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Diabetes can weaken bones, and some diabetes medications also can weaken bones. Here are five things every diabetic needs to know about the heightened risk of osteoporosis.

Osteoporosis can be an unexpected complication of poor diabetic control. Unfortunately, overly zealous diabetic control can also weaken bones. There is a relatively narrow path for healthy diabetes management to maintain healthy bones. Here are five things diabetics need to know.

1. Keeping your HbA1C below 7.0 percent isn’t important only for control of diabetes. It’s also important for bone health.

HbA1C is a measure of the percentage of red blood cells that are “sticky” with advanced glycation end products or AGE’s. The higher the average blood sugar level, the higher the proportion of “sticky” red blood cells and the higher the HbA1C. These destructive molecules stimulate the activity of osteoclasts, the cells that break down bone. They also stick to the collagen fibers that hold the mineral crystals of bone together. This makes them stiff, and in turn the bone becomes more prone to fracture. Controlling blood sugar levels indirectly helps to keep bones strong in diabetes.

There are different effects of high HbA1C in type 1 and type 2 diabetics. Type 1 diabetics with poor control have lower bone mineral density and more fractures. Type 2 diabetics tend not to lose bone mineral density if their blood sugar levels are poorly controlled, but also have more fractures despite their more nearly normal bone mineralization.

2. Drastic reductions in blood sugar levels, however, can trigger inflammatory reactions that cause bone loss and other problems

Sixty-five-year-old type 2 diabetic Robert decided he was going to get his diabetes under control once and for all. For three months, he followed his 1800-calorie-a-day diet to the letter. He exercised every day. He lost 40 pounds. He took his metformin, Farxiga, Novolog, and Levemir, and he measured his blood sugar levels five times a day.

At his next checkup, Robert’s endocrinologist applauded his progress. He had lowered his A1C from 8.5 percent to 5.7 percent. But three weeks later Robert suffered a vitreous hemorrhage, leaving him temporarily blind in one eye, and three weeks after that, Robert broke his hip. The orthopedic surgeon told him that he had developed osteoporosis.

Sudden changes in blood sugar levels generate inflammation. This inflammation can attack the heart, the eyes, the nerves, or bone. It’s not the case that diabetics “just can’t win.” But it is important not to make too many changes too quickly.

3. GLP-1 inhibitors can slow down bone regeneration and focus bone loss for easier fractures

The latest class of diabetes drugs is the glucagon-like peptide or GLP inhibitors. Medications in this class include:

  • exenatide (Byetta, Bydureon)
  • liraglutide (Victoza, Saxenda),
  • lixisenatide (Lyxumia)
  • albiglutide (Tanzeum)
  • dulaglutide (Trulicity)
  • semaglutide (Ozempic)

GLP-1 is a counterregulator to insulin. It keeps insulin from taking blood sugar levels too low. GLP-1 inhibitors prevent glucagon-like proteins from raising blood sugar levels higher. They also interfere with the ability of bone to absorb minerals.

The problem with GLP-1 inhibitors is that the protein they inhibit does more than just to help to regulate blood sugar levels. It also regulates the development of “baby” bone-building cells, osteoblasts, into fully functional bone-building cells.  It also slows down the development of premature bone-destructive cells, osteoclasts, into their fully functional form. It reduces the area of bone that these osteoclasts break down. Glucagon-like peptides ensure that bones take advantage of relatively abundant food supplies to build up new mineral structure, leaving the task of breaking down old, dysfunctional bone for times when blood sugar levels are low. When diabetics take inhibitors of these naturally occurring peptides, they achieve lower blood sugar levels, but they also slow down bone regeneration and focus the action bone-recycling into tiny areas that are more easily fractured.

4. Thiazolidinediones (TZDs) are also linked to bone loss

In the 1990’s, the thiazolidinediones (also known as TZDs) were thought to be something of a wonder drug for diabetes. Millions of diabetics took Actos, Avandia, or the now-banned Rezulin and watched their blood sugar levels plummet even if they ate what they wanted. After a few months of treatment with these drugs, they also watched their weight soar 40, 50, and sometimes 100 pounds, not without dietary noncompliance, but out of proportion to caloric excess.

It turned out that these drugs activated a substance called PPAR-gamma. This substance helps fat cells store sugar. But it also causes stem cells to become fat cells. Stem cells that were intended by the body to become bone cells became fat cells inside the bone. Fat in bone resulted in fractures. Years after discontinuing TZDs, diabetics may still have this ectopic fat in their bones, and they continue to be at elevated risk for broken bones. There is nothing to be done to remove fat once it has developed inside bones. Diabetics who have ever taken Actos, Avandia, or Rezulin need to be vigilant about maintaining bone health, and diabetics who are offered the still-legal Actos or Avandia should ask their doctors about the associated risk of osteoporosis.

5. Not every functional food is appropriate for type 2 diabetics.

Functional foods are foods that act like medicines. Most functional foods are beneficial for diabetics and non-diabetics alike, but one food is a problem for type 2’s: whey protein. Commonly added to smoothies for muscle recovery after a workout, whey protein stimulates insulin production. Why is that a bad thing? In type 2 diabetes, at least at first, the problem is not that the body does not make enough insulin. Instead the problem is that the body makes too much insulin, so much that cells become resistant to it. Whey proteins aggravate this problem. Type 2 diabetics are better off using protein from peas, rice, or hemp.

  • Holst JJ. The physiology of glucagon-like peptide 1. Physiol Rev. (2007) 87:1409–39. 10.1152/physrev.00034.2006.
  • Mabilleau G, Perrot R, Mieczkowska A, Boni S, Flatt PR, Irwin N, et al. . Glucose-dependent insulinotropic polypeptide (GIP) dose-dependently reduces osteoclast differentiation and resorption. Bone(2016) 91:102–12. 10.1016/j.bone.2016.07.014
  • Mieczkowska A, Irwin N, Flatt PR, Chappard D, Mabilleau G. Glucose-dependent insulinotropic polypeptide (GIP) receptor deletion leads to reduced bone strength and quality. Bone (2013) 56:337–42. 10.1016/j.bone.2013.07.003
  • Westberg-Rasmussen S, Starup-Linde J, Hermansen K, Holst JJ, Hartmann B, Vestergaard P, et al. . Differential impact of glucose administered intravenously or orally on bone turnover markers in healthy male subjects. Bone (2017) 97:261–66. 10.1016/j.bone.2017.01.027.
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