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The conventional understanding of osteoporosis used to be that it was reliably associated with thin bones and low weight. Unexpected side effects of modern medications, however, are leading to exceptions to the rules.

Osteoporosis has been always been associated with small bones and lower body weight. One of the ways that medical researchers know this is through observation.

A study at the Baystate Medical Center and the Harvard School of Public Health in the late 1990s found that:

  • Obese women (who had a BMI greater than 30) had a 78 percent lower risk of developing osteoporosis than women of normal weight.
  • Overweight women (who had a BMI of 25 to 30) had a 54 percent lower risk of developing osteoporosis than women of normal weight.
  • Unusually thin women (who had a BMI of 18 or lower) had an 80 percent greater risk of developing osteoporosis than women of normal weight.
For every unit of BMI (about 5 to 8 pounds, or 2 to 3 kilos) less weight, the risk of osteoporosis goes up about 12 percent. This would seem to be a reason not to diet. Heavier people build stronger bones to carry their added weight around. Heavier, thicker bones are less likely to break. Body fat seems to protect bones. But these observations were made before modern medications arrived that had the unexpected side effect of filling bone marrow with ectopic (misplaced) fat.

Fatty bones from faulty medication

One of the "miracle drugs" of the 1990s was a class of medications called the thiazolidinediones (TZDs) for diabetes. These drugs activated a receptor protein on fat cells that acted like a pharmacological vacuum cleaner to remove glucose from circulation. People were able to eat as they pleased and keep their blood sugar levels nearly normal. There was at least one major problem. All that sugar turned into fat.

It was not unusual for diabetics placed on Actos, Avandia, or the now-banned Rezulin to gain 30, 50, or even 100 pounds (12 to 40 kilos) of weight during their first year on the medication. Of course, you don't gain weight if you aren't eating too much. But the great blood sugar readings TZD-users saw every day caused them to abandon appropriate caution in their eating habits. If you have gone years without your pie and ice cream, and suddenly you can eat them without fear of soaring blood sugar levels, dietary restraint is going to be hard to accomplish.

Overweight type 2 diabetics became morbidly obese diabetics. And many morbidly obese diabetics started breaking bones. The problem was a form of secondary osteoporosis caused by the diabetes drugs. A previously unknown side effect of TZDs was that they caused baby stem cells that were supposed to mature into baby bone cells to become baby fat cells lodged inside bone. Fat weakens bone. Weak bones break.

It took about 10 years for researchers to confirm that Actos and Avandia (Rezulin had been banned because of cardiovascular deaths) could trigger rapid bone loss in overweight people. Avandia (rosiglitazone) caused excessive foot, hand, and wrist fractures in women who used it. The evidence regarding breaks in the hip and spine was inconclusive. Actos (pioglitazone) was associated with increasing numbers of fractures, but the numbers were not statistically significant.

Actos and Avandia are still on the market, although most countries require them to be dispensed with a "black box" warning. Over the years, however, medical watchdogs have confirmed a bone-fat connection for users of an even more commonly used class of drugs, the glucocorticoids. These drugs increase marrow fat. Marrow fat weakens the core of bone. Dieting increases marrow fat, as do alcohol abuse and inactivity.

Are you taking a drug that can put fat in your bones? If you are taking one of these medications, you are.

Glucocorticoids (with US trade names):

  • cortisone
  • dexamethasone (Dexamethasone Intensol, DexPak 10 Day, DexPak 13 Day, DexPak 6 Day)
  • ethamethasoneb (Celestone)
  • hydrocortisone (Cortef)
  • prednisone (Prednisone Intensol)
  • prednisolone (Orapred, Prelone)
  • triamcinolone (Aristospan Intra-Articular, Aristospan Intralesional, Kenalog) Methylprednisolone (Medrol, Depo-Medrol, Solu-Medrol)

Similar effects are possible with mineralocorticoid medications such as fludrocortisone (Florinef). If you are taking one of these drugs, you are at risk of osteoporosis even if you are "big boned" and overweight, because the medication is stimulating the growth of fat in the marrow of your bones.

Dieting is not the answer

How much you weigh is a major risk factor for osteoporosis. If you weigh too little, then your bones don't get enough stimulation to stay strong. it is especially important for you to avoid excessive alcohol use, to get regular low-impact exercise, and to seek alternatives to the medications listed earlier in this article. You don't necessarily have to gain weight, but you do need to make sure you eat enough protein and get enough calcium and other micronutrients.

If you weigh too much, your medications may pose as great a risk to your bones as weighing too little. Sometimes a problem medication just can't be avoided. If you are overweight, and you have any other risk factors osteoporosis, avoid the above-listed drugs if you can. Even if you can't, take these basic steps in osteoporosis prevention:

Avoid excessive alcohol use. Don't be a couch potato. Get gentle, low-impact, fall-free exercise regularly. But don't starve yourself to lose weight or take thiazide diuretics to deal with fluid retention. Make sure you get adequate protein without too many total calories every day, supplement with calcium, vitamin D, magnesium, zinc, copper, and vitamin K2 in moderate amounts. and seek medical care to keep your bones healthy.

  • Asomaning K, Bertone-Johnson ER, Nasca PC, Hooven F, Pekow PS. The association between body mass index and osteoporosis in patients referred for a bone mineral density examination. J Womens Health (Larchmt). 2006 Nov. 15(9):1028-34.PMID: 17125421.
  • Kawai M, de Paula FJ, Rosen CJ. New insights into osteoporosis: the bone-fat connection. J Intern Med. 2012 Oct.272(4):317-29. doi: 10.1111/j.1365-2796.2012.02564.x. Epub 2012 Jul 29. Review. PMID: 22702419 . Qiu W, Andersen TE, Bollerslev J, Mandrup S, Abdallah BM, Kassem M. Patients with high bone mass phenotype exhibit enhanced osteoblast differentiation and inhibition of adipogenesis of human mesenchymal stem cells. J Bone Miner Res. 2007 Nov.. 2(11):1720-31. PMID: 17680723.
  • Savopoulos Ch, Dokos Ch, Kaiafa G, Hatzitolios A. Adipogenesis and osteoblastogenesis: trans-differentiation in the pathophysiology of bone disorders. Hippokratia. 2011 Jan.15(1):18-21. PMID: 21607030.
  • Schwartz AV. TZDs and Bone: A Review of the Recent Clinical Evidence.PPAR Res. 2008. 2008:297893. doi: 10.1155/2008/297893.
  • Photo courtesy of SteadyHealth

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