Hyperparathyroidism, a condition characterized by excessive parathyroid hormone (PTH) production, can have far-reaching effects on the body. The parathyroid glands, typically four pea-sized glands located behind the thyroid, are responsible for producing PTH, which regulates calcium and phosphorus levels. When these glands become overactive, it can lead to hypercalcemia (elevated calcium levels) and a range of associated symptoms. While hyperparathyroidism is often linked to weight gain, some individuals may experience weight loss. This article explores the complex relationship between hyperparathyroidism and weight changes, delving into the potential mechanisms and underlying factors.
Understanding Hyperparathyroidism
Hyperparathyroidism arises when the parathyroid glands produce an excess of parathyroid hormone (PTH). This hormonal imbalance often leads to elevated calcium levels in the blood (hypercalcemia). The causes of hyperparathyroidism typically involve enlargement of the parathyroid glands, which may stem from benign growths (adenomas) or, in rare instances, parathyroid gland cancers.
A rise in PTH often triggers a rise in calcium. This increased amount of calcium may begin to build up in your kidneys, which causes increased urination and thirst. An imbalance in the levels of PTH and calcium in your body can also cause the feeling of a foggy brain. Calcium is also involved in the normal day to day functioning of the gastrointestinal tract. Thus, when PTH rises and triggers a surge in calcium, the digestive system can be affected. Some patients experience nausea, vomiting, and constipation, which may all cause a decreased appetite. Hyperparathyroidism can cause your bones to release excessive amounts of calcium in the blood (hypercalcemia). When your bones release their calcium, they lose the strength needed to maintain normal function. Many patients who experience hyperparathyroidism often report mood changes. Some people even report feeling depressed.
Types of Hyperparathyroidism
There are two main types of hyperparathyroidism:
- Primary hyperparathyroidism: The problem originates in the parathyroid gland itself, often due to a non-cancerous tumor (adenoma).
- Secondary hyperparathyroidism: Another condition, such as kidney failure, lowers calcium levels, causing the body to produce extra PTH in response.
- Tertiary hyperparathyroidism: Long-term secondary hyperparathyroidism begins to act like primary.
Both primary and secondary hyperparathyroidism may be associated with weight loss for some people.
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Metabolic Syndrome and Parathyroid Diseases
Parathyroid diseases, including hyperparathyroidism (hyperPTH), hypoparathyroidism (hypoPTH), and pseudohypoparathyroidism (pseudoPTH), are common clinical conditions that may share common pathways with metabolic syndrome (MetS). MetS is a cluster of conditions that increase the risk of heart disease, stroke, and type 2 diabetes.
Metabolic syndrome (MetS) is a set of diseases of high cardiometabolic risk, with steadily increasing incidence in the adult population, considerable social impact and health care costs. It depends on geographic and sociodemographic factors, European MetS prevalence has been estimated as 41% in men and 38% in women.
The most recent International Diabetes Federation (IDF) criteria states that central obesity (waist circumference ≥ 94 cm for men and ≥ 80 cm for women) allows the diagnosis of metabolic syndrome along with two of the following: systolic blood pressure ≥ 130 mmHg and/or diastolic blood pressure ≥ 85 mmHg, fasting blood glucose ≥ 100 mg/dl (5.6 mmol/L), HDL cholesterol < 40 mg/dl in men or < 50 mg/dl in women, triglycerides > 150 mg/dl. Therefore, MetS is characterized by the coexistence of abdominal obesity, atherogenic dyslipidemia, elevated blood pressure and glucose alterations, which together increase the risk of developing chronic conditions such as type 2 diabetes mellitus and cardiovascular disease.
Parathyroid hormone (PTH) is involved in the calcium homeostasis, increasing calcium resorption from the skeleton and calcium kidney resorption. Both metabolic and cardiovascular complications of parathyroid diseases may share common pathogenetic mechanisms with the features of MetS. Although kidney and bone represent the primary target organs for PTH, many additional tissues also express PTH receptors, thus additional effects of PTH should be considered. PTH promotes phospholipase C-b, increasing the amount of free intracellular calcium in both adipocytes and skeletal muscle. There is evidence that the increase of intracellular calcium in adipocytes interferes with insulin-stimulated glucose uptake. Furthermore, in view of the common progenitor between adipocytes and osteoblasts, it has been postulated that PTH might play a role on their differentiation. Noteworthy, a possible association between elevated PTH levels and increased body weight has been proposed by a meta-analysis in which body weight values were elevated in both hypercalcemic and eucalcemic populations with hyperPTH. Also, Elevated PTH levels may promote hypertension, due to its correlation with aldosterone levels PTH could directly stimulate aldosterone synthesis. PTH may also contribute to endothelial dysfunction increasing peripheral vascular resistance.
Weight Loss and Hyperparathyroidism: Exploring the Connection
While many associate hyperparathyroidism with weight gain, weight loss can also occur. Several factors may contribute to this phenomenon:
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Nausea and Vomiting
An imbalance in the levels of PTH and calcium in your body can also cause the feeling of a foggy brain. Calcium is also involved in the normal day to day functioning of the gastrointestinal tract. Thus, when PTH rises and triggers a surge in calcium, the digestive system can be affected. Some patients experience nausea, vomiting, and constipation, which may all cause a decreased appetite. Some people may develop nausea and have trouble eating. Reduced food intake may cause weight loss.
Leptin Changes
Leptin is a hormone primarily secreted by fat cells that makes you feel full. It’s thought that increased levels of leptin resistance in people with obesity may exacerbate secondary hyperparathyroidism.
Associated Conditions Like Kidney Failure
Secondary hyperparathyroidism is commonly caused by kidney failure. Loss of appetite is common in people with kidney failure. Reduced appetite generally leads to a lower calorie intake and weight loss. Muscle wasting is also common in people with kidney failure. Muscle wasting is the loss of muscle mass and strength.
Changes to Fat Tissue
Most of the fat in your body is classified as white fat. Your body uses white fat as an energy reserve. Brown fat is another type of fat that helps you create heat and maintain your body temperature.
Some evidence suggests that parathyroid hormone may stimulate the conversion of white fat tissue to brown fat. This change may trigger:
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- increased energy expenditure
- loss of muscle and fat
- weight loss
Elevated intact parathyroid hormone (iPTH) levels could also trigger adipose tissue browning, which leads to increased energy expenditure and ultimately results in weight loss.
Impact of PTHrP
Previous research has highlighted that primary hyperparathyroidism (PHPT) and weight loss are directly influenced by the action of a parathyroid hormone-related protein (PTHrP), which stimulates the browning of white adipose tissue (WAT).
Hypercalcemia and Gastrointestinal Symptoms
Previous studies have indicated that gastrointestinal symptoms associated with hypercalcemia, primarily presenting as anorexia, nausea, and vomiting, often result in reduced food intake and subsequent weight loss.
Affecting Appetite
Moreover, hyperglycemia and weakness induced by PHPT contributed to a decreased appetite, further exacerbating the weight loss.
Secondary Hyperparathyroidism and Wasting
However, secondary hyperparathyroidism seems to demonstrate another mechanism of wasting, especially among chronic dialysis patients; bodyweight loss might be a mediator between elevated PTH levels and mortality.
Study on Hemodialysis Patients
Elevated PTH was associated with subsequent weight loss, a hallmark of wasting. This relationship was sustained after adjustment for numerous covariates, was robust regardless of whether patients were hospitalized or not, and was more pronounced in persons with preserved appetite. Furthermore, the association between PTH and weight loss partly mediated the higher risk of mortality associated with elevated PTH levels.
In an international DOPPS cohort of over 42 000 haemodialysis patients, it was found that elevated PTH was associated with subsequent weight loss, a hallmark of wasting. This relationship was sustained after adjustment for numerous covariates, was robust regardless of whether patients were hospitalized or not, and was more pronounced in persons with preserved appetite. Furthermore, the association between PTH and weight loss partly mediated the higher risk of mortality associated with elevated PTH levels.
Brown Tumors and Weight Loss
In a case study, a 68-year-old woman experienced unusual bodyweight loss in the past 6 months (56kg-40kg) and bone pain. She was diagnosed with osteitis fibrosa cystica associated with PHPT due to a parathyroid adenoma. PHPT can be presented with multiple fractures, bone pain, and bodyweight loss.
The role of elevated PTH levels
Elevated parathyroid hormone (PTH) levels, leading to weight loss, may influence mortality rates in patients with secondary hyperparathyroidism or in those undergoing long-term dialysis in the absence of parathyroid diseases.
Factors Influencing Weight Changes in Hyperparathyroidism
Several factors can influence whether an individual with hyperparathyroidism experiences weight gain or weight loss:
- Severity of hypercalcemia: Severe hypercalcemia is more likely to cause gastrointestinal symptoms and weight loss.
- Underlying conditions: Conditions like kidney failure can independently contribute to weight loss.
- Individual metabolism: Differences in metabolism can affect how the body responds to hormonal imbalances.
- Lifestyle factors: Diet and physical activity levels play a significant role in weight management.
Hyperparathyroidism and Other Metabolic Conditions
Prevalence of impaired glucose tolerance and diabetes in hyperPTH patients resulted higher compared with general population, with a prevalence of 25 and 10%, respectively. In particular, prevalence of impaired fasting glucose, impaired glucose tolerance and diabetes is increased in all hyperPTH patients, both symptomatic and asymptomatic. However, the lack of long-term prospective trials leads to a reduced understanding of glucose metabolism alterations in these patients. Several studies demonstrated that patients with hyperPTH present a reduced insulin sensitivity, basal and after stimulus. The impact of therapy on glucose metabolism in these patients remains unclear, since the regression of diabetes and of impaired glucose tolerance after parathyroidectomy has been observed only in a study on 34 patients.
Regarding lipid metabolism, several studies have identified an atherogenic lipid profile in patients with hyperPTH, characterized by an increase in LDL cholesterol and triglycerides levels and a reduction in HDL cholesterol. However, an improvement in these parameters has not been observed after 3, 6 and 12 months after parathyroidectomy, even after the exclusion of patients already treated with lowering cholesterol drugs. These data suggest that surgery seems to play a marginal role in dyslipidemia in hyperPTH patients. Contrasting results have been observed in patients with mild hyperPTH, since several studies find a reduction in total cholesterol, LDL cholesterol (even in patients on treatment) and triglycerides levels and an increase in HDL cholesterol levels. Although parathyroidectomy improves dyslipidemia only in patients with mild hyperPTH, a role of PTH in lipid metabolism should be considered.
In several studies, hyperPTH is associated with an increased risk of hypertension, since this feature has been observed with a prevalence of 40-65% in hyperPTH patients, higher than general population. Several mechanisms have been proposed to explain this relationship. Calcium is a regulator of the renin-angiotensin-aldosterone system (RAAS). Indeed, chronic hypercalcemia causes an increase in renin activity, through stimulation of Calcium Sensing Receptor (CaSR). Also, elevated PTH levels contribute to hypertension, because this hormone correlates with aldosterone levels in these patients and the possible underlying mechanism is that PTH may directly stimulate aldosterone synthesis. Moreover, PTH action on hypertension could be explained through endothelial dysfunction, increasing sympathetic activity or with a direct effect on vascular smooth muscle cells, leading to an increased peripheral vascular resistance with hypertension. Several studies evaluated reversibility of cardiovascular disease and hypertension in patients with hyperPTH undergoing surgery. Indeed, patients presented a reduction of plasmatic renin activity, angiotensin and aldosterone levels, and consequently a significative reduction in systolic and diastolic blood pressure after parathyroidectomy. Parathyroidectomy improved blood pressure in several studies; blood pressure improvement has been observed already 6 months after surgery in two series of 147 and 726 patients. This improvement is maintained over time in a study that evaluated 501 patients after 2 years from surgery.
Vitamin D Deficiency
Vitamin D deficiency has been proposed as a possible factor that can contribute to the development of MetS. Indeed, adipocyte, pancreatic beta cells and muscle cells are target tissues for this vitamin. Several epidemiological studies suggest an association between obesity, insulin resistance, diabetes and a reduced vitamin D activity. In particular, Meng et al. observed lower total 25(OH)D and vitamin D binding protein levels (p < 0.001) in patients with hyperPTH. Moreover, vitamin D concentrations present an inverted correlation with obesity-related parameters as BMI and waist circumference and vitamin D may contribute to build the sarcopenic obesity phenotype. In a similar way, vitamin D deficiency is associated with insulin resistance and diabetes, although vitamin D integration is not recommended to prevent or improve diabetes. Vitamin D deficiency has been also associated with hypertension. Several studies demonstrated that vitamin D levers are inversely correlated to renin and angiotensin II levels. Based on these results, a trial aimed to verify the effect of correcting vitamin D deficiency, but no benefit was found on blood pressure after 8 weeks of therapy, demonstrating that vitamin D isn’t a modifiable target for lowering blood pressure in deficient patients. In the evaluation of the vitamin D impact on blood pressure, some author observed that blood pressure modifications were mostly correlated with PTH levels and not with vitamin D, suggesting that hypertension is primarily influenced by PTH levels.
Hypoparathyroidism and Pseudohypoparathyroidism
Literature data analyzing the metabolic aspects and associated cardiovascular risk in patients with hypoPTH are lacking and mainly regard the influence of PTH treatment in these patients. On the basis of animal and human studies in which osteocalcin (OC) and undercarboxylated osteocalcin (ucOC) has been shown to regulate glucose metabolism Harsløf et al. conducted a randomized trial enrolling 62 patients with hypoPTH and assigned them double-blind to treatment with 100 g PTH (1-84) administered once daily subcutaneously or placebo for 24 weeks (24w), both groups received optimal calcium and vitamin D supplement (Table 3). Patients underwent at baseline and after 24w measures of body composition (body weight, truncal fat, and total body fat) and dosage of glucose, insulin, adiponectin, leptin, HOMA-IR, OC, and ucOC. In response to treatment, ucOC increased (p < 10-50) and body weight decreased significantly in the PTH-treated group; additionally, in the placebo group body weight increased (p:0.04). Changes in ucOC were inversely linked with changes in total body fat mass (p = 0.03) and body weight (p = 0.004). Therefore, PTH treatment seems to affect body weight independently of glyc…
Diagnosis and Treatment
A physical exam and blood test can diagnose hyperparathyroidism. Your doctor can help you arrange a blood test to check the levels of PTH, phosphorus, and calcium in your body. Although it’s a rare condition, hyperparathyroidism can lead to feeling confused, depression, bone pain and other serious health problems. Fortunately, medication or surgery treats this condition effectively. Even still, getting screened for hyperparathyroidism remains the best way to protect yourself from this disease.
If you have hyperparathyroidism, you don’t need to follow any particular diet. It’s a good idea to eat a balanced diet filled with plenty of nutrient-dense and minimally processed foods. For example, the Mediterranean diet is a dietary pattern that’s consistently associated with good health outcomes.
You may need to take a vitamin D supplement if you’re low in vitamin D. Your healthcare professional can advise you on how much you may need to take.
If you have an underlying condition like kidney failure, you may need to make additional dietary changes. For example, you may benefit from reducing salt intake.
It’s important to seek medical attention if you develop potential symptoms of hyperparathyroidism without a known cause. Most of the symptoms of hyperparathyroidism are general and require a proper medical evaluation to find the underlying cause. It’s especially important to see a doctor if you suspect you may have kidney failure. Early symptoms of kidney failure can include:
- fatigue
- swelling in your feet and legs
- shortness of breath
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