Abstract
This is due in part to vitamin D deficiency (vitamin D is a primary modulator of intestinal calcium and phosphate absorption), which is caused by a lack of sunlight combined with low vitamin D dietary intake and cutaneous synthesis. Secondary hyperparathyroidism is caused by low calcium intake and vitamin D deficiency, which is characterised as a serum 25-hydroxyvitamin D (25 (OH) D concentration below 12 ng/ml and is related to increased bone turnover and, indirectly, an increased risk of fracture. Furthermore, recent findings indicate that vitamin D deficiency is more widespread than previously thought, owing to a revision of the traditional 25 (OH) D threshold level below which parathyroid hormone secretion (PTH) begins to increase. The value of z is 2.44949, the value of p is 0.01428 and the result is significant at p < 0.05 are obtained for the calcium levels of pre and post-test results of all study groups when compared against BMI. The value of z is 1.36471, the value of p is 0.00321 and the result is significant at p < 0.05 are obtained for the T-values of pre and post-test results of all study groups when compared against BMI. After observing the findings, it is clear that after eating prescribed nutritional food for three months, the ionised Calcium levels, overall Calcium levels, and bone density have increased significantly as compared to before taking nutritional food. As a result, the nutrient food given is a good source of calcium and helps postmenopausal women strengthen their bones. Furthermore, it is recommended that all age groups consume the recommended food kit to minimise the risk of osteoporosis and bone fracture.
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