Have you ever wondered if there’s a natural way to lower your high blood pressure, guard against Alzheimer's, lose weight, and feel better? Well as it turns out there is. Michael Greger, M.D. FACLM, founder of NutritionFacts.org, and author of the instant New York Times bestseller “How Not to Die” celebrates evidence-based nutrition to add years to our life and life to our years.

Today, we look at bone mineral density screening, the safety and efficacy of oral and injected medications, which foods may help protect our bones, and more.

Nearly 1 in 5 adults in the world may have osteoporosis. That’s hundreds of millions of people. The word “osteo-porosis” literally means porous bone. Now, most of our bone is actually porous to begin with.

Bone mineral density is considered to be the standard measure for the diagnosis of osteoporosis. Although the bone mineral density cut-off for an osteoporosis diagnosis is kind of arbitrary, using the standard definition, osteoporosis may affect about 1 in 10 women by age 60, 2 in 10 by age 70, 4 in 10 by age 80, and 6 or 7 out of 10 by 90. Osteoporosis is typically thought of as a disease in women, but one third of hip fractures occur in men. The lifetime risk for osteoporotic fractures (for 50-year-old white women and men) are 40 percent and 13 percent, respectively.

The good news, is that osteoporosis need not occur. Based on a study of the largest twin registry in the world, less than 30 percent of osteoporotic fracture risk is heritable, leading the researchers to conclude, “Prevention of fractures [even] in the oldest elderly should focus on lifestyle interventions.” This is consistent with the enormous variation in hip fracture rates around the world, with the incidence of hip fracture varying 10-fold, or even 100-fold between countries, suggesting that excessive bone loss is not just an inevitable consequence of aging.

The United States Preventive Services Task Force, an independent scientific panel that sets evidence-based, clinical prevention guidelines, recommends osteoporosis screening (such as a DXA bone mineral density scan) for all women aged 65 years and older and potentially starting even earlier than 65 for women at increased risk (such as having a parental history of hip fracture, being a smoker or an excessive alcohol consumer, or having low body weight). What should you do if you’re diagnosed, or more importantly, what should you do to never be diagnosed? Before exploring the drugs on offering to treat osteoporosis, there are some drugs that may cause it; so, let’s start there.

Stomach acid-blocking “proton pump inhibitor” drugs, so-called PPIs—with brand names like Prilosec, Prevacid, Nexium, Protonix, and AcipHex—are among the most popular drugs in the world, raking in billions of dollars a year…But then, in 2006, two observational studies out of Europe suggested an association between intake of this class of drugs and increased risk of hip fracture, and by 2010, the growing evidence forced the US Food and Drug Administration to issue a safety alert implicating PPI use with fractures of the hip, wrist, and spine. By now, there’s been dozens such studies involving more than two million people that, overall, show higher hip fracture rates, among both long- and short-term users…at all, dose, levels.

The irony is that most people taking these drugs shouldn’t even be on them in the first place. These PPIs are only FDA-approved for 10 days of use for the treatment of H. pylori, up to 2 weeks for heartburn, up to 8 weeks for acid reflux disease, and for 2 to 6 months for ulcers. Yet, in a community survey, most users remained on these drugs for more than a year, and more than 60 percent of patients were taking them for inappropriate reasons, (often wrongly prescribed for quote-unquote “indigestion,” for instance).

Calls to stop this massive overuse from regulatory authorities have fallen on deaf doctor ears. And now that they’re available over the counter, the problem of overuse may have gotten even worse. They can be hard to stop taking since many patients experience withdrawal symptoms that can last for weeks. In fact, if you take normal, healthy volunteers without any symptoms and put them on these drugs for two months and then covertly switch them to a placebo without their knowledge, all of a sudden, they can develop acid-related symptoms, such heartburn or acid regurgitation, so ending up worse off than they were before they even started taking the drugs.

In addition to bone fractures, this class of drugs has also been linked to increased risk of other possible long-term adverse effects, such as pneumonia, intestinal infections, kidney failure, stomach cancer, and cardiovascular disease. (In fact, the blood vessel effects could explain the case report “Abrupt-Onset, Profound Erectile Dysfunction in a Healthy Young Man After Initiating Over-the-Counter Prilosec.”) Oh, and also, premature death.

There are individuals with conditions like Zollinjer-Ellison syndrome—stricken with tumors that cause excess stomach acid secretion—for whom the risk versus benefit of long-term use may be acceptable, but that’s a far cry from the 100 million PPIs prescribed annually in the United States alone.

To deal with acid reflux without drugs, recommendations include weight loss, smoking cessation, avoiding fatty meals, especially within 2 to 3 hours of bedtime, increased fiber consumption, and, overall, a more plant-based diet because non-vegetarianism is associated with twice the odds of acid reflux-induced inflammation.

Other classes of drugs that have been associated with hip fracture risk include antidepressants, anti-Parkinson’s drugs, antipsychotics, anti-anxiety drugs, oral corticosteroids, and the other major class of heartburn drugs, the H2 blockers, such as Pepcid, Zantac, Tagamet, and Axid.

OK, so excessive bone loss is not just an inevitable-consequence-of-aging, and one of the things we can do to lower our risk and that of our patients is to take into account the potential skeletal side effects of the drugs we take and prescribe.

What about the drugs prescribed to treat osteoporosis? First, let me address efficacy:

Drug therapy for osteoporosis is recommended for those 50 and older with a history of past hip or spine fractures, those with hip or spine “T-scores” of negative 2.5 or less, and postmenopausal women or men 50 and older who don’t make that cut-off—but, have an estimated 20 percent or higher risk of a major osteoporotic fracture over the subsequent decade, or an estimated 3 percent or greater risk of hip fracture, specifically.

A T-score is a measure of how dense your bones are compared to a 30-year-old white woman. Since that’s the standard, and we tend to lose bone as we age, you can be labeled as having osteoporosis even if you have completely normal bone density for your age. Of course, just because your bone density may be normal doesn’t mean it’s necessarily optimal, which is why the National Osteoporosis Foundation set out these guidelines for drug treatment. Though, another reason, perhaps, is because it gets substantial funding from the drug industry, which rakes in literally billions of dollars in profits from osteoporosis drugs. What, does the science say?

The primary drug class used to treat osteoporosis is the bisphosphonates, sold as such brands as Fosamax, Actonel, Boniva, and Reclast. They are most effective at reducing vertebral fractures, cutting the risk in postmenopausal women from 2.8 percent down to 1.4 percent. That’s a relative risk reduction of 50 percent, but an absolute risk reduction of only 1.4 percent, meaning you’d have to treat 71 women to prevent just one woman from getting a vertebral fracture.

Unfortunately, the diagnosis of vertebral fracture is kind of wishy-washy. Depending on how you define the changes on x-ray, the prevalence of vertebral fractures can vary by as much as 3 percent to 90 percent in the same elderly population—almost none, to almost all. They’re also poorly predictive of back pain or disability. Vertebral fractures can certainly lead to back pain and reduced physical function, but only about a third are symptomatic—at all. The most harmful fractures are hip fractures.

Despite most of the clinical trials for osteoporosis treatment being funded by the drug companies themselves, no primary prevention benefit from bisphosphonates has been found for hip fractures. In other words, taking these drugs has not been convincingly shown to prevent fracturing your hip in the first place. However, having a prior fracture doubles your risk of breaking another bone; so, for those at high risk, bisphosphonate drugs may decrease the odds of hip fracture by 25 percent, though the absolute risk reduction is, again, only about 1 percent. It may take treating 91 people for three years to prevent one hip fracture.

An overconfidence in the power of pills and procedures for disease prevention may be one of the reasons doctors and patients alike may undervalue diet and lifestyle approaches.

In a study of those undergoing bone density scans, the average five-year fracture risk that would motivate most participants to consider preventative medication was 50 to 60 percent—much higher than their actual risk. Most patients want to be told the truth. They want to be told what the chances are that the drugs will actually benefit them, but there is a tension between the patient’s right to know and the likely reduction in their willingness to take the drug if they knew the truth.

In the bone density scan survey, participants greatly overestimated their own personal risk for hip fracture, thinking it was around 19 percent over the next five years, which is more than ten times higher than their actual risk, of 1.4 percent. Rather than disabusing them of this overestimate, some suggest physicians should do the opposite: stoke fears in patients who “refuse to comply with medication recommendations” by increasing their “perceived susceptibility to fragility fractures” as well as their “perceived severity of suffering from a fragility fracture.” Since emotion can be more motivating than reason, and anecdotal evidence can be more effective than evidence evidence, a “graphic scenario of suffering and incapacitation after a hip fracture will enhance emotional perception of this threat.”

But hip fractures can indeed be devastating and are associated with a significant risk of ensuing death. So, what about all of the lives these drugs must be saving? Well, only about a quarter of the deaths following fractures may be attributable to the fracture itself; so, most of the mortality risk may just be a consequence of the comorbidities—that is, the other diseases and poor health status of people who tend to fracture their hips. So, they may have died anyway in that same time frame even if they hadn’t broken any bones. This may help explain why there are no saved lives. Osteoporosis drug treatments, particularly bisphosphonates, fail to significantly reduce overall mortality.

OK, so the efficacy of the primary drug class used to treat osteoporosis is so slight on an individual basis, that most patients, if truly fully informed, likely wouldn’t take them. And that’s before even talking about the side effects, which I’ll turn to right now.

Potential lack of efficacy is not the only reason why most people prescribed bisphosphonate drugs for osteoporosis, like Fosamax, Actonel, Boniva, or Reclast, may stop taking them within a year. There are two rare but devastating side effects— osteonecrosis of the jaw, and atypical femur fractures—that contributed to around a 50 percent drop in the use of this class of drugs when they came to light. The New York Times article noting the decline explained the reasoning: “Reports of the drugs causing jawbones to rot and thighbones to snap in two have shaken many osteoporosis patients so much, that they say they would rather take their chances with the disease.”

The jaw-rot syndrome that prevents many from initiating treatment for fear of “their jaw falling off” can severely impact many aspects of quality of life but is exceedingly rare, affecting at most 1 in a thousand patients treated for osteoporosis. Atypical femur fractures can occur more frequently, though, as many as 1 in 300 users treated for three years. They are called “atypical” because they occur not after a fall or trauma, but just during routine activities, like walking, twisting at the waist or even just standing still. Your femur, your thigh bone, the biggest bone in your body—just breaks in half. Too cruel an irony from a drug that’s supposed to protect your bones.

Bisphosphonates work by inhibiting the action of a type of bone cell called osteoclasts. Your entire skeleton is constantly being remodeled with bone added in some spots and taken away in others to conform to changing demands. The cells that are continually laying down new bone are called osteoblasts, and the ones that chisel away old bone are the osteoclasts. It makes sense, then, that curbing the ‘clasts would prevent bone loss. But by reducing the active remodeling process, bisphosphonates might “freeze” the skeleton, allowing for the accumulation of microcracks over time, resulting in stress fractures. Other osteoporosis drugs like den-o-sumab (sold, as “Prolia”) prevent the new formation of osteoclasts in the first place, and have been plagued by the same kinds of rare but disturbing side effects.

As with anything in life, it all comes down to risks versus benefits. How many hip fractures are prevented for every femur that snaps? It depends on your race and how long you’re on these drugs. After five years in white women, 36 hip fractures are prevented for every atypical femur fracture. Hispanic women only get half the benefit, with about 18 to 1, and for Asian women it’s only about 5 hip fractures prevented for every femur fracture caused. (The study claims it failed to accrue enough data on Black women.) At ten years of drug exposure, the ratios get worse, 16:1 for white women, 5:1 for Hispanic women, and only about 1.5:1 for Asian women, meaning that the devastating fractures prevented and caused in Asian women are nearly comparable.

A nationwide survey of resident physicians found that knowledge regarding osteoporosis diagnosis and treatment was poor, with a particularly striking lack of knowledge regarding the two serious drug side effects. The good news is that after stopping the drugs, the risk of femur fracture rapidly drops by 70 percent within a year, leading to the suggestion that a drug “holiday” be considered after a few years on the drug to help mediate the risk.


How crazy is that atypical femur fracture data? I just cannot get over the irony of it all. OK, so between the lack of sufficient efficacy and these rare but devastating side effects, what can we do personally, and how can we counsel our patients to protect their skeletons?

In 12 short years, government panels have gone from suggesting widespread calcium supplementation may be necessary to protect our bones to “Do Not Supplement”. What happened? It all started with a 2008 study in New Zealand. Short-term studies had showed that calcium supplementation may drop blood pressures by about a point. Though the effect appears to be transient, disappearing after a few months, it’s better than nothing. And excess calcium in the gut can cause fat malabsorption, by forming soap fat, reducing saturated fat absorption and increasing fecal saturated fat content. And, indeed, if you take a couple Tums along with your half bucket of KFC, up to twice as much fat would end up in your stool, and with less saturated fat absorbed in your system, your cholesterol might drop. So, the New Zealand researchers were expecting to lower heart attack rates by giving women calcium supplements. To their surprise, there appeared to be more heart attacks in the calcium supplement group.

Was this just a fluke? All eyes turned to the Women’s Health Initiative, the largest and longest randomized controlled trial of calcium supplementation. The name might sound familiar—that’s the study that uncovered how dangerous hormone replacement therapy was. Would it do the same for calcium supplements? The Women’s Health Initiative reported no adverse effects. However, the majority of the participants were already taking calcium supplements before the study started; so, effectively the study was just comparing higher versus lower dose calcium supplementation, calcium supplements versus  no calcium supplements. But what if you go back and just see what happened to the women who started out not taking supplements and then were randomized to the supplement group? Those who started calcium supplements suffered significantly more heart attacks or strokes. Thus, high dose or low dose, any calcium supplementation seemed to increase cardiovascular disease risk.

So, researchers went back, digging through other trial data for heart attack and stroke rates in women randomized to calcium supplements with or without vitamin D added, and confirmed the danger, and most of the population studies agreed—users of calcium supplements tended to have increased rates of heart disease, stroke, and death.

The supplement industry was not happy, accusing the researchers of relying in part on self-reported data—like they just ask if people had a heart attack or not rather than verifying it. And indeed long-term calcium supplementation causing all sorts of gastrointestinal distress including twice the risk of being hospitalized with acute symptoms that may have been confused with a heart attack. But no, the increased risk was seen consistently across the trials whether the heart attacks were verified or not.

OK, but why do calcium supplements increase heart attack risk but not calcium you get in your diet? Perhaps because when you take calcium pills, you get a spike of calcium in your bloodstream that you don’t get just eating calcium rich foods. Within hours of taking supplemental calcium, the calcium levels in the blood shoot up and can stay up as long as eight hours. This evidently produces what’s called a hypercoagulable state; your blood clots more easily, which could increase the risk of clots in the heart or brain. And, indeed, higher calcium blood levels are tied to higher heart attack and stroke rates. So, the mechanism may be calcium supplements lead to unnaturally large, rapid, and sustained calcium levels in the blood, which can have a variety of potentially problematic effects.

Calcium supplements have been widely embraced on the grounds that they are a natural and, therefore, safe way of preventing osteoporotic fractures. But, it is now becoming clear that taking calcium in one or two daily doses is not natural, in that it does not reproduce the same metabolic effects as calcium in food, the way nature intended. And furthermore, the evidence is also becoming steadily stronger that calcium supplementation may not be safe. That’s why most organizations providing advice regarding bone health now recommend that individuals should obtain their calcium requirement from diet in preference to supplements. But if we can’t reach it through diet in preference to supplements


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