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Ginkgo has many alleged nootropic properties, and is mainly used as memory[25] and concentration enhancer, and anti-vertigo agent. However, studies differ about its efficacy. The largest and longest independent clinical trial to assess ginkgo biloba's ability to prevent memory loss has found that the supplement does not prevent or delay dementia or Alzheimer's disease.[26] Some controversy has arisen over the conclusions drawn by some studies that were allegedly funded by a firm which marketed Ginkgo.[27] In 2002, a long-anticipated paper appeared in JAMA (Journal of the American Medical Association) titled "Ginkgo for memory enhancement: a randomized controlled trial." This Williams College study, sponsored by the National Institute on Aging rather than Schwabe, examined the effects of ginkgo consumption on healthy volunteers older than 60. The conclusion, now cited in the National Institutes of Health's ginkgo fact sheet, said: "When taken following the manufacturer's instructions, ginkgo provides no measurable benefit in memory or related cognitive function to adults with healthy cognitive function." ... The impact of this seemingly damning assessment, however, was ameliorated by the almost simultaneous publication of a Schwabe-sponsored study in the less prestigious Human Psychopharmacology. This rival study, conducted at Jerry Falwell's Liberty University, was rejected by JAMA, and came to a very different-if not exactly sweeping-conclusion: There was ample evidence to support "the potential efficacy of Ginkgo biloba EGb 761 in enhancing certain neuropsychological/memory processes of cognitively intact older adults, 60 years of age and over." According to some studies, in a few cases, Ginkgo can significantly improve attention in healthy individuals.[28][29] Allegedly, the effect is almost immediate and reaches its peak in 2.5 hours after the intake.[30] [edit] In dementia A 2004 conference paper[31] summarizes how various trials indicate that Gi

August of this year, the BBC reported that the British Advertising Standards Authority attacked a vegetarian organization for making "alarmist" and "unsubstantiated" claims about the risks of eating meat. Headlines like "Vegetarian group slammed over advertising" splashed across the evening news. What "exaggerated" claims were targeted by the Agency? The vegetarian group claimed that meat-eaters were at increased risk of dying from heart disease and stroke, and that vegetarians lived longer than meateaters. How could the agency possibly find fault with such incontrovertible facts? Because, simply put, our "facts" aren't true. The latest science and the best science that we have that we have suggests that we vegetarians do not live longer than our meat-eating counterparts. The latest published results came out January, 2002 in a journal called Public Health Nutrition. Eight thousand vegetarians were followed for 18 years, and no survival advantage was found. Then April, 2002 the results of a study twice that size were released at the International Congress on Vegetarian Nutrition held at Loma Linda University. A study involving seventeen thousand vegetarians followed for about 9 years confirms the bad news-no survival advantage for vegetarians. Even more worrisome, both this huge studies found that vegetarians had an increased risk of dying from degenerative brain diseases

An ecologic study of dietary and solar ultraviolet-B links to breast carcinoma mortality rates. Grant WB. Cancer. 2002 Jan 1;94(1):272-81. PMID: 11815987 CONCLUSIONS It is hypothesized that animal products are associated with risk for breast carcinoma because they are associated with greater amounts of insulin-like growth factor-1and lifetime doses of estrogen. Vegetable products contain several risk reduction components including antioxidants and phytoestrogens. The association with latitude is very likely because of solar UV-B radiation and vitamin D. Alcohol modulates estrogen's effects on breasts. Fish intake is associated with risk reduction through vitamin D and n-3 oils. These results are consistent with those of many case-control and cohort studies but should be assessed in well designed cohort studies.

"Results of the first placebo-controlled, multicenter clinical trial of the compound coenzyme Q10 suggest that it can slow disease progression in patients with early-stage Parkinson's disease (PD). While the results must be confirmed in a larger study, they provide hope that this compound may ultimately provide a new way of treating PD. The phase II study, led by Clifford Shults, M.D., of the University of California, San Diego (UCSD) School of Medicine, looked at a total of 80 PD patients at 10 centers across the country to determine if coenzyme Q10 is safe and if it can slow the rate of functional decline. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS) and appears in the October 15, 2002, issue of the Archives of Neurology"

Estimation and fortification of vitamin D3 in pasteurized process cheese. Upreti P, Mistry VV, Warthesen JJ. J Dairy Sci. 2002 Dec;85(12):3173-81. PMID: 12512590 The objective of this study was to develop methods for the estimation and fortification of vitamin D3 in pasteurized Process cheese. Vitamin D3 was estimated using alkaline saponification at 70°C for 30 min, followed by extraction with petroleum ether:diethyl ether (90:10 vol/vol) and HPLC. The retention time for vitamin D3 was approximately 9 min. A standard curve with a correlation coefficient of 0.972 was prepared for quantification of vitamin D3 in unknown samples. In the second phase of the study, pasteurized Process cheeses fortified with commercial water- or fat-dispersible forms of vitamin D3 at a level of 100 IU per serving (28 g) were manufactured. There was no loss of vitamin D3 during Process cheese manufacture, and the vitamin was uniformly distributed. No losses of the vitamin occurred during storage of the fortified cheeses over a 9-mo period at 21 to 29°C and 4 to 6°C. There was an approximately 25 to 30% loss of the vitamin when cheeses were heated for 5 min in an oven maintained at 232°C. Added vitamin D3 did not impart any off flavors to the Process cheeses as determined by sensory analysis. There were no differences between the water- and fat-dispersible forms of the vitamin in the parameters measured in fortified cheeses

Sunlight and vitamin D: both good for cardiovascular health. Holick MF. J Gen Intern Med. 2002 Sep;17(9):733-5. PMID: 12220371 doi: 10.1046/j.1525-1497.2002.20731.x.

Evolutionary health promotion. Eaton SB, Strassman BI, Nesse RM, Neel JV, Ewald PW, Williams GC, Weder AB, Eaton SB 3rd, Lindeberg S, Konner MJ, Mysterud I, Cordain L. Prev Med. 2002 Feb;34(2):109-18. Review. PMID: 11817903 doi:10.1006/pmed.2001.0876

Mercury, fish oils, and the risk of myocardial infarction. Guallar E, Sanz-Gallardo MI, van't Veer P, Bode P, Aro A, Gómez-Aracena J, Kark JD, Riemersma RA, Martín-Moreno JM, Kok FJ; Heavy Metals and Myocardial Infarction Study Group. N Engl J Med. 2002 Nov 28;347(22):1747-54. PMID: 12456850 Conclusions The toenail mercury level was directly associated with the risk of myocardial infarction, and the adipose-tissue DHA level was inversely associated with the risk. High mercury content may diminish the cardioprotective effect of fish intake.

Estimation of the net acid load of the diet of ancestral preagricultural Homo sapiens and their hominid ancestors. Sebastian A, Frassetto LA, Sellmeyer DE, Merriam RL, Morris RC Jr. Am J Clin Nutr. 2002 Dec;76(6):1308-16. PMID: 12450898

Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA. 2002 Nov 27;288(20):2569-78. Review. PMID: 12444864 [PubMed - indexed for MEDLINE]

The 'carnivore connection'--evolutionary aspects of insulin resistance. Colagiuri S, Brand Miller J. Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S30-5. Review. PMID: 11965520

Maté: a risk factor for oral and oropharyngeal cancer. Goldenberg D. Oral Oncol. 2002 Oct;38(7):646-9. Review. PMID: 12167417

Amelioration of cisplatin induced nephrotoxicity in mice by ethyl acetate extract of a polypore fungus, Phellinus rimosus. Ajith TA, Jose N, Janardhanan KK. J Exp Clin Cancer Res. 2002 Jun;21(2):213-7. PMID: 12148580

Arginine: Clinical potential of a semi-essential amino. Appleton J. Altern Med Rev. 2002 Dec;7(6):512-22. Review. PMID: 12495375

Impact of fish oil enriched total parenteral nutrition on DNA synthesis, cytokine release and receptor expression by lymphocytes in the postoperative period. Schauder P, Röhn U, Schäfer G, Korff G, Schenk HD. Br J Nutr. 2002 Jan;87 Suppl 1:S103-10. PMID: 11895146 doi:10.1079/BJN2001463

Vieth R, Fraser D. Vitamin D insufficiency: no recommended dietary allowance exists for this nutrient. CMAJ. 2002 Jun 11;166(12):1541-2. PMID: 12074121 In fact, current recommendations for vitamin D are not designed to ensure anything. They are simply based on the old, default strategy for setting a nutritional guideline, which is to recommend an amount of nutrient similar to what healthy people are eating. This approach underlies the circular logic behind a familiar refrain about nutrition: "If you eat a good diet, you won't need supplements." By this logic, the answer to the question, "How much nutrient do you need?" is, "Whatever healthy people happen to be eating." The essential point, lost in the confusing terminology of modern nutrient recommendations, is that a recommended daily allowance (RDA) does not yet exist for vitamin D. Instead, the recommendations for it are referred to as "adequate intake" (AI).12,13 The AI for young adults (5 µg or 200 IU) was chosen to approximate twice the average vitamin D intake reported by 52 young women in a questionnaire-based study reported from Omaha, Neb., in 1997.13,14 Because the available evidence was acknowledged as weak, the Food and Nutrition Board of the US Institute of Medicine called its recommendation an AI.

Lin X, Gingrich JR, Bao W, Li J, Haroon ZA, Demark-Wahnefried W. Effect of flaxseed supplementation on prostatic carcinoma in transgenic mice. Urology. 2002 Nov;60(5):919-24. PMID: 12429338 [PubMed - indexed for MEDLINE]

The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, Volek JS. J Nutr. 2002 Jul;132(7):1879-85. PMID: 12097663

These data indicate that fish oil feeding downregulated the endogenous PPAR-activation system and increased antioxidant gene expressions to protect against ROS excess Fish oil feeding alters liver gene expressions to defend against PPARalpha activation and ROS production. Takahashi M, Tsuboyama-Kasaoka N, Nakatani T, Ishii M, Tsutsumi S, Aburatani H, Ezaki O. Am J Physiol Gastrointest Liver Physiol. 2002 Feb;282(2):G338-48. PMID: 11804856

Vitamin D poisoning by table sugar. Vieth R, Pinto TR, Reen BS, Wong MM. Lancet. 2002 Feb 23;359(9307):672. PMID: 11879864 doi:10.1016/S0140-6736(02)07814-5