Osteoporosis literally means porous bone. Although the entire skeleton may be involved, bone loss is usually greatest in the spine, hips and ribs. Since these bones bear a great deal of weight, they are then susceptible to pain, deformity or fracture.
Normally there is a decline in bone mass after the age of 40. This bone loss is accelerated in patients with osteoporosis. Many factors can result in excessive bone loss and different variants of osteoporosis exist. All of these other causes of accelerated bone loss should be ruled out before a diagnosis of osteoporosis is made. Postmenopausal osteoporosis is the most common form of osteoporosis currently.
Although considered by many to be just a loss of calcium in the bones, osteoporosis involves both the mineral (inorganic) and the non-mineral (organic matrix) of bone. This is the first clue that there is more to osteoporosis than a lack of dietary calcium. In fact, lack of dietary calcium in the adult results in a separate condition known as osteomalacia or "softening of the bone." The two conditions, osteomalacia and osteoporosis, are different in that in osteomalacia there is only a deficiency of calcium in the bone. In contrast, in osteoporosis there is a lack of both calcium and other minerals as well as a decrease in the non-mineral framework (organic matrix) of bone. Primarily composed of collagen and other proteins, little attention has been given to the important role this organic matrix plays in maintaining bone structure.
It is currently estimated 15 million persons in the United States have osteoporosis with nearly one-third of all women over the age of 60 being affected. Although many physicians recommend estrogen replacement for their postmenopausal women, at present time it is generally agreed the risk outweighs the benefit in the majority of women who are at risk for osteoporosis. Instead, a greater emphasis should be placed on those nutritional and lifestyle factors. In the severe case, improvement may result by the administration of estrogen, 1,25- (OH)2D3, or calcitonin (all of these are prescription medications).
Many general dietary factors have been implicated in the development of osteoporosis: low calcium-high phosphorus intake, high protein diet, high acid-ash diet, and trace mineral deficiencies to name a few. In addition to these strong dietary associations with osteoporosis, other things implicated in the development of osteoporosis include: hypochlorhydria; a disturbance in vitamin D metabolism; and several hormonal factors.
The absorption of calcium is dependent first on becoming ionized in the intestines. This has been the major problem with the most widely used form of calcium used for supplementation, calcium carbonate. In order for calcium carbonate and other insoluble calcium salts to be absorbed they must first be solubilized and ionized by stomach acid. This is where the problem arises for many individuals. In studies with postmenopausal women, it has been shown about 40% are severely deficient in stomach acid a condition known as hypochlorhydria. It has been shown that patients with insufficient stomach acid output can only absorb about 4% of an oral dose of calcium as calcium carbonate while a person with normal stomach acid can typically absorb about 22%. Patients with low stomach acid secretion need a form of calcium already in a soluble and ionized state, like calcium citrate, calcium lactate or calcium gluconate. About 45% of the calcium is absorbed from calcium citrate in patients with reduced stomach acid compared to 4% absorption for calcium carbonate. This clearly demonstrates ionized calcium is much more beneficial than insoluble calcium salts like calcium carbonate in patients with reduced stomach acid secretion. It has also been demonstrated calcium is more bioavailable from calcium citrate than from calcium carbonate in normal subjects as well. In any event, calcium citrate appears to be the best form to supplement with at this time for best absorption.
Vitamin D stimulates the absorption of calcium. Since vitamin D can be produced in our bodies by the action of sunlight on 7-dehydrocholesterol in the skin, many experts consider it more of a hormone than a vitamin. The sunlight changes the 7-dehydrocholesterol into vitamin D3 (cholecalciferol). It is then transported to the liver and converted by an enzyme into 25-hydroxycholcalciferol (25-OHD3) which is five times more potent than cholecalciferol (D3). The 25-hydroxycholecalciferol is then converted by an enzyme in the kidneys to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3), which is ten times more potent than cholecalciferol and the most potent form of vitamin D3. Disorders of the liver or kidneys results in impaired conversion of cholecalciferol to more potent vitamin D compounds. In many patients with osteoporosis there are high levels of 25- OHD3 while the level of 1,25-(OH)2D3 is quite low. This signifies an impairment in conversion of 25-OHD3 to 1,25-(OH)2D3 by the kidney in osteoporosis. Many theories have been proposed to account for this decreased conversion including relationships to estrogen and magnesium deficiency.
The concentration of calcium in the blood is strictly maintained within very narrow limits. If levels start to decrease there is an increase in the secretion of parathyroid hormone by the parathyroid glands (there are four parathyroid glands nestled in the thyroid gland that secretes this hormone) and a decrease in the secretion of calcitonin by the thyroid and parathyroids. If calcium levels in the blood start to increase there is a decrease in the secretion of parathyroid hormone and an increase in the secretion of calcitonin. An understanding of how these hormones increase (parathyroid hormone) and decrease (calcitonin) serum calcium levels is necessary in understanding osteoporosis.
Parathyroid hormone increases serum calcium levels primarily by increasing the activity of the cells that breakdown bone (osteoclasts), although it also decreases the excretion of calcium by the kidneys and increases the absorption of calcium in the intestines. In the kidneys, parathyroid hormone increases the conversion of 25-OHD3 to 1,25-(OH)2D3. One if the theories relating bone loss to estrogen deficiency is as follows: an estrogen deficiency makes the cells that breakdown bone (osteoclasts) more sensitive to parathyroid hormone resulting in increased bone breakdown thereby raising serum calcium levels. This leads to a decreased parathyroid hormone level which results in diminished levels of active vitamin D and increased calcium excretion as well. Evidence in osteoporosis patients seems to support this theory.
Calcitonin acts on lowering serum calcium levels by increasing the activity of the cells building bone (osteoblasts). Obviously this is a very desirable effect. Low calcitonin levels are found in postmenopausal osteoporosis and may be responsible for this type of bone loss. Recently calcitonin (isolated from salmon) has demonstrated remarkable effects in clinical studies and holds much promise in treating severe osteoporosis. Since calcitonin secretion can be increased by an elevation in serum calcium levels, this may be one of the ways calcium supplementation exerts its protective effect.
Lifestyle factors in the development of osteoporosis
Coffee, ethanol, and smoking induce a negative calcium balance and are associated with an increase risk of developing osteoporosis. As smokers tend to drink more coffee and ethanol, and consume a diet high in refined carbohydrate, it is very difficult to control for these other variables when trying to determine why smokers have a 15-30% lower bone mineral content compared to non-smokers. Smoking in relationship to causing osteoporosis is probably a greater statement of a lifestyle than a direct causal relationship.
Physical exercise consisting of one hour of moderate activity three times a week has been shown to prevent bone loss. In fact, this type of exercise has actually been shown to increase the bone mass in postmenopausal women. Walking is probably the best exercise to start with. In contrast to exercise, immobilization doubles the rate of urinary and fecal calcium excretion resulting in a significant negative calcium balance.
Signs & Symptoms
Osteoporosis is a condition without major signs and symptoms until the disease has progressed to a very serious extent at which time such things as severe backache, loss of height due to vertebral compression and develop of a "widow's hump." Severe bone loss may result in spontaneous fractures of the vertebrae or hip.
Structure & Function:
Bone Support &
Multi Vitamin/Multi Mineral Formulas
Adult Bee propolis* Calcium (citrate) 1,000 mg DHEA* Folic acid 900 mcg Magnesium (citrate) 500 mg Melatonin* N-A Glucosamine* Proanthocyanidins* Vitamin B-6 25 mg Vitamin B-12 1,000 mcg
* Please refer to the respective topic for specific nutrient amounts.
Supplementation of calcium has been shown to be effective in reducing age-related bone loss. Many experts are recommending a daily calcium intake of 1,500 mg. This typically means supplementation in the range of 1,000 to 1,200 mg is required. As mentioned above, the absorption and retention of calcium is dependent on a complex interplay of hormones and other factors. The initial approach is supplementation with the most bio-available form of calcium. At this time, calcium citrate appears to be the best form of calcium to supplement with both in regards to better absorption and decreased risk of developing kidney stones.
Concern has arisen that increased calcium supplementation may result in increased calcium oxalate nephrolithiasis. Calcium citrate appears to bypass this justifiable concern. While urinary calcium will rise in patients consuming calcium citrate, some of citrate's effects inhibit the formation of kidney stones. Specifically citrate has the ability to reduce urinary saturation of calcium oxalate and calcium phosphate, and retard the nucleation and crystal growth of calcium salts. While the use of non-citrate calcium supplements may increase the risk of developing calcium oxalate kidney stones while on the other hand calcium citrate appears to greatly reduce this risk.
One natural source is dolomite, although concerns have been expressed about other minerals within the same rock sample.
Magnesium supplementation is as important as calcium supplementation. Osteoporotics have lower bone magnesium content and other indicators of magnesium deficiency than people without osteoporosis. In human magnesium deficiency, there is a decrease in serum concentration of the most active form of vitamin D (1,25-dihydroxycholecalciferol or 1,25-(OH)2D3). This could be either due to the enzyme needed in the conversion of 25-OHD3 to 1,25-(OH)2D3 or mediation of parathyroid hormone and calcitonin secretion. Intake of dairy foods fortified with vitamin D results in decreased magnesium absorption. This combined with the high number of osteoporotics that cannot tolerate milk (27-47%) indicates that milk may not be an appropriate food to prevent osteoporosis.
Vitamin B-6, folic acid, and vitamin B-12
Low levels of these nutrients are quite common in the elderly population and may cause osteoporosis. These vitamins are important in the conversion of the amino acid methionine to cysteine. If deficient in these vitamins or if a defect exists in the enzymes responsible for this conversion, there will be an increase in homocysteine. This compound has been implicated in a variety of conditions including arteriosclerosis (hardening of the arteries) and osteoporosis. Increased homocysteine concentrations in the blood have been demonstrated in postmenopausal women and is thought to play a role in osteoporosis by interfering with collagen cross-linking leading to a defective bone matrix. Since osteoporosis is known to be a loss of both the organic and inorganic phases of bone, this theory has much credence as it is one of the few that addresses both factors. Folic acid supplementation has been shown to reduce homocysteine levels but vitamin B-6 and B-12 are necessary for this to occur.
It should be noted ( for those who like to obtain their nutrients from natural sources) that brewer's yeast has been stated to be contra-indicated for osteoporosis.
The major non-collagen protein in bone is osteocalcin. This protein is dependent on vitamin K to be in its active form. Vitamin K is necessary for the gamma-carboxylation of the glutamic acid portion of osteocalcin allowing the osteocalcin to chelate the calcium and hold it into place within the bone. A deficiency of vitamin K could lead to impaired mineralization of the bone due to inadequate osteocalcin levels. Vitamin K is found in green leafy vegetables and may be one of the protective factors of a vegetarian diet. Vitamin K deficiency is quite high in individuals with chronic gastrointestinal disorders or poor fat absorption.
Note: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
Low levels of B-complex (Vitamin B-6, folic acid, and vitamin B-12) are quite common in the elderly population and may contribute to osteoporosis.
It is important to maintain an adequate diet rich in calcium and vitamin D while taking e.g. Calcitonin.
Osteoporotics have lower bone magnesium content and other indicators of magnesium deficiency than people without osteoporosis.
The major non-collagen protein in bone is osteocalcin. This protein is dependent on vitamin K to be in its active form. Vitamin K deficiency is quite high in individuals with chronic gastrointestinal disorders or poor fat absorption.
Alendronic acid is generally well tolerated; although mild gastrointestinal adverse events predominate, the frequency of these is low.
Table: Benefits and Disadvantages of HRT
Positive Effects Negative Effects (Decreased) (Increased) Bone loss Vaginal bleeding, nausea, breast tenderness [estrogen] Fracture rate Fluid retention, weight gain, PMS [progestogen] Menopausal symptoms Breast cancer Heart disease mortality Venous thromboembolism Alzheimer's disease
Biphosphonates [e.g. alendronic and etidronic acids [Etidronate (Didronel)] inhibit bone resorption. Several others are expected on the market within the next few years (e.g. clodronic acid, ibandronic acid, pamidronic acid, risedronic acid, tiludronic acid and zoledronic acid). Treatments have resulted in modest gains in bone mineral density (5-8% over 3 years) but reduced new vertebral fractures by half. (Black, 1996 and Harris, 1993)
As a class they are poorly absorbed from the gastrointestinal tract and need to be taken on an empty stomach at least 2 hours before the next meal. (Sahota, 1997)
Many general dietary factors have been implicated in the development of osteoporosis: low calcium-high phosphorus intake, high protein diet, high acid-ash diet and trace mineral deficiencies to name a few. Therefore, a High Calcium Diet is recommended.
A vegetarian diet (both lacto-ovo and vegan) is associated with a lower risk of osteoporosis. Although bone mass in vegetarians does not differ significantly from omnivores in the third, fourth, and fifth decades, there are significant differences in the later decades. This indicates the decreased incidence of osteoporosis in vegetarians is not due to increased initial bone mass, but rather decreased bone loss.
Several factors are probably responsible for this decrease in bone loss observed in vegetarians. Most important is probably a lowered intake of protein and phosphorus. A high-protein diet or a diet high in phosphates is associated with increasing the excretion of calcium in the urine. Raising daily protein from 47 to 142 grams doubles the excretion of calcium in the urine. A diet this high in protein is common in the United States and may be a significant factor in the increased number of people suffering from osteoporosis in this country.
Following sugar intake, there is an increase in the urinary excretion of calcium. Considering the average American consumes in one day 150 grams of sucrose, plus other refined simple sugars, and a glass of a carbonated beverage loaded with phosphates, along with the high-protein, it is little wonder that so many suffer from osteoporosis in this country. When lifestyle factors are also taken into consideration, it is very apparent why osteoporosis has become a major medical problem.
In general, a diet high in vegetables, but low in fat and animal products, should be adopted. Refined carbohydrate and ethanol intake should be held to a low level and carbonated beverages loaded with phosphates should be completely eliminated.
Long Term Treatment
1. Calcarea carbonica - 30C
2. Calcarea fluorica tinct. - 30C
Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.
X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.
Boericke, D.E., 1988. Homeopathic Materia Medica.
Coulter, C.R., 1986. Portraits of Homeopathic Medicines.
Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.
Koehler, G., 1989. Handbook of Homeopathy.
Shingale, J.N., 1992. Bedside Prescriber.
Smith, Trevor, 1989. Homeopathic Medicine.
Ullman, Dana, 1991. The One Minute (or so) Healer.
Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.
Procyanidins are responsible for the deep red-blue color of many berries including: hawthorn berries, blackberries, blueberries (bilberry), etc. Procyanidins are remarkable in their ability to stabilize collagen structures. Since collagen is the major protein structure in bone, stabilization of its integrity and structure appears very much indicated. Supplementation with a concentrated extract of those berries rich in these types of flavonoids may offer significant benefit in preventing osteoporosis. Hawthorn berry (Crataegus oxycantha) is a particularly rich source.
Horsetail provides silica.
Newall has compiled a list of hormonally Active Herbs:
Herb Effect Agnus Castus Hormonal imbalance disorders Alfalfa Estrogenic, in vivo Aniseed Estrogenic Bayberry Mineralocorticoid Cohosh, Black Estrogenic Fucus / Kelp Hyper-/hypothyroidism reported. Ginseng Estrogenic, human Horseradish May depress thyroid activity Licorice Mineralocorticoid activity, human. estrogenic in vivo, in vitro Motherwort oxytocic Pleurisy Root Estrogenic Red Clover Estrogenic in vivo Saw Palmetto Estrogenic and anti-androgenic in vivo, human use in prostate cancer. Vervain Inhibition of gonadotrophic activity Wild Carrot Estrogenic
Newall CA, Anderson LA, Phillipson JD. Herbal Medicines: A Guide for Health-care Professionals. London: The Pharmaceutical Press, 1996.
Aromatherapy - Essential Oils
Chamomile Essence, Cardamom Essence, Cypress Essence, Lavender Essence, Melissa Essence, Rosemary Essence, Sandalwood Essence, Thyme Essence.
Related Health Conditions
Ache Hyperthyroidism Acromegaly Inflammation Aging Malnutrition Alcoholism Menke's syndrome Anemia Oral contraceptives Backache Paget's disease Fracture Pain Cushing's syndrome Pulmonary disease Diabetes mellitus Scurvy Epilepsy Stress
Aloia, J., S. Cohn, A. Vaswani, et al: Risk factors for postmenopausal osteoporosis. Am J Med 78:95-100. 1985.
Anderson, J.B. & Metz, J. A.: Contributions of Dietary Calcium and Physical Activity to Primary Prevention of Osteoporosis in Females. Journal of the American College of Nutrition, 1993;12(4):378-383.
Anderson JJ et al., Roles of diet and physical activity in the prevention of osteoporosis. Scand J Rheumatol Suppl, 1996, 103:, 65-74.
Anonymous: Clinical practice guidelines for the diagnosis and management of osteoporosis. Scientific Advisory Board, Osteoporosis Society of Canada. Can Med Assoc J, 1996 Oct 15, 155:8, 1113-33.
Barker, H., O. Frank, I.C. Thind, et al: Vitamin profiles in elderly persons living at home or in nursing homes versus profile in healthy young subjects. J Am Geriatrics Society 10:444-50, 1979.
Baron, J. Smoking and estrogen-related disease. A J Epid 119:9-22, 1984.
Bell, R., Beirne, O.R. J Oral Maxillofac Surg., 1988; 46: 589-594.
Bellantoni MF: Osteoporosis prevention and treatment. Am Fam Physician, 1996 Sep 1, 54:3, 986-92, 995-6.
Bikle DD: Role of vitamin D, its metabolites, and analogs in the management of osteoporosis. Rheum Dis Clin North Am, 1994 Aug, 20:3, 759-75.
Bilezikian JP: Current and future nonhormonal approaches to the treatment of osteoporosis. Int J Fertil Menopausal Stud, 1996 Mar-Apr, 41:2, 148-55.
Binkley NC & Suttie JW: Vitamin K nutrition and osteoporosis. J Nutr, 1995 Jul, 125:7, 1812-21.
Bonjour JP et al., Nutritional aspects of hip fractures. Bone, 1996 Mar, 18:3 Suppl, 139S-144S.
Bowman MA & Spangler JG: Osteoporosis in women. Prim Care, 1997 Mar, 24:1, 27-36.
Brattstrom, L., B. Hultberg & J. Hardebo. Folic acid responsive postmenopausal homocysteinemia. Metabolism 34:1073-7, 1985.
Boyle-IT: Secondary osteoporosis. Baillieres-Clin-Rheumatol. 1993 Oct; 7(3): 515-34.
Bunker VW: The role of nutrition in osteoporosis. Br J Biomed Sci, 1994 Sep, 51:3, 228-40.
Cohen, L. & R. Kitzes. Infrared spectroscopy and magnesium content of bone mineral in osteoporotic women. Isr J Med Sci 17:1123-5, 1981.
Dambacher MA et al., Can the fast bone loss in osteoporotic and osteopenic patients be stopped with active vitamin D metabolites? Calcif Tissue Int, 1997 Jan, 60:1, 115-8.
Deal CL: Osteoporosis: prevention, diagnosis, and management. Am J Med, 1997 Jan 27, 102:1A, 35S-39S.
DeMeo MT et al., Three cases of comprehensive dietary therapy and pharmacotherapy of patients with complex obesity-related diseases. Nutr Rev, 1997 Aug, 55:8, 297-302.
Dixon, A. Brit Med J., 1983; 286: 999-1000.
Donaldson, C., S. Hulley, J. Vogel, et al: Effect of prolonged bed rest on bone mineral. Metabolism 19:1071-84, 1976.
Durance, R.A., et al. Clin Trials J., 1973; 3: 67-73.
Editoral. Citrate for calcium nephrolithiasis. Lancet i:955. 1986.
Editoral. The function of the vitamin K-dependent proteins, bone GLA protein (BGP) and kidney GLA proteins (KGP). Nutr Rev 42:230-3, 1984.
Ellis, F., S. Holesh, & J. Ellis. Incidence of osteoporosis in vegetarians and omnivores. Am J Clin Nutr 25:55-8, 1972.
Epstein, O. et al. Am J Clin Nutr., 1982; 36: 426-430.
Feng, W. et al: Low Follicular Estrogen Levels in New Zealand Women Consuming High Fiber Diets: A Risk Factor For Osteopenia. The New Zealand Medical Journal, October 13, 1993;106(965):319- 322.
Francis RM: Is there a differential response to alfacalcidol and vitamin D in the treatment of osteoporosis? Calcif Tissue Int, 1997 Jan, 60:1, 111-4.
Fujita T: Clinical guidelines for the treatment of osteoporosis in Japan. Calcif Tissue Int, 1996, 59 Suppl 1:, 34-7.
Fujita T: Vitamin D in the treatment of osteoporosis revisited. Proc Soc Exp Biol Med, 1996 Jun, 212:2, 110-5.
Furst, P.: Dietary L-Lysine Supplementation: A Promising Nutritional Tool in the Prophylaxis and Treatment of Osteoporosis. Nutrition, January/February 1993;9(1):71-72.
Gallagher JC: The role of vitamin D in the pathogenesis and treatment of osteoporosis. J Rheumatol Suppl, 1996 Aug, 45:, 15-8.
Gallagher, J., L. Riggs, J. Eisman, et al: Intestinal calcium absorption and serum vitamin D metabolites in normal subjects and osteoporotic patients: Effect of age and dietary calcium. J Clin Invest 64, 1979.
Gallagher-Allred CR & Emley SJ: Specific dietary interventions. Diabetes, osteoporosis, renal disease. Prim Care, 1994 Mar, 21:1, 175-89.
Germine, M., Parsons, J.R. J Biomed Mater Res., 1988; 22; 55-67.
Grossman, M., J. Kirsner & I. Gillespie. Basal and histalog-stimulated gastric secretion in control subjects and in patients with peptic ulcer or gastric cancer. Gastroenterology 45:15-26, 1963.
Haines ST et al., Alternatives to estrogen replacement therapy for preventing osteoporosis. J Am Pharm Assoc (Wash), 1996 Dec, NS36:12, 707-15.
Hathcock JN: Vitamins and minerals: efficacy and safety. Am J Clin Nutr, 1997 Aug, 66:2, 427-37.
Heaney, R. Nutritional factors and estrogen in age-related bone loss. Clin Invest Med 5:147-55, 1981.
Hilund U et al., Importance of diet and sex in prevention of coronary artery disease, cancer, osteoporosis, and overweight or underweight: a study of attitudes and practices of Danish primary care physicians. Am J Clin Nutr, 1997 Jun, 65:6 Suppl, 2004S-2006S.
Hussain-A & Barer-DH.: Nutritional assessment in patients admitted with proximal femoral fractures [letter] Gerontology. 1994; 40(5): 289.
Infante-Rivard, C., M. Krieger, M. Gascon-Barre & G.E. Rivard. Folate deficiency among institutionalized elderly, public health impact. J Am Geriatrics Society 34:211-4, 1986.
Johansson, G., U. Backman, B. Danielson, et al. Biochemical and clinical effects of the prophylactic treatment of renal calcium stones with magnesium hydroxide. J Urol 124:770-4, 1980.
Jones G et al., Prevention and management of osteoporosis: consensus statements from the Scientific Advisory Board of the Osteoporosis Society of Canada. 8. Vitamin D metabolites and analogs in the treatment of osteoporosis. Can Med Assoc J, 1996 Oct 1, 155:7, 955-61.
Kessenich CR: Update on pharmacologic therapies for osteoporosis. Nurse Pract, 1996 Aug, 21:8, 19-24.
Kirschmann, J.D. 1990. Nutrition Almanac: Nutrition Search. McGrew-Hill: New York.
Klesges RC Changes in bone mineral content in male athletes. Mechanisms of action and intervention effects. JAMA, 1996 Jul 17, 276:3, 226-30.
Krasinski, S.D., R.M. Russell, B.C. Furie, et al. The prevalence of vitamin K deficiency in chronic gastrointestinal disorders. Am J Clin Nutr 41:639-43, 1985.
Krolner, B., B. Toft, S. Nielsen & E. Tondevold. Physical exercise as prophylaxis against involutional vertebral bone loss. A controlled trial. Clin Sci 64:541-6, 1983.
Lee, C.J., G.S. Lawler, & G.H. Johnson. Effects of supplementation of the diets with calcium and calcium-rich foods on bone density of elderly females with osteoporosis. Am J Clin Nutr 34:819-23, 1981.
Licata, A., E. Bou, F. Bartter, & F. West. Acute effects of dietary protein on calcium metabolism in patients with osteoporosis. J Geron 36:14-9, 1981.
Lore, F., R. Nuti, A. Vattimo & Caniggia. Vitamin D metabolites in postmenopausal osteoporosis. Horm Metabol Res 16:58, 1984.
Marcus, R. The relationship of dietary calcium to the maintenance of skeletal integrity in man - An interface of endocrinology and nutrition. Metabol 31:93-102, 1982.
Marsh, A., T. Sanchez, F. Chaffe, et al. Bone mineral mass in adult lacto ovo-vegetarian and omnivorous adults. Am J Clin Nutr 37:453-6, 1983.
Melton ME & Kochman ML: Reversal of severe osteoporosis with vitamin B12 and etidronate therapy in a patient with pernicious anemia. Metabolism, 1994 Apr, 43:4, 468-9.
Murray TM: Prevention and management of osteoporosis: consensus statements from the Scientific Advisory Board of the Osteoporosis Society of Canada. 4. Calcium nutrition and osteoporosis. Can Med Assoc J, 1996 Oct 1, 155:7, 935-9.
Newcomer, A., S. Hodgson, D. McGill, & Thomas P: Lactase deficiency: Prevalence in osteoporosis. Ann Int Med 89:218-20, 1978.
Nicar, M.J. & C.Y.C. Pak. Calcium bioavailability from calcium carbonate and calcium citrate. J of Clin Endocrinolgy & Metabolism 61:391-3, 1985.
Nilsen, E.M., et al. Brit Med J., 1978; 2: 1124.
Packard PT & Heaney RP: Medical nutrition therapy for patients with osteoporosis. J Am Diet Assoc, 1997 Apr, 97:4, 414-7.
Pak & Fuller. Idiopathic hypocitraturic calcium-oxalate nephrolithiasis successfully treated with potassium citrate. Ann Int Med 104:33-7, 1986.
Peris P et al., Aetiology and presenting symptoms in male osteoporosis. Br J Rheumatol, 1995 Oct, 34:10, 936-41.
Pines, A., et al. Curr Med Res Opinion, 1984; 8: 734-742.
Pizzorno, Joseph E. & Murray, Michael T. A Textbook of Natural Medicine. JBC Publications, Seattle, WA, 1985.
Prior JC et al., Prevention and management of osteoporosis: consensus statements from the Scientific Advisory Board of the Osteoporosis Society of Canada. 5. Physical activity as therapy for osteoporosis. Can Med Assoc J, 1996 Oct 1, 155:7, 940-4.
Rao, C., V. Rao & B. Steinman. Influence of bioflavonoids on the metabolism and crosslinking of collagen. Ital J Biochem 30:259-70, 1981.
Recker, R. Calcium absorption and achlorhydria. New England Journal of Medicine 313:70-3, 1985.
Reid IR: Therapy of osteoporosis: calcium, vitamin D, and exercise. Am J Med Sci, 1996 Dec, 312:6, 278-86.
Rico-H et al: Biochemical markers of nutrition in type-I and type-II osteoporosis. J-Bone-Joint-Surg-Br. 1995 Jan; 77(1): 148-51.
Romberg, R.W., et al. Biochem., 1986; 25: 1176-1180.
Rousseau ME: Dietary prevention of osteoporosis. Lippincotts Prim Care Pract, 1997 Jul-Aug, 1:3, 307-19.
Rude RK & Olerich M: Magnesium deficiency: possible role in osteoporosis associated with gluten-sensitive enteropathy. Osteoporos Int, 1996, 6:6, 453-61.
Rude, R.K., J.S. Adams, E. Ryzen, et al. Low serum concentration of 1,25-dihydroxy vitamin D in human magnesium deficiency. J Clin Endo Metabol 61:933-40.
Sambrook, P. et al: Prevention of Corticosteroid Osteoporosis: A Comparison of Calcium, Calcitriol, and Calcitonin. New England Journal of Medicine, June 17, 1993;328(24):1747-1752.
Sampson HW: Alcohol, osteoporosis, and bone regulating hormones. Alcohol Clin Exp Res, 1997 May, 21:3, 400-3.
Seaborn, C. D.& Nielsen, F. H.: Silicon: A Nutritional Beneficence for Bones, Brains and Blood Vessels. Nutrition Today, July/August 1993;13-18.
Seater, R. & R. Martin. Senile osteoporosis: The effects of exercise. Postg Med 75:147-9, 1984.
Seelig, M.S. Magnesium deficiency with phosphate and vitamin D excess. Role in pediatric cardiovascular nutrition. Cardio Med 3:637-50, 1978
Smith, D.F., Reid, D.M. Scot Med J., 1989; 438-439.
Spencer & Kramer: Antacid-induced calcium loss. Arch. Intern. Med. 1983, 143(4): 657-659.
Stellon, A., et al. Postgrad Med J., 1985; 61: 791-796.
Thom, J., J. Morris, A. Bishop & Blacklock. The influence of refined carbohydrate on urinary calcium excretion. Br J Urol 50:459-64, 1978.
Walji, H. 1992. Vitamin Guide: Essential Nutrients for Healthy Living. Rockport, MA: Element, Inc.
Watts NB: Osteoporosis: prevention, detection and treatment. J Med Assoc Ga, 1997 Sep, 86:3, 224-6.
Windsor, A.C.M., et al. Age Aging, 1987; 2: 230-234.
- Product Categories
- Detox & Immunity
- Digestive Health
- Joint Health
- Weight Loss
- Popular Products
- CellRenew Collagen Hyaluronic Acid
- Foundation Blue-Green Algae
- Dream Health System
- Liver Cleanse
- Reference Materials
- Product Testimonials
- Health Journal Archive
- Health Briefs
- Health Basics
- Frequent Product Q&A's
- Med-Scope (health database)
- Health Conditions
- Natural Solutions
- Alternative Therapies
- Toxicity Sources
- Foods Advice
- Anatomy & Fitness
We test only on humans