Vitamin D Supplements for Increasing Aging Muscle Strength

We have known for more than 400 years that muscle weakness is a common presenting symptom of vitamin D deficiency. Bones aren’t the only organs that respond to vitamin D—muscles do, too. However, as we age, our muscles lose vitamin D receptors, perhaps helping to explain the loss in muscle strength as we age. Indeed, vitamin D status does appear to predict the decline in physical performance as we get older, with lower vitamin D levels linked to poorer performance. As I discuss in my video in my video Should Vitamin D Supplements Be Taken to Prevent Falls in the Elderly?, maybe the low vitamin D doesn’t lead to weakness. Rather, maybe the weakness leads to low vitamin D. Vitamin D is the sunshine vitamin, so being too weak to run around outside could explain the correlation with lower levels. To see if it’s cause and effect, you have to put it to the test.

As you can see at 1:01 in my video, about a dozen randomized controlled trials have tested vitamin D supplements versus sugar pills. After putting them all together, we can see that older men and women taking vitamin D get significant protection from falls, especially among those who had started out with relatively low levels. This has led the conservative U.S. Preventive Services Task Force, the official prevention guideline setting body, and the American Geriatric Society to “recommend vitamin D supplementation for persons who are at high risk of falls.”

We’re not quite sure of the mechanism, though. Randomized controlled trials have found that vitamin D boosts global muscle strength, particularly in the quads, which are important for fall prevention, though vitamin D supplements have also been shown to improve balance. So, it may also be a neurological effect or even a cognitive effect. We’ve known for about 20 years that older men and women who stop walking when a conversation starts are at particularly high risk of falling. Over a six-month timeframe, few who could walk and talk at the same time would go on to fall, but 80 percent of those who stopped walking when a conversation was initiated ended up falling, as you can see at 2:14 in my video.

Other high-risk groups who should supplement with vitamin D include those who have already fallen once, are unsteady, or are on a variety of heart, brain, and blood pressure drugs that can increase fall risk. There’s also a test called “Get-Up-and-Go,” which anyone can do at home. Time how long it takes you “to get up from an armchair, walk 10 feet, turn around, walk back, and sit down.” If it takes you longer than ten seconds, you may be at high risk.

So, how much vitamin D should you take? As you can see at 3:00 in my video, it seems we should take at least 700 to 1,000 units a day. The American Geriatric Society (AGS) recommends a total of 4,000 IU a day, though, based on the rationale that this should get about 90 percent of people up to the target vitamin D blood level of 75 nanomoles per liter. Although 1,000 IU should be enough for the majority of people, 51 percent, the AGS recommends 4,000 IU to capture 92 percent of the population. That way, you don’t have to routinely test levels, since 4,000 IU will get most people up to the target level and “is considerably below the proposed upper tolerable intake of 10,000 IU/d.” The AGS does not recommend periodic mega-doses.

Despite the AGS’s recommendation, because it’s hard to get patients to comply with pills, why not just give people one megadose, like 500,000 units, once a year, perhaps when they come in for their flu shot? That way, every year, you can at least guarantee an annual spike in vitamin D levels that lasts a few months, as you can see at 4:00 in my video. It’s unnatural but certainly convenient, for the doctor at least. The problem is that it actually increases fall risk, a 30 percent increase in falls in those first three months of the spike. Similar results were found in other mega-dose trials. It may be a matter of too much of a good thing. See, “vitamin D may improve physical performance, reduce chronic pain, and improve mood” so much that people start moving around more and, thereby, increase fall risk. When you give people a whopping dose of vitamin D, they get a burst in physical, mental, and social functioning, and it may take time for their motor control to catch up to their improved muscle function. It would be like giving someone a sports car when they’ve been used to driving a beater. You’ve got to take it slow.

It’s possible, too, that such unnaturally high doses may actually damage the muscles. The evidence the researchers cite in support is a meat industry study showing you can improve the tenderness of steaks by feeding cattle a few million units of vitamin D. The concern is that such high doses may be over-tenderizing our own muscles, as well. Higher vitamin D levels are associated with a progressive drop in fracture risk, but too much vitamin D may be harmful, as you can see at 5:29 in my video.

The bottom line is that vitamin D supplementation appears to help, but the strongest and most consistent evidence for prevention of serious falls is exercise. If you compare the two, taking vitamin D may lower your fall risk compared to placebo, but strength and balance training with or without vitamin D may be even more powerful, as you can see at 5:41 in my video.


Other studies in which vitamin D supplements have been put to the test in randomized placebo-controlled studies, effectively proving—or disproving—their efficacy, are featured in videos such as:

That brings up a number of important questions, which I answer in these videos:

Unfortunately, most supplements are useless—or worse. Here are some additional videos on supplements I’ve produced that may be of interest to you:

For more on the benefits of exercise, see Longer Life Within Walking Distance and How Much Should You Exercise?

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live presentations:

How Phytoestrogens Can have Anti-Estrogenic Effects

When the Women’s Health Initiative study found that menopausal women taking hormone replacement therapy suffered “higher rates of breast cancer, cardiovascular disease, and overall harm,” a call was made for safer alternatives. Yes, the Women’s Health Initiative found that estrogen does have positive effects, such as reducing menopausal symptoms, improving bone health, and reducing hip fracture risk, but negative effects were also found, such as increasing the blood clots in the heart, brain, and lungs, as well as breast cancer.

Ideally, to get the best of both worlds, we’d need what’s called a selective estrogen receptor modulator—something with pro-estrogenic effects in some tissues like bone but at the same time anti-estrogenic effects in other tissues like the breast. Drug companies are trying to make these, but phytoestrogens, which are natural compounds in plants, appear to function as natural selective estrogen receptor modulators. An example is genistein, which is found in soybeans, which happen to be structurally similar to estrogen. How could something that looks like estrogen act as an anti-estrogen?

The original theory for how soy phytoestrogens control breast cancer growth is that they compete with our own estrogens for binding to the estrogen receptor. As more and more soy compounds are dripped onto breast cancer cells in a petri dish, less and less actual estrogen is able to bind to them. So, the estrogen-blocking ability of phytoestrogens can help explain their anti-estrogenic effects. How do we then explain their pro-estrogenic effects on other tissues like bone? How can soy have it both ways?

The mystery was solved when it was discovered there are two different types of estrogen receptors in the body and the way in which a target cell responds depends on which type of estrogen receptor they have. The existence of this newly discovered estrogen receptor, named “estrogen receptor beta…to distinguish it from the ‘classical’ estrogen receptor alpha,” may be the “key to understanding the health-protective potential of soy” phytoestrogens. And, unlike our body’s own estrogen, soy phytoestrogens preferentially bind to the beta receptors.

For instance, within eight hours or so of eating about a cup of cooked whole soybeans, genistein levels in the blood reach about 20 to 50 nanomoles. That’s how much is circulating throughout our body, bathing our cells. About half is bound up to proteins in the blood, so the effective concentration is about half the 20 to 50 nanomoles. What does that mean for estrogen receptor activation?

In my video Who Shouldn’t Eat Soy?, I feature a graph explaining the mysterious health benefits of soy foods. Around the effective levels we would get from eating a cup of soybeans, there is very little alpha activation, but lots of beta activation. What do we find when we look at where each of these receptors are located in the human body? The way estrogen pills increase the risk of fatal blood clots is by causing the liver to dump out extra clotting factors. But guess what? The human liver contains only alpha estrogen receptors, not beta receptors. So, perhaps eating 30 cups or so of soybeans a day could be a problem, but, at the kinds of concentrations we would get with just normal soy consumption, it’s no wonder this is a problem with drug estrogens but not soy phytoestrogens.

The effects on the uterus also appear to be mediated solely by alpha receptors, which is presumably why no negative impact has been seen with soy. So, while estrogen-containing drugs may increase the risk of endometrial cancer up to ten-fold, phytoestrogen-containing foods are associated with significantly less endometrial cancer. In fact, protective effects are found for these types of gynecological cancers in general: Women who ate the most soy had 30 percent less endometrial cancer and appeared to cut their ovarian cancer risk nearly in half. 

Soy phytoestrogens don’t appear to have any effect on the lining of the uterus and can still dramatically improve some of the 11 most common menopausal symptoms (as compiled by the Kupperman Index).

In terms of bone health, human bone cells carry beta estrogen receptors, so we might expect soy phytoestrogens to be protective. And, indeed, they do seem to “significantly increase bone mineral density,” which is consistent with population data suggesting that “[h]igh consumption of soy products is associated with increased bone mass…” But can soy phytoestrogens prevent bone loss over time?

In a two-year study, soymilk was compared to a transdermal progesterone cream. The control group lost significant bone mineral density in their spine over the two years, but the progesterone group lost significantly less than that. The group drinking two glasses of soymilk a day, however, actually ended up even better than when they started.

In what is probably the most robust study to date, researchers compared the soy phytoestrogen genistein to a more traditional hormone replacement therapy (HRT) regimen. Over one year, in the spine and hip bones, the placebo group lost bone density, while it was gained in both the soy phytoestrogen and HRT estrogen groups. The “study clearly shows that genistein prevents bone loss…and enhances new bone formation…in turn producing a net gain of bone mass.”

The main reason we care about bone mass is that we want to prevent fractures. Is soy food consumption associated with lower fracture risk? Yes. In fact, a significantly lower risk of bone fracture is associated with just a single serving of soy a day, the equivalent of 5 to 7 grams of soy protein or 20 to 30 milligrams of phytoestrogens, which is about a cup of soymilk or, even better, a serving of a whole soy food like tempeh, edamame, or the beans themselves. We don’t have fracture data on soy supplements, though. “If we seek to derive the types of health benefits we presume Asian populations get from eating whole and traditional soy foods,” maybe we should look to eating those rather than taking unproven protein powders or pills.

Is there anyone who should avoid soy? Yes, if you have a soy allergy. That isn’t very common, though. A national survey found that only about 1 in 2,000 people report a soy allergy, which is 40 times less than the most common allergen, dairy milk, and about 10 times less than all the other common allergens, such as fish, eggs, shellfish, nuts, wheat, or peanuts.


What if you’re at high risk for breast cancer? See BRCA Breast Cancer Genes and Soy

What if you already have breast cancer? See:

What if you have fibroids? See Should Women with Fibroids Avoid Soy?.

What about hot flashes? See Soy Phytoestrogens for Menopause Hot Flashes.

What about genetically modified soy? See GMO Soy and Breast Cancer.

Not all phytoestrogens are beneficial, though. See What Are the Effects of the Hops Phytoestrogen in Beer? and The Most Potent Phytoestrogen Is in Beer.

How deleterious is hormone replacement therapy? See How Did Doctors Not Know About the Risks of Hormone Therapy?.

Synthetic estrogens used in animal agriculture are also a concern. For more on this, see Zeranol Use in Meat and Breast Cancer.

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations:

Why Some Dairy Products are More Closely Linked to Parkinson’s Disease

Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Each year in the United States, approximately 60,000 new cases are diagnosed, bringing the total number of current cases up to about a million, with tens of thousands of people dying from the disease every year. The dietary component most often implicated is milk, as I discuss in my video Could Lactose Explain the Milk and Parkinson’s Disease Link?, and contamination of milk by neurotoxins has been considered the “only possible explanation.” High levels of organochlorine pesticide residues have been found in milk, as well as in the most affected areas in the brains of Parkinson’s victims on autopsy. Pesticides in milk have been found around the world, so perhaps the dairy industry should require toxin screenings of milk. In fact, inexpensive, sensitive, portable tests are now available with no false positives and no false negatives, providing rapid detection of highly toxic pesticides in milk. Now, we just have to convince the dairy industry to actually do it.

Others are not as convinced of the pesticide link. “Despite clear-cut associations between milk intake and PD [Parkinson’s disease] incidence, there is no rational explanation for milk being a risk factor for PD.” If it were the pesticides present in milk that could accumulate in the brain, we would assume that the pesticides would build up in the fat. However, the link between skimmed milk and Parkinson’s is just as strong. So, researchers have suggested reverse causation: The milk didn’t cause Parkinson’s; the Parkinson’s caused the milk. Parkinson’s makes some people depressed, they reasoned, and depressed people may drink more milk. As such, they suggested we shouldn’t limit dairy intake for people with Parkinson’s, especially because they are so susceptible to hip fractures. But we now know that milk doesn’t appear to protect against hip fractures after all and may actually increase the risk of both bone fractures and death. (For more on this, see my video Is Milk Good for Our Bones?.) Ironically, this may offer a clue as to what’s going on in Parkinson’s, but first, let’s look at this reverse causation argument: Did milk lead to Parkinson’s, or did Parkinson’s lead to milk?

What are needed are prospective cohort studies in which milk consumption is measured first and people are followed over time, and such studies still found a significant increase in risk associated with dairy intake. The risk increased by 17 percent for every small glass of milk a day and 13 percent for every daily half slice of cheese. Again, the standard explanation is that the risk is from all the pesticides and other neurotoxins in dairy, but that doesn’t explain why there’s more risk attached to some dairy products than others. Pesticide residues are found in all dairy products, so why should milk be associated with Parkinson’s more than cheese is? Besides the pesticides themselves, there are other neurotoxic contaminants in milk, like tetrahydroisoquinolines, found in the brains of people with Parkinson’s disease, but there are higher levels of these in cheese than in milk, though people may drink more milk than eat cheese.

The relationship between dairy and Huntington’s disease appears similar. Huntington’s is a horrible degenerative brain disease that runs in families and whose early onset may be doubled by dairy consumption, but again, this may be more milk consumption than cheese consumption, which brings us back to the clue in the more-milk-more-mortality study.

Anytime we hear disease risks associated with more milk than cheese—more oxidative stress and inflammation—we should think galactose, the milk sugar rather than the milk fat, protein, or pesticides. That’s why we think milk drinkers specifically appeared to have a higher risk of bone fractures and death, which may explain the neurodegeneration findings, too. Not only do rare individuals with an inability to detoxify the galactose found in milk suffer damage to their bones, but they also exhibit damage to their brains.


Other than avoiding dairy products, what can we do to reduce our risk of Parkinson’s? See Is Something in Tobacco Protective Against Parkinson’s Disease? and Peppers and Parkinson’s: The Benefits of Smoking Without the Risks?.

You may also be interested in my videos Treating Parkinson’s Disease with Diet and Parkinson’s Disease and the Uric Acid Sweet Spot.

For the effect of foods on another neurodegenerative disease that affects our ability to move normally, see ALS (Lou Gehrig’s Disease): Fishing for Answers and Diet and Amyotrophic Lateral Sclerosis (ALS).

In health,
Michael Greger, M.D.

PS: If you haven’t yet, you can subscribe to my free videos here and watch my live, year-in-review presentations: