Hypothyroidism and Hyperparathyroidism

Paul L. Reller L.Ac. / Last Updated: August 03, 2017


Hyperparathyroidism and Hypothyroid syndromes

A growing incidence of subclinical hyperparathyroid disorder is also seen in the population, often associated with subclinical hypothyroidism and hypothalamic dysfunction. The parathyroid glands are small hormone excreting glands located on the sides of the larger thyroid gland. These glands predominantly secrete parathyroid hormone, an 84 amino acid protein built on tyrosine and arginine, that is a key regulator of calcium and phosphorous. Activation of the stored preprohormone in the parathyroid, and release of the active parathyroid hormone in circulation, is dependent on a number of factors, including low concentration of calcium in the blood, concentration of phosphate in the blood, hypothalamic function, kidney and adrenal function, thyroid function, and parathyroid receptor function. By 2013, large studies of the U.S. population found that the incidence of primary hyperparathyroidism had risen to an estimated 1-7 per 1000 adults, with women experiencing hyperparathyroidism 2-3 times more than men, and increased occurrence in aging. Secondary hyperparathyroidism, meaning hyperparathyroidism caused by another disorder, once considered very rare, is also seen in increased incidence, with kidney dysfunction and accumulation of phosphorus in circulation stimulating increased parathyroid secretion and cell proliferation, especially in the presence of hormone Vitamin D deficiency.

Adrenal insufficiency, excess phosphates from sodas and baked goods, deficient hormone Vitamin D3, subclinical hypothyroidism, and poor hypothalamic function may all contribute to hyperparathyroidism. A subclinical hyperparathyroidism, often accompanied by a subclinical hypothyroidism, presents as fatigue, depression, weakness, aches and pains, and potentially loss of appetite, and mild confusion. Clinical cases are often described in medical texts as moans, groans, stone and bones, with psychic overtones, indicating the wide variety of potential dysfunctions with a serious lack of regulation of the calcium and phosphorous balance in the body. Symptoms of skin disorder and restless leg syndrome are also commonly noted, especially in cases of chronic kidney dysfunction. Most cases of hyperparathyroidism are slowly developing and do not present significant danger, but when the gland malfunctions clinically in excess, which is rare, immediate response is needed. A 2002 study by the Henry Ford Hospital in Detroit, Michigan (cited in the section Additional Information), found that there has been a steady rise in the incidence of hyperparathyroidism in the United States and Europe, and a dramatic shift in the presentation of the primary disease, with a majority of patients asymptomatic in studies. Such findings point to the fact that many cases of hyperparathyroidism go undiagnosed. These experts concluded from this study that dietary and environmental changes were responsible for this rise in incidence of the disease, with evidence that hormone Vitamin D deficiency was integral to this rise in incidence of subclinical hyperparathyroidism. These experts also concluded from a meta-review of studies around the world that a hormone Vitamin D deficiency was inversely related to the size of the parathyroid gland enlargement, or adenoma. To understand more about the hormone Vitamin D metabolism, you may refer to a separate article on this website entitled Vitamin D, the true story. The persistent misinformation from standard medicine concerning this hormonal cascade simply termed Vitamin D is phenomenal, and we should be ashamed that such basic aspects of public health, the "Vitamin" D hormone metabolism, the affects of iodine deficiency, and adverse effects of synthesized chemicals in food, industrial use, pesticides and herbicides has been so stubbornly and thoroughly ignored and a campaign of misinformation allowed.

In a clinical primary hyperparathyroid disorder, the usual therapy is removal of the parathyroids (parathyroidectomy), whereby other tissues in the thyroid start to produce parathyroid hormone (PTH) and calcium phosphate levels are usually normalized. In recent years, minimally invasive approaches and partial parathyroid removal have been used and outcomes after 3 months appear to be the same for these procedures. Minimally invasive procedures locate the enlarged parathyroid glands and remove only these, using advanced scanning and ultrasound. Since the parathyroids are small and located usually on the sides of the thyroid, but sometimes in the interior of the thyroid, and sometimes away from the thyroid, locating the parathyroids correctly has been questioned in the past. Recurrent and persistent secondary hyperparathyroidism has an incidence of 10-70 percent, though, after either complete or partial removal of the parathyroid glands, and repeat surgeries are often utilized. Obviously, more needs to be done to correct hyperparathyroidism and the growth of abnormal tissue in the thyroid gland. Late-onset calcium deficiencies after minimally invasive parathyroidectomy have been noted in patients with Vitamin D3 deficiency, and monitoring with appropriate supplementation is recommended. Up to 40 percent of patients studied after parathyroidectomy develop elevated PTH levels but normal calcium levels in circulation, which is poorly understood, but appears to be related to kidney resistance to PTH mediated conversion of Vitamin D3 to its active hormonal form. While parathyroidectomy is considered safe and effective for both primary and secondary hyperparathyroidism (rare cases of adenoma or carcinoma), few studies have assessed quality of life in long-term outcomes. Some studies in Taiwan suggest that neuromuscular and neuropsychiatric abnormalities are common. Presently, these subjects are finally being explored. While parathyroidectomy is recommended and considered highly successful for primary parathyroidism, where an overstimulated parathyroid has become enlarged, it would be unwise to ignore the health problems associated with this condition, and many patients are now also seeking a holistic approach to restoring healthy hormonal balance after the parathyroidectomy, or minimally invasive partial parathyroidectomy.

Separating the thyroid from the parathyroid is a convenient simplification in modern medicine, but obviously, glands that are part of the thyroid gland do not function independently from the parent gland. In fact, in a significant portion of the population, the parathyroid glands are found inside, or part of, the thyroid gland itself. Parathyroid hormone acts only in balance with the thyroid hormone calcitonin, a 32-amino acid protein that modulates parathyroid hormone effects and is stimulated by both increases in circulating calcium and the stomach hormone gastrin. Because of this, both chronic intake of excess calcium supplement that is not quickly assimilated, and increases circulating calcium levels, and stomach dysfunction, which may alter calcitonin stimulation, may be implicated in parathyroid dysfunction. Hyperparathyroid dysfunction may be directly associated with chronic kidney dysfunction, Vitamin D deficiency (which is not actually a vitamin, but a prohormone), excess phosphorous in the diet (e.g. excess meat as a percentage of food intake), and chronic use of a thiazide diuretic to control high blood pressure, which may elevate circulating calcium. There is also speculation that chronic supplementation with calcium when there is poor calcium regulation may directly contribute to parathyroid dysfunction, especially when there is poor thyroid function, although high dose calcium carbonate has been used with some success to reduce PTH concentrations over time, producing an inhibitory feedback. More commonly, supplementation with D3 cholecalciferol is used in therapy, and some study of high dose D3 cholecalciferol is being conducted. Since D3 hormone is a potent regulator of calcium, this may reduce the need for parathyroid hormone and reduce stimulation of the parathyroids by the hypothalamus and pituitary.

The key to the connection between thyroid and parathyroid dysfunction appears to be the hypothalamus, a portion of the brain that signals the release of hormones that stimulate the production or release of other hormones. The hypothalamus thus regulates the activity, underactivity, or hyperactivity of the various endocrine glands, such as the thyroid and parathyroid. The hypothalamus is the common denominator. Much study has revealed a number of mechanisms by which the hypothalamus becomes deficient in function, as well as a number of nutrient medicines and herbs that stimulate improved hypothalamic function. Of course, if there is a nutritional deficiency, metabolic problem, or hormonal imbalance that is negatively affecting the hypothalamic function, this needs to be addressed to restore healthy function. Taking only one substance that may stimulate better hypothalamic function without correcting the other causes will not have a good overall outcome. This is why the comprehensive holistic approach is needed with Complementary Medicine. Scientific study also has shown that acupuncture stimulation may have a dramatic effect on hypothalamic function, and should be incorporated into the treatment protocol (see links to scientific studies below). Since the hypothalamus is also affected by the limbic system in the brain, which helps regulate mood and emotion, problems with emotional stress and control of anxiety and depression should also be addressed when needed. Such a comprehensive approach will produce long-lasting positive results over time.

Serum PTH (parathyroid hormone) is often seen at the upper limit of normal on blood tests in the targeted high-risk population, and so diagnosis of hyperparathyroid disease should be confirmed with confirmation of common symptoms as well as a full analysis of labs. Common symptoms included fatigue, weakness, mild constipation, abdominal pain, changes in short term memory or cognitive function, depression, bone pain, osteopenia, increased urination at night, joint pain, and high blood pressure, although only some of these symptoms are seen in most individual cases. Lab tests should analyze circulating calcium, alkaline phosphatase, circulating Vitamin D3, phosphate and other electrolytes, and blood cell counts. Active metabolite tests may be run, analyzing Vitamin D3 metabolites, as well as a hormone and thyroid panel to gauge overall hormonal balance. The occurrence of hyperparathyroidism with normal calcium levels is not infrequent, and studies have shown that there is a link between Metabolic Syndrome, glucose intolerance, high triglycerides and other metabolic disturbances and excess PTH. A more careful analysis and monitoring of patients with abnormal PTH and calcium levels in circulation is needed, and a more holistic approach to correction of this problem.

The parathyroid hormones along with the activated D3 hormone produced by the kidney are the main regulators of calcium in circulation (Vitamin D3 molecules, such as cholecalciferol, are the precursor, or prohormone, or preprohormone, to the D3 calcitriol). Calcium is the most highly regulated molecule in the body because it is large and a highly charged ion. There is abundant calcium in our bodies, in every cell, and much is stored in the bone matrix. Deficiency of calcium is perhaps not possible, although deficient calcium in the bone and in circulation is. When the calcium regulation is not functioning well, the patient may have excess calcium in circulation, or hypercalcemia, as well. Studies have shown that 90 percent of patients with hypercalcemia have hyperparathyroidism or a cancerous malignancy. Certain types of malignant cancer cells may produce a molecule that is very similar to parathyroid hormone, and excess may stimulate excess release of calcium from the bone. These parathyroid-like proteins have been increasingly studied in recent years and are found to compete at parathyroid hormone receptors, perhaps contributing to excess parathyroid hormone release in the absence of parathyroid hypertrophy. In addition to hyperparathyroidism, thyrotoxicosis, or toxic inflammation of the thyroid, may also cause excess calcium in circulation. Adrenal insufficiency and chronic kidney dysfunction are also causes, as well as Sarcoidosis (granulatomatous disease), Vitamin A & D excess, and chronic use of the medications such as a Thiazide diuretic, Tamoxifen and Lithium. All of these may contribute to a hormonal dysfunction and the Hyperparathyroid and Hypothyroid syndrome. Correct diagnosis and analysis is very important.

Besides calcium regulation, parathyroid hormone exerts a number of effects in the body. It regulates phosphates, stimulates and regulates synthesis of D3 hormone in the kidney, stimulates and regulates liver and blood cell proliferation, helps maintain mineral balance and acid-base balance, and is involved in immunoreactivity. All of these processes involve feedback regulation and need homeostatic balance. Of course, it is well known that PTH helps maintain healthy bones, along with hormone Vitamin D produced by the kidneys, by regulating the calcium homeostasis. There is also a relationship between blood pressure and parathyroid hormone, and indirect relationships with the health of brain cells and function. While all these hormonal mechanisms are still not well understood, the metabolism of the parathyroid, and the thyroid, are very important to overall health and well being. While modern medicine is still mostly concerned with primary Hyperparathyroidism and Hypothyroidism, and monitoring and treatment is geared almost entirely to severe problems and allopathic means of correction, the patient needs to pay attention to hormonal health and balance to achieve the best results when problems arise. Many patients will experience secondary subclinical Hyperparathyroidism, though, and these patients will need to look to less invasive and drastic measures to correct the problem, addressing more complex underlying causes, and restoration of homeostatic balance. To correct these problems, a more comprehensive approach is needed, utilizing Complementary and Integrative Medicine (CIM/TCM). Don't expect that the treatment protocol will be as simple as taking a synthetic thyroid hormone or having the parathyroids removed. Expect to be proactive when utilizing CIM/TCM, learn about your body, and seek help to do all the things necessary to restore balance, or homeostasis.

The rise in secondary hyperparathyroidism around the world in the last decade or so has been phenomenal. Standard medicine has been slow to assess this public health problem, and the little research devoted to it has mainly concerned the rise in chronic kidney disease. While this is a significant problem, the rise in chronic kidney disease and eventual kidney failure and need for dialysis, which involves hyperparathyroidism and dysfunction of mineral balance, we cannot simply ignore less serious problems with hyperparathyroidism, or the apparent cycle of dysfunction and relationship between slowly developing parathyroid problems and slowly advancing kidney disease. Studies have shown that over half of patients with chronic renal failure and a need for dialysis experience clinical hyperparathyroidism. Attention to the whole cycle of dysfunction, or a more holistic approach, would obviously result in better outcomes even for these patients. What such research should also reveal, though, is the need to address hypothyroidism and hyperparathyroidism with a more holistic treatment approach, as obviously kidney health and function is integral to this systemic cycle of dysfunction, and a strong association between diabetes, cardiovascular disease and hyperparathyoidism in chronic kidney disease is evident. An assessment by experts at the University of Kansas School of Medicine in 2009 stated that: "Secondary hyperparathyroidism is a frequently encountered problem in the management of patents with chronic kidney disease (CKD). Its pathophysiology is mainly due to hyperphosphatemia and vitamin D deficiency and resistance" (JABFM 2009, Sept-Oct; 22(5): 574-581). Integration of restorative medicine could greatly reduce this 'epidemic of rising kidney disease'.

A large retrospective study of the population and prevalence of parathyroid disorders, utilizing a bone health screening panel was conducted in 2016 by experts at the Aga Khan University School of Medicine, in Karachi, Pakistan. This large study noted that 68 percent of the patients in this screening study showed abnormal parathyroid hormone (PTH) secretions. Primary hyperparathyroidism was noted in just 1 percent, but subclinical hyperparathyroidism with normal circulating calcium levels were noted in 8.5 percent, and secondary hyperparathyroidism was noted in 18 percent, while secondary hypoparathyroidism was noted in 39 percent. These experts stressed that parathyroid disorders are mostly metabolic and subclinical and are not explained by a simple Vitamin D deficiency, as medical doctors continue to stress. The treatment of these problems needs a more thoughtful and holistic approach, not just a cynical advice to measure circulating "Vitamin" D and take a supplement. To see this important study, click here: http://www.ncbi.nlm.nih.gov/pubmed/27018622 .

Phosphate, or phosphorus homeostasis, is an important part of hyperparathyroidism, as excess phosphorous will stimulate excess excretion of parathyroid hormone (PTH) and lead to excess tissue growth in the parathyroid glands. In the last decade we have discovered that phosphorous homeostasis involves not only the balance of PTH and the hormone Vitamin D, but is regulated by growth factors as well. Fibroblast growth factor, or FGF-23, is a protein hormone with strong phosphaturic activity, and is mainly secreted by bone osteocytes. FGF-23 stimulates cells in the kidneys to increase excretion of phosphorous as needed, and inhibits the enzyme 1-alpha hydroxylase, which many cause the low hormone Vitamin D level in circulation. Excess phosphates are the principal stimulator of excess hormone Vitamin D, and excess phosphates in circulation are the principal stimulator of excess FGF-23. Here too is a cycle of dysfunction that needs restoration of homeostatic controls. Obviously, a holistic approach is needed in therapy. A phosphate is a salt or ester of phosphoric acid, and soft drinks contain a high amount of phosphoric acid, so soft drinks need to be eliminated in hyperparathyroidism and kidney disease. Phosphorus is a highly reactive, toxic nonmetallic element in phosphates. Other foods with high phosphate concentration include soft drinks made of fruit juice using fruit syrup, chocolates and other candies, ice cream, pastries, ketchup, mayonnaise, processed fish and cheese foods, frozen pizzas, hot dogs, and most processed meats. A smaller amount of phosphate is found in some whole unprocessed foods, and excess intake should be avoided, such as egg yolks, milk, nuts, wheat germ, soy, lentils, beans, corn, oats and organ meats. Avoidance of phosphates in the diet alone will not solve the problem, though, as the cycle of dysfunction described above is the chief concern.

The relationship between hypothyroidism and hyperparathyroidism has long been known. In a 1992 study at Loyola University, laboratory animals with induced elevation of TSH showed a 95 percent incidence of parathyroid hyperplasia, which would induce hyperparathyroidism. More recent studies have identified a relationship between levels of TSH in the upper normal range and incidence of hyperparathyroidism with normal circulating levels of calcium. Despite these findings, there has been very little research focused on understanding this relationship. More research has been devoted to the relationship between deficiency of Vitamin D3 (which is not really a vitamin, but a prohormone), and both hyperparathyroidism and hypothyroidism. Deficiency of calcidiol, the active form of the Vitamin D3 hormone produced in the kidney, is a significant risk factor for the development of secondary hyperparathyroidism, as well as primary hyperparathyroidism. Circulating levels of D3 are taken more frequently to assess this risk, and other risks. High dose supplementation with D3 cholecalciferol has created higher levels of calcidiol, but not as high as the patient might need. This implies that improved kidney and adrenal health is also necessary to restore this hormone imbalance. A combination of acupuncture stimulation, herbal therapy and nutrient medicine is ideal to achieve the best restoration of kidney function along with the taking of cholecalciferol (Vitamin D3) to achieve a lasting effect on calcidiol. A 2005 study at the University of Auckland, New Zealand, Department of Medicine, found that replenishing cholecalciferol in hyperparathyroidism did not cause an increase in serum calcium, modestly reduced parathyroid hormone in circulation, as well as decreasing bone turnover (osteopenia). How PTH was reduced by taking cholecalciferol was not well understood, underscoring how complex these interactions are in the hormonal system. Only be restoring hormonal balance can we insure that we get the healthy results that we are looking for. A thorough holistic approach to such restoration of hormonal balance could be invaluable, but is rarely utilized.

A 2010 study at the University of Dundee, Scotland, United Kingdom, found that overall mortality and morbidity (related health problems) were increased in patients with mild primary hyperparathyroidism. Comorbidities of concern included cardiovascular disease, osteoporotic fractures, and multiple endocrine neoplasia, such as the growth and spread of leiomyoma cells, commonly called uterine fibroid tumors. In standard medicine there is still no effective treatment for this disorder, other than partial removal of the parathyroid glands surgically, which causes hormonal imbalances and symptoms where there were none in asymptomatic patients. With Complementary and Integrative Medicine (CIM/TCM), this condition may be treated successfully in many cases, utilizing an intelligent comprehensive protocol. This protocol is discussed in the next section of this article. Prevention of hyperparathyroidism, which is often asymptomatic or undiagnosed, could have amazing long-term benefits and improve quality of life.