These Drugs Poison Your Bones

By Dr. Al Sears

Would you use a drug that gives you the problem it’s supposed to prevent?

Well, that’s exactly what’s going on with the new osteoporosis drugs.

Fosomax, Boniva, Reclast, Actonel. These medications are supposed to help stop you from getting bone fractures as you get older. But we now have evidence that they cause bone breaks.

Researchers studied women taking these medications – called bisphosphonates – who experienced some sort of fracture. Over 65 percent had the same rare fracture in the same area of their thigh bones. And these were the women who had been on the drugs for the longest periods.¹

Plus they’ve also found that if you’re on the drugs for a long time and you do get a bone break, you’ll heal very slowly. Sometimes it can take two years!

It’s another example of how modern medicine doesn’t learn from its mistakes. They refuse to take a whole-body approach to healing. Instead they opt to treat individual symptoms with drugs designed only for those symptoms.

And bone density drugs are a perfect example of this. I’ll tell you how they work in a moment, but first I want to tell you a little bit about how your body makes bone.

Your bones have cells called osteoclasts. Their job is to remove old bone tissue. This allows the bone to grow strong because other cells called osteoblasts then rebuild the bone.

With osteoporosis and other bone diseases, there is an imbalance – either your osteoblasts aren’t making new cells fast enough, or osteoclasts are removing too much tissue.

So drug companies came up with a way to stop osteoclasts from removing the old tissue, which also artificially increases your bone density: bisphosphonate drugs.

There are two problems with this.

1. By keeping your old bone tissue, you increase bone mass but make bones act older.

2. The drugs do the job by poisoning your osteoclast cells.

What happens is that you take the medicine, the osteoclasts absorb it, and it poisons the osteoclast cells by cutting off their blood supply. The cells then either work very slowly or die.

Because they don’t take away the old tissue, your bones become denser. But they’re dense with old tissue. And the osteoblasts can’t make new tissue if the old tissue is still there.

After a while, the old-bone tissue becomes brittle and fragile, like glass, because it’s not as strong as the newer bone that would have formed without the drugs.

You end up with technically “dense” but weak bones that can fracture.

The other thing that can happen that most people don’t know about is osteonecrosis. This is what happens when your bones are too dense with old tissue. There’s not enough space in the inner bone for your bone marrow, which keeps your bones alive. Your bones then start to die. This often happens in the jaw.

Look, poisoning your body is hardly ever a good idea. This is why in my practice, I never use these drugs. I’ve helped thousands of patients – both men and women – increase their bone mineral density naturally. Here’s what I tell them:

1. Vitamin D3 (calcifediol) is your number-one bone nutrient. Your body uses it in the process of making osteoclast and osteoblast cells. I always recommend sunshine as the best source of vitamin D. But because it’s winter and you might not be able to get that much sun on your skin, you can:

·         Eat some mushrooms: They’re the only vegetable that has vitamin D.

·         Eat seafood: Everyone knows by now that cold-water fish have lots of vitamin D. But did you know that oysters have as much vitamin D as salmon? You get about 350 IU for every 3.5 ounces.

·         Eat liver: Pork and beef liver are good sources. Braunschweiger pork sausage has 27 IU for every 2 slices, and beef liver has 42 IU for every 3 oz.

·         Supplement: I recommend 3,000-5,000 IU of vitamin D3 per day.

2. Vitamin K is also important when it comes to maintaining strong bones. Vitamin K comes in two forms: K1 is found in leafy green vegetables and helps with blood clotting. K2 on the other hand aids with your bones’ absorption of calcium to help make them stronger. You can find K2 in a variety of different foods including egg yolks, organ meat, and organic milk. I recommend 90 mcg a day.

3. Sex hormones are building blocks for strong bones.

·         Estrogen and testosterone control the amount of calcium absorbed into your bones. And by maintaining proper levels in your body, the less likely your bones are to weaken and fracture.

·         Progesterone also plays a role. Studies show that the cycle of ovulation is also a cycle of bone formation. Progesterone levels drop after giving birth, and after menopause, so returning your levels to normal can be, according to one study, “extraordinarily effective in reversing osteoporosis.”²

4. The more protein you eat, the easier it is for your bones to absorb calcium and the stronger your bones will become.³ You want to eat as many different kinds of protein as you can. When choosing animal protein, be sure to opt for natural, hormone-free meat and eggs. Grass-fed beef, free-range chicken, and cage-free eggs are good choices.

5. Weight-bearing exercise is one of the most effective ways to increase your bone strength and help prevent fractures. These include walking, bicycling, sprints, swimming or weight training. Focus on increasing intensity in all of these exercises.

Another benefit for your bones is that if you focus on increasing intensity, instead of increasing duration, you’ll lose weight and shed fat faster. This will reduce the amount of stress on your bones and joints, helping you prevent future injuries down the road.

Sources

1 Lenart, B., Lorich, D., Lane, J., et al, “Atypical Fractures of the Femoral Diaphysis in Postmenopausal Women Taking Alendronate,” New England Journal of Medicine 2008
2 Lee, J.R., "Is natural progesterone the missing link in osteoporosis prevention and treatment?" Med. Hypotheses. Aug 1991;35(4):316-8
3 Kerstetter, Jane, E., O’Brien, Kimberly, O., Insogna, Karl, L., “Supplements Dietary Protein, Calcium Metabolism, and Skeletol Homeostasis Revisited,” American Journal of Clinical Nutrition Sept. 2003;78(3):584S-592S