Bob, Vitamin D supplements may well help with Lupus as it does with MS and Chron's disease.
Ivan. SUMMARY An abundance of scientific evidence indicates that vitamin D deficiency is associated with MS onset and progression. Such evidence includes epidemiology which demonstrates that high prevalence rates of MS closely track areas of low intake of vitamin D. Animal experiments reveal that vitamin D hormone can suppress a variety of animal autoimmune diseases including EAE, the animal equivalent of MS. Furthermore, associated immunological studies have shown that vitamin D hormone has a number of immunomodulating functions, all of which contribute to the suppression of inflammatory autoimmune reactions. Small clinical trials have suggested that vitamin D has some efficacy in slowing autoimmune disease progression although no properly controlled trials have been conducted. Vitamin D can be readily attained from exposure to sunlight and studies have shown that the optimal intake of vitamin D is about 4000- 6000 IU a day. This results in a circulation concentration of 25(OH)D ( a vitamin D metabolite) of 100-125 nmol/litre and this level seems to be required for the proper functioning of all vitamin D-dependent systems. In colder, low sunlight areas such an intake from the sun is impossible for most of the year and it is important to use supplements to makeup the shortfall in vitamin D supply. Currently suggested supplement levels of 200-400 IU are much too low. A daily supplement of 4000 IU of vitamin D3 seems warranted for people who do not get a lot of exposure to sunlight throughout the year. This amount is well below the no observed adverse effect level which is conservatively placed at 10000 IU/day and thus such supplementation is safe for anyone who is not hypersensitive to vitamin D. Throughout most of the two million years of human development, humans had a relatively high intake of vitamin D (~5000-10,000 IU/day) from the sun. Major environmental changes brought on by the agricultural, industrial and technological revolutions have resulted in large populations in northern climates experiencing a subclinical and chronic vitamin D deficiency and this deficiency is more pronounced in persons with MS. Vitamin D deficiency is just one of a number of nutrient-related factors which play a role in MS. Notably the dietary regimens which contain the most pro-inflammatory food types (e.g. gluten, dairy, saturated fat) and the least anti-inflammatory nutrients ( vitamin D, omega 3 fats) occur in areas in which MS and other autoimmune diseases are most common. To combat MS, a person must change their lifestyle with diet revision being perhaps the most useful modification. As part of this change, it is important to ensure that sufficient vitamin D (4000 IU/day) is acquired through sun exposure and supplements. **Full article and references to be found at: http://www.direct-ms.org/vitamind.html Vitamin D and the Risk of Developing Multiple Sclerosis for British and Irish Migrants to Australia Ashton F. Embry, Ph.D., Reinhold Vieth, Ph.D. and Colleen Hayes, Ph.D. Hammond et al. (2000) recently documented that British and Irish immigrants to Queensland, Australia, situated at latitude 120-280, had a striking 75% reduction in their risk of developing multiple sclerosis (MS) when compared with that of their native countrymen. Importantly, this reduction affected both adult and child immigrants. Furthermore, using migration data from the other Australian provinces, they elegantly demonstrated that the reduction in MS risk for the relatively genetically homogeneous British and Irish immigrants progressively lessened with increasing latitude, finally reaching zero risk reduction in the Hobart area of Tasmania, the highest latitude area (420) of Australia. These results, which overcome weaknesses in previous migration study designs (Gale and Martyn 1995), provide the strongest evidence to date that an environmental factor, which protects both adults and children against the development of MS, is abundant in Queensland at latitude 120-280, but lacking in Tasmania at latitude 420 **Full article at: http://www.direct-ms.org/british.html Drug interactions and vitamin D, should any one be interested: http://clinical.caregroup.org/altmed/interactions/Nutrients/Vitamin_D.htm Vitamin D Deficiency and Bowel Diseases Connected April 18, 2000 San Diego, Calif. --- Research with mice at Penn State has demonstrated a connection between vitamin D deficiency and two bowel diseases that occur in one out of every 1,000 people in North America and Europe. Dr. Margherita T. Cantorna, assistant professor of nutrition and director of the research project, says "Our experiments show that vitamin D deficiency worsens the symptoms of Chrons disease and ulcerative colitis. Treatment with Vitamin D for as little as two weeks lessens the symptoms of these inflammatory bowel diseases in mice." **Full article: http://www.psu.edu/ur/2000/vitamind.html **An interesting piece: http://westonaprice.org/Nutr_D.html **And finally a rather long article which details vitamin D effects on bones. (I would have posted the link but it is a MedLine retrieval) Dietary and Nutritional Influences on Skeletal Health A Review of Current Knowledge and Future Perspectives Susan A. New, PhD The role of dietary intake and nutritional status on skeletal health, in the earlier and later years of the life cycle, remains to be fully quantified. As a "modifiable" lifestyle factor, influencing both peak bone mass development in the younger population and the rate of bone loss in older age groups, it is an area of considerable public health concern.[1] A number of key papers were presented at the 22nd Annual General Meeting of the American Society for Bone and Mineral Research held in Toronto, Canada (September 22-26, 2000), on nutrition and bone health. Evidence of Vitamin D "Insufficiency" Among Population Groups: Consequences for Bone Health Vitamin D is derived from 2 sources, namely endogenous (skin) and exogenous (diet), with the major source being the exposure of skin to the ultraviolet B-rays contained in sunlight.[2] The action of sunlight on the skin converts 7-dehydrocholesterol to previtamin D, which is then metabolized to vitamin D by a temperature-dependent isomerization. The vitamin D is transported, via the general circulation, to the liver, where the enzyme 25-hydroxylase converts it to 25-hydroxyvitamin D (25-[OH]D). Further conversion to 1,25 (OH)2D3 occurs in the kidney. 25-OHD is the main circulating vitamin D metabolite and is the best indicator of clinical status, whereas 1,25 OH2D3 is the active form of the vitamin, which is involved in calcium homeostasis.[3] The amount and strength of ultraviolet light is known to vary with both latitude and season; thus, differences have been reported to be lower in the winter and to vary with different geographic areas worldwide. However, the variation, globally, of vitamin D status and the clinical diagnosis of vitamin D deficiency remains unclarified because of the large interlaboratory differences in assays for serum 25-(OH)D. Of considerable interest in the area of vitamin D research were the findings of a global study of vitamin D status and parathyroid function in postmenopausal women with osteoporosis presented by Lips and colleagues,[4] on behalf of the MORE [Multiple Outcomes of Raloxifene Evaluation] Study Group. Data were collected from the international MORE trial, a large prospective clinical intervention trial. Baseline data on serum 25-(OH)D and serum parathyroid hormone (PTH), obtained from 7564 postmenopausal women, were analyzed. These women were from 25 countries spanning 5 continents. Serum 25-(OH)D was found to be lower than 25nmol/L (the lower level of the normal range) in 4.1% of all women in the MORE study (with 8.3% of women coming from Southern Europe). Bone mineral density (BMD) was found to be 4% lower in women with serum 25(OH)D below 25nmol/L. The results also suggested that women with low vitamin D levels (< 25 nmol/L) had 30% higher serum PTH values and higher levels of alkaline phosphatase (a marker of bone formation). Vitamin D status is affected by the aging process, and there is now evidence in the literature to show that vitamin D levels: (1) fall with age,[5] (2) have a seasonal variation (being lowest in the fall/winter),[6] and (3); are inversely related to PTH[7] (which is also known to have a seasonal variation).[8] Menopausal bone loss has been shown to be partially regulated by dietary intake of vitamin D.[9] The elderly population is of considerable concern with respect to the nutritional status of vitamin D, and there is now good data to suggest that this is a group who is at considerable risk of vitamin D "insufficiency/deficiency."[10] Despite several key published studies which show convincingly that vitamin D supplementation (with calcium) reduces fracture rates in institutionalized[11] and free-living elderly populations[12] and improves calcium absorption, lowers PTH levels, and reduces wintertime bone loss in postmenopausal women,[13] there is still a considerable lack of awareness of this public health nutrition message. In an interesting paper presented by Grados and colleagues,[14] supplementation with 500 mg of calcium and 400 IU of vitamin D3, twice a day for 12 months in a group of 95 elderly women with vitamin D insufficiency (mean age, 74.2 years +/- 6.4 years) resulted in (1) significant increases in BMD at the femoral neck, femoral trochanter, and whole body sites and (2) significant alterations in bone remodeling. Krall and colleagues[15] presented data from a study examining the use of calcium and vitamin D supplements on oral health in elderly women. There is evidence to suggest that oral bone loss and tooth loss are associated with bone loss at non-oral sites, but few studies have analyzed the effect of these nutrients in reducing tooth loss. Supplement use was significantly associated with a decrease in tooth loss risk in 145 subjects (62 men and 83 women) aged 65 years and older. This study has important implications for the health of the aging population because improvements in tooth retention will assist in reducing the risk of malnutrition in the elderly. This is a particularly pertinent point because it is well established that malnutrition is a characteristic of hip (and vertebral) fracture patients.[16] The effective level of UV energy decreases north to south because of the reduced zenith angle of the sun and because much of the UV in sunlight is absorbed by clouds, ozone, and other forms of atmospheric pollution. For example, in areas of Southern Europe, there is no UV radiation of the appropriate wavelength from the end of October to the end of March. Furthermore, for the remaining months of the year, 60% of the effective UV radiation is present between 11 AM and 3 PM.[17] Thus, adequate storage of vitamin D during the spring and summer months is essential. Although it is known that the vitamin D precursor (calciferol) of active vitamin D metabolites is stored in adipose tissue, no data exist on the storage of the active metabolites (calcidiol and calcitriol). Schroder and colleagues[18] presented findings using animal models in vivo, verifying that both calcidiol and calcitriol are stored in adipose tissue (which can in turn be released for target tissue uptake). It is well known that obesity is a protective factor for osteoporosis, which may be explained, in part, by the storage and release of active vitamin D metabolites in the adipose tissue. Vitamin D is vital for optimum growth and development in the younger population. Until recently, however, vitamin D deficiency was considered a problem only in those children from cultures where skin exposure to sunlight is limited. However, evidence is emerging that vitamin D "insufficiency" is more prevalent in children and adolescents than previously thought. Data presented by El-Hajj Fuleihan and colleagues[19] from a study of 169 adolescents aged 10-16 years revealed that 21% of the population had serum 25(OH)D below 10 ng/mL and 44% had values between 10 and 20 ng/mL during the winter months. Corresponding changes were also seen in PTH and biochemical markers of bone turnover, which in turn have important implications for optimal skeletal growth and maximum peak bone mass attainment. The effect of vitamin D3 supplementation on vitamin D levels in male adolescents was investigated by Guillemant and colleagues.[20] Serum 25-(OH)D in the placebo-treated group showed marked decreases from 61 +/- 15.5 nmol/L (September) to 20.2 +/- 0.5 nmol/L (March), which was mirrored by an increase in intact PTH (iPTH) compared with no significant changes in either 25-(OH)D or iPTH in the supplemented group. Furthermore, there is growing concern that atmospheric pollution, particularly in developing countries, may have important implications for the vitamin D status of population groups. In a paper presented by Puliyel and colleagues,[21] both 25-(OH)D and PTH were significantly different in children from high-pollution areas (HPA) compared with those from low-pollution areas (LPA). For example, serum 25-(OH)D: HPA 12.6 +/- 7 ng/mL vs LPA 28.2 +/- 7 ng/mL (P <.001); serum PTH: HPA 42.9 +/- 68 vs LPA 14.7 +/- 9 pg/mL (P < .01). The data presented on vitamin D status in children and adolescents have important implications for skeletal health and clearly suggest a need for consideration of vitamin D supplementation programs in certain younger population groups. Influence of Food Groups on Bone Health The approach consistently used to examine the relationship between nutrition and skeletal health has been to focus on specific (or a variety of) nutrients commonly consumed in the human diet. Although this has assisted in the understanding of specific nutrients (eg, calcium) and their effect on bone health, there are still considerable gaps in our knowledge. An alternative approach to elucidating this complexity is to consider the foods we consume rather than the nutrients contained within them.[22] Clearly, this is a sensible approach to investigating diet:disease relationships, because it is well known that the direct hedonic pleasure derived from food is an important determinant of food choice. Dietary data from the Framingham Offspring Study were presented by Tucker and colleagues.[23] Cluster analysis was performed on specific food groups, and iterative analyses enabled separation of participants into eating pattern groups, which were listed as (1) fruit, vegetables, milk, and cereal (termed the "Healthy Group"); (2) soda, pizza, and salty snacks; (3) cheese and other dairy; (4) meat, bread, and potatoes; (5) baked goods and sweets, and (6) alcohol. Bone mass in both males (n = 601) and females (n = 905) was significantly higher in the Healthy Group. The lowest bone mass was found in the meat group for men and in the soda/pizza/salty snacks group for women. These data support the findings of both the original older Framingham cohort[24] and the baseline analyses of the APOSS (Aberdeen Perimenopausal Osteoporosis Screening Study) population.[25,26] There is growing evidence of a positive link between fruit and vegetable consumption and bone health from population-based studies[24-29] as well as from the findings of the fruit and vegetable intervention trial (DASH - Dietary Approaches to Stopping Hypertension), which demonstrated a reduction of urinary calcium excretion from 157 mg/day to 110 mg/day when the daily serving of fruit and vegetable intake was increased from 3.6 mg/day to 9.5 mg/day.[30] The mechanisms behind this fruit and vegetable link point to the role that bone plays in acid-base balance.[31] The skeleton has been referred to as "a giant ion exchange column" loaded with "alkali buffer," because 80% of body carbonate, 80% of body citrate, and 35% of body sodium are contained in solution in the hydration shell of bone, and these substances are then released in response to metabolic acid.[32] Thus, it has been proposed that the bone loss that occurs with aging may be attributable, at least in part, to the life-long mobilization of skeletal salts to balance the endogenous acid generated from foods that are acid-producing.[33] The paper presented by Tucker and associates provides further evidence of a positive link between alkaline-forming foods and the skeleton. There is now an urgent need for population-based intervention trials using fruit and vegetables as the supplementation vehicle with a focus on measurement of indices of bone health (markers of bone metabolism/assessment of axial and peripheral skeletal sites). Calcium and the Skeleton There is considerable interest and indeed controversy regarding the role that calcium plays in both peak bone mass attainment and postmenopausal bone loss,[34,35] a debate that has been in force for well over a decade.[36,37] One important aspect that remains unclarified is the ideal vehicle for supplementation. Although calcium supplements alone are useful in quantifying the exact relationship of this single nutrient to skeletal health, from a public health nutrition policy perspective, they are often perceived as "medication." Milk and milk products are a useful, practical alternative. Supplementation with milk or milk-derived products has been shown to improve the nutritional quality of the diet to a much greater extent than calcium alone.[38] Furthermore, the additional protein contained in milk may have anabolic effects on bone via interactions with insulin-like growth factor 1 (IGF1).[39-41] Just published is the finding that milk basic protein directly suppresses osteoclast-mediated bone resorption, resulting in the prevention of bone loss in the animal model.[42] However, the consumption of dairy products is limited, particularly among young females, because of the perception that they may be high in fat, thus predisposing the individual to obesity. Data from a 7-year longitudinal field study on bone health of 258 white young females aged 11-18 years was presented by Badenhop-Stevens and colleagues[43] The data had been examined for differences in body composition between individuals with low and high dairy consumption at different ages. In the young women 18 years of age, no differences were found between the 2 consumption groups with respect to body composition, and no evidence existed of a higher rate of body fat accumulation in those individuals consuming larger amounts of dairy products. Furthermore, the data suggested that patterns of dairy consumption, once set, showed trends of maintainability, although subjects in the high dairy consumption group showed a slight decline in calcium intake over time. Work presented by Saxon and colleagues[44] examined the combined effect of exercise and calcium on bone mass in prepubertal and early pubertal girls. Results suggested a synergistic effect at important weight-bearing bone mass sites. For example, a total of 20 minutes of high-impact exercise (eg, jumping) 3 times a week, together with an additional 540 mg of calcium, resulted in an increase in bone mass. The effects of the exercise regimen and additional calcium supplementation worked independently and synergistically. Influence of Nutrient-Gene Interactions and Other Micronutrients on Bone Genetic factors have gained increasing prominence in the etiopathogenesis of osteoporosis, with the focus of attention on polymorphisms of the vitamin D receptor gene, collagen I alpha 1 receptor gene, and estrogen receptor gene. Public health strategies targeting dietary advice at those women with a genetic predisposition to low peak bone mass attainment or increased perimenopausal bone loss would clearly be a sensible approach, but more data are required. There is evidence in the literature that calcium absorption in older women is dependent on vitamin D receptor (VDR) genotype.[45] In a paper presented by Macdonald and colleagues,[46] calcium intake was found to be a determinant of BMD in perimenopausal and early postmenopausal women with bb VDR genotype but not those with BB genotype; this finding was exclusive to those women not taking exogenous estrogen. Little is known about the role of other micronutrients on bone, but clearly, as bone minerals, magnesium and phosphorus are important. Carpenter and colleagues[47] presented data from the NHANES III (National Health and Nutrition Examination Survey), the largest and most recent US nutrition and bone health database, on the association between intake of Mg and bone mass. Significant positive correlations were found between Mg intake in non-Hispanic white men and women and femoral neck bone mass at a variety of sites. These data support previous findings of other large population datasets[24-26] and emphasize further the importance of investigating the impact nutrients other than calcium have on skeletal integrity. Clinical Significance The clinical relevance of the papers presented and discussed at the 22nd Annual General Meeting of the ASBMR can be summarized as follows: Vitamin D insufficiency/deficiency remains a problem for the aging population and is a particular concern for those living in institutionalized homes. There is evidence that in many countries and regions, vitamin D cannot be synthesized in the winter and fall months, and there is a clear requirement for careful monitoring of the nutritional status of vitamin D (via measurement of serum 25-(OH)D) as well as PTH levels. There is a growing body of evidence that vitamin D insufficiency is more prevalent in children and adolescents than previously thought. Although there is a need for further research in this area, consideration of vitamin D supplementation programs in younger population groups is required. There is evidence to suggest that consumption of dairy products in amounts that are required to meet dietary calcium intake recommendations will not lead to obesity. High-impact exercise and increased calcium intake together appear to work synergistically on peak bone mass development in the younger population. Additional intervention trials in older age groups are required. Data presented at this conference provide further support of a positive link between fruit and vegetable intake and bone health. Although the exact mechanisms and the level of intake required for optimum bone status remain unclear, high intake of alkaline-forming foods may be helpful to bone health maintenance. Nutrient-gene interactions require further quantification, but data are emerging to suggest that it may be useful to target future nutrition advice to those individuals who are genetically more susceptible to poor bone health. References New SA. Bone health: the role of micronutrients. Br Med Bull. 1999;55:619-633. Loveridge N. Vitamin D (calciferols). The fat soluble vitamins. In: Garrow JS, James WPT, Ralph A, eds. Human Nutrition and Dietetics. 10th Ed. London: Churchill Livingstone.2000: 211-248. Gallagher JC. Vitamin D treatment in osteoporosis and osteomalacia. In: Stevenson JC, Lindsay R, eds. Osteoporosis. London: Chapman & Hall Medical. 1998; 243-262. Lips P, Duong R, Oleksik A, et al. A global study of vitamin D status and parathyroid function in postmenopausal women with osteoporosis: baseline data from the MORE trial [abstract]. J Bone Miner Res. 2000;15(suppl 1):S140. McKenna MJ, Freaney R, Meade A, Muldowney FP. Hypovitaminosis D and elevated serum alkaline phosphatase in elderly Irish people. Am J Clin Nutr. 1985;41:101-109. Davies M, Mawer EB, Hann JT, Taylor JL. Seasonal changes in the biochemical indices of vitamin D deficiency in the elderly: a comparison of people in residential homes, long stay wards and attending a day hospital. Age & Ageing. 1986;15:77-83. Khaw KT, Sneyd MJ, Compston J. Bone density, parathyroid hormone and 25 hydroxyvitamin D concentrations in middle aged women. Br Med J. 1992;305:273-277. Krall EA, Sahyoun N, Tannenbaum S, Dallal GE, Dawson-Hughes B. Effect of vitamin D intake on seasonal variations in parathyroid hormone secretion in postmenopausal women. N Engl J Med. 1989;321:1777-1783. Lukert BP, Higgins J, Stosopf M. Menopausal bone loss is partially regulated by dietary intake of vitamin D. Calcif Tissue Int. 1992;51:173-179. Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D insufficiency in an adult population. Osteoporos Int. 1997;7:439-443. Chapuy MC, Arlot ME, Duboeuf F, et al. Vitamin D and calcium to prevent hip fractures in elderly women. N Engl J Med. 1992;327:1637-1642. Dawson-Hughes B, Harris SS, Krall EA, Dallal GE. Effect of Ca and vitmain D supplementation on bone density in men and women aged 65 years and older. N Engl J Med. 1997;337:670-676. Dawson-Hughes B, Dallas GE, Krall EA, Harris S, Sokoll LJ, Kakoner C. Effect of vitamin D supplementation in wintertime and overall bone loss in healthy post-menopausal women. Ann Intern Med. 1991;115:505-512. Grados F, Brazier M, Kamel S, et al. Effect of vitamin D and Ca supplementation on bone mass and bone remodelling markers in ambulatory women with vitamin D insufficiency [abstract]. J Bone Miner Res. 2000;15(suppl 1):S316. Krall EA, Randall C, Harris SS, Garcia RI, Dawson-Hughes B. Calcium and vitamin D supplements reduce tooth loss in the elderly [abstract]. J Bone Miner Res. 2000;15(suppl 1):S191. Bunker VW, Laswon MS, Stansfield MF, Clayton BE. The intake and excretion of Ca, Mg and P in apparently healthy elderly people and those who are housebound. J Clin Exp Gerontol. 1989;11:71-86. Department of Health. Dietary References Values for Food Energy and Nutrients for the United Kingdom. Report on Health and Social Subjects: 41. London: HMSO; 1991. Schroder C, Segovis C, Barsony J. Active vitamin D metabolites are stored and released from the adipose tissue [abstract]. J Bone Miner Res. 2000;15(suppl 1):S316. El-Hajj Fuleihan GA, Nabulsi M, Shoucair M, Salamoun M, Hajj Shahine C. Hypovitaminosis D in healthy school children [abstract]. J Bone Miner Res. 2000;15(suppl 1):S572. Guillemant J, Allemandou A, Peres G, Guillemant SE. Wintertime vitamin D deficiency in male adolescents: response to vitamin D3 supplements [abstract]. J Bone Miner Res. 2000;15(suppl 1):S450. Pulliyel JM, Agarwal K, Upadhyay P, Mawer EB, Berry JL, Mughal Z. The impact of atmospheric pollution related haze on vitamin D status of two-year-olds in Delhi, India [abstract]. J Bone Miner Res. 2000;15(suppl 1):S356. New SA. Impact of food clusters. In: Burckhardt P, Dawson-Hughes B, Heaney RP, eds. Nutritional Aspects of Osteoporosis 2000. Proceedings of the 4th International Symposium on Nutritional Aspects of Osteoporosis, Switzerland, 2000. Rome, Italy: Ares-Serono Symposia Publications (in press). Tucker KL, Hannan MT, Chen H, McLean RR, Felson DT, Kiel DP. Diet patterns groups are related to bone mineral density (BMD) among adults: the Framingham Study [abstract]. J Bone Miner Res. 2000;15(suppl 1):S222. Tucker KL, Hannan MT, Chen H, Cupples A, Wilson PWF, Kiel DP. Potassium, magnesium and fruit and vegetables are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr. 1999;69:727-736. New SA, Bolton-Smith C, Grubb DA, Reid DM. Nutritional influences on bone mineral density: a cross-sectional study in premenopausal women. Am J Clin Nutr. 1997;65:1831-1839. New SA, Robins SP, Campbell MK, et al. Dietary influences on bone mass and bone metabolism: further evidence of a positive link between fruit and vegetable consumption and bone health? Am J Clin Nutr. 2000;71:142-151. New SA, Smith R, Foulds E, Reid DM. Association between present dietary intake and bone health in elderly Scottish men and women. Current research in osteoporosis and bone mineral measurement [abstract]. Presented at the 5th UK Conference on Osteoporosis. Ring EFJ, Elvins DM, Bhalla AK, eds. British Institute of Radiology. London. 1998; 3. Michaelsson K, Holmberg L, Maumin H, Wolk A, Bergstrom R, Ljunghall S. Diet, bone mass and osteocalcin: a cross-sectional study. Calcif Tissue Int. 1995;57:86-93. Eaton-Evans J, McIlrath EM, Jackson WE, Bradley P, Strain JJ. Dietary factors and vertebral bone density in perimenopausal women from a general medical practice in Northern Ireland. Proc Nutr Soc. 1993;52:44A. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. N Engl J Med. 1997;336:1117-1124. Bushinsky DA. Acid-base imbalance and the skeleton. In: Burckhardt P, Dawson-Hughes B, Heaney RP, eds. Nutritional Aspects of Osteoporosis '97. Proceedings of the 3rd International Symposium on Nutritional Aspects of Osteoporosis, Switzerland, 1997.Rome, Italy: Ares-Serono Symposia Publications; 1998: 208-217. Barzel US. The skeleton as an ion exchange system: implications for the role of acid-base imbalance in the genesis of osteoporosis. J Bone Miner Res. 1995;10:1431-1436. Wachman A, Bernstein DS. Diet and osteoporosis. Lancet. 1968;I:958-959. Heaney RP. There should be a dietary guideline for Ca. Am J Clin Nutr. 2000;71:658-670. Speaker BL. Should there be a dietary guideline for calcium intake? No. Am J Clin Nutr. 2000;71:661-664. Kanis J, Passmore R. Calcium supplementation of the diet I and II. Br Med J. BMJ. 1989;298:137-140, 205-208. Nordin BEC, Heaney RP. Calcium supplementation of the diet is justified by present evidence. BMJ. 1990;300:1056-1060. Devine A, Prince RL, Bell R. Nutritional effect of Ca supplementation by skim milk powder or Ca tablets on total nutrient intake in postmenopausal women. Am J Clin Nutr. 1996;64:731-737. Bonjour JP, Carrie AL, Ferrari A, Rizzoli R. Ca-enriched foods and bone mass growth in prepubertal girls: a randomized, double blind, placebo controlled trial. J Clin Invest. 1997;99:1287-1294. Chan GM, Hoffman K, McMurry M. Effects of dairy products on bone and body composition in pubertal girls. J Pediatr. 1995;126:551-556. Cadogan J, Eastell R, Jones N, Barker M. Milk intake and bone mineral acquisition in adolescent girls: randomised controlled intervention trial. BMJ. 1997;315:1255-1260. Toba Y, Takada Y, Yamamura J, et al. Milk basic protein: a novel protective function of milk against osteoporosis. Bone. 2000;27:403-408. Badenhop-Stevens NE, Landoll JD, Ha E, Matkovic V. Body composition changes and dietary calcium intake of young females over seven years [abstract]. J Bone Miner Res. 2000;15(suppl 1):S534. Saxon L, Iuliano-Burns S, Naughton G, Oliver D, Bass S. Exercise and increased dietary calcium intake: a synergistic effect at the loaded sites in pre and early pubertal girls [abstract]. J Bone Miner Res. 2000;15:S230. Dawson-Hughes B, Harris SS, Finneran S. Calcium absorption on high and low calcium intakes in relation to vitamin D receptor genotype. J Clin Endocrinol Metab. 1995;80:3657-3661. Macdonald HM, New SA, McGuigan FE, et al. Femoral neck bone loss and dietary Ca intake in peri and early post-menopausal Scottish women: an association dependent on VDR geneotype [abstract]. J Bone Miner Res. 2000;15(suppl 1):S202. Carpenter TO, Barton CN, Park YK. Usual dietary magnesium intake in NHANES III is associated with femoral bone mass [abstract]. J Bone Miner Res. 2000;15:S292. > -----Original Message----- > From: Robert L. Berger [mailto:bober...@swbell.net] > Sent: Saturday, 14 July 2001 02:24 > To: Silver-list; k...@kenashley.com; William Ashley Jr. > Subject: CS>Lupus help needed!! > > > Greetings Ya'all. > > Does anyone have information as to the safety of using CS when a person > has Lupus?? > > The present medicine is to stop the autoimmune system from attaching and > destroying her vital organs. > > "Ole Bob" > > > -- > The silver-list is a moderated forum for discussion of colloidal silver. > > To join or quit silver-list or silver-digest send an e-mail message to: > silver-list-requ...@eskimo.com -or- silver-digest-requ...@eskimo.com > with the word subscribe or unsubscribe in the SUBJECT line. > > To post, address your message to: silver-list@eskimo.com > Silver-list archive: http://escribe.com/health/thesilverlist/index.html > List maintainer: Mike Devour <mdev...@eskimo.com> > >
