There is a growing body of information about hormones, which regulate the appetite. This base of information suggests that various hormones are secreted with eating. In normal or thin subjects, the amount of hormones produced is directly related to the amount of food ingested. These hormones are supposed to suppress the appetite. Thus, the more food eaten, the more hormones released, and the more the appetite is decreased.
A number of hormones have been identified, which may act in this system. The group includes a gut hormone, called GLP1, a hormone from the pancreas called amylin, and a hormone made by fat cells, known as leptin. All three hormones reduce the appetite in various experimental models, in both humans and animals.
Heavy people may have defects in the secretion or action of these hormones. The secretion of GLP1 and amylin may be inadequate. Leptin secretion is actually increased in heavy people; however, its ability to penetrate the brain and affect the appetite center may be decreased.
New approaches to treatment of obesity with existing drugs and new drug development both offer optimism about more successful treatment of obesity in the future. There may be less negative judgment about patients in this area of therapy.
This site is the diabetes portal for Endocrine Consultants, PC. Here our patients and friends can find timely news stories on diabetes, resources for managing diabetes, and dates of upcoming events in the Columbus, Georgia areas. Patients may schedule appointments, send questions, and report blood sugars from this site.
Thyroid Function in Normal, Hypothyroid, and Hyperthyroid States
The thyroid is the “gas pedal” of the body. Thyroid hormone governs the rate at which the metabolic processes of the body work. Thyroid hormone influences heart rate, body temperature, mental alertness and total body salt and water content. It also governs more subtle functions, as taste, bowel habits, and neurological reflex time. We handle complicated thyroid conditions and cancer.
The most common cause of excessive mineral loss from bone is hyperthyroidism, or too much thyroid hormone in the blood. This is true whether the cause of the excess is due to intrinsic thyroid disease or the use of excessive doses of thyroid hormone medication. Thyroid hormone can mobilize calcium out of bone. It is then excreted in the urine. Long-standing hyperthyroidism will cause an excessive loss of bone mineral content in the urine. Correcting the hyperthyroidism leads to repair of bone mineral content over time.
Osteoporosis occurs when one of two situations exits: the amount of mineral per unit area of bone protein is deficient, and the bone becomes too soft; or the thickness of the spicules becomes too thin, although what spicule bone is there is properly constructed. In the second case, the bone is fragile and more easily fractured than normal.
The thickness of bone and the degree to which it has mineral content grows from the start of puberty and reaches a peak in early adulthood. After early adulthood, bone mass gradually declines. In some ways, the risk of getting osteoporosis is related to the height of the peak in bone mass, and the rate at which bone mass declines from the peak. People who do not experience a growth in bone mass as vigorously as is desirable are at greater risk to develop osteoporosis later in life, because their peak bone mass is less than desirable. Also, people who, for some reason, have a more rapid decline in bone mass than is desirable will have a greater risk of osteoporosis later in life.
The dietary calcium intake during adolescence and the vigor with which puberty occurs in each individual helps determine how high the peak of bone mass will be. Teenagers with incomplete or inadequate hormonal surge of puberty are at risk for having a lower peak in their bone mass than desired. Therefore, we recommend that teenagers take an oral calcium supplement daily during adolescence. This is especially true if their puberty is mild or incomplete.
Factors, which determine the adequacy of maintenance of the mineralization of bone, or the degree to which new bone protein is manufactured to renew the bone mass determine in part how fast the bone mass declines from the peak over the course of adulthood. Conditions, which tend to pull mineral out of the bone instead of replacing mineral in the bone will tend to lower the mineral content of the bone over time. Conditions, which reduce the synthesis of new bone protein, tend to make the bone thin and brittle over time.
Conditions Which Reduce Mineral Content
There is a long list of conditions, which decrease how much mineral is placed into bone over time. Inadequate dietary calcium intake is perhaps the most common, but, interestingly, it is common only in a limited segment of the population – the elderly. Adequate dietary calcium intake is thought to be more than 1500 mg of calcium per day. Calcium intake often parallels the intake of vitamin D, because many (but not all) foods high in calcium content often have high concentrations of vitamin D. Adequate vitamin D intake is thought to be 600 units per day.
Studies have shown that most of the American population takes in adequate amounts of vitamin D and calcium, except for people more than 65 years of age. A large minority of people in that age group take in far less calcium and vitamin D per day than is recommended. Aged persons, who are shut-ins, because of incapacity or disability, are at the highest risk for nutritional deficiency of calcium or vitamin D. Therefore, close attention to dietary supplements with calcium and vitamin D in older people, particularly shut-ins, is recommended.
The second most common cause of excessive bone mineral loss is a condition known as “idiopathic hypercalciuria”. This is a condition in which the kidney wastes an excess of circulating calcium in the urine. There is nothing else necessarily wrong with the kidney, and this disorder does not lead to progressive loss of kidney function. The kidney normally processes constituents of blood in forming urine and regulates how much calcium in the blood will be excreted in the urine. Persons with this condition lose an excess of blood calcium in the urine. This body compensates for this continuous loss of blood calcium by increasing a hormone called “parathyroid hormone” or PTH. PTH pulls calcium out of bone and places it in blood. Thus, people with this condition have a slow, excessive loss of bone mineral over the course of their lives, which leads to deficient mineralization of bone. The treatment is to take drugs from the thiazide class of diuretics. These drugs have a side effect, which remedies idiopathic hypercalciuria. They block calcium excretion by the kidney.
PTH is made by four tiny glands in the neck. These glands surround the thyroid gland. Hence, they are called “parathyroid glands” for the Latin preposition “para”, which means around something. Four to seven percent of people with decreased bone mineralization have this condition. As in any condition, whether primary hyperparathyroidism or idiopathic hypercalciuria, in which there is an excess secretion of PTH, there is an excess mobilization of mineral from bone. Surgical removal of the offending parathyroid gland helps repair the bone.
Vitamin D Resistance
One of the main actions of vitamin D is to stimulate the small intestine to produce a protein, called calcium binding protein (CBP). Unlike most other minerals, calcium does not simply pass across the gut into the blood. It must be “ferried” across the gut or it cannot pass. CBP is the factor that “ferries” calcium across the gut. The amount of CBP produced is determined by how much active vitamin D is in the blood, and by how responsive the gut cells are to vitamin D. People who do not get enough vitamin D in their diet or sunlight exposure will not make enough CBP because there is an insufficient amount of vitamin D to stimulate the adequate synthesis of CBP (nutritional rickets). People with gut cells that do not respond normally to vitamin D have vitamin D resistance.
The effect of nutritional rickets and vitamin D resistant rickets (VDRR) on the bone is the same. Lacking an adequate flow of calcium from the diet into the blood, the body increases PTH secretion to cause an excess mobilization of bone calcium to flow into the blood. Over a period of years, this leads to decreased bone mineral content.
Conditions With Reduced Bone Spicule Thickness
Sex hormone deficiency in women or men will lead to normal bone (what bone is present), but decreased bone spicule thickness. This is due to decreased synthesis of new bone protein. Bone is under constant reconstruction. Daily minor traumas to the bone result in “micro-fractures”, or little defects and pits in the bone that require repair. The body sends in a “demolition team”, called osteoclasts, to remove the defective bone locus and then sends in a reconstruction team, known as osteoblasts, to lay down new, healthy bone. The osteoblasts must first synthesize new bone protein. In certain ways, sex hormone (estrogen or testosterone) directly or indirectly enhance the ability of the osteoblasts to make new bone protein. A deficiency of sex hormone leads to a decreased production of new bone protein. Therefore, the bone spicules are thin and weak. This condition is osteoporosis.
Other hormones affect the synthesis of bone protein. Growth hormone and growth factors do. And PTH does. Insufficient amounts of either of those hormones may lead to decreased bone protein production.
There are three basic treatment approaches in osteoporosis. The first is to determine if a person has a specific cause of osteoporosis and to prescribe treatments to address that cause. An example would be to use thiazide diuretics to treat idiopathic hypercalciuria, because these drugs block the excretion of calcium in the urine. For all other patients, (who constitute the majority of patients with osteoporosis or osteopenia), the treatment choices fall into two classes of drugs: anti-resportive agents; and accretive agents. Anti-resorptive agents are drugs, which block the bone from tearing up “old bone”. In this way, they reduce the rate of bone turnover, and increase the bone density. Many studies show that, up to a point, these drugs improve bone density and reduce bone fracture. Fosamax, Actonel, and Boniva are drugs in this class. However, there is growing concern that overly long use of these agents might harm the bone, because they inhibit normal bone metabolism. There is a consequence of this therapy called “porcelain bone syndrome”, which can lead to death of the bone, particularly the jaw. This occurs after many years of therapy. The alternate treatment approach is to use accretive drugs, or drugs, which stimulate the bone to form new bone. Drugs in this class include estrogen (which also has anti-resportive effects), testosterone for men, and the injectable agents, Forteo and growth hormone. These drugs do not increase bone density as much as they increase bone strength and reduce fracture risk.
A new theory that is starting to emerge in the specialty medical literature is “pulsatile therapy”, or alternating one group of treatments with the other over a period of time. This concept is early, but it would involve, for example, using Forteo for two years and then a drug as Boniva for two years. We believe that the best approach to osteoporosis will become more sophisticated and more complex over time than just prescribing one class of drugs to every patient, without an analysis of their individual characteristics or treatment needs.