This website uses cookies so that we can provide you with the best user experience possible. Cookie information is stored in your browser and performs functions such as recognizing you when you return to our website and helping our team to understand which sections of the website you find most interesting. We do not share any your subscription information with third parties. It is used solely to send you notifications about site content occasionally.

bone mineral density

  • According to the U.S. Department of Agriculture (USDA), Americans have failed to meet the RDA for several key nutrients, including calcium, magnesium, and zinc.1 Other research on both athletes and sedentary individuals indicated that their food intake was RDA-deficient in more than one-third of the seven minerals analyzed.2 In addition, research done by the USDA has shown that over a period of about 90 years, a 3–7 percent decrease in magnesium, zinc and potassium levels occurred in our food supply.3 Furthermore, studies from various sources demonstrated that growing conditions, agricultural technologies and nutrient content of the soil can reduce some minerals in some crops by as much as 300 percent.4,5,6,7,8

    This data clearly indicates that Americans are not getting sufficient minerals in their diet, which can have a number of health implications. One such implication is the loss of bone mineral density, a common occurrence as we age, and more prevalent in women than men.9 Consequently, supplementation with mineral supplements can help to fill the missing mineral gap and promote healthy bone density. In doing so, it is important to note that calcium is not the only nutrient necessary for helping to build bone density. The following text will elucidate some of the key nutrients necessary for healthy bone density, including calcium.

    Potassium
    Potassium is necessary to help maintain normal osmotic pressure of body fluids, the acid-base balance of the body, and for transmission of nerve impulses and muscle contraction. In addition, at least four cross-sectional studies have reported significant positive associations between dietary potassium intake and bone mineral density (BMD) in populations of premenopausal, perimenopausal, and postmenopausal women as well as elderly men.10,11,12 In studies on postmenopausal women, supplementation with potassium decreased urinary acid and calcium excretion, resulting in increased biomarkers of bone formation and decreased biomarkers of bone resorption.13 Other studies have reported that supplementation with potassium decreased urinary acid excretion and biomarkers of bone resorption in postmenopausal women.14

    Calcium
    Calcium is necessary for the formation of bones and teeth, blood clotting, and for normal muscle and nerve activity. Adequate calcium, along with regular exercise and a healthy diet, helps maintain good bone health, and may help teen and young adult women reduce their high risk for osteoporosis later in life.15,16,17 Furthermore, daily calcium supplementation has been shown to effectively slow bone loss.18,19,20,21 Calcium’s role in the prevention and treatment of osteoporosis is also well established.22 Research overwhelmingly supports the use of calcium supplementation, alone or in combination with other therapies, for slowing or stopping the progression of osteoporosis.23 As a matter of fact, FDA-approved therapy for the treatment of postmenopausal osteoporosis includes calcium supplementation.24 In addition, osteoporosis can lead to an increased incidence of fractures. Research has clearly shown that calcium supplementation can help to reduce the risk of, and even prevent fractures in osteoporosis.25,26,27,28

    Regarding the types of calcium, hydroxyapatite, calcium citrate, and calcium malate are good choices. Research using calcium citrate/malate has demonstrated a high level of absorption and an ability to effectively promote the consolidation and maintenance of bone mass in adults.29

    In addition, some research has shown that calcium citrate has greater absorption than other forms such as calcium gluconolactate and carbonate.30,31,32 Then, there is hydroxyapatite (HA), a whole bone concentrate that provides calcium, phosphorus and a variety of other naturally occurring bone nutrients. Research indicates that women who use HA gain significant cortical bone thickness as compared to women who used calcium alone (as calcium gluconate).33

    Iodine
    Iodine is an essential component of thyroid hormones, which regulate metabolic rate and other functions. Thyroid hormones have many interactions with the skeleton, and play a role in bone growth and development in the fetal growth plate and the normal mechanisms of mature bone remodeling.34

    Magnesium
    Magnesium is necessary for normal functioning of muscle and nervous tissue and participates in the formation of bones and teeth.35,36 Given its role in bone health, it is not surprising that people with osteoporosis were reported to be at high risk for magnesium malabsorption.37 Furthermore, bone38 and blood levels of magnesium have also been reported to be low in people with osteoporosis.39 Research has shown that supplementing with magnesium reduces indications of bone loss.40 Other research has shown that supplementing with magnesium daily also stopped bone loss, and even increased bone mass in twenty-seven of thirty-one people with osteoporosis in a two-year study.41

    Zinc
    Zinc is a versatile trace mineral required as a cofactor by more than 100 enzymes in every organ of the body. It is also associated with the hormone insulin, involved in making genetic material and proteins, immune reactions, transport of vitamin A, taste perception, wound healing, the making of sperm, and the normal development of the fetus. The highest concentrations of zinc in the body are in bone, the prostate gland, and the eyes.42

    Low blood and bone levels of zinc have been reported in people with osteoporosis.43 Also, research indicates that urinary loss of zinc may be high in people with osteoporosis.44 Other research found that men consuming a good amount of zinc in their diet had almost half the risk of osteoporosis-related fractures compared with those consuming significantly less dietary zinc.45 Furthermore, in one study the use of supplemental zinc with calcium was more effective than calcium supplementation by itself in protecting against the loss of bone density.46

    Selenium
    Selenium functions as a constituent of the antioxidant enzyme glutathione peroxidase, which detoxifies products of oxidized fats, and is found in the red blood cells. Selenium plays a fundamental role in regulating thyroid and other functions of the human body including reproduction, autoimmunity, glucose metabolism and bone metabolism.47 Specifically, it is the selenoproteins that are involved in bone metabolism.48

    Copper
    Copper is necessary with iron for the formation of red blood cells and nerve fibers. It is also necessary in the formation of the hair and skin pigment melanin. Furthermore, copper is needed for normal bone synthesis, and one study reported that daily copper prevented bone loss.49 The potential importance of copper for people with osteoporosis requires further research, although consumption of some copper can still be recommended at this time at least for general nutritional purposes.

    Manganese
    Manganese is an activator of enzymes (cofactor), and is involved in fatty acid metabolism and protein synthesis. It also plays a role in bone health.50 Unpublished research indicated that manganese deficiency occurred in a small group of women with osteoporosis,51 and published research using a combination of minerals including manganese was reported to halt bone loss.52

    Chromium
    Chromium participates in glucose metabolism by enhancing the effects of insulin.53 Since some data suggest that insulin is a potential anabolic agent in bone, this insulin-enhancing effect of chromium may contribute to bone health.54

    Molybdenum
    In humans, molybdenum is known to function as a cofactor for three enzymes: sulfite oxidase, xanthine oxidase, and aldehyde oxidase. Sulfite oxidase catalyzes the transformation of sulfite to sulfate, a reaction that is necessary for the metabolism of sulfur-containing amino acids (methionine and cysteine). Xanthine oxidase catalyzes the breakdown of nucleotides (precursors to DNA and RNA) to form uric acid, which contributes to the plasma antioxidant capacity of the blood. Aldehyde oxidase and xanthine oxidase catalyze hydroxylation reactions that involve a number of different molecules with similar chemical structures. Xanthine oxidase and aldehyde oxidase also play a role in the metabolism of drugs and toxins.55

    Silica
    Silica has been recognized as playing a significant role in bone formation.56 Also, supplementation with silica has increased bone formation in animal research.57 In human research, supplementation with silica increased bone mineral density in a group of eight women with osteoporosis.58 Bamboo stem extract is a rich source of silica, and is used in this formulation.

    Boron
    Chronically low intakes of the trace mineral boron may predispose people to osteoporosis.59 Changes caused by boron deprivation include reduced blood levels of calcium, as well as an increase in urinary excretion of calcium. Boron deprivation causes changes similar to those seen in women with postmenopausal osteoporosis, and this mineral is needed to prevent the excessive bone loss, which often occurs in postmenopausal women and older men.60 In addition, studies have reported possible improvements in bone mineral density in women who were supplemented with boron.61 For example, research has found that supplementation with 3 mg daily of the boron reduced urinary loss of both calcium and magnesium.62

    Vanadium
    Vanadium is a trace mineral that appears to be important in normal bone growth and as a cofactor for various enzyme reactions. The highest concentrations of vanadium are found in the liver, kidney, and bone.63 Some evidence suggests that vanadium can mimic the actions of insulin, possibly by causing phosphorylation of insulin receptor proteins.64 Since some data suggest that insulin is a potential anabolic agent in bone, this insulin-mimicking action of vanadium may further contribute to bone health.65

    References:

    1. Moshfegh AJ, Tippett KS, Borrud LG, Perloff BP. Food and Nutrient Intakes by Individuals in the United States, by Sex and Age, 1994-96. Agriculture Research Service; http://www.nalusda.gov/ttic/tektran/data/000009/29/0000092962.html.
    2. Misner B. Food Alone May Not Provide Sufficient Micronutrients for Preventing Deficiency. Journal of the International Society of Sports Nutrition 2006;3(1):51-55.
    3. Gerrior, S. and Bente, L. 1997. Nutrient Content of the U.S. Food Supply, 1909-94. U.S. Department of Agriculture, Center for Nutrition Policy and Promotion. Home Economics Report No. 53.
    4. USDA National Nutrient Database for Standard Reference, Release 15 , USDA Nutrient Data Laboratory, Last updated December 11, 2002; http://www.nal.usda.gov/fnic/foodcomp/.
    5. Barta DJ, Tibbitts TW, Barta DJ. Calcium localization and tipburn development in lettuce leaves during early enlargement. Journal of the American Society for Horticultural Science2000;125(3):294-8
    6. McKeehen JD, Smart DJ, Mackowiak CL, et al. Effect of CO2 levels on nutrient content of lettuce and radish. Advances in space research: the official journal of the Committee on Space Research 1996; 18(4-5):85-92.
    7. Kubota J, Allaway WH. Geographic distribution of trace element problems. In J.J.Mortvedt, ed., Micronutrients in Agriculture: Proceedings of Symposium held at Muscle Shoals, Alabama, Madison, WI: Soil Science Society of America; 1972:525–554.
    8. Composition of Foods: Raw, Processed, Prepared. USDA National Nutrient Database for Standard Reference, Release 15. December 2002. U.S. Department of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, Nutrient Data Laboratory.
    9. Pietschmann P, Rauner M, Sipos W, Kerschan-Schindl K. Osteoporosis: an age-related and gender-specific disease—a minireview. Gerontology 2008;55(1):3-12.
    10. 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(6):1831–9.
    11. 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(1):142–51.
    12. Tucker KL, Hannan MT, Chen H, Cupples LA, Wilson PW, Kiel DP. Potassium, magnesium, and fruit and vegetable intakes are associated with greater bone mineral density in elderly men and women. Am J Clin Nutr 1999;69(4):727–36.
    13. Sebastian A, Harris ST, Ottaway JH, Todd KM, Morris RC, Jr. Improved mineral balance and skeletal metabolism in postmenopausal women treated with potassium bicarbonate. N Engl J Med 1994;330(25):1776–81.
    14. Marangella M, Di Stefano M, Casalis S, Berutti S, D’Amelio P, Isaia GC. Effects of potassium citrate supplementation on bone metabolism. Calcif Tissue Int 2004;74(4):330–35.
    15. Tortora G, Anagnostakos N. Principles of Anatomy And Physiology. New York: Harper & Row Publishers; 1981: 655.
    16. Whitney E, Rolfes S. "Understanding Nutrition," sixth edition. St. Paul: West Publishing, 1983:384–390.
    17. Rules and Regulations. Federal Register 1993; Vol. 58, No. 3, pp. 2677.
    18. Reid IR. Pharmacological management of osteoporosis in postmenopausal women: a comparative review. Drugs & Aging 1999; 15(5):349–63.
    19. Prince R. The calcium controversy revisited: implications of new data. Medical Journal of Australia 1993; 159(6):404–7.
    20. Dawson-Hughes B. Calcium supplementation and bone loss: a review of controlled clinical trials. American Journal Of Clinical Nutrition 1991; 54(1 Suppl):274S.
    21. Cumming RG. Calcium intake and bone mass: a quantitative review of the evidence. Calcified Tissue International 1990; 47(4):194-201.
    22. Whitney E, Cataldo C, Rolfes S. Understanding Normal and Clinical Nutrition. Belmont, California: Wadsworth Publishing; 1998: 426-433, 439–448.
    23. Laulert L, Almeida M de A, Araujo VG, Francisco CM. [Osteoporosis: a silent epidemic which will turn public] Osteoporose:a epidemia silenciosa que devese tornar publica. Revista brasileira de enfermagem 1995; 48(2):161–7.
    24. Wisneski LA. Clinical management of postmenopausal osteoporosis. Southern Medical Journal 1992; 85(8):832–9.
    25. Blank RD, Bockman RS. A review of clinical trials of therapies for osteoporosis using fracture as an end point. Journal Of Clinical Densitometry 1999; 2(4):435–52.
    26. Scheiber LB 2nd, Torregrosa L. Evaluation and treatment of postmenopausal osteoporosis. Seminars in arthritis and rheumatism 1998; 27(4):245–61.
    27. Cumming RG, Nevitt MC. Calcium for prevention of osteoporotic fractures in postmenopausal women. Journal of Bone and Mineral Research 1997; 12(9):1321–9.
    28. Wark JD. Osteoporotic fractures: background and prevention strategies. Maturitas 1996; 23(2):193–207.
    29. Reinwald S, Weaver CM, Kester JJ. The health benefits of calcium citrate malate: a review of the supporting science. Adv Food Nutr Res 2008;54:219–346.
    30. Hansen C, Werner E, Erbes HJ, Larrat V, Kaltwasser JP. Intestinal calcium absorption from different calcium preparations: influence of anion and solubility. Osteoporos Int 1996;6:386–93.
    31. Gonnelli S, Cepollaro C, Camporeale A, et al. Acute biochemical variations induced by two different calcium salts in healthy perimenopausal women. Calcif Tissue Int 1995;57(3):175–7.
    32. Harvey JA, Zobitz MM, Pak CY. Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate. J Bone Miner Res (1988) 3(3):253–8.
    33. Epstein O, Y Kato, R Dick, and S Sherlock. Vitamin D, hydroxyapatite, and calcium gluconate in treatment of cortical bone thinning in postmenopausal women with primary biliary cirrhosis. Am J Clin Nutr 1982;36:426–30.
    34. Wexler JA, Sharretts J. Thyroid and bone. Endocrinol Metab Clin North Am 2007;36(3):673–705.
    35. Tortora G, Anagnostakos N. "Principles of anatomy and physiology." New York: Harper & Row Publishers; 1981: 655.
    36. Wilson ED, Fisher KH, Garcia PA. "Principles of Nutrition," fourth edition. New York: John Wiley & Sons, New York; 1979:274.
    37. Cohen L, Laor A, Kitzes R. Magnesium malabsorption in postmenopausal osteoporosis. Magnesium 1983; 2:139–43.
    38. Cohen L, Kitzes R. Infrared spectroscopy and magnesium content of bone mineral in osteoporotic women. Isr J Med Sci 1981;17:1123–25.
    39. Geinster JY, Strauss L, Deroisy R, et al. Preliminary report of decreased serum magnesium in postmenopausal osteoporosis. Magnesium 1989; 8:106–9.
    40. Dimai H-PPorta S, Wirnsberger G, et al. Daily oral magnesium supplementation suppresses bone turnover in young adult males. J Clin Endocrinol Metab 1998; 83:2742–48.
    41. Stendig-Lindberg G, Tepper R, Leichter I. bone density in a two year controlled trial of peroral magnesium in osteoporosis. Magnesium Res (1993) 6:155–63.
    42. Whitney E, Cataldo C, Rolfes S. "Understanding Normal and Clinical Nutrition," Fifth Edition. Belmont, California:West/ Wadsworth; 1998:463–8.
    43. Sahap Atik O. Zinc and senile osteoporosis. J Am Geriatr Soc 1983; 31:790–91.
    44. Relea P, et al. Zinc, biochemical markers of nutrition and type 1 osteoporosis. Age Ageing (1995) 24:303–7.
    45. Elmståhl S, et al. Increased Incidence of Fractures in Middleaged and Elderly Men with Low Intakes of Phosphorus and Zinc. Osteoporos Int 1998; 8:333–40.
    46. Strause L, Saltman P, Smith KT, et al. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr1994; 124:1060–4.
    47. Kaprara A, Krassas GE. Selenium and thyroidal function; the role of immunoassays. Hell J Nucl Med 2006;9(3):195–203.
    48. Köhrle J, Jakob F, Contempré B, Dumont JE. Selenium, the thyroid, and the endocrine system. Endocr Rev2005;26(7):944–84.
    49. Eaton-Evans J, McIlrath EM, Jackson WE, et al. Copper supplementation and bone-mineral density in middle-aged women. Proc Nutr Soc 1995;54:191A.
    50. Gold M. Basketball bones. Science 1980; 80:101–2. 51. Raloff J. Reasons for boning up on manganese. Science News 1986;27:199.
    51. Strause L, Saltman P, Smith KT, et al. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr 1994;124:1060–4.
    52. Food and Nutrition Board, Institute of Medicine. Chromium. Dietary reference intakes for vitamin A, vitamin K, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, D.C.: National Academy Press; 2001:197–223.
    53. Thrailkill KM, Lumpkin CK Jr, Bunn RC, Kemp SF, Fowlkes JL. Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues. Am J Physiol Endocrinol Metab 2005;289(5):E735–45.
    54. Eckhert C. Other trace elements In: Shils ME, Shike M, Ross AC, Caballero B, Cousins RJ, eds. "Modern Nutrition in Health and Disease." 10th ed. Philadelphia: Lippincott, Williams & Wilkins; 2006:338–350.
    55. Carlisle EM. Silicon localization and calcification in developing bone. Fed Proc 1969;28:374.
    56. Hott M, de Pollak C, Modrowski D, Marie PJ. Short-term effects of organic silicon on trabecular bone in mature ovariectamized rats. Calcif Tissue Int 1993;53:174–9.
    57. Eisinger J, Clairet D. Effects of silicon, fluoride, etidronate and magnesium on bone mineral density: a retrospective study. Magnes Res 1993;6:247–9.
    58. Bunker VW. The role of nutrition in osteoporosis. British Journal Of Biomedical Science 1994; 51(3):228–40.
    59. Nielsen FH. Studies on the relationship between boron and magnesium, which possibly effects the formation and maintenance of bones. Magnesium And Trace Elements 1990; 9(2):61–9.
    60. Volpe SL, Taper LJ, Meacham S. The relationship between boron and magnesium status and bone mineral density in the human: a review. Magnesium Research 1993; 6(3):291–6.
    61. Nielson FH, Hunt CD, Mullen LM, Hunt JR. Effect of dietary boron on mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEB J 1987;1:394–7.
    62. Food and Nutrition Board, Institute of Medicine. "Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc." Washington, DC: National Academy Press, 2002. Available at: www.nap.edu/books/0309072794/html.
    63. Harland BF, Harden-Williams BA. Is vanadium of human nutritional importance yet? J Am Diet Assoc 1994;94:891–4.
    64. Thrailkill KM, Lumpkin CK Jr, Bunn RC, Kemp SF, Fowlkes JL. Is insulin an anabolic agent in bone? Dissecting the diabetic bone for clues. Am J Physiol Endocrinol Metab 2005;289(5):E735–45.

  • Dehydroepiandrosterone (DHEA) is an important hormone produced in the adrenal glands and liver1, and in men, the testes. DHEA and its sulfate ester, dehydroepiandrosterone sulfate (DHEA-S), are interconvertible. DHEA-S is the storage form of DHEA.2,3 DHEA can then be metabolized to androstenedione, the major human precursor to androgens and estrogens4,5—although DHEA doesn’t have direct estrogenic or androgenic activity.6 In most individuals, the production of DHEA normally peaks during the mid-’20s and then begins a steady, progressive decrease of up to 90 percent with aging.7 This decrease is associated with a host of age-related syndromes and conditions, including a concurrent reduction in protein formation, a decrease in muscle mass, and an increase in body fat.8 There are no good dietary sources of DHEA other than by way of supplementation.

    7-keto DHEA is a metabolite of DHEA and may prove to be a safer alternative. Unlike DHEA, 7-keto-DHEA is not converted to androgens and estrogens.9,10,11 Oral or topical administration of 7-keto-DHEA does not affect plasma levels of steroid hormones.12,13Similarly to DHEA, 7-keto-DHEA is rapidly converted to the sulfated form, known as 7-keto-DHEAS14.

    Areas Of Benefit
    Clinical studies have been conducted on supplementation with both DHEA and 7-keto-DHEA. Based upon that research, DHEA offers potential benefits for adrenal support, youthful skin, sexual support, bone mineral density, mood support/ mental function, healthy inflammatory response in body tissues, fatigue reduction, menopause, weight loss, and insulin sensitivity. Clinical studies on 7-keto DHEA have identified three major areas of potential benefit, including weight loss, cognitive function, and immune function. Following is an overview of the research on each of these dietary supplement ingredients.

    DHEA: Adrenal Support
    In individuals with suboptimal adrenal function, daily supplementation with 20–50 mg DHEA seems to improve feelings of well-being, skin and hair, and sexuality responsiveness.15,16 DHEA also helps support healthy maturation of the adrenal glands in children with suboptimal adrenal function.17

    DHEA: Youthful Skin
    As previously discussed. DHEA levels decline with age. In research with individuals 60–79 years old, taking 50 mg DHEA daily helped reverse certain parameters of aging skin. Subjects experienced an increase in epidermal thickness, sebum production, skin hydration, and decrease facial skin pigmentation.18

    DHEA: Sexual Support
    Aging males supplemented with 50 mg DHEA daily for six months experienced improvements in parameters of male performance, including erection, orgasmic function, sexual desire, and overall sexual satisfaction. DHEA helped improve male performance in men with suboptimal blood pressure balance or whose performance was suboptimal for unknown reasons, but did not improve performance in individuals with diabetes or neurological disorders.19,20

    In postmenopausal women, clinical evidence has demonstrated that a single 300 mg dose of DHEA improved sexual response, including significantly greater mental and physical sexual arousal.21 Furthermore, vaginal application of DHEA was found to be effective in reducing vaginal atrophy in elderly postmenopausal women.22

    DHEA: Bone Mineral Density
    Loss of bone mineral density (BMD) is common with aging. Daily supplementation with 50–100 mg DHEA has been shown to improve BMD in older women and men with suboptimal BMD.23,24 It also helps improve BMD in younger women with eating disorders.25

    DHEA: Mood Support / Mental Function
    Experiencing moodiness or “the blues” is common during the lifecycle but can increase with age.26Some clinical research suggests that taking DHEA orally might improve symptoms of moodiness in elderly subjects.27,28,29 Taking DHEA orally seems to improve healthy mental function in individuals with suboptimal perception or expression of reality.30

    DHEA: Healthy Inflammatory Response In Body Tissues
    Some individuals experience acute and chronic inflammation of various tissues of the body resulting from an attack by their body’s own immune system. Taking DHEA orally in conjunction with conventional treatment may help support a healthy inflammatory response in various tissues.31,32,33,34,35,36,37 It may also help promote the normalization of symptoms such as muscle ache.38 In addition, DHEA also seems to improve bone mineral density in such individuals whose conventional medications adversely affect bone mineral density.39,40,41

    DHEA: Fatigue Reduction
    Some individuals, who experience a period of high physical and/or emotional stress, also experience the onset of fatigue of a chronic nature. DHEA may be able to help. In a clinical study, supplementation with DHEA led to a significant reduction in associated pain, fatigue, limitations in activities of daily living, helplessness, anxiety, difficulty thinking, poor memory, and sexual problems over the period of the study.42

    DHEA: Menopause
    In a clinical study, 25 mg of DHEA daily increased the levels of all the hormones that derive from DHEA metabolism. It also increased neurosteroids and endorphin levels. The results were an improvement of vasomotor symptoms such as hot flashes, as well as psychological symptoms throughout 12 months of therapy.43

    DHEA: Weight Loss & Insulin Sensitivity
    In a randomized, double-blind, placebo-controlled study, fiftysix elderly subjects took 50 mg DHEA daily for six months. Subjects taking the DHEA experienced a significant decrease in abdominal fat, and improvements in insulin sensitivity compared to those using the placebo.44

    7-keto: Weight Loss
    7-keto-DHEA is thought to be beneficial in weight loss by increasing metabolism and thermogenesis. Early evidence in animals suggests 7-keto-DHEA can increase thermogenesis, possibly by stimulation of thermogenic enzymes in the liver45 ; however this effect has not yet been reported in humans. Clinical evidence suggests 7-keto-DHEA might increase basal metabolism.

    In obese patients, 7-keto-DHEA can significantly increase the thyroid hormone triiodothyronine (T3) when used over four weeks.46 This effect on thyroid function may positively influence metabolism47, helping patients reduce body weight and body fat. In fact, one clinical study seems to support the hypothesis that the supplement can enhance weight loss.

    Thirty overweight adults were randomized into a prospective, double-blind, placebo controlled eight-week study.48 Fifteen subjects received 100 mg 7-Keto DHEA twice per day whereas the other 15 subjects received a matching placebo. All subjects exercised three times per week, 60 minutes per session of cross-training (aerobic and anaerobic) under the supervision of an exercise physiologist. The exercise plus 7-Keto DHEA group lost a significant amount of body weight as compared with the exercise plus placebo group.

    When analyzed per a four-week interval, the 7-Keto DHEA group lost 3.17 lbs per interval, whereas placebo lost 1.09 lbs. In terms of actual body composition changes, the exercise plus 7-Keto DHEA group lost 1.8 percent body fat as compared to 0.57 percent for the placebo group. When viewed as a change in body fat per four-week interval, the 7-Keto DHEA group lost 0.89 percent body fat per interval as compared to 0.29 percent for the placebo.

    In a later randomized, double-blind, placebo-controlled, crossover trial49, 7-Keto DHEA was tested in overweight adults maintained on a calorie-restricted diet to determine efficacy in increasing the resting metabolic rate (RMR). The results were that RMR increased significantly by 1.4 percent in the 7-Keto DHEA group, whereas RMR decreased by 3.9 percent in the placebo group. In this study, 7-Keto reversed the decrease in RMR normally associated with dieting and was generally well tolerated with no serious adverse events.

    7-Keto: Cognitive Function
    Research has indicated that that DHEA administration might be beneficial in terms of neuroprotection against agerelated loss of brain functions like learning and memory.50 Furthermore, DHEA showed insignificant effects on both learning/memory ability in aging rats.51 Higher DHEAS levels are also independently and favorably associated with executive function, concentration, and working memory in humans.52 In addition, other research suggests that 7-keto-DHEA improves chemically-induced and age-related memory impairment.53

    7-Keto: Immune Function
    7-keto DHEA has also been studied for its potential immuneboosting properties. This includes immunomodulatory effects by stimulating interleukin-2 production by human lymphocytes in-vitro.54 Researchers think that it may also stimulate the activity and effectiveness of T-lymphocytes. These T-lymphocytes may in turn stimulate additional immune system functions.55 Studies based on these observations suggest that 7-keto DHEA may have a future as an important immune system enhancer.56,57 Thus, 7-keto DHEA could prove to be therapeutically useful in a wide range of conditions. Studies suggest that DHEA may reduce the replication of certain types of viruses.58

    References

    1. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
    2. Moffat SD, Zonderman AB, Harman M, et al. The relationship between longitudinal declines in dehydroepiandrosterone sulfate concentrations and cognitive performance in older men. Arch Int Med 2000;160:2193–8.
    3. Pepping J. DHEA: dehydroepiandrosterone. Am J Health Syst Pharm 2000;57:2048-50, 2053– 4, 2056.
    4. Oelkers W. Dehydroepiandosterone for adrenal insufficiency (editorial). N Engl J Med 1999;341:1073– 4.
    5. van Vollenhoven RF. Dehydroepiandrosterone in systemic lupus erythematosus. Rheum Dis Clin North Am 2000;26:349- 62.
    6. Tchernof A, Labrie F. Dehydroepiandrosterone, obesity and cardiovascular disease risk: a review of human studies. Eur J Endocrinol 2004;151:1– 14.
    7. Mortola J, Yen SSC. The Effects of Oral Dehydroepiandrosterone on Endocrine-Metabolic Parameters in Postmenopausal Women. J Clin Endocrin 1990;71(3): 696–704.
    8. Morales AJ, Nolan JJ, Nelson JC, Yen SS. Effects of replacement dose of dehydroepiandrosterone in men and women of advancing age. J Clin Endocrin 1994;78(6):1360– 7.
    9. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
    10. Davidson MH, Weeks C, Lardy H, et al. Clinical Safety and Endocrine Effects of 7-KETO-DHEA. Abstract presented at: Experimental Biology 98, April 19-22, 1998, San Francisco, CA. Abstract obtained from Humanetics Corporation website.
    11. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
    12. Davidson M, Marwah A, Sawchuk RJ, et al. Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers. Clin Invest Med 2000;23:300–10.
    13. Sulcova J, Hill M, Masek Z, et al. Effects of transdermal application of 7-oxo-DHEA on the levels of steroid hormones, gonadotropins and lipids in healthy men. Physiol Res 2001;50:9– 18.
    14. Davidson M, Marwah A, Sawchuk RJ, et al. Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers. Clin Invest Med 2000;23:300–10.
    15. Arlt W, Callies F, van Vlijmen JC, et al. Dehydroepiandosterone replacement in women with adrenal insufficiency. N Engl J Med 1999;341:1013–20.
    16. Johannsson G, Burman P, Wiren L, et al. Low dose dehydroepiandrosterone affects behavior in hypopituitary androgen-deficient women: a placebo-controlled trial. J Clin Endocrinol Metab 2002;87:2046– 52.
    17. Kim SS, Brody KH. Dehydroepiandrosterone replacement in Addison’s disease. Eur J Obstet Gynecol Reprod Biol 2001;97:96– 7.
    18. Baulieu EE, Thomas G, Legrain S, et al. Dehydroepiandrosterone (DHEA), DHEA sulfate, and aging. Contribution of the DHEAge study to a sociobiomedical issue. Proc Natl Acad Sci U S A 2000;97:4279- 84.
    19. Reiter WJ, Pycha A, Schatzl G, et al. Dehydroepiandosterone in the treatment of erectile dysfunction: A prospective, double-blind, randomized, placebo-controlled study. Urol 1999;53:590– 5.
    20. Reiter WJ, Schatzl G, Mark I, et al. Dehydroepiandrosterone in the treatment of erectile dysfunction in patients with different organic etiologies. Urol Res 2001;29:278–81.
    21. Hackbert L, Heiman JR. Acute dehydroepiandrosterone (DHEA) effects on sexual arousal in postmenopausal women. J Womens Health Gend Based Med 2002;11:155– 62.
    22. Labrie F, Diamond P, Cusan L, et al. Effect of 12 month dehydroepiandrosterone replacement therapy on bone, vagina, and endometrium in postmenopausal women. J Clin Endocrinol Metab 1997;82:3498–505.
    23. Sun Y, Mao M, Sun L, et al. Treatment of osteoporosis in men using dehydroepiandrosterone sulfate. Chin Med J (Engl) 2002;115:402–4.
    24. Villareal DT, Holloszy JO, Kohrt WM. Effects of DHEA replacement on bone mineral density and body composition in elderly women and men. Clin Endocrinol (Oxf) 2000;53:561– 8.
    25. Gordon CM, Grace E, Emans SJ, et al. Effects of oral dehydroepiandrosterone on bone density in young women with anorexia nervosa: a randomized trial. J Clin Endocrinol Metab 2002;87:4935– 41.
    26. Hybels CF and Blazer DG. Epidemiology of late-life mental disorders. Clinics in Geriatric Medicine 2003; 19:663– 696.
    27. Wolkowitz OM, Reus VI, Keebler A, et al. Double-blind treatment of major depression with dehydroepiandosterone. Am J Psychiatry 1999;156:646–9.
    28. Bloch M, Schmidt PJ, Danaceau MA, et al. Dehydroepiandrosterone treatment of midlife dysthymia. Biol Psychiatry 1999;45:1533–41.
    29. Wolkowitz OM, Reus VI, Manfredi F, et al. Dehydroepiandrosterone (DHEA) treatment of depression. [Abstract] Biol Psychiatry 1997;41:311–8.
    30. Strous RD, Maayan R, Lapidus R, et al. Dehydroepiandrosterone augmentation in the management of negative, depressive, and anxiety symptoms in schizophrenia. Arch Gen Psychiatry 2003;60:133– 41.
    31. van Vollenhoven RF, Morabito LM, Engleman EG, et al. Treatment of systemic lupus erythematosus with dehydroepiandrosterone: 50 patients treated up to 12 months. J Rheumatol 1998;25:285– 9.
    32. van Vollenhoven RF, Engleman EG, McGurie JL. Dehydroepiandrosterone in Systemic Lupus Erythematosus. Arth Rheum 1995;38:1826– 31.
    33. van Vollenhoven RF, Engleman EG, McGuire JL. Dehydroepiandrosterone in systemic lupus erythematosus. Arthritis Rheum1994;37:1305–10.
    34. an Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe lupus erythematosus. Lupus 1999;8:181–7.
    35. Mease PJ, Merrill JT, Lahita RG, et al. GL701 (prasterone, dehydroepiandrosterone) improves systemic lupus erythematosus. 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29–November 2. Abstract 1230.
    36. Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858–68.
    37. Petri MA, Lahita RG, Van Vollenhoven RF, et al. Effects of prasterone on corticosteroid requirements of women with systemic lupus erythematosus: a double-blind, randomized, placebo-controlled trial. Arthritis Rheum 2002;46:1820–9.
    38. Petri MA, Mease PJ, Merrill JT, et al. Effects of prasterone on disease activity and symptoms in women with active systemic lupus erythematosus. Arthritis Rheum 2004;50:2858–68.
    39. Mease PJ, Merrill JT, Lahita RG, et al. GL701 (prasterone, dehydroepiandrosterone) improves systemic lupus erythematosus. 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29-November 2. Abstract 1230.
    40. Mease PJ, Ginzler EM, Gluck OS, et al. Improvement in bone mineral density in steroid-treated SLE patients during treatment with GL701 (prasterone, dehydroepiandrosterone). 2000 American College of Rheumatology Meeting. Philadelphia, PA. October 29-November 2. abstract 835.
    41. van Vollenhoven RF, Park JL, Genovese MC, et al. A double-blind, placebo-controlled, clinical trial of dehydroepiandrosterone in severe lupus erythematosus. Lupus 1999;8:181–7. 42. Himmel PB, Seligman TM. A Pilot Study Employing Dehydroepiandrosterone (DHEA) in the Treatment of Chronic Fatigue Syndrome. [Abstract] J Clin Rheumatol 1999:5:56–9.
    42. Genazzani AD, Stomati M, Bernardi F, et al. Long-term low-dose dehydroepiandrosterone oral supplementation in early and late postmenopausal women modulates endocrine parameters and synthesis of neuroactive steroids. Fertil Steril 2003;80:1495–501.
    43. Villareal DT, Holloszy JO. Effect of DHEA on abdominal fat and insulin action in elderly women and men. JAMA 2004;292:2243–8.
    44. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci U S A 1995;92:6617–9.
    45. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
    46. Lardy H, Partridge B, Kneer N, Wei Y. Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci USA 1995;92(14):6617–9.
    47. Colker CM, Torina GC, Swain MA, Kalman DS. Double-Blind Study Evaluating the Effects of Exercise Plus 3-Acetyl-7-oxodehydroepiandrosterone on Body Composition and the Endocrine System in Overweight Adults. Journal of Exercise Physiology Online 1999;2(4):Abstract #30.
    48. Zenk JL, Frestedt JL, Kuskowski MA. HUM5007, a novel combination of thermogenic compounds, and 3-acetyl-7-oxodehydroepiandrosterone: each increases the resting metabolic rate of overweight adults. J Nutr Biochem. 2007;18(9):629–34.
    49. Taha A, Mishra M, Baquer NZ, Sharma D. Na+ K(+)-ATPase activity in response to exogenous dehydroepiandrosterone administration in aging rat brain. Indian J Exp Biol. 2008;46(12):852–4.
    50. Chen C, Lang S, Zuo P, Yang N, Wang X. Treatment with dehydroepiandrosterone increases peripheral benzodiazepine receptors of mitochondria from cerebral cortex in D-galactose-induced aged rats. Basic Clin Pharmacol Toxicol 2008;103(6):493–501.
    51. Davis SR, Shah SM, McKenzie DP, Kulkarni J, Davison SL, Bell RJ. Dehydroepiandrosterone sulfate levels are associated with more favorable cognitive function in women. J Clin Endocrinol Metab 2008;93(3):801–8.
    52. Shi J, Schulze S, Lardy HA. The effect of 7-oxo-DHEA acetate on memory in young and old C57BL/6 mice. Steroids 2000;65:124–9.
    53. Nelson R, Herron M, Weeks C, Lardy H. Dehydroepiandrosterone and 7-KETO-DHEA augment Interleukin 2 (IL2) Production by Human Lymphocytes In Vitro. Abstract presented at: The 5th Conference on Retroviruses and Opportunistic Infections, February 1–5, 1998, Chicago, IL. Abstract obtained from Humanetics Corporation.
    54. Whittington R, Faulds D. Interleukin-2. A review of its pharmacological properties and therapeutic use in patients with cancer. Drugs 1993;46(3):446–514.
    55. Nelson R, Herron M, Weeks C, Lardy H. Dehydroepiandrosterone and 7-keto DHEA Augment Interleukin 2 (IL2) Production by Human Lymphocytes in Vitro. The 5th Conference on Retroviruses and Opportunistic Infections. Chicago, IL. Feb 1998;598:49.
    56. Hampl R. 7-Hydroxydehydroepiandrosterone--a natural antiglucocorticoid and a candidate for steroid replacement therapy? Physiol Res 2000;49 Suppl 1:S107–12.
    57. Henderson E, Yang JY, Schwartz A. Dehydroepiandrosterone (DHEA) and synthetic DHEA analogs are modest inhibitors of HIV-1 IIIB replication. AIDS Res Hum Retroviruses1992;8(5):625–31.