scholarly journals THU0489 The impact of calcium intake and physical exercise on peak bone mineral density

Author(s):  
L. Brites ◽  
M.L. Marques ◽  
A. Marques ◽  
A. Daniel ◽  
M. Santiago ◽  
...  
2011 ◽  
Vol 165 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Helene Holmer ◽  
Vera Popovic ◽  
Bertil Ekman ◽  
Cecilia Follin ◽  
Ann Britt Siversson ◽  
...  

ContextData on bone mineral density (BMD) are lacking in adults with childhood onset (CO)–craniopharyngioma (CP) with hypothalamic damage from the tumor. In patients with CO GH deficiency, BMD increases during GH treatment.ObjectiveThe aims were to evaluate BMD in adults with CO–CPs on complete hormone replacement, including long-term GH and to evaluate the impact of hypothalamic damage on these measures.Design and participantsBMD (dual-energy X-ray absorptiometry), markers of bone turn over, physical activity and calcium intake were assessed in 39 CO–CP adults (20 women), with a median age of 28 (17–57) years, in comparison with matched population controls.ResultsLate puberty induction was recorded in both genders, but reduced androgen levels in females only. Only CP women had lower BMD (P=0.03) at L2–L4, and reduced Z-scores at femoral neck (P=0.004) and L2–L4 (P=0.004). Both genders had increased serum leptin levels (P=0.001), which significantly correlated negatively with BMD at L2–L4 (P=0.003; r=−0.5) and 45% of CP women had Z-score levels ≤−2.0 s.d. Furthermore, 75% of those with a Z-score ≤−2.0 s.d. had hypothalamic involvement by the tumor. Calcium intake (P=0.008) and physical activity (P=0.007) levels were reduced in CP men only. Levels of ostecalcin and crossLaps were increased in CP men only.ConclusionsDespite continuous GH therapy, low BMD was recorded in CO–CP females. Insufficient estrogen and androgen supplementation during adolescence was the main cause, but hypothalamic involvement with consequent leptin resistance was also strongly associated with low BMD in both genders.


2006 ◽  
Vol 175 (4S) ◽  
pp. 41-42
Author(s):  
Anna Orsola ◽  
Jacques Planas ◽  
Carlos Salvador ◽  
José M. Abascal ◽  
Enrique Trilla ◽  
...  

Author(s):  
MINAKSHI JOSHI ◽  
SHRADHA BISHT ◽  
MAMTA F. SINGH

Thyroid hormone serves as an indispensable component for the optimum functioning of various biological systems. They curb body’s metabolism, regulates the estrogen level, regulates bone turnover, essential for skeletal development and mineralization. Within the scope of knowledge, it is intimately familiar that thyroid disorders have widespread systemic manifestations, among which in hypothyroidism, even though elevated TSH (thyroid-stimulating hormone) may reduce estrogen level which in turn stimulates osteoclasts and thus cause osteoporosis, while hyperthyroidism accelerates bone turnover. Hypothyroidism does not directly interfere with the skeletal integrity, but treatment with levothyroxine for the suppression of TSH to bring the hypothyroid patient to euthyroid state for a long haul; lead to simultaneous reduction in bone mass and in (bone mineral density) BMD. After the initial relevation of the correlation between thyroid disorders and osteoporosis in numerous studies have emphasized that both hypo and hyperthyroidism either directly or indirectly affects the bone mineral density or leads to the progression of osteoporosis. Therefore the present study is aimed and so designed to review all the possible associations between them and the impact of thyroid disorders on estrogen level and bone mineral density. The main findings of this review indicate that both excesses as well as deficiency of thyroid hormone can be potentially deleterious for bone tissue.


2012 ◽  
Vol 25 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Susan Ziglar ◽  
Tracy S. Hunter

Maximizing bone mass in youth is touted as the best strategy to offset the natural losses of aging and the menopausal transition. Not achieving maximum peak bone mineral density (BMD) is an independent risk factor for osteoporosis and thus a public health concern. Adolescence is a critical time of bone mineralization mediated by endogenous estradiol. Research has shown that the highest velocity of bone mass accrual occurs 1 year before menarche and after the first 3 years. Low-peak attainment of BMD in young women is associated with contributing factors such as diets low in calcium, eating disorders, lack of exercise, smoking, and low estrogen states. Oral contraceptives (OCs) suppress endogenous estradiol production by suppressing the hypothalamic–pituitary–ovarian axis. Thus, OCs, by replacing endogenous estradiol with ethinyl estradiol (EE), establish and maintain new hormone levels. The early initiation and the use of very low dose of EE raises the possibility that bone mass accrual at a critical time of bone mineralization in young women or adolescents may be jeopardized. This review examines the studies of BMD in adolescents and young women that use combination hormonal contraception. Some studies had inherent limitations, such as small trial, poor control of confounders, failure to exclude women with prior use of hormonal contraceptives, or prior pregnancy from control groups. The vast majority of reviewed studies showed OCs containing 20 to 30 µg of EE interfere with acquisition of peak BMD. Limited numbers of studies examine the effects of OCs containing 35 µg on adolescents and young adults. Additionally, studies are needed evaluating the progestin component of OCs as their differing androgenic properties may affect bone mineralization as well.


Sign in / Sign up

Export Citation Format

Share Document