Mineral decline, bone

Bone strength however declines much earlier in life beginning approximately age 20 for both men and women (8j. In animals bone strength is directly related with its mineral content (9-12). 

Clinical trials have been reported, and these are not subject to the same levels of uncertainty. They have concentrated on bone mineral density, because this parameter is an acceptable measure of bone mass, is sensitive to the occurrence of osteoporosis and correlates well with the likelihood of bone fracture in patients affected by osteoporosis. Bone mineral density is known to increase in childhood and adolescence, to reach a maximum around the age of 40, then to decline [110,111]. In women in the years immediately following the menopause, it may sharply reduce, and if it reaches a level TA standard deviations below the young adult mean value, the condition is defined by the WHO as osteoporosis [110,111]. 

After Completion of Puberty Regression of the pubertal effects of testosterone depends on both the degree and the duration of testosterone deficiency. When the deficiency is severe, libido and energy decrease within a week or two, but other testosterone-dependent characteristics decline more slowly. A clinically detectable decrease in muscle mass does not occur for several years. A pronounced decrease in hematocrit and hemoglobin will occur within several months. A decrease in bone mineral density probably is detectable within 2 years by dual-energy x-ray absorptiometry, but an increase in fracture incidence would not be likely to occur for many years. A loss of sexual hair takes many years. 

In general, peak bone mass occurs between 30 and 40 years of age (3,6) and is dependent on genetic factors as well as proper intake of calcium, maintenance of quality nutrition, and participation in weight-bearing exercise (6). Thereafter, peak bone mass progressively declines at the rate of 0.3 to 0.5% of cortical bone per year (3). After menopause, bone loss is accelerated (2% per year in the spine) (6) for a period of 5 to 10 years because of the loss of estrogen. This can result in up to a 30% decrease in bone mineral density. 

This finding is in agreement with studies in both preterm infants 0 and term infants that demonstrated a decrease in SOS (Eliakim et al. 2002, Litmanovitz et al. 2003, Liao et al. 2005) and DEXA (Rauch and Schoenau 2001). The reason for these phenomena is not clear. It was suggested that the decline in bone mineral density (BMD) in healthy newborns is associated with a relative physiological decrease in the cortical area and a redistribution of bone tissue from the endocortical to the periosteal surface rather than with bone loss (Liao et al. 2005). It is also possible that this decrease represents a delay between rapid linear bone growth and mineralization. 

Lead—Apparently, lead poisoning htis dogged man for a longer time than most people might suspect, because toxic levels of this nonessential mineral were found in the disinterred bones of ancient Romans. In fact, the use of lead for household utensils and wine containers by the Romans is suspected of having been responsible for widespread lead poisoning which, it is conjectured, may have led to weakness and infertility, and the eventual decline of the empire. 

Fractional calcium absorption increases in response to low intake but varies throughout life. It is highest during infancy (60%) and puberty (25-35%), stable at approximately 25% in adults, and then declines with age (by approximately 2% per decade after menopause). There is little difference in calcium absorption efficiency between Caucasians and African Americans. The lower urinary calcium and better calcium conservation in African Americans probably contributes to their higher bone mineral density. 

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