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.^12,13 Similarly 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 sub-optimal 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 sub-optimal blood pressure balance or whose performance was sub-optimal 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 sub-optimal 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.²⁶ Some 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 sub-optimal 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, 56 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 age-related loss of brain functions like learning and memory.⁵⁰ Furthermore, DHEA showed insignificant effects on both learning/memory ability in aging rats.⁵¹ Higher DHEA-S 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 immune-boosting 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

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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 Rheum 1994;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.
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The post Understanding DHEA and 7-Keto DHEA appeared first on Total Health Magazine.

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:

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