LAF and elevated parathyroid hormone level

BOSTON, MASSACHUSETTS. The parathyroid glands are four or more small glands, each about the size of a grain of rice, located on the backside of the thyroid gland. They are named for their proximity to the thyroid, but serve a completely different role. While the thyroid gland is involved in regulating metabolism, the major function of the parathyroid glands is to maintain the body’s calcium level within a very narrow range so that the nervous and muscular systems can function properly. The parathyroid glands perform their function by releasing a hormone, parathyroid hormone (also known as parathormone or PTH), in response to a low blood level of calcium. The glands have sensors for measuring calcium level in the blood and, if found to be low, the release of PTH will result in removal of calcium from the bones (resorption) and/or the conversion of 25-hydroxy vitamin D (cholecalciferol) to its active form 1,25 dihydroxycholecalciferol (calcitriol), which will increase intestinal calcium absorption.

The parathyroid gland also releases PTH if it senses a magnesium deficiency and, somewhat paradoxically, magnesium is also required for the synthesis and secretion of PTH. Finally, there is some indication from animal experiments that vitamin K2 can counteract an increase in PTH by stimulating renal calcium absorption. In addition to its direct effects on calcium homeostasis, PTH also acts as a cardiac hormone. It accelerates heart rate and increases the force of heart contractions. There is also evidence of an association between PTH and hypertension, disturbances in the RAAS (renin-angiotensin-aldosterone system), left ventricular hypertrophy, and heart failure. The normal level of PTH is 10-55 pg/mL.

A group of researchers at the Massachusetts General Hospital now report an association between elevated PTH levels and lone atrial fibrillation (AF). Their study included 230 lone afibbers and 150 controls. The mean age of the participants was 56 years, 80% were male, and 88% had paroxysmal AF. About a third (37%) of the lone afibbers had hypertension. All participants had blood samples drawn for PTH measurement and underwent a physical examination as well as electrocardiography and echocardiography at entry to the study. The PTH level was higher in afibbers than in the control group (56 pg/mL vs. 50 pg/mL) and higher in afibbers with hypertension than in those without (59 pg/mL vs. 54 pg/mL). PTH levels were also higher in permanent afibbers than in paroxysmal ones (61 pg/mL vs. 55 pg/mL).

At the time of the blood draw, 164 afibbers were in sinus rhythm and 50 were in AF. PTH levels were substantially higher in those not in normal sinus rhythm (64 pg/mL vs. 54 pg/mL) and the difference in PTH level between afibbers in sinus rhythm and the controls was statistically non-significant.

The researchers conclude that PTH levels are higher in lone afibbers than in controls. The difference was particularly marked in afibbers actually experiencing AF at the time of blood sampling, in permanent afibbers, and in afibbers with hypertension. They also observed that a higher PTH level was associated with a larger left atrium. They suggest that their observations support the hypothesis that AF causes an increase in PTH, but concede that the possibility that an elevated PTH level causes AF cannot be excluded.

Rienstra, M, Ellinor, PT, et al. Elevation of parathyroid hormone levels in atrial fibrillation. Journal of the American College of Cardiology, Vol. 57, No. 25, June 21, 2011, pp. 2542-43

Editor’s comment: The finding that atrial fibrillation and PTH levels are associated confirms an earlier report by Israeli researchers. The team from Tel Aviv University found that PTH levels were significantly elevated during a bout of paroxysmal AF. They also observed a direct correlation between blood glucose level and duration of an AF episode. The higher the glucose level, the longer it took to convert to normal sinus rhythm[1].

Assuming that AF causes the release of PTH rather than vice versa, it would be interesting to speculate as to why AF would increase PTH. In my 2003 report “Aldosterone: Villain of the Peace”, I suggested that the wildly beating heart would release substantial amounts of ANP (atrial natriuretic peptide) and, to a lesser extent, BNP (brain natriuretic peptide). Inasmuch as ANP and BNP are strong diuretics, their release would be accompanied by copious urination (the big pee) which, in turn, would cause a substantial loss of sodium and, a somewhat lesser loss, of calcium, magnesium and phosphorous. The disproportional loss of sodium would rebalance the potassium/sodium ratio and eventually terminate the AF episode. The loss of calcium would result in a lowering of its concentration in the blood which would cause the release of PTH in order to correct the imbalance by drawing calcium from the bones[2,3].

So what do these findings mean, in practical terms, to afibbers?

  • The release of PTH is normally associated with low levels of calcium in the blood and serves to restore normal levels by causing the release of calcium from the bones (resorption). Presumably, PTH release associated with AF would have the same effect, and thus be a risk factor for osteopenia and osteoporosis, especially in the case of permanent afibbers.

  • If PTH released via AF has the same effect as PTH released due to low calcium levels than AF-related PTH release could presumably cause the common symptoms of hypercalcemia, including kidney stones, hypertension, development of cardiac structure abnormalities, myocardial calcification, and disturbances to the RAAS (renin-angiotensin-aldosterone system).

  • The observation that an AF episode lasts longer at high levels of blood glucose would lead to the conclusion that consuming high glycemic index foods during or immediately prior to an AF episode is a bad idea. Thus attempting to stop an episode by eating a banana or drinking orange juice is clearly not recommended.

While there is, as far as I know, no clinical data proving that AF-related PTH release could lead to the above complications, it would seem prudent to take steps to reduce PTH levels. Fortunately, this can easily be accomplished by supplementing with vitamin D. A recent study by Japanese researchers found that daily supplementation with 800 – 1200 IU of vitamin D3 reduced PTH levels by an average of 5.6 pg/mL in a group of 107 subjects without disorders affecting vitamin D metabolism. The increase in blood levels of vitamin D and the decline in PTH was accompanied by a slight increase in circulating calcium from 9.5 mg/dL (2.33 mmol/L) to 9.6 mg/dL (2.35 mmol/L)[4]. Another group of Japanese researchers has reported that vitamin K2 also retards an increase in PTH level and the resulting bone resorption[5].

Thus it would seem prudent for afibbers to ensure an adequate intake of vitamin D and K2. Inasmuch as PTH can also be released as a result of a magnesium deficiency, continued magnesium supplementation would also be in order.

  1. Shor, R, et al. Serum parathyroid hormone-related protein levels before and after paroxysmal atrial fibrillation. American Journal of Emergency Medicine, Vol. 26, March 2008, pp. 361-63
  2. Larsen, HR. Aldosterone: Villain of the Peace?
  3. Richards, AM, et al. Renal, haemodynamic, and hormonal effects of human alpha atrial natriuretic peptide in healthy volunteers. The Lancet, Vol. 1, No. 8428, March 9, 1985, pp. 545-49
  4. Okazaki, R, et al. Vitamin D insufficiency defined by serum 25-hydroxyvitamin D and parathyroid hormone before and after oral vitamin D3 load in Japanese subjects. Journal of Bone and Mineral Metabolism, Vol. 29, 2011, pp. 103-10
  5. Iwamoto, J, et al. Effects of vitamin K2 on the development of osteopenia in rats as the models of osteoporosis. Yonsei Medical Journal, Vol. 47, No. 2, 2006, pp. 157-66