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Serum 25-hydroxyvitamin D status of the US population: 1988-1994 compared with 2000-2004. Looker AC, Pfeiffer CM, Lacher DA, Schleicher RL, Picciano MF, Yetley EA. Am J Clin Nutr. 2008 Dec;88(6):1519-27. PMID: 19064511 doi:10.3945/ajcn.2008.26182 Conclusions: Overall, mean serum 25(OH)D was lower in 2000-2004 than 1988-1994. Assay changes unrelated to changes in vitamin D status accounted for much of the difference in most population groups. In an adult subgroup, combined changes in BMI, milk intake, and sun protection appeared to contribute to a real decline in vitamin D status. In summary, age-standardized mean serum 25(OH)D concentrations based on observed values were significantly lower in 2000-2004 than in 1988-1994 in all groups examined. Adjustment for assay changes noticeably reduced the difference between surveys. However, mean serum 25(OH)D concentrations remained significantly lower in males (except Mexican Americans) in NHANES 2000-2004 than in NHANES III, even after adjustment for assay differences. This remaining difference likely represents a real decline in vitamin D status. Changes in BMI, milk intake, and sun protection appeared to contribute to this decline in a subgroup of non-Hispanic white adults. The possibility that trends in overweight, sun protection, and milk intake may continue supports the need to continue monitoring the serum 25(OH)D status of the population

Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Ginde AA, Liu MC, Camargo CA Jr. Arch Intern Med. 2009 Mar 23;169(6):626-32. PMID: 19307527 Conclusions National data demonstrate a marked decrease in serum 25(OH)D levels from the 1988-1994 to the 2001-2004 NHANES data collections. Racial/ethnic differences have persisted and may have important implications for known health disparities. Current recommendations for vitamin D supplementation are inadequate to address the growing epidemic of vitamin D insufficiency.

Demographic differences and trends of vitamin D insufficiency in the US population, 1988-2004. Ginde AA, Liu MC, Camargo CA Jr. Arch Intern Med. 2009 Mar 23;169(6):626-32. PMID: 19307527 Conclusions National data demonstrate a marked decrease in serum 25(OH)D levels from the 1988-1994 to the 2001-2004 NHANES data collections. Racial/ethnic differences have persisted and may have important implications for known health disparities. Current recommendations for vitamin D supplementation are inadequate to address the growing epidemic of vitamin D insufficiency.

Matsuoka, L. Y., Wortsman, J., Hanifan, N. & Holick, M. F. (1988) Chronic sunscreen use decreases circulating concentrations of 25-hydroxyvitamin D: a preliminary study. Arch. Dermatol. 124:1802-1804

Fish oil and tocopherol-induced changes in natural killer cell-mediated cytotoxicity and PGE2 synthesis in young and old mice. Meydani SN, Yogeeswaran G, Liu S, Baskar S, Meydani M. J Nutr. 1988 Oct;118(10):1245-52. PMID: 3183771

Association between vitamin D and age-related macular degeneration in the Third National Health and Nutrition Examination Survey, 1988 through 1994. Parekh N, Chappell RJ, Millen AE, Albert DM, Mares JA. Arch Ophthalmol. 2007 May;125(5):661-9. PMID: 17502506

A few researchers are turning their attention to the sunshine vitamin as a culprit, prompted by the experience of immigrants that have moved from their equatorial country to two northern latitude locations As evidence of widespread vitamin D deficiency grows, some scientists are wondering whether the sunshine vitamin-once only considered important in bone health-may actually play a role in one of neurology's most vexing conditions: autism. The idea, although not yet tested or widely held, comes out of preliminary studies in Sweden and Minnesota. Last summer, Swedish researchers published a study in Developmental Medicine and Child Neurology that found the prevalence of autism and related disorders was three to four times higher among Somali immigrants than non-Somalis in Stockholm. The study reviewed the records of 2,437 children, born between 1988 and 1998 in Stockholm, in response to parents and teachers who had raised concerns about whether children with a Somali background were overrepresented in the total group of children with autism

The most common imbalance in the acid-base balance in the industrialized countries is mild chronic metabolic acidosis caused by the diet rich in the animal protein. Proteins are metabolized to organic acids. The typical American diet produces after metabolism approximately 100 meq of acid every day (Barzel 1995). This kind of a diet has been proved to cause aciduria and calciuria as a consequence of acidosis and thus a loss of total calcium of the body (Breslau et al. 1988, Schuette et al. 1980, Licata et al. 1981). Cola drinks that contain phosphoric acid are another acidosis-inducing ingredient of diet, especially among young people (Barzel 1995).

Dietary long-chain (n-3) fatty acids facilitate immune cell activation in sedentary, but not exercise-trained rats. Robinson LE, Field CJ. J Nutr. 1998 Mar;128(3):498-504. PMID: 9482755

Conversion of dietary phylloquinone to tissue menaquinone-4 in rats is not dependent on gut bacteria. Davidson RT, Foley AL, Engelke JA, Suttie JW. J Nutr. 1998 Feb;128(2):220-3. PMID: 9446847 These data offer conclusive proof that the tissue-specific formation of MK-4 from K is a metabolic transformation that does not require bacterial transformation to menadione as an intermediate in the process