Celiac disease is associated with reduced bone mineral density and increased FRAX scores in the US National Health and Nutrition Examination Survey.

We investigated the association between celiac disease (CD) and bone mass density (BMD) and risk of osteoporotic fractures in the general US population. In children and men ≥18 years, CD was associated with reduced BMD, and in men ≥40 years, CD was associated with increased risk of osteoporotic fractures. INTRODUCTION: Celiac disease (CD) is an autoimmune condition, characterized by inflammation of the small intestine. CD has an increasing prevalence, and if unrecognized or untreated, CD can lead to complications from malabsorption and micronutrient deficiencies. We aimed to study whether CD is an independent predictor of reduced bone mineral density (BMD) and FRAX scores in the general US population. METHODS: We used data from the National Health and Nutrition Examination Survey, 2009-2010 and 2013-2014. CD was defined by positive tissue transglutaminase IgA antibody test. Multivariable models of BMD and FRAX scores were adjusted for BMI, serum 25-hydroxyvitamin D, vitamin D and calcium supplements, milk intake, serum calcium, and smoking status, when available. RESULTS: In children, aged 8-17 years, CD was associated with decreased Z-scores, by 0.85 for hip and 0.46 for spine (both P < 0.001). In men aged ≥ 18 years, CD was associated with 0.06 g/cm2 decrease in BMD in hip and with 0.11 g/cm2 decrease in BMD in spine (P = 0.08 and P < 0.001, respectively). In women, there were no statistically significant differences in the multiple-adjusted model. In men aged ≥ 40 years, CD predicted FRAX scores, resulting in increased scores by 2.25 % (P = 0.006) for hip fracture and by 2.43 % (P = 0.05) for major osteoporotic fracture. CD did not predict FRAX scores in women aged ≥40 years. CONCLUSION: CD is independently associated with reduced BMD in children and adults aged ≥18 years and is an independent risk factor of osteoporotic fractures in men aged ≥40 years.

Supplementation with vitamin D does not increase serum testosterone levels in healthy males.

Cross-sectional studies indicate a positive relation between serum 25-hydroxyvitamin D [25(OH)D] and testosterone. It is not known if this relation is causal, which in theory could be in both directions. A cross-sectional population based study was designed with pooled data from 3 vitamin D randomized clinical trials (RCTs) performed in Tromsø with weight reduction, insulin sensitivity, and depression scores as endpoints, and one testosterone RCT in subjects with low serum testosterone (<11.0 nmol/l) and with body composition as endpoint. Serum 25(OH)D and androgens were measured in 893 males in the cross-sectional part, at baseline and after 6-12 months of supplementation with vitamin D 20 000 IU-40 000 IU per week vs. placebo in the vitamin D RCTs (n=282), and at baseline and after one year treatment with testosterone undecanoate 1 000 mg or placebo injections (at baseline and after 6, 16, 28, and 40 weeks) in the testosterone RCT (n=37). In the cross-sectional study, serum 25(OH)D was found to be a significant and positive predictor of serum testosterone. In the vitamin D RCTs, no significant effect on serum total or free testosterone levels was seen, and in the testosterone RCT no significant effect on serum 25(OH)D was seen. This was unchanged in sub-analyses in subjects with low serum 25(OH)D (or testosterone) levels. In conclusion, in subjects without significant vitamin D deficiency, there is no increase in serum testosterone after high dose vitamin D supplementation. Similarly, in subjects with moderately low serum testosterone levels, substitution with testosterone does not increase serum 25(OH)D.

Insulin sensitivity in subjects with secondary hyperparathyroidism and the effect of a low serum 25-hydroxyvitamin D level on insulin sensitivity.

To investigate the relation between secondary hyperparathyroidism (SHPT) and insulin sensitivity, 15 subjects with SHPT (serum PTH >6.4 pmol/l, serum calcium <2.40 mmol/l, and normal serum creatinine) and 15 control subjects were investigated with an oral glucose tolerance test (OGTT) and a 3-h hyperglycemic clamp. Body composition was measured with dual-energy X-ray absorptiometry. No differences were found between the SHPT and control groups on any indices of glucose or insulin metabolism. However, when dividing the 30 subjects in the upper and lower halves according to serum 25-hydroxyvitamin D levels (<59 and >58 nmol/l), those in the lower half had significantly higher 2-h serum insulin value at the OGTT, significantly higher insulin secretion during the last hour of the clamp, and significantly lower insulin sensitivity index (ISI; glucose infusion rate/insulin secretion during the last hour of the clamp). In a multiple linear regression analysis correcting for age, gender, and body mass index (BMI), the serum 25-hydroxyvitamin D level was significantly and positively associated with the ISI. The amounts of total body and truncal fat were negatively and significantly associated with the ISI, whereas no association between measures of lean body mass were associated with insulin secretion or sensitivity.

Effects of acute hypercalcaemia on blood pressure in subjects with and without parathyroid hormone secretion.

AIM: Acute hypercalcaemia increases the blood pressure, but the mechanism is uncertain. It may partly be the result of the concomitant fall in parathyroid hormone (PTH) secretion as PTH has been reported to have a vasodilator effect. To elucidate this, we infused calcium intravenously in subjects with and without PTH secretion. METHODS: Seven thyroparathyroidectomized subjects with undetectable PTH levels and 10 controls were studied twice, once with a calcium clamp technique that increased plasma ionized calcium in two steps of 0.1 mmol L(-1), each step lasting 60 min, and once with a placebo infusion. RESULTS: On the placebo day, blood pressure and all other variables were unaffected in both groups. On the calcium day, systolic blood pressure increased gradually and significantly from end of baseline till end of the calcium infusion in the controls (123.5 +/- 19.8 and 134.2 +/- 17.6 mmHg, P < 0.004) but not in the thyroparathyroidectomized subjects (124.9 +/- 15.7 and 126.0 +/- 20.6 mmHg, P = ns). Serum PTH levels fell promptly in the controls, and in both groups there was a significant increase in serum phosphate. The diastolic blood pressure and pulse rate, and the plasma adrenaline and noradrenaline, plasma renin activity, and serum aldosterone levels were unaffected by the calcium infusion. CONCLUSION: During acute hypercalcaemia the blood pressure increase appears unrelated to catecholamine secretion and the renin-aldosterone system, whereas the fall in PTH secretion may play a contributory role.

Serum parathyroid hormone (PTH) levels in smokers and non-smokers. The fifth Tromsø study.

OBJECTIVE: Smoking is associated with reduced bone density and calcium absorption, and reduced serum levels of vitamin D. A compensatory increase in serum parathyroid hormone (PTH) would therefore be expected as a result of an altered calcium balance. However, reports on PTH levels in smokers are conflicting. As serum PTH levels give important information on the calcium balance, the PTH levels in smokers are of interest. SUBJECTS AND METHODS: In the fifth Tromsø study, smoking status was recorded and serum PTH measured in 7896 subjects. Intakes of calcium and vitamin D were evaluated with a food-frequency questionnaire. In a follow-up study on 205 subjects, serum 25-hydroxyvitamin D, calcium absorption, and renal excretion of calcium were measured in addition. RESULTS: The serum PTH levels were significantly lower in smokers than non-smokers (3.1+/-1.4 vs 3.6+/-1.9 pmol/l in males; 3.1+/-1.5 vs 3.6+/-1.8 pmol/l in females (P < 0.001) after correcting for confounding variables, linear regression). In the smokers, there was no association between number of cigarettes smoked and serum PTH. One year after quitting smoking, serum PTH levels were similar to those of people who had never smoked. The smokers had significantly lower intake of vitamin D, lower serum levels of 25-hydroxyvitamin D and lower calcium absorption. The intake of calcium and the renal excretion of calcium were similar to that in non-smokers. CONCLUSIONS: Smokers have lower serum PTH levels than non-smokers. This cannot be explained by the predictors of serum PTH measured in our study.