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This complex system of regulatory hormones responds to changes in blood calcium and phosphorus, acting not only on bone but also on other tissues such as the intestine and the kidney. The system is illustrated for calcium regulation in Figure Under normal conditions only part of the dietary calcium is absorbed and some calcium is secreted into the intestinal tract so that the net amount of calcium entering the body normally is only a small proportion of dietary calcium.
In healthy young adults there is calcium balance, where the amount taken in is equal to the amount excreted. The bones are constantly remodeling, but breakdown and formation are equal. The kidney filters the blood, including a large amount of calcium, but most of this is taken back into the body by the kidney cells. Too many withdrawals can weaken the bone. The regulatory hormones also play critical roles in determining how much bone is formed at different phases of skeletal growth and how well bone strength and mass is maintained throughout life.
For example, sex hormones and the growth hormone system described below are increased during puberty, a time of rapidly increased skeletal growth. Finally, it is important to remember that the effects of hormones and mechanical forces on the skeleton are closely linked. For example, the ability of bone to respond to mechanical loading is impaired in animals lacking the receptor for estrogen Lee et al. Regulation of the Calcium Levels in the Body Fluids.
The extracellular fluid ECF calcium level is regulated not only by bone, but also by the intestine and kidney as shown in this figure. In addition to the limited absorption of calcium from the more The stronger the bones are at this time, the better able they are to deal with any withdrawals of calcium and phosphorus that are needed and with any other changes to bone that occur with aging. What follows is a brief description of the most important regulating hormones with respect to bone health.
Three calcium-regulating hormones play an important role in producing healthy bone: PTH is produced by four small glands adjacent to the thyroid gland. These glands precisely control the level of calcium in the blood. They are sensitive to small changes in calcium concentration so that when calcium concentration decreases even slightly the secretion of PTH increases. PTH acts on the kidney to conserve calcium and to stimulate calcitriol production, which increases intestinal absorption of calcium. PTH also acts on the bone to increase movement of calcium from bone to blood. Excessive production of PTH, usually due to a small tumor of the parathyroid glands, is called hyperparathyroidism and can lead to bone loss.
PTH stimulates bone formation as well as resorption. When small amounts are injected intermittently, bone formation predominates and the bones get stronger Rubin, Cosman et al. This is the basis for a new treatment for osteoporosis see Chapter 9. This hormone normally regulates cartilage and bone development in the fetus, but it can be over-produced by individuals who have certain types of cancer.
PTHrP then acts like PTH, causing excessive bone breakdown and abnormally high blood calcium levels, called hypercalcemia of malignancy Stewart Calcitriol is the hormone produced from vitamin D Norman, Okamura et al. Calcitriol, also called 1,25 dihydroxy vitamin D, is formed from vitamin D by enzymes in the liver and kidney. Calcitriol acts on many different tissues, but its most important action is to increase intestinal absorption of calcium and phosphorus, thus supplying minerals for the skeleton. Vitamin D should not technically be called a vitamin, since it is not an essential food element and can be made in the skin through the action of ultra violet light from the sun on cholesterol.
Many people need vitamin D in their diet because they do not derive adequate levels from exposure to the sun. This need occurred as people began to live indoors, wear clothes, and move further north. Vitamin D deficiency leads to a disease of defective mineralization, called rickets in children and osteomalacia in adults. These conditions can result in bone pain, bowing and deformities of the legs, and fractures. Treatment with vitamin D can restore calcium supplies and reduce bone loss. Calcitonin is a third calcium-regulating hormone produced by cells of the thyroid gland, although by different cells than those that produce thyroid hormones Sexton, Findlay et al.
Calcitonin can block bone breakdown by inactivating osteoclasts, but this effect may be relatively transient in adult humans. Calcitonin may be more important for maintaining bone development and normal blood calcium levels in early life. Excesses or deficiencies of calcitonin in adults do not cause problems in maintaining blood calcium concentration or the strength of the bone. However, calcitonin can be used as a drug for treating bone disease.
Along with calcium-regulating hormones, sex hormones are also extremely important in regulating the growth of the skeleton and maintaining the mass and strength of bone.
The female hormone estrogen and the male hormone testosterone both have effects on bone in men and women Falahati-Nini, Riggs et al. The estrogen produced in children and early in puberty can increase bone growth. The high concentration that occurs at the end of puberty has a special effect—that is, to stop further growth in height by closing the cartilage plates at the ends of long bone that previously had allowed the bones to grow in length.
Estrogen acts on both osteoclasts and osteoblasts to inhibit bone breakdown at all stages in life. Estrogen may also stimulate bone formation. The marked decrease in estrogen at menopause is associated with rapid bone loss. Hormone therapy was widely used to prevent this, but this practice is now controversial because of the risks of increased breast cancer, strokes, blood clots, and cardiovascular disease with hormone therapy see Chapter 9. Testosterone is important for skeletal growth both because of its direct effects on bone and its ability to stimulate muscle growth, which puts greater stress on the bone and thus increases bone formation.
Testosterone is also a source of estrogen in the body; it is converted into estrogen in fat cells. This estrogen is important for the bones of men as well as women. In fact, older men have higher levels of circulating estrogen than do postmenopausal women. Growth hormone from the pituitary gland is also an important regulator of skeletal growth.
It acts by stimulating the production of another hormone called insulin-like growth factor-1 IGF-1 , which is produced in large amounts in the liver and released into circulation. IGF-1 is also produced locally in other tissues, particularly in bone, also under the control of growth hormone. The growth hormone may also directly affect the bone—that is, not through IGF-1 Wang et al. Growth hormone is essential for growth and it accelerates skeletal growth at puberty. Decreased production of growth hormone and IGF-1 with age may be responsible for the inability of older individuals to form bone rapidly or to replace bone lost by resorption Yakar and Rosen Thyroid hormones increase the energy production of all body cells, including bone cells.
They increase the rates of both bone formation and resorption. Deficiency of thyroid hormone can impair growth in children, while excessive amounts of thyroid hormone can cause too much bone breakdown and weaken the skeleton Vestergaard and Mosekilde The pituitary hormone that controls the thyroid gland, thyrotropin or TSH , may also have direct effects on bone Abe et al. It has complex effects on the skeleton Canalis and Delany Small amounts are necessary for normal bone development, but large amounts block bone growth. Synthetic forms of cortisol, called glucocorticoids, are used to treat many diseases such as asthma and arthritis.
They can cause bone loss due both to decreased bone formation and to increased bone breakdown, both of which lead to a high risk of fracture Kanis et al. There are other circulating hormones that affect the skeleton as well. Insulin is important for bone growth, and the response to other factors that stimulate bone growth is impaired in individuals with insulin deficiency Lu et al. A recently discovered hormone from fat cells, leptin, has also been shown to have effects on bone Elefteriou et al. Maintaining a strong and healthy skeleton is a complicated process that requires having the right amount of bone with the right structure and composition in the right place.
There are many things that can go wrong along the way. Genetic abnormalities can produce weak, thin bones, or bones that are too dense. The disease osteogenesis imperfecta is caused by abnormalities in the collagen molecule that make the matrix weak and can lead to multiple fractures. In another congenital disorder, osteopetrosis, the bones are too dense because of failure of osteoclast formation or function. This failure of the remodeling process results in persistence of trabecular bone in the marrow space so that the marrow cavity may not be large enough to form red and white blood cells normally.
These dense bones cannot remodel well in response to mechanical forces or micro damage and hence may be weaker and subject to fracture even though bone mass is increased. There are also other abnormalities of the genes that affect the size and shape of the skeleton and can cause deformities or abnormal growth. Nutritional deficiencies, particularly of vitamin D, calcium, and phosphorus, can result in the formation of weak, poorly mineralized bone. In children, vitamin D deficiency produces rickets in which there is not only a marked weakness of bone and fractures but also bowing of the long bones and a characteristic deformity due to overgrowth of cartilage at the ends of the bones.
In adults, vitamin D deficiency leads to a softening of the bone a condition known as osteomalacia that can also lead to fractures and deformities. Many hormonal disorders can also affect the skeleton. Overactive parathyroid glands or hyperparathyroidism can cause excessive bone breakdown and increase the risk of fractures. In severe cases, large holes or cystic lesions appear in the bone, which makes them particularly fragile. Loss of gonadal function or hypogonadism in children and young adults can cause severe osteoporosis due to loss of the effects of testosterone and estrogen.
Use of glucocorticoids as medication is a common cause of bone disease. Excess glucocorticoids will stop bone growth in children and cause marked thinning of the bone in adults, often leading to fracture. Many bone disorders are local, affecting only a small region of the skeleton. Inflammation can lead to bone loss, probably through the production of local resorbing factors by the inflammatory white cells. This process can occur around the affected joints in patients with arthritis.
Bacterial infections, such as severe gum inflammation or periodontal disease, can produce loss of the bones around the teeth, and osteomyelitis can produce a loss of bone at the site of infection.
Buy Life And Death of A Parathyroid Gland (Calcium Man) (A Simple Guide to Medical Conditions): Read 1 Kindle Store Reviews - www.farmersmarketmusic.com The function of the thyroid gland is to take iodine and convert it into It lowers blood calcium and phosphorus by decreasing the rate of . out that thyroid problems are far more common in women than in men Removing a parathyroid adenoma, a fairly simple surgery, can .. Jon's Guide to Supplements.
This type of bone loss is due to the direct damaging effect of bacterial products as well as the production of resorbing factors by white cells. The osteoblasts try to repair this damage by increasing bone formation. However, the normal bone architecture has been disrupted, leading to weak bones and the potential for fractures and deformities even though the bones may appear dense on an x-ray. In addition, the new bone may not be in the right place to provide strength. Osteoporosis is by far the most common bone disease. The composition of the mineral and matrix, the fine structure of the trabecular bone, the porosity of the cortical bone, and the presence of micro-fractures and other forms of damage in bone are all important in determining bone strength.
Changes in the fine structure or micro-architecture of trabecular bone are particularly important since the most common fractures in osteoporosis occur at the spine, wrist, and hip, sites where trabecular bone predominates. As shown in Figure , the structure of normal trabecular bone consists of well-connected plates or broad bands that provide great strength. In individuals with osteoporosis these bands are disrupted and often become thin, weakened rods. Some of these rods are no longer connected to another piece of bone, meaning that they no longer contribute to bone strength.
These pictures, called scanning electron micrographs, are from biopsies of a normal and an osteoporotic patient. The normal bone shows a pattern of strong interconnected plates of bone. Much of this bone is lost in more Unfortunately, however, it is not possible to measure bone strength directly, or to detect changes in the micro-architecture of bone in living patients.
The mass of bone, its density, and its general shape can be determined by radiographs and absorptiometry see Chapter 8. There are a number of different ways in which osteoporosis can develop, with the skeleton becoming more fragile and the risk of fracture increasing Raisz and Rodan Some of the most important mechanisms that lead to skeletal fragility and fractures are listed in Table Many people have relatively weak bones even as young adults because of their genes or because of suboptimal nutrition and lifestyle.
However, fractures due to bone fragility rather than severe injury are uncommon in young adults. It is typically not until later in life that bone loss begins due to bone breakdown, a process that accelerates around the time of menopause in women. At the same time, bone formation tends to decrease with age in both men and women, typically failing to keep up with the rate of bone resorption. An imbalance between bone resorption and bone formation results in loss of bone mass, leading to the development of structural abnormalities that make the skeleton more fragile.
There are a number of different combinations of increased resorption and decreased formation that can result in a weakened skeletal structure see Figure Each of these pathways can be involved in producing skeletal fragility at different times or sites within an individual patient.
Since bone breakdown is the first step in this process, blocking bone resorption is one way to decrease bone loss and prevent fractures. It is currently the most widely used therapeutic approach in osteoporosis. Stimulation of bone formation can also reverse skeletal fragility; new therapies based on this approach have recently been developed Chapter 9.
This brief overview of the basics of bone health and disease provides a framework for the discussion of what is known about the causes, prevention, and treatment of skeletal disorders today. Many knowledge gaps remain, and it is still unclear precisely why so many people suffer fractures. Fortunately there have recently been a number of exciting new discoveries about skeletal regulation, and there are undoubtedly many more to come.
These discoveries will further increase our understanding of bone health and disease. For example, recent discoveries have shown how osteoblastic and osteoclastic cells communicate and provide signals to begin the process of resorption Figure The osteoblastic cells produce macrophage colony stimulating factor M-CSF and receptor activator of nuclear factor kappa B ligand RANKL Khosla , proteins that bind to receptors on the osteoclast precursors, stimulate their proliferation and differentiation, and increase osteoclast activity.
Osteoblastic cells also produce a protein called osteoprotegerin that can bind RANKL and prevent it from interacting with osteoclastic cells. The hormones and local factors that stimulate bone resorption act on this system. While RANKL excess or osteoprotegerin deficiency would be expected to cause bone loss, measurements of the amounts of these proteins in circulating blood do not support this theory.
The activated link is defined as Active Tab. Hormones can be thought of as chemical messages that communicate with the body and bring about changes Your metabolism is influenced by your age, gender, muscle-to-fat ratio, the food you eat, physical activity and hormone function Most cases of Addison's disease are caused by an autoimmune response that attacks and damages the adrenal glands over time Some people have Cushing's syndrome symptoms when they take glucocorticoid hormones to treat inflammatory conditions such as asthma, lupus or rheumatoid arthritis Cortisol helps to maintain blood pressure, immune function and the body's anti-inflammatory processes Acromegaly is caused by an excess of growth hormone in adults, which causes the overgrowth of bones in the face, hands, feet and internal organs Some athletes and bodybuilders wrongly believe that taking synthetic growth hormone will help build up their muscles Generally, pituitary tumours are benign and slow growing, and pituitary cancers are extremely rare Symptoms of a goitre can include enlargement of the throat, swallowing problems and breathing problems The parathyroid glands make hormones that regulate calcium, phosphorus and magnesium in the bones and blood If the thyroid gland is overactive or sluggish, the metabolism will be affected, leading to a variety of symptoms Hypothyroidism means the thyroid gland is underactive which causes the person?
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The bottom line is that the only connection the parathyroids have with the thyroid is their physical location. Specifically, the parathyroid glands are located behind the thyroid, and they are intimately connected to the covering of the thyroid gland. There are two on each side.
They are supplied by the same blood vessels that supply the thyroid. Each parathyroid is about the size of a large kernel of rice. They can be extremely difficult for surgeons to locate and identify. And something that can make the job even harder is that the parathyroid glands sometimes "disengage" from the thyroid gland and migrate down into the chest cavity, making them difficult to find and remove.
So what do the parathyroids do? The chief cells principal cells produce parathormone PTH, parathyroid hormone. The oxyphil cells produce…???? In fact, the function of the oxyphil cells is as yet unknown. PTH has one simple function. It regulates the levels of calcium and phosphorus in the blood. It accomplishes this by increasing the cells of the bone osteoclasts , which reabsorb calcium. It also increases urinary re-absorption of calcium by the kidneys. In addition, it causes the kidneys to form calcitrol, a hormone made from vitamin D that increases absorption of calcium from the GI tract.
And finally, it increases excretion of phosphorus by the kidneys which, in turn increases calcium levels. Calcium and phosphorus always go in opposite directions -- in a defined relationship called the solubility constant. Calcitonin from the thyroid gland participates in the negative feedback system that regulates the parathyroids by forcing calcium back into the bones. Hyperparathyroidism refers to increased PTH production, usually because of a benign tumor of one or more of the parathyroid glands parathyroid adenoma.
If PTH is produced in excess, calcium is reabsorbed from the kidneys, bones, and stomach back into the blood. This leads to a condition that many endocrinologists call " Stones, bones, groans, and moans. Hyperparathyroidism is almost always caused by parathyroid adenoma. Removing a parathyroid adenoma, a fairly simple surgery, can cause an immediate and drastic return to normal function and the disappearance of all symptoms. Another form of hyperparathyroidism is called parathyroid hyperpiesia, in which all four parathyroid glands overproduce PTH for no obvious reason. In other words, there is no adenoma causing the problem.
Surgeons usually attempt to fix the problem by removing most of the parathyroid glands. On the other hand, if the surgeon makes a mistake and removes too much or all of the parathyroid tissue by accident, you can end up with hypoparathyroidism. Hypoparathyroidism leads to low serum calcium levels and an elevated state of excitement for nerves and muscles, resulting in twitching and over-activity of the muscular and nervous systems. In the extreme, this can lead to convulsions and death.
Again, it is caused primarily by inadvertent surgical removal. This is an extremely difficult condition to live with, as it is almost impossible to self regulate. Fortunately, there is one medical alternative that works in some cases…if the surgeon recognizes the error in time. Removed parathyroid glands can be chopped up and implanted into muscle tissue in other areas of the body such as the forearm , where sometimes, they will survive and start producing PTH again. If that doesn't work, hypoparathyroid patients require lifelong calcium and vitamin D injections, which are almost impossible to manage accurately.
When it comes to maintaining the health of the thyroid and parathyroid glands, you want to address several key issues. In our next issue, we'll move on down the body into the pancreas. In our previous newsletters on the digestive system, we explored the pancreas' production of digestive enzymes. But the pancreas has two distinct functions in the body. In addition to producing digestive juices, it also is part of the endocrine system and produces several key hormones, most notably insulin and ghrelin the appetite hormone.
We will explore those hormones in our next newsletter. Enjoy the following links to complete the entire newsletter series on the Endocrine System: Ive had my thyriods removed the docters meds. Dont work for me and its been hard for years. Just dont know what to do anymore. Here is a page with links to many articles: Hello, My son has Alopecia Areata an Autoimmune do you believe that transfer factors could work well for my son, to help regulate my child's immune system.
For obvious legal reasons, we cannot diagnose or prescribe for specific medical conditions—merely provide information. With that in mind…Alopecia areata appears to have both a genetic component and an immune system component. Obviously, no supplement can address any genetic aspects of an illness, but as the article above mentions. L-caronsine, Cetyl myristoleate, and Transfer Factor all function as immune system modulators that can help to throttle back an overactive immune system.
In fact, Transfer Factor is used to treat atopic dermatitis, an autoimmune condition. I recently started taking thytrophin pmg. I feel great, but learned that my antibodies doubled since beginning this product. Have you seen this before? Should I continue use?
I have had rapid deterioration or my endo system. I hemmoraged with my last to the extent I had to have 2 blood transfusions. Any ideas or comments please feel free to contact me. I fear at times I will end up in trouble with the law if I continue this way. Child birth has not only depleted your Magnesium, but your iron as well and then more We all have health issues of many years duration, we can help each other and then from 34K more very knowledgable members including health professionals.. I feel for you.
This is a very interesting article For immune modulation how long do people usually use cetyl-myristoleate and or L-carnosine? And for thyroid autoimmune like hashimoto's how long do people usually use the Thryrotrophin PMG. I find all of your articles very educational.. Thank you so much too as the reading keeps our brains working in tip top shape. Cetyl-myristoleate, L-carnosine, and Thytrophin-PMG, unless you are having any side effects that would indicate otherwise, can all be used for as long as needed or desired.
Thank you BaselineFoundation for your input on my question. However I was leaning towards a more definitive educational answer from Jon Barron. I hope this will be forthcoming. Again I thank you for your consideration. What can be done about recurring primary hyperparthyroidism, other than surgery? I had an adenoma on a parathyroid 16 years ago. Then also the thyroid was resected for papillary-follicular cancer. Only 1 parathyroid is left and now malfunctioning, can be an adenoma again.
For obvious legal reasons, we can neither diagnose or prescribe for specific medical conditions—merely provide information, with that in mind, the follow link might be useful.