Parathyroid Bioidentical Hormone Replacement Therapy


					about us \| contact us \| schedule an appointment
								(330) 552-7202 kent, ohio

what is HRT	supplements	HRT for women	HRT for men	advanced internal medicine	FAQs	ask the physician

Supplements		Parathyroid Bioidentical Hormones
activin and inhibin calcitonin cortisol DHEA estrogens growth hormones human chrionic gonadotropin hCG insulin melatonin oxytocin parathyroid pregnenolone progestin progesterone TA 65 & telomerase testosterone thyroid vitamin D schedule a consultation		About Parathyroid Parathyroid (PTH) is secreted by the chief cells of the parathyroid gland as a polypeptide. It acts to increase the concentration of calcium (Ca2+) in the blood, whereas calcitonin, a hormone produced by the parafollicular cells (C cells) of the thyroid gland, decreases calcium concentration. PTH acts to increase the concentration of calcium in the blood by acting upon the parathyroid hormone 1 receptor (high levels are found in bone and kidney) and the parathyroid hormone 2 receptor (high levels are found in the central nervous system, pancreas, testis, and placenta). What Can We Do at Forever Ageless We closely monitor parathyroid hormone, calcium and phosphorus levels and optimize them when necessary in order to improve bone health and energy level and prevent ectopic calcification.

Why Optimize Parathyroid Hormone Levels with Bioidentical Hormone Replacement Therapy

Parathyroid Hormones and Bone Health - Parathyroid hormone enhances the release of calcium from the large reservoir contained in the bones. Bone resorption is the normal destruction of bone by osteoclasts, which are indirectly stimulated by PTH. Stimulation is indirect since osteoclasts do not have a receptor for PTH; rather, PTH binds to osteoblasts, the cells responsible for creating bone. Binding stimulates osteoblasts to increase their expression of RANKL and inhibits their expression of osteoprotegerin (OPG). OPG binds to RANKL (Receptor activator of nuclear factor kappa-B ligand) and blocks it from interacting with RANK, a receptor for RANKL. The binding of RANKL to RANK (facilitated by the decreased amount of OPG) stimulates these osteoclast precursors to fuse, forming new osteoclasts, which ultimately enhances bone resorption.

Parathyroid Hormones and Kidneys - Parathyroid hormone enhances the active reabsorption of calcium and magnesium from distal tubules and the thick ascending limb. As bone is degraded, both calcium and phosphate are released. PTH also decreases the reabsorption of phosphate, with a net loss in plasma phosphate concentration. When the calcium phosphate ratio increases, more calcium is free in the circulation.

Parathyroid Hormone and Intestine via Kidney - Parathyroid hormone enhances the absorption of calcium in the intestine by increasing the production of activated vitamin D. PTH up-regulates 25-hydroxyvitamin D3 1-alpha-hydroxylase, the enzyme responsible for 1-alpha hydroxylation of 25-hydroxy vitamin D, converting vitamin D to its active form (1,25-dihydroxy vitamin D). This activated form of vitamin D increases the absorption of calcium (as Ca2+ ions) by the intestine via calbindin.

Clinical Significance

Hyperparathyroidism - Hyperparathyroidism is the presence of excessive amounts of parathyroid hormone in the bloodstream, occurs in two very distinct sets of circumstances. Primary hyperparathyroidism is due to the autonomous and abnormal hypersecretion of PTH in the parathyroid gland while secondary hyperparathyroidism is an appropriately high PTH level seen as a physiological response to hypocalcemia or hyperphosphatemia. Hyperparathyroidism is a frequently undiagnosed cause of chronic fatigue and premature osteoporosis.

Hypoparathyroidism - A low level of PTH in the blood is known as hypoparathyroidism and is most commonly due to damage to or the removal of parathyroid glands during thyroid surgery. Severe decreases in serum magnesium also produce symptoms of hypoparathyroidism.

Advanced Osteoporosis- In osteoporotic women and men, administration of an exogenous parathyroid hormone analogue (teriparatide (Forteo)) by daily injection, superimposed on estrogen hormone replacement therapy, produced an increase in bone mass and reduced vertebral and nonvertebral fractures by 45 to 65%.

*DISCLAIMER: The information provided on this website is intended for educational purposes only. The educational material contained in this site is based on readily available information and the experience of Forever Ageless Age Management and Bioidentical HRT. This information is not intended to self diagnose any conditions or treatments and it is recommended that you seek a professional's opinion. This information is not intended to diagnose, treate or prevent any disease.