| ||Calcium regulation of androgen receptor expression in the human prostate cancer cell line LNCaP|
| ||The role of calcium, pH, and cell proliferation in the programmed (apoptotic) death of androgen-independent prostatic cancer cells induced by thapsigarin|
| ||Programmed cell death as a new target for prostatic cancer therapy|
| ||Hypercalcemia in carcinoma of the prostate: Case report and review of the literature|
| ||Calcium excretion in metastatic prostatic carcinoma|
| ||Chemoprevention of colorectal tumors: role of lactulose and of other agents.|
| ||[Overview--suppression effect of essential trace elements on arteriosclerotic development and it's mechanism]|
| ||Different effects of PTH on erythrocyte calcium influx|
| ||Hypercalcemia due to constitutive activity of the parathyroid hormone (PTH)/PTH-related peptide receptor: Comparison with primary hyperparathyroidism|
| ||Osteoclast cytomorphometry in patients with femoral neck fracture|
| ||The PTH-calcium relationship curve in secondary hyperparathyroidism, an index of sensitivity and suppressibility of parathyroid glands|
| ||Role of parathyroid hormone-related peptide (PTHrP) in hypercalcemia of malignancy and the development of osteolytic metastases|
| ||Experimental study of glucocorticoid-induced rabbit osteoporosis|
| ||24,25 dihydroxyvitamin D supplementation corrects Intradialytic calcium balances with different calcium dialysate levels. Effects on cardiovascular stability and parathyroid function|
| ||Biochemical effects of calcium and vitamin D supplementation in elderly, institutionalized, vitamin D-deficient patients|
| ||Calcium, phosphate, vitamin D, and the parathyroid|
| ||The BsmI vitamin D receptor restriction fragment length polymorphism (bb) influences the effect of calcium intake on bone mineral density|
| ||Bone mineral density changes during lactation: Maternal, dietary, and biochemical correlates|
| ||Postprandial parathyroid hormone response to four calcium-rich foodstuffs|
| ||Complementary medical treatment for Colles' fracture: A comparative, randomized, longitudinal study|
| ||Treatment of postmenopausal osteoporosis: Spoilt for choice? Part 1 - Foundations for an individually adapted management concept|
| ||Calcium and vitamin D in the prevention and treatment of osteoporosis|
| ||Calcium intake and fracture risk: Results from the study of osteoporotic fractures|
| ||Bone loss and turnover after cardiac transplantation|
| ||What's hip in diet and osteoporosis?|
| ||A high dietary calcium intake is needed for a positive effect on bone density in Swedish postmenopausal women|
| ||Amelioration of hemiplegia-associated osteopenia more than 4 years after stroke by 1alpha-hydroxyvitamin D3 and calcium supplementation|
| ||The usefulness of bone turnover in predicting the response to transdermal estrogen therapy in postmenopausal osteoporosis|
| ||Osteoporotic vertebral fractures in postmenopausal women|
| ||Proteins and bone health|
| ||Osteoporosis: Prevention, diagnosis, and management|
| ||Connections between phospho-calcium metabolism and bone turnover. Epidemiologic study on osteoporosis (second part)|
| ||Calcium regulation and bone mass loss after total gastrectomy in pigs|
| ||Management of osteoporosis in the elderly|
| ||Effect of measuring bone mineral density on calcium intake|
| ||Osteoporosis: Its pediatric causes and prevention opportunities|
| ||Estimated dietary calcium intake and food sources for adolescent females: 1980-92|
| ||The pathogenesis of age-related osteoporotic fracture: Effects of dietary calcium deprivation|
| ||Osteoporosis prevention and treatment. Pharmacological management and treatment implications|
| ||Calcium metabolism in the elderly|
| ||Therapy of osteoporosis: Calcium, vitamin D, and exercise|
| ||Pathophysiology of osteoporosis|
| ||Risk for osteoporosis in black women|
| ||Age considerations in nutrient needs for bone health: Older adults|
| ||Dietary calcium intake and its relation to bone mineral density in patients with inflammatory bowel disease|
| ||Harmonization of clinical practice guidelines for the prevention and treatment of osteoporosis and osteopenia in Europe: A difficult challenge|
| ||Clinical practice guidelines for the diagnosis and management of osteoporosis|
| ||Current and potential future drug treatments for osteoporosis|
| ||Calcium nutrition and osteoporosis|
| ||Osteoporosis of Crohn's disease: A critical review|
| ||The preparation and stability of compound active calcium tablets|
| ||Immunosuppression: Tightrope walk between iatrogenic side effects and therapy|
| ||Secondary osteoporosis in rheumatic diseases|
| ||Does lactose intolerance predispose to low bone density? A population-based study of perimenopausal Finnish women|
| ||Glucocorticoid-induced osteoporosis|
| ||Current treatment options for osteoporosis|
| ||Treatments for oestoporosis|
| ||Estrogen replacement may be an alternative to parathyroid surgery for the treatment of osteoporosis in elderly postmenopausal women presenting with primary hyperparathyroidism: A preliminary report|
| ||The effect of calcium supplementation and Tanner Stage on bone density, content and area in teenage women|
| ||Osteoporosis and calcium ingest|
| ||Vitamin D and calcium in the prevention of corticosteroid induced osteoporosis: A 3 year followup|
| ||Novelties and issues in the drug market 1995|
| ||Influence of life style in the MEDOS study|
| ||Roles of diet and physical activity in the prevention of osteoporosis|
| ||The problem: Health impact of osteoporosis|
| ||Prophylaxis of osteoporosis with calcium, estrogens and/or eelcatonin: Comparative longitudinal study of bone mass|
| ||Nutritional prevention of aging osteoporosis|
| ||Osteoporotic fractures: Background and prevention strategies|
| ||Energy and nutrient intake in patients with CF|
| ||Current and future nonhormonal approaches to the treatment of osteoporosis|
| ||Transient osteoporosis of the hip. Case report and review of the literature|
| ||Osteomalacia and osteoporosis in a woman with ankylosing spondylitis|
| ||Calcium and vitamin D nutritional needs of elderly women|
| ||Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis|
| ||Calcium deficiency in fluoride-treated osteoporotic patients despite calcium supplementation|
| ||Axial bone mass in older women|
| ||Bone mineral density in mother-daughter pairs: Relations to lifetime exercise, lifetime milk consumption, and calcium supplements|
| ||Reduced bone mass in women with premenstrual syndrome|
| ||Calcium-regulating hormones across the menstrual cycle: Evidence of a secondary hyperparathyroidism in women with PMS|
| ||Calcium supplementation in premenstrual syndrome: A randomized crossover trial|
| ||Multiple sclerosis: vitamin D and calcium as environmental determinants of prevalence (a viewpoint). I.: Sunlight, dietary factors and epidemiology |
| ||Calcium, phosphorus and magnesium intakes correlate with bone mineral content in postmenopausal women |
| ||Effect of glucocorticoids and calcium intake on bone density and bone, liver and plasma minerals in guinea pigs|
| ||Relationship between liver cirrhosis death rate and nutritional factors in 38 countries|
| ||Prophylaxis of recurring urinary stones: hard or soft mineral water|
| ||Prospective study of nutritional factors, blood pressure, and hypertension among US women.|
| ||Association of macronutrients and energy intake with hypertension.|
| ||Relations between magnesium, calcium, and plasma renin activity in black and white hypertensive patients|
| ||Effect of renal perfusion pressure on excretion of calcium, magnesium, and phosphate in the rat.|
| ||Nonpharmacologic treatment of hypertension.|
| ||Micronutrient effects on blood pressure regulation.|
| ||Role of magnesium and calcium in alcohol-induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P-NMR, spectroscopy and a unique magnesium ion-selective electrode.|
| ||Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review).|
| ||Effect of dietary magnesium supplementation on intralymphocytic free calcium and magnesium in stroke-prone spontaneously hypertensive rats.|
| ||Impact of increasing calcium in the diet on nutrient consumption, plasma lipids, and lipoproteins in humans|
| ||Electrolytes and hypertension: results from recent studies.|
| ||Augmentation of the renal tubular dopaminergic activity by oral calcium supplementation in patients with essential hypertension.|
| ||The pathogenesis of eclampsia: the 'magnesium ischaemia' hypothesis.|
| ||Intracellular Mg2+, Ca2+, Na2+ and K+ in platelets and erythrocytes of essential hypertension patients: relation to blood pressure.|
| ||A prospective study of nutritional factors and hypertension among US men|
| ||Electrolytes in the epidemiology, pathophysiology, and treatment of hypertension.|
| ||Minerals and blood pressure.|
| ||The effect of Ca and Mg supplementation and the role of the opioidergic system on the development of DOCA-salt hypertension.|
| ||Dietary modulators of blood pressure in hypertension|
| ||Daily intake of macro and trace elements in the diet. 4. Sodium, potassium, calcium, and magnesium|
| ||Calcium intake: covariates and confounders|
| ||Nutrition and the elderly: a general overview.|
| ||Blood pressure and nutrient intake in the United States.|
| ||Serum calcium, magnesium, copper and zinc and risk of cardiovascular death.|
| ||Endothelial function in deoxycorticosterone-NaCl hypertension: effect of calcium supplementation.|
| ||Prevention of preeclampsia with calcium supplementation and its relation with the L-arginine:nitric oxide pathway.|
| ||[Guidelines on treatment of hypertension in the elderly, 1995--a tentative plan for comprehensive research projects on aging and health-- Members of the Research Group for "Guidelines on Treatment of Hypertension in the Elderly", Comprehensive Research Projects on Aging and Health, the Ministry of Health and Welfare of Japan]|
| ||Management of acute myocardial infarction in the elderly|
| ||Supraventricular tachycardia after coronary artery bypass grafting surgery and fluid and electrolyte variables|
| ||The effects of calcium channel blockers on blood fluidity.|
| ||Concentrations of magnesium, calcium, potassium, and sodium in human heart muscle after acute myocardial infarction.|
| ||Nutrient intake and food use in an Ojibwa-Cree community in Northern Ontario assessed by 24h dietary recall|
| ||Mgsup 2sup +-Casup 2sup + interaction in contractility of vascular smooth muscle: Mgsup 2sup + versus organic calcium channel blockers on myogenic tone and agonist-induced responsiveness of blood vessels|
| ||Antacids drugs: Multiple but too often unknown pharmacological properties|
| ||Trace elements in prognosis of myocardial infarction and sudden coronary death|
| ||Intakes of vitamins and minerals by pregnant women with selected clinical symptoms.|
| ||[Amyotrophic lateral sclerosis--causative role of trace elements]|
| ||Aluminum Deposition in Central Nervous System of Patients with Amyotrophic Lateral Sclerosis From the Kii Peninsula of Japan|
| ||[Deficiency of certain trace elements in children with hyperactivity]|
| ||Augmented Ca2+ in-flux is involved in the mechanism of enhanced proliferation of cultured vascular smooth muscle cells from spontaneously diabetic Goto-Kakizaki rats|
| ||The central role of calcium in the pathogenesis of cardiovascular disease|
| ||Dietary calcium, vitamin D, and the risk of colorectal cancer in Stockholm, Sweden|
| ||Natural products and their derivatives as cancer chemopreventive agents|
| ||New agents for cancer chemoprevention|
| ||Frequently nebulized beta-agonists for asthma: effects on serum electrolytes.|
| ||Effect of nebulized albuterol on serum potassium and cardiac rhythm in patients with asthma or chronic obstructive pulmonary disease.|
| ||Long-term treatment with calcium-alpha-ketoglutarate corrects secondary hyperparathyroidism|
| ||Oral vitamin D or calcium carbonate in the prevention of renal bone disease?|
| ||Comparison of effects of calcitriol and calcium carbonate on secretion of interleukin-1beta and tumour necrosis factor-alpha by uraemic peripheral blood mononuclear cells|
| ||Effect of dietary calcium on urinary oxalate excretion after oxalate loads|
| ||The lack of influence of long-term potassium citrate and calcium citrate treatment in total body aluminum burden in patients with functioning kidneys|
The problem: Health impact of osteoporosis
Scandinavian Journal of Rheumatology, Supplement (Norway), 1996, 25/103 (3‑5)
Osteoporosis constitutes a major public health problem through its association with age related fractures. These fractures typically occur at the hip, spine and distal forearm. It has been estimated from incidence rates derived in North America that the lifetime risk of a hip fracture in caucasian women is 17.5%, with a comparable risk in men of 6%. Hip fractures lead to an overall reduction in survival of around 15% and the majority of excess deaths occur within the first six months following the fracture. They are also associated with considerable morbidity: they invariably necessitate hospitalization and the average length of hospital stay is around 30 days. Although all vertebral deformities do not come to clinical attention, the lifetime risk of clinically diagnosed vertebral fractures is around 15% in caucasian women. These fractures tend to be associated with back pain and result in kyphosis. They are also associated with impairment of survival, although this is likely to be due to the clustering of comorbidity which predisposes independently to osteoporosis and premature death. Around a quarter of clinically diagnosed vertebral deformities result in hospitalization. Hip fractures typically follow a fall from the standing position and their incidence rises exponentially with age. Above the age of 50 years there is a female to male ratio of around 2:1. There is marked seasonality in hip fracture incidence, with substantial increases in rates during winter months in temperate countries. Nevertheless, the majority of hip fractures follow falls indoors and are not related to slipping on icy pavements. Age‑ and sex‑adjusted hip fracture rates are generally higher in caucasian than in Asian populations. Furthermore, the pronounced female preponderance in fracture incidence observed in white populations is not seen amongst blacks or Asians in whom age‑adjusted female to male incidence ratios approximate unity. Urbanisation in certain parts of Africa has led to a secular increase in hip fracture incidence rates, bt even recently derived African rates are considerably lower than those found in North American or European whites. The incidence of clinically diagnosed vertebral fractures also rises steeply with age and the female to male incidence ratio after age adjustment is also around 2:1. The ultimate determinants of osteoporotic fractures are bone strength and trauma. Bone strength is related to the quality of bone, its architecture and its mass. These characteristics cannot easily be assessed in vivo, but correlate closely with bone mineral density. There is now convincing longitudinal evidence that a reduction in bone density is an important determinant of fracture risk. The determinants of bone density can be categorised into those influencing the peak which is attainable during growth and consolidation; and the subsequent rate of bone loss. There is a genetic feeling to the peak bone density which can be obtained during the first 25 years of life, which is modified by nutrition, mechanical factors and hormonal status. Important determinants of bone loss include estrogen deficiency in women, low body mass index, cigarette smoking, alcohol consumption, poor dietary calcium intake, physical inactivity, certain drugs such as corticosteroids, and illnesses such as rheumatoid arthritis. The information on individual risk factors which has been carefully characterised over the last decade permits translation into coherent public health strategies for the prevention of osteoporosis both in individuals and in the general population.
Prophylaxis of osteoporosis with calcium, estrogens and/or eelcatonin: Comparative longitudinal study of bone mass
Maturitas (Ireland), 1996, 23/3 (327‑332)
Objective: To evaluate three different therapeutic regimens for the prevention of osteoporosis in natural and surgical postmenopausal women who had been found to have rapid bone loss in analytical studies. Methods: A total of 104 naturally or surgically postmenopausal women were studied, and subsequently followed‑up during 1 year for avoidance of the influence of seasonal variation on bone mass, a factor overlooked in several studies. They were randomized into four groups of 26 patients each: the untreated control group (mean age 50 + or - 5 years); the hormonal replacement treatment (HRT) group (mean age 48 plus or minus 6 years), which was treated for 24 days each month with transdermal 17beta‑estradiol, 50 mg/day, together with medroxiprogesterone, 10 mg during 12 days; the calcium group (mean age 50 + or - 4 years), which was treated with elemental calcium, 1 g/day; and the calcitonin group (mean age 50 plus or minus 5 years), which was treated for 10 days each month with eel calcitonin, 40 IU/day and with elemental calcium, 500 mg/day. Full‑body bone densitometry, for measuring total body bone mineral content (TBBMC), was carried out in all the women at baseline and 1 year. TBBMC was corrected for body weight by dividing its value by body weight (TBBMC/W). Results: After 1 year TBBMC/W was lower in every group: ‑2.14% (P < 0.001) in the control group; ‑0.14% (P = NS) in the HRT group (P < 0.05 vs. controls); ‑0.18% (P = NS) in the calcium group (P < 0.05 vs. controls); and ‑0.06% (P = NS) in the calcitonin group (P < 0.01 vs. controls; P < 0.05 vs. calcium and HRT). Conclusions: These findings show that all three treatments are effective in the prevention of postmenopausal loss of bone mass.
Nutritional prevention of aging osteoporosis
Cahiers de Nutrition et de Dietetique (France), 1996, 31/2 (98‑101)
Aging is accompanied by a decrease in bone mass, with the risk of developing osteoporosis, of which the consequence is atraumatic fractures. These fractures, particularly those of the proximal femur, are associated with an important socioeconomic impact.Calcium supplements contribute to prevent bone loss in the elderly. On the other hand, protein repletion administered to compensate highly frequent malnutrition in the elderly can decrease medical complications following a fracture of the proximal femur, and exerts a favorable influence on bone mineral density.
Osteoporotic fractures: Background and prevention strategies
Maturitas (Ireland), 1996, 23/2 (193‑207)
Objectives: To review current knowledge of the epidemiology, pathogenesis, prevention and treatment of osteoporosis, with particular reference to issues related to the menopause. Methods: Peer‑reviewed publications were assessed. Results: Much international variation exists in the prevalence of osteoporosis and the incidence of fracture. Risk fractures for oesteoporosis are numerous. The menopause and other causes of hypogonadism in both women and men strongly predispose to osteoporosis. Various endocrinopathies, especially glucocorticoid excess, also are important. The contribution of family history may be explained by one or more markers. Poor vitamin D and calcium nutrition, smoking, high alcohol consumption and inactivity increase risk. Reduced bone mass is a major risk factor for fracture, although the magnitude of that risk may vary between populations. In addition, bone fragility, length of the femoral neck (for hip fracture), history of prior fracture (for vertebral fracture) and falls affect fracture risk. Useful methods for measuring bone density are available for both epidemiologic surveillance and for clinical practice. Dual energy x‑ray absorptiometry is the most desirable method in clinical care settings. Some risk factors can be modified for prevention of osteoporosis. Postmenopausal bone loss can be inhibited with estrogen or estrogen plus progestin therapy. Bone loss in the elderly may be moderated with calcium and vitamin D supplementation. Maintenance of muscle tone and strength through exercise may reduce falls.Conclusion: Osteoporosis is a large and growing health problem in many countries. Prevention of osteoporosis is a high priority, especially because treatment of the established disease remains sub‑optimal. Prevention requires immediate, intermediate‑term and long‑term strategies. First line therapy for established osteoporosis in women in many countries is estrogen or estrogen plus progestin, calcium and vitamin D. Prospects for improved prevention of osteoporotic fractures are encouragng.
Energy and nutrient intake in patients with CF
Monatsschrift fur Kinderheilkunde (Germany), 1996, 144/4 (396‑402)
Background: Nutritional assessment and management remain important issues in the treatment of CF patients despite newer developments as lung transplantation, inhalation with DNase and gene therapy. Methods: The nutritional status of 26 patients (mean age 15,8 years; 16 male; 46% homozygous, 38% heterozygous for DeltaF 508, remaining unknown; 3 pancreas sufficient, Shwachman score intermediate to excellent) of our CF clinic was analyzed using a three days protocol, the precise weighing method and comparison of data with the official dietary recommendations. Results: The average energy intake was below the 130% officially recommended and the fat intake was below the aimed 40% of total energy intake. The regression analysis revealed positive correlations between energy intake and SDS(Height) and Shwachman score and SDS(Weight) respectively. Food contained an insufficient amount of unsaturated fatty acids. Water soluble vitamins were supplemented adequately besides folic acid, but intake of fat soluble vitamins E and A often was insufficient despite extra vitamin capsules. Every second patient did not take enough minerals as calcium, magnesium or iron. Conclusions: This analysis underlines how important the regular assessment of the nutritional status can be for the individual nutritional management of CF patients even if clinical symptoms of deficiencies could not be detected. An increase of fat intake as a main source of energy, essential fatty acids and fat soluble vitamins has to be encouraged as well as the increased use of milk and milk products for the prevention of osteoporosis. Iron and folic acid are further critical nutrients.
Current and future nonhormonal approaches to the treatment of osteoporosis
International Journal of Fertility and Menopausal Studies (USA), 1996, 41/2 (148‑155)
Osteoporosis is the most important metabolic bone disease of women. Still, approaches to successful therapy are limited. The 'gold standard' for prevention of osteoporosis in the menopausal years is estrogen. None of the other agents should be regarded as true alternatives to estrogens. Current recommendations for dietary calcium and vitamin D will be given as well as the following therapies: bisphosphonates, fluoride, calcitonin, and parathyroid hormone.
Transient osteoporosis of the hip. Case report and review of the literature
Acta Orthopaedica Belgica (Belgium), 1996, 62/1 (56‑59)
We present a case of idiopathic transient osteoporosis of the hip in a 43‑year‑old male. The patient presented with pain in the hip and limb. Hip x ray showed osteoporosis and scintigraphy revealed a diffuse uptake in the femoral head. Magnetic resonance imaging showed decreased signal intensity on the T1 weighted images and increased signal intensity on T2 weighted images in the femoral head and neck. Blood tests were normal. Healing was achieved by restricting weight‑bearing and administering calcitonin and calcium. Radiographic remineralization occurred simultaneously with clinical resolution.
Osteomalacia and osteoporosis in a woman with ankylosing spondylitis
Journal of Bone and Mineral Research (USA), 1996, 11/5 (697‑703)
Three months postpartum, a 33‑year‑old woman with ankylosing spondylitis (AS) suffered multiple vertebral fractures. Bone mineral density was 61‑67% of age‑matched normal values at the lumbar spine and proximal femur, and an initial iliac crest bone biopsy revealed osteoporosis and osteomalacia. Secondary causes of bone disease were excluded, and the patient was treated with calcium, vitamin D, and nasal spray calcitonin (400 u/day). Over 4 years, she has shown partial recovery of bone mass and almost complete resolution of osteomalacia. Osteoporosis and fracture occur in patients with AS, yet this case represents a rare association between AS and both osteomalacia and postpregnancy spinal osteoporosis.
Calcium and vitamin D nutritional needs of elderly women
Journal of Nutrition (USA), 1996, 126/4 SUPPL. (1165S‑1167S)
Because osteoporosis is irreversible, the most effective approach to reduce morbidity and mortality from this disease is to maximize peak bone mass and minimize bone loss. This presentation reviews the evidence that calcium and vitamin D influence rates of bone loss in postmenopausal women. In the first five or more years after menopause, women lose bone very rapidly. During this period, high dose calcium supplementation modestly reduces cortical loss from long bones but has minimal effect on more trabecular sites such as the spine. In addition, vitamin D appears to enhance the effectiveness of supplemental calcium. Late postmenopausal women are generally more responsive to added calcium, and those with the lowest dietary calcium intakes benefit the most. In calcium‑replete women, supplementation with vitamin D reduces bone loss and fracture incidence. Available evidence indicates that postmenopausal women should consume 1000‑1500 mg of calcium and 400 to 800 IU of vitamin D per day to minimize bone loss.
Heated oyster shell‑seaweed calcium (AAA Ca) on osteoporosis
Calcified Tissue International (USA), 1996, 58/4 (226‑230)
A randomized, prospective, double‑blind lest was curried out to compare the effects of heated oyster shell‑seaweed calcium (AAA Ca), calcium carbonate, and placebo in 58 elderly, hospitalized women with the mean age of 80 divided into three groups. Group A received 900 mg/day Ca as AAA Ca. Group B 900 mg/day Ca as CaCO3, and Group C placebo besides regular hospital diet containing approximately 600 mg Ca/day for 24 months. From the 25th to the 30th month, all groups were given AAA Ca. Lumbar spine and radial bone mineral density (BMD) were measured at 3‑month intervals. Urinary Ca/Cr and serum alkaline phosphatase, intact and midportion serum parathyroid hormone (PTH), and calcitonin were also measured at intervals. From the 6th to the 24th month of the study, the ratio of lumbar spine BMD (L2‑L4 by DPX, Lunar) to the basal pretest value was consistently mid significantly higher in Group A than Group C but not higher in Group B than in Group C. PTH, measured 12 months after the beginning of the study, was lower in Group A than in Group C, but no significant difference was found between Groups B and C. At 3 months after the placebo was switched to AAA Ca in Group C. serum PTH was significantly decreased from the level during placebo supplement. Morning urine Ca/Cr decreased in Groups A after 18 months and in B after 12 months, but not in C. Serum alkaline phosphatase decreased in Group A significantly compared with Group C, but not in Group B. AAA Ca appears to be effective for increasing BMD in elderly subjects.
Calcium deficiency in fluoride‑treated osteoporotic patients despite calcium supplementation
Journal of Clinical Endocrinology and Metabolism (USA), 1996, 81/1 (269‑275)
To test the hypothesis that the osteogenic response to fluoride can increase the skeletal requirement for calcium, resulting in a general state of calcium deficiency and secondary hyperparathyroidism, we assessed calcium deficiency, spinal bone density by quantitative computed tomography, and serum PTH in three groups of osteoporotic subjects. Two of the three groups had been treated with fluoride and calcium (at least 1500 mg/day) for 32 + or - 19 months. Group I consisted of 16 fluoride‑treated subjects who had shown rapid increases in spinal bone density (+3.8 + or - 2.6 mg/cm3 month), group II consisted of 10 fluoride‑treated subjects who had shown decreases or only slow increases in spinal bone density (‑0.05 + or - 0.6 mg/cm3 month), and group III consisted of 10 age‑matched untreated osteoporotic controls. Calcium deficiency was assessed by measurement of calcium retention after calcium infusion. The results of our studies showed that 1) 94% of the subjects in Group I were calcium deficient compared with only 30% in groups II and III (P < 0.01 for each); 2) the subjects in group I retained more calcium (79%) than the subjects in group II (60%, P < 0.001) or the subjects in group III (64%, P < 0.005); 3) calcium retention was proportional to serum PTH (r = 0.37, n = 36, P < 0.03); and 4) calcium retention was proportional to the (previous) fluoride‑dependent increase in quantitative computed tomography spinal bone density (in groups I and II, r = 0.48, n = 26, P < 0.02). To test the hypothesis that the calcium deficiency and the secondary hyperparathyroidism that were associated with the positive response to fluoride would respond to concomitant calcitriol treatment, a subgroup of 7 calcium‑deficient subjects were selected from group I and treated with calcitriol (plus fluoride and calcium) for an average of 7 months. The calcitriol therapy reduced the calcium deficit in all 7 subjects, decreasing calcium retention from 80% to 62% (P < 0.02), and decreasing PTH from 50 to 28 pg/mL (P < 0.02). Together, these data indicate that fluoride‑treated osteoporotic subjects may develop calcium deficiency in proportion to the effect of fluoride to increase bone formation, and this calcium deficit is responsive to calcitriol therapy.
Medecine et Hygiene (Switzerland), 1996, 54/2100 (85‑95)
The medical therapy of hyperprolactinemia and of acromegaly is improving due to emerging new drugs and to a better understanding of the biological mechanisms underlying their action. Somatotropic replacement therapy in growth hormone‑deficient adults results in favorable changes in body composition, physical resistance and quality of life. If can be predicted that this treatment will be made available to most adults with pathological growth hormone failure. The immune modulation exerted by anti‑thyroid drugs in Grave's disease remains controversial and the prolonged use of large doses systematically does not seem to be justified. On the other hand, the biological markers of autoimmunity, of recognized diagnostic interest, appeared to be of little prognostic value. The ob protein is an anorexigenic hormone from adipose tissue that has also been identified in man. It seems to be involved in the development of obesity, and it could be of considerable importance in the management of this condition. Progress in the treatment of osteoporosis of facilitated by the availability of dependable techniques to assess bone metabolism. The role of calcitonin, fluoride, bisphosphonates, calcium, and vitamin D in the treatment of each type of patients can thus be defined more appropriately.
Axial bone mass in older women
Annals of Internal Medicine (USA), 1996, 124/2 (187‑196)
Objective: To determine the anthropometric, historical, and lifestyle factors associated with bone mineral density (BMD) of the spine and proximal femur in older women. Design: Cross‑sectional analyses. Setting: Four clinical centers in Baltimore, Maryland; Minneapolis, Minnesota; Portland, Oregon; and the Monongahela Valley, Pennsylvania. Participants: 7963 ambulatory, nonblack women 65 years of age or older. Measurements: Medical history was obtained by questionnaire and interview, and physical and anthropometric data were obtained by examination. Lumbar spine and proximal femoral BMDs were measured using dual‑energy x‑ray absorptiometry. Results: The multivariable models could predict 21% and 25% of the difference between participants in BMD at the femoral neck and lumbar spine, respectively. Weight was most highly associated with BMD. Postmenopausal estrogen use and other indicators of total estrogen exposure were strongly associated with increased BMD. Use of diuretics (both thiazide and nonthiazide), activity levels and muscle strength, alcohol intake, and dietary calcium intake were associated with higher BMD. A family history of osteoporotic fracture was strongly associated with low BMD. European ancestry and blond hair, childbirth or breast feeding, a history of hyperthyroidism, and progestin use were not associated with axial BMD. Conclusions: Weight is strongly associated with BMD. Estrogen exposure, physical activity, and calcium intake are also positively associated with BMD, whereas a family history of osteoporosis is associated with reduced BMD. These associations suggest ways to better identify risk for fracture.
Bone mineral density in mother‑daughter pairs: Relations to lifetime exercise, lifetime milk consumption, and calcium supplements
American Journal of Clinical Nutrition (USA), 1996, 63/1 (72‑79)
This study investigated associations between lifetime milk consumption, calcium intake from supplements, lifetime weight bearing exercise, and bone mineral density (BMD) among 25 elderly women (mean age 72 y) and their premenopausal daughters (mean age 41 y).The BMD of the total, axial, and peripheral skeleton was measured by dual energy X‑ray absorptiometry. Lifetime milk consumption, supplemental calcium intake, and weight‑bearing exercise were estimated retrospectively by questionnaire and interview. In multiple linear‑regression analyses, mothers' total and peripheral BMD were positively associated with supplemental calcium intake after age 60 y, body weight, current estrogen replacement therapy (ERT), and past oral contraceptive (OC) use, and negatively associated with age and height (all P < 0.05). Mothers' axial BMD was positively correlated with body weight and past OC use. Among daughters, lifetime weight‑ bearing exercise was a predictor of total and peripheral BMD, whereas total lean mass was a predictor of axial BMD. Mothers' lifetime milk consumption was positively associated with that of their daughters. Mothers' and daughters' peripheral BMD values were positively correlated after adjustment for daughters' exercise, and mothers' age, body weight, and ERT. These results suggest that calcium supplementation and exogenous estrogen positively influence bone mass in postmenopausal years. Our findings lend support to recommendations for physical activity as a means of osteoporosis prevention. In the age groups studied, the effects of behavioral and hormonal factors on BMD appeared to dominate over familial similarity, which suggests thai women may successfully enhance their genetically determined bone mass through weight‑bearing exercise, post menopausal ERT, and adequate calcium intake.
Journal of Women's Health (USA), 1995, 4/2 (161-168)
Recent evidence has demonstrated the efficacy of calcium in the relief of premenstrual syndrome (PMS) symptomatology. We therefore, hypothesized that PMS might be a clinical manifestation of a calcium deficiency state resulting in potential bone loss. The present study was designed to determine whether women with established PMS have reduced bone mineral density (BMD) measurements compared to asymptomatic controls. Women with PMS and asymptomatic controls were evaluated with dual-photon absorptiometry at two sites, the lumbar vertebrae and the proximal femur. During the luteal phase, concentrations of the calciotropic hormones iPTH, 1,25(OH)2D, 25OHD, and total serum calcium were obtained. Dietary calcium intake and 24-hour urine calcium excretion were measured as well in all participants. Controls and women with PMS had similar age, race, body mass index (BMI), and physical activity, Compared to controls, women with PMS had significantly lower vertebral bone mass measurements at L2-4 (1.18 plus or minus 0.11 vs. 1.28 plus or minus 0.11 g/cm2, p = 0.0016), and at the femur in Ward's triangle (0.84 plus or minus 0.10 g/cm2 vs. 0.91 plus or minus 0.16 g/cm2, p = 0.0458). In contrast, BMD at the femoral neck and trochanter was not different between groups. Women with PMS also had significantly lower 25OHD concentrations (19.5 plus or minus 7.5 vs. 25.3 plus or minus 8.3 ng/mL, p = 0.018) than controls. There were no differences between the two groups in the mean concentrations of iPTH, 1,25(OH)2D, calcium excretion, or dietary calcium intake. These data suggest that PMS is associated with reduced bone mass measurements and a calcium deficiency state. Further research in calcium metabolism may be worthwhile in elucidating the pathophysiology of PMS.
Journal of Clinical Endocrinology and Metabolism (USA), 1995, 80/7
Calcium metabolism across one menstrual cycle was studied in 12 healthy, premenopausal women. Seven women had documented premenstrual syndrome (PMS), and five were asymptomatic controls. Fasting blood samples were drawn at six points throughout the ovulatory cycle. In both the asymptomatic and the PMS groups, total and ionized calcium declined significantly at midcycle with the increase of estradiol. In the PMS group only, peak midcycle intact PTH was significantly elevated by approximately 30% compared with early follicular levels (49 plus or minus 25 vs. 37 plus or minus 22 ng/L, t = 3.79, P = 0.009). In the asymptomatic group, iPTH did not vary during the menstrual cycle. Midcycle iPTH was significantly higher in the PMS group compared with that of the control group (49 plus or minus 25 vs. 26 plus or minus 7 ng/L, Wilcoxon Z = 2.28, P = 0.02). Multivariate analysis showed that total and ionized calcium both varied significantly across the menstrual cycle. Significant differences between groups were found for total calcium, 25OHD, and 1,25-(OH)2D. One woman with PMS was treated with oral elemental calcium and cholecalciferol daily for 3 months, with amelioration of her symptoms. Midcycle iPTH and 1,25-(OH)2D declined after repletion of 25OHD. In conclusion, we found that concentrations of total and ionized calcium significantly fluctuate during the menstrual cycle both in symptomatic and in asymptomatic women. We also found that concentrations of iPTH, 25OHD, and 1,25-(OH)2D differed between groups during specific phases of the menstrual cycle. Our data suggest that women with PMS have mid-cycle elevations of iPTH with a transient, secondary hyperparathyroidism.
J. GEN. INTERN. MED. (USA), 1989, 4/3 (183-189)
Objective: To determine the efficacy of calcium supplementation in women with premenstrual syndrome (PMS). Design: Randomized, double-blind crossover trial. Setting: Outpatient medical clinic of a large city hospital. Participants: Seventy-eight women were initially screened. Trial selection was based on a history of recurrent PMS symptoms and on the results of a prospective assessment of daily symptom scores. Only women with symptom scores during the late luteal phase that were at least 50% greater than those during the intermenstrual phase were selected. Thirty- three women completed the trial. Intervention: A preliminary evaluation included physical examination, routine laboratory tests, dietary assessment, and psychiatric-evaluation. Each participant received six months of treatment involving three months of daily calcium supplementation (1,000 mg of calcium carbonate) and three months of placebo. Measurements: Efficacy was assessed prospectively by changes in daily symptom scores over a six-month period and retrospectively by an overall global assessment. Multivariate repeated measures analysis of variance on symptom ratings derived from daily PMS symptom scores demontrated a reduction in symptoms on calcium treatment during both the luteal (p = 0.011) and the menstrual phases (p = 0.032) of the reproductive cycle. Calcium supplementation had no effect during the intermenstrual phase. Retrospective assessment of overall symptoms confirmed this reduction: 73% of the women reported fewer symptoms during the treatment phase on calcium, 15% preferred placebo, and 12% had no clear preference. Three premenstrual factors (negative affect (p = 0.045); water retention (p = 0.003); pain (p = 0.036)) and one menstrual factor (pain (p = 0.02)) were significantly alleviated by calcium. Conclusion: Calcium supplementation is a simple and effective treatment for premenstrual syndrome, but further studies will be needed to determine its precise role in PMS.
Multiple sclerosis: vitamin D and calcium as environmental determinants of prevalence (a viewpoint). I.: Sunlight, dietary factors and epidemiology
INT.J.ENVIRON.STUD. (ENGLAND), 1974, 6/1 (19‑27)
A new theory for the etiology of multiple sclerosis (MS) has been developed which is compatible with epidemiologic, biochemical and genetic evidence. A predisposition for the disease is held to result from the development of abnormal myelin during puberty. Vitamin D and calcium are proposed as being essential for normal myelination. Curtailed supplies of these substances (from inadequate sunlight and phytate rich diets) correlate with geographic regions of high risk of MS. Conversely the prevalence of MS is lower where vitamin D is abundant, as in sunny climates, high altitudes, and littorals with dietaries rich in fish oils.
GYNECOL. ENDOCRINOL. (United Kingdom), 1994, 8/1 (55-58)
Qualitative and quantitative differences in the dietary habits of postmenopausal women were studied to assess their influence on bone health and osteoporosis. A total of 194 postmenopausal women were studied with forearm DEXA densitometry. 70 were osteoporotic and 124 served as controls. Women had been menopausal for 5-7 years and had never been treated with hormone replacement or drug therapy. A 3-day dietary recall was completed on Sunday, Monday and Tuesday after the examination: the results were processed by computer and daily calcium, phosphorus and magnesium intakes were related to bone mineral content (BMC). Data were compared with Student's t-test and significance was assessed at p < 0.05. Regression analysis was performed to correlate BMC and intake levels. The dietary intake of calcium phosphorus and magnesium was significantly reduced in osteoporotic women and correlated with BMC. Calcium and magnesium intakes were lower than the recommended daily allowance even in normal women. The results suggest that nutritional factors are relevant to bone health in postmenopausal women, and dietary supplementation may be indicated for the prophylaxis of osteoporosis. Adequate nutritional recommendations and supplements should be given before the menopause, and dietary evaluation should be mandatory in treating postmenopausal osteoporosis.
J. NUTR. (USA), 1979, 109/7 (1175-1188)
The purpose of this study was to see what effect glucocorticoids would have on bone density and mineral distribution in guinea pigs. Adult female guinea pigs were given prednisolone, a synthetic analogue of cortisol, for up to 24 weeks. Bone density and bone, liver and plasma levels of zinc, copper, iron, manganese, chromium, magnesium and calcium were studied in these animals. In one study, the effect of menopause was simulated by using ovariectomy. In another study, dietary calcium was varied to investigate its effect with glucocorticoids. Animals treated with 1 mg prednisolone/kg body weight showed increased femur density compared with controls, but no changes in tissue mineral concentrtions. Animals fed 100 mg prednisolone/kg body weight experienced decreased femur density. Differences in effects were not observed between ovariectomized and intact animals. Bone loss was greatest in animals fed the cereal-based closed-formula diet and least in animals fed the low-calcium diet. Changes in mineral content of femurs observed in animals which lost bone mass were increased iron concentration and decreased magnesium concentration. Total liver stores of zinc and magnesium increased. Liver copper increased in concentration per gram as well as in total content. Liver concentration of manganese decreased. Plasma changes in animals fed the high level of drug were decreased iron and calcium, and increased copper. Hemoglobin and hematocrit increased with increasing drug levels. It is suggested that glucocorticoids have marked effects on mineral metabolism which may be related to the bone loss and that these effects may be modified by dietary changes.
INT. J. EPIDEMIOL. (United Kingdom), 1988, 17/2 (414-418)
The relationship between liver cirrhosis death rates and certain nutritional factors was studied in 38 countries where mortality statistics were considered to be reliable. A partial correlation analysis showed that several food commodity consumption factors were independently and negatively (p < 0.01) associated with liver cirrhosis death rates after adjustment for alcohol consumption. These factors were total calories, protein, fat, calcium, vitamin A and vitamin B2. The significant association of protein, vitamin A, vitamin B2 and calcium with the cirrhosis death rates is of importance since they were not intercorrelated with alcohol consumption. Further results showed that animal protein was more significantly related to cirrhosis death rates than vegetable protein. However, in view of certain limitations of this study, the findings do not necessarily reflect causal relationships but rather support the consideration by scientists that protein and vitamin deficiency may have certain effects on liver cirrhosis.
MINERVA MED. (Italy), 1987, 78/24 (1823-1829)
The influence of a calcium-rich mineral water on urine crystallisation in patients with recurring kidney stones was investigated. A calcium and magnesium rich water like the one tested increases the calcium and magnesium content of the urine but decreases oxaluria even after a dietary oxalate load.
Prospective study of nutritional factors, blood pressure, and hypertension among US women.
Hypertension (UNITED STATES) May 1996, 27 (5) p1065‑72
We examined prospectively the relation of nutritional factors with hypertension and blood pressure levels among 41,541 predominantly white US female nurses, aged 38 to 63 years, who completed a detailed semiquantitative food frequency questionnaire in 1984 and were without diagnosed hypertension, cancer, or cardiovascular disease. During 4 years of follow‑up, from 1984 to 1988, 2,526 women reported a diagnosis of hypertension. Age, relative weight, and alcohol consumption were the strongest predictors for the development of hypertension. Dietary calcium, magnesium, potassium, and fiber were not significantly associated with risk of hypertension, after adjusting for age, body mass index, alcohol, and energy intake. Among women who did not report hypertension during the follow‑up period, calcium, magnesium, potassium, and fiber were each significantly inversely associated with self‑reported systolic and diastolic pressures, after adjusting for age, body mass index, alcohol consumption, and energy intake. When the four nutrients were added simultaneously to the regression model, only fiber and magnesium intakes retained significant inverse associations with systolic and diastolic pressures. In analyses of food groups, intakes of fruit and vegetables were inversely associated with systolic and diastolic pressures, and intakes of cereals and meat were directly associated with systolic pressure. These results support hypotheses that age, body weight, and alcohol consumption are strong determinants of risk of hypertension in middle‑aged women. They are compatible with the possibilities that magnesium and fiber as well as a diet richer in fruits and vegetables may reduce blood pressure levels.
Association of macronutrients and energy intake with hypertension.
J Am Coll Nutr (UNITED STATES) Feb 1996, 15 (1) p21‑35
Hypertension, a major public health problem, becomes more prevalent during aging. Epidemiological studies suggest that environmental factors such as nutrition may play a major role in blood pressure (BP) regulation. It is generally accepted that obesity and sodium/alcohol consumption are important factors, and many believe that calcium, magnesium and potassium consumption are regulatory as well. Less emphasis has been placed on whether macronutrients influence blood pressure significantly. This review focused on the ability of excess calories and consumption of carbohydrates, fats, and proteins to regulate blood pressure. (207 Refs.)
Relations between magnesium, calcium, and plasma renin activity in black and white hypertensive patients
Miner Electrolyte Metab (SWITZERLAND) 1995, 21 (6) p417‑22
The heterogeneous status of magnesium and calcium metabolism in the hypertensive population may be related to the plasma renin activity (PRA). This study investigates the relationships between serum and erythrocyte magnesium (Mg2+) and calcium (Ca2+) concentrations and PRA in black and white essential hypertensive patients. Thirty‑nine normotensive (20 black, 19 white) and 47 hypertensive (25 black, 22 white) subjects were studied. The PRA was measured by radioimmunoassay, Mg2+ and Ca2+ by atomic absorption spectroscopy, and serum ionized Ca2+ by a specific electrode. PRA and ionized Ca2+ were significantly lower in the black hypertensive as compared with the white hypertensive group (1.99 +/‑ 0.33 vs. 5.96 +/‑ 1.02 ng/ml/h for PRA; 1.28 +/‑ 0.07 vs. 1.42 +/‑ 0.01 mmol/l for ionized Ca2+: black hypertensives vs. white hypertensives p < 0.05). Ionized Ca2+ was significantly increased (p < 0.05) in the white hypertensive patients as compared with the normotensive controls (1.42 +/‑ 0.01 vs. 1.29 +/‑ 0.04 mmol/l). In the black hypertensive group, serum and erythrocyte Mg2+ were significantly (p < 0.05) decreased as compared with the other groups. The erythrocyte Ca2+ concentration was significantly elevated in both black and white hypertensive patients. In the group as a whole, serum Mg2+ and PRA were negatively correlated and ionized Ca2+ and PRA and ionized Ca2+ and erythrocyte Ca2+ positively correlated. However, in the subgroups, these correlations were only significant in the white group: r = ‑0.67 and p < 0.05 serum Mg2+ vs. PRA; r = 0.64, and p < 0.05 ionized Ca2+ vs. PRA; r = 0.82 and p < 0.01 ionized [Ca2+]i vs. erythrocyte Ca2+. These data suggest a relationship between PRA, Mg2+, and Ca2+ which may be more important in white than in black hypertensive patients.
Effect of renal perfusion pressure on excretion of calcium, magnesium, and phosphate in the rat.
Clin Exp Hypertens (UNITED STATES) Nov 1995, 17 (8) p1269‑85
Abnormalities in renal handling of calcium, magnesium, or phosphate have been implicated in the development and/or maintenance of human hypertension. We have shown recently that renal excretion of these ions is correlated to blood pressure in Dahl salt‑sensitive as well as salt‑resistant rats. The present study was designed to determine whether renal perfusion pressure per se could affect excretion of these ions. Urinary excretion of calcium, magnesium, and phosphate was studied in anaesthetized Sprague‑Dawley rats under basal conditions and during an intravenous infusion of angiotensin II (ANG II), vasopressin (AVP) or phenylephrine (PE). A cuff, placed around the aorta between the two renal arteries, allowed maintenance of normal perfusion pressure in the left kidney, while that in the right kidney was allowed to rise. Infusion of pressor agents raised mean arterial blood pressure to comparable levels (means +/‑ SE): ANG II (n = 7), before = 102 +/‑ 4, during = 133 +/‑ 3 mmHg, AVP (n = 8), before = 110 +/‑ 7, during = 136 +/‑ 5 mmHg, PE (n = 6), before = 111 +/‑ 6, during = 141 +/‑ 6 mmHg. Although there was no difference in excretion of calcium, magnesium and phosphate between the two kidneys under basal conditions, infusion of ANG II or PE induced hypercalciuria, hypermagnesiuria and hyperphosphaturia in the right kidney which was exposed to the increased arterial pressure. Such effects did not appear in the pressure‑controlled left kidney. Infusion of AVP was associated with reduced excretion of calcium and magnesium, and increased excretion of phosphate, in the normotensive kidney. The response to the similarly increased renal perfusion pressure in this group was also reduced for calcium and magnesium, and enhanced for phosphate. The results indicate (1) renal excretion of calcium, magnesium and phosphate is renal perfusion pressure‑dependent; the higher the renal perfusion pressure, the greater the excretion of these ions. (2) Independently of perfusion pressure, AVP can inhibit phosphate reabsorption and stimulate divalent cation reabsorption.
Nonpharmacologic treatment of hypertension.
Curr Opin Nephrol Hypertens (UNITED STATES) Oct 1992, 1 (1) p85‑90
A variety of lifestyle modifications will lower both the blood pressure and various other cardiovascular risk factors that are frequently present in patients with hypertension. Numerous recent studies document the overall efficacy of some (weight reduction, sodium restriction, physical activity, moderation of alcohol) and the relative lack of effect of others (stress management and calcium, magnesium, and fish oil supplements). In particular, the Trials of Hypertension Prevention, Phase I (a control trial funded by the National Heart, Lung, and Blood Institute) provides important new data on the ability of these various modalities to prevent the development of hypertension, an equally or even more important goal than the reduction of already‑established disease. (32 Refs.)
Micronutrient effects on blood pressure regulation.
Nutr Rev (UNITED STATES) Nov 1994, 52 (11) p367‑75
Five micronutrients have been shown to directly influence blood pressure: sodium, calcium, potassium, magnesium, and chloride. The data presented here are based on accumulated findings from epidemiologic, laboratory, and clinical investigations, many of which focused primarily on a single nutrient. However, as also discussed here, nutrients are not consumed in isolation, and their physiologic interactions and combined effects on blood pressure are the subjects of much of the current research in the area of diet and hypertension. (71 Refs.)
Role of magnesium and calcium in alcohol‑induced hypertension and strokes as probed by in vivo television microscopy, digital image microscopy, optical spectroscopy, 31P‑NMR, spectroscopy and a unique magnesium ion‑selective electrode.
Alcohol Clin Exp Res (UNITED STATES) Oct 1994, 18 (5) p1057‑68
It is not known why alcohol ingestion poses a risk for development of hypertension, stroke and sudden death. Of all drugs, which result in body depletion of magnesium (Mg), alcohol is now known to be the most notorious cause of Mg‑wasting. Recent data obtained through the use of biophysical (and noninvasive) technology suggest that alcohol may induce hypertension, stroke, and sudden death via its effects on intracellular free Mg2+ ([Mg2+]i), which in turn alter cellular and subcellular bioenergetics and promote calcium ion (Ca2+) overload. Evidence is reviewed that demonstrates that the dietary intake of Mg modulates the hypertensive actions of alcohol. Experiments with intact rats indicates that chronic ethanol ingestion results in both structural and hemodynamic alterations in the microcirculation, which, in themselves, could account for increased vascular resistance. Chronic ethanol increases the reactivity of intact microvessels to vasoconstrictors and results in decreased reactivity to vasodilators. Chronic ethanol ingestion clearly results in vascular smooth muscle cells that exhibit a progressive increase in exchangeable and cellular Ca2+ concomitant with a progressive reduction in Mg content. Use of 31P‑NMR spectroscopy coupled with optical‑backscatter reflectance spectroscopy revealed that acute ethanol administration to rats results in dose‑dependent deficits in phosphocreatine (PCr), the [PCr]/[ATP] ratio, intracellular pH (pHi), oxyhemoglobin, and the mitochondrial level of oxidized cytochrome oxidase aa3 concomitant with a rise in brain‑blood volume and inorganic phosphate. Temporal studies performed in vivo, on the intact brain, indicate that [Mg2+]i is depleted before any of the bioenergetic changes. Pretreatment of animals with Mg2+ prevents ethanol from inducing stroke and prevents all of the adverse bioenergetic changes from taking place. Use of quantitative digital imaging microscopy, and mag‑fura‑2, on single‑cultured canine cerebral vascular smooth muscle, human endothelial, and rat astrocyte cells reveals that alcohol induces rapid concentration‑dependent depletion of [Mg2+]i. These cellular deficits in [Mg2+]i seem to precipitate cellular and subcellular disturbances in cytoplasmic and mitochondrial bioenergetic pathways leading to Ca2+ overload and ischemia. A role for ethanol‑induced alterations in [Mg2+]i should also be considered in the well‑known behavioral actions of alcohol. (90 Refs.)
Consequences of magnesium deficiency on the enhancement of stress reactions; preventive and therapeutic implications (a review).
J Am Coll Nutr (UNITED STATES) Oct 1994, 13 (5) p429‑46
Stress intensifies release of catecholamines and corticosteroids that increase survival of normal animals when their lives are threatened. When magnesium (Mg) deficiency exists, stress paradoxically increases risk of cardiovascular damage including hypertension, cerebrovascular and coronary constriction and occlusion, arrhythmias and sudden cardiac death (SCD). In affluent societies, severe dietary Mg deficiency is uncommon, but dietary imbalances such as high intakes of fat and/or calcium (Ca) can intensify Mg inadequacy, especially under conditions of stress. Adrenergic stimulation of lipolysis can intensify its deficiency by complexing Mg with liberated fatty acids (FA), A low Mg/Ca ratio increases release of catecholamines, which lowers tissue (i.e. myocardial) Mg levels. It also favors excess release or formation of factors (derived both from FA metabolism and the endothelium), that are vasoconstrictive and platelet aggregating; a high Ca/Mg ratio also directly favors blood coagulation, which is also favored by excess fat and its mobilization during adrenergic lipolysis. Auto‑oxidation of catecholamines yields free radicals, which explains the enhancement of the protective effect of Mg by anti‑oxidant nutrients against cardiac damage caused by beta‑catecholamines. Thus, stress, whether physical (i.e. exertion, heat, cold, trauma‑‑accidental or surgical, burns), or emotional (i.e. pain, anxiety, excitement or depression) and dyspnea as in asthma increases need for Mg. Genetic differences in Mg utilization may account for differences in vulnerability to Mg deficiency and differences in body responses to stress. (259 Refs.)
Effect of dietary magnesium supplementation on intralymphocytic free calcium and magnesium in stroke‑prone spontaneously hypertensive rats.
Clin Exp Hypertens (UNITED STATES) May 1994, 16 (3) p317‑26
The effects of dietary magnesium (Mg) supplementation on intralymphocytic free Ca2+ ([Ca2+]i) and Mg2+ ([Mg2+]i) were examined in the stroke‑prone spontaneously hypertensive rats (SHRSP) at the age of 10 weeks. After 40 day Mg supplementation (0.8% Mg in the diet), systolic blood pressure (SBP) was significantly lower in Mg supplemented group (Mg group) than the control group (0.2% Mg). [Ca2+]i was significantly lower and [Mg2+]i was significantly higher in Mg group than in the control group. Further, [Ca2+]i was positively and [Mg2+]i was negatively correlated with SBP. These results suggest that dietary Mg supplementation modifies [Ca2+]i and [Mg2+]i, and modulates the development of hypertension.
Impact of increasing calcium in the diet on nutrient consumption, plasma lipids, and lipoproteins in humans
Am J Clin Nutr (UNITED STATES) Apr 1994, 59 (4) p900‑7
This study examined the feasibility of increasing food‑derived calcium to 1500 mg/d and the impact of this change on plasma lipids and nutrient consumption in hypertensive (n = 130) and normotensive (n = 196) participants. Three interventions were applied in a randomized, parallel, placebo‑controlled fashion: 1) counseling to increase dietary calcium through food consumption to 1500 mg/d (n = 106), 2) a 1000‑mg/d calcium supplement (n = 109), or 3) placebo (n = 111). Plasma lipids were measured before and after 12 wk of intervention whereas nutrient intake was monitored throughout the study. At baseline, hypertensive patients reported lower intakes of carbohydrates, calcium, magnesium, phosphorus, potassium, iron, vitamin D, thiamin, and riboflavin (all P < 0.05). They also had lower HDL (P = 0.014) and higher LDL (P < 0.05) compared with normotensive subjects. During intervention, calcium, magnesium, phosphorus, potassium, thiamin, riboflavin, and vitamins C and D increased (P < 0.01) in the group receiving food calcium but not in the placebo or supplement groups. No changes occurred in plasma lipids or lipoproteins after 12 wk of intervention.
Electrolytes and hypertension: results from recent studies.
Am J Med Sci (UNITED STATES) Feb 1994, 307 Suppl 1 pS17‑20
The effects of dietary electrolytes on blood pressure may start as early as the prenatal period as there is evidence to suggest that a high maternal calcium, magnesium, and potassium intake is reflected in lower infant blood pressure levels. One randomized trial in newborn infants suggested that, in this early phase, high sodium intake is associated with an increased blood pressure change. Such a sodium effect is not present when children grow older, and between 6 and 16 years a high potassium intake appears to limit the increase in blood pressure. Recent observational population studies have shown that the association between dietary sodium intake and blood pressure level in adults is less than initially reported. In randomized trials, the average fall in blood pressure from moderate sodium restriction is small, although benefits may be larger in the elderly. A high potassium intake has consistently been shown to reduce blood pressure levels in treated and untreated hypertensive subjects, although the overall effects are modest. The available data on calcium are difficult to interpret. From observational studies an inverse association between dietary calcium intake and blood pressure levels has repeatedly been reported. Also, several disturbances in calcium metabolism in hypertensive subjects have been demonstrated. Findings in randomized trials are less consistent and indicate a marked heterogeneity in response. (36 Refs.)