitors to block PPARalpha signaling diminished the synergistic cytotoxicity of clioquinol and DHA. These results provide pharmacological evidence that the synergistic anticancer action of clioquinol and DHA is mediated by PPARalpha signaling in human cancer cells. PPARalpha signaling mediates the synergistic cytotoxicity of clioquinol and docosahexaenoic acid in human cancer cells. Tuller ER, Brock AL, Yu H, Lou JR, Benbrook DM, Ding WQ. Biochem Pharmacol. 2009 May 1;77(9):1480-6. Epub 2009 Feb 13. PMID: 19426685

These results suggest that combination chemotherapy (FO+Cur or Lim) may favorably modulate CD4+ T-cell-mediated inflammation.D ietary curcumin and limonin suppress CD4+ T-cell proliferation and interleukin-2 production in mice. Kim W, Fan YY, Smith R, Patil B, Jayaprakasha GK, McMurray DN, Chapkin RS. J Nutr. 2009 May;139(5):1042-8. Epub 2009 Mar 25. PMID: 19321585 doi:10.3945/jn.108.102772

Ginger inhibits cell growth and modulates angiogenic factors in ovarian cancer cells. Rhode J, Fogoros S, Zick S, Wahl H, Griffith KA, Huang J, Liu JR. BMC Complement Altern Med. 2007 Dec 20;7:44. PMID: 18096028 doi:10.1186/1472-6882-7-44

"ScienceDaily (Nov. 30, 2009) - Universitat Autònoma de Barcelona (UAB) researchers have confirmed that a diet rich in polyphenols and polyunsaturated fatty acids, patented as an LMN diet, helps boost the production of the brain's stem cells -neurogenesis- and strengthens their differentiation in different types of neuron cells. The research revealed that mice fed an LMN diet, when compared to those fed a control diet, have more cell proliferation in the two areas of the brain where neurogenesis is produced, the olfactory bulb and the hippocampus, both of which are greatly damaged in patients with Alzheimer's disease. These results give support to the hypothesis that a diet made up of foods rich in these antioxidant substances could delay the onset of this disease or even slow down its evolution. The study will be published in the December issue of the Journal of Alzheimer's Disease and was directed by Mercedes Unzeta, professor of the UAB Department of Biochemistry and Molecular Biology"

"Cancer lies dormant in all of us," he wrote in his new book, "Anticancer: A New Way of Life" (Viking, $25.95). "But our bodies are also equipped with a number of mechanisms that detect and keep such (defective) cells in check." Cancer rears its ugly head when things get out of balance, Servan-Schreiber said in an interview. And that can happen if the bad guys that promote the growth of cancer cells (tobacco, excessive alcohol, excessive sugar, hydrogenated fats, environmental pollutants) outnumber the good guys that support our natural defenses (cancer-fighting phytochemicals found in fruits, vegetables, herbs and teas; physical activity; and stress management techniques). But conventional treatment, while indispensable, focuses on a single target: destroying cancer cells. Doctors rarely address the other side: teaching patients how to fortify themselves using nutrition, exercise and stress-management techniques to create an inhospitable environment for cancer.

ScienceDaily (Feb. 22, 2009) - Cancer cells need a lot of nutrients to multiply and survive. While much is understood about how cancer cells use blood sugar to make energy, not much is known about how they get other nutrients. Now, researchers at the Johns Hopkins University School of Medicine have discovered how the Myc cancer-promoting gene uses microRNAs to control the use of glutamine, a major energy source. The results, which shed light on a new angle of cancer that might help scientists figure out a way to stop the disease, appear Feb. 15 online at Nature

Inhibitions of vascular endothelial growth factor expression and foam cell formation by EGb 761, a special extract of Ginkgo biloba, in oxidatively modified low-density lipoprotein-induced human THP-1 monocytes cells. Liu HJ, Wang XL, Zhang L, Qiu Y, Li TJ, Li R, Wu MC, Wei LX, Rui YC. Phytomedicine. 2009 Jan 7. [Epub ahead of print] PMID: 19135347