It’s time for the NutritionFacts grab bag – where we look at the science on a wide variety of topics. Today, we start with the results of a study that has correlated low calcium intake and vitamin D exposure with higher bone fracture rates in British vegans. Here’s the story.
Vegetarians had slightly lower bone mineral density in their spines. Although the difference was basically within the margin of error for the test, if the bone quality really is compromised, it could lead to collapsed vertebrae and increased spinal fracture risk, but there is no evidence for this. The incidence of vertebral fracture was ascertained in older women who had been vegan for most of their lives—34 years on average. And despite their calcium intake being terrible, about half that of the non-vegans, and a quarter of them vitamin D deficient, the incidence of vertebral fractures was not significantly different. Although the vegans had a higher prevalence of vitamin D deficiency, and lower dietary calcium intakes, the two factors were not associated with bone loss. In fact, the annual loss in bone mineral density in the hips of vegans was less than half that of the meat-eaters, though the difference did not reach statistical significance.
Vegetarian women had not been found to be at higher risk of any kind of fractures, including wrist fractures, in this case, though among vegetarians, those who consumed the least vegetable protein intake were at the highest risk for fracture. Those who ate beans every day, or nuts, or something like veggie burgers, only had a third of the wrist fractures compared to vegetarians who only ate beans or other higher protein foods less than three times a week. So, those who consume a vegan or vegetarian diet may be at increased risk of fracture unless care is taken to ensure that an adequate quantity and variety of foods high in protein (such as whole grains, nuts, and beans, split peas, chickpeas, or lentils) are in the diet. That’s one of the reasons in my free Daily Dozen app, I recommend whole grains and legumes every day.
Hip fractures are even more serious. Those eating legumes, like beans, every day reduced their risk of hip fracture by more than 60 percent, compared to 40 percent lower risk from meat protein, with plant-based meats coming in in between, with about 50 percent lower risk of hip fracture.
What’s the bottom line on plant-based diets and bone health, according to this 2020 review? Theoretically, a long-term plant-based diet may reduce the risk of osteoporosis, but that has yet to be demonstrated. What we do know is that plant-based diets, when ensuring adequate calcium and vitamin D levels, don’t appear to have any detrimental effects on bone health. But this was published in August 2020. In November 2020, the 12-year follow-up to the study I talked about in my last video on comparative fracture risk in vegetarians vs. non-vegetarians was published, finding that non-meat eaters, especially vegans, had higher risks of total bone fractures, including at sites associated with osteoporosis such as hip fractures. It comes out to be about 20 more cases in vegans for every 1000 people over 10 years. So, if indeed this is cause-and-effect, eating vegan there would be an annual 1 in 500 chance of having a bone fracture that you otherwise might not have had.
Was it because they weren’t eating enough beans? Apparently not, since vegans getting more protein still apparently had higher risk. Maybe it was because they weren’t getting enough calcium? Apparently not, since vegans getting more calcium still apparently had higher risk.
What about bone and vitamin B12? If you remember, EPIC-Oxford, where the bone data come from, is the same group of British vegans who have rampant B12 deficiency. More than half the vegans were B12-deficient because they weren’t adequately supplementing with B12 or B12-fortified foods. This can lead to high homocysteine levels, which not only increase stroke risk, but may increase the activity of bone-eating cells. This was in a petri dish, but you do indeed see low bone mineral density in those born with a birth defect that leads to high homocysteine levels in the blood. Therefore, high serum homocysteine may be regarded as a factor that can reduce both bone mass and quality. But you don’t know, until you put it to the test. And homocysteine-lowering treatment failed to reduce the risk of bone fracture. So, in the end, the effect of B12 deficiency in bone health remains to be established.
Okay, so, how do we explain the higher fracture rates found among vegans? The investigators conclude that their findings suggest that bone health in vegans requires further research, but there were some clues. The elevated fracture risk, both for total fractures and for hip fractures specifically, was only significant for those under a BMI of 22.5, which is like under about 130 pounds for a woman of average height. So, part of the problem is that vegans tend to be so slender on average. Why are overweight and obese individuals protected from fractures? Think about it. They have a cushioning during a fall. There’s more of a cushion on your hips. Also, there’s an enzyme in fatty tissue that churns out estrogen, which is why women increase their breast cancer risk a percentage point for every pound they gain in adulthood. But estrogen can also have a bone-preserving effect. You can get the best of both worlds consuming soy foods, preventing bone loss while at the same time associated with lessening breast cancer risk for both estrogen receptor positive tumors and estrogen receptor negative tumors. Finally, overweight and obese individuals also may have stronger bones just from the increased weight bearing. Carrying 100 extra pounds, you’re doing major weight-bearing exercise just walking across the room! So, the risk differences they saw between vegans and meat eaters were likely at least partially due to differences in BMI.
My money, however, is on vitamin D. Great Britain is at Canadian latitudes. The sun’s rays are at such an angle during the winter months up there that the vitamin D levels among British vegans in the wintertime drop down to suboptimal levels. Ideally, we should be up around 75 nanomoles per liter or 30 nanograms per milliliter, depending on what units you’re using, which the vegans nail in the summer. It is the sunshine vitamin, after all. But in the winter, not getting the vitamin D added to dairy or found naturally in oily fish, if vegans aren’t supplementing, at that latitude during the winter, their vitamin D levels may drop too low.
Now, randomized controlled trials show that vitamin D alone doesn’t seem to reduce fracture rates, but boosting people’s vitamin D and calcium at the same time does. So, maybe it was a combination of the relatively low vitamin D and calcium intakes among the vegans that led to their higher fracture rates. We won’t know for sure until it’s actually put to the test, and when it is, you can be sure I’ll do a video.
Did you know that our body can make vitamin K2 from the K1 in green leafy vegetables? Here’s the story.
Vitamin K. Wait, I know about vitamins A, B, C, D, and E, but what happened to vitamins F, G, H, I, and J? It’s not alphabetical. Vitamin K stands for coagulation––or at least it does in German. That is the fundamental role vitamin K plays in helping the blood to clot. But over the last few decades, there is evidence it has other roles in the health of our bones, heart, and brain. It kind of reminds me of vitamin D. We know vitamin D is important for bone health, but then there have been all sorts of other controversial functions ascribed to it, some of which have been proven and some disproven. What about vitamin K? For bone health, for example, is the link between vitamin K and osteoporosis myth or reality?
It turns out the findings on vitamin K and bone are conflicting and unclear. It doesn’t help that some of the major trials were found to be problematic to say the least, as in “likely fraudulent,” containing “impossible data,” with investigators admitting to complete fabrication. And so, if you do a systematic review eliminating any fraud, we find that there is no evidence that vitamin K supplementation affects bone mineral density or vertebral fractures.
What about the heart? Researchers studied vitamin K supplementation for the prevention of cardiovascular disease. There is a vitamin K-activated protein in your blood that binds up excess calcium, and helps prevent calcium from being deposited into the walls of your arteries and stiffening them. So, if you give people extra vitamin K, will that protect people’s arteries from calcification? It sounds good in theory, but no; vitamin K does not appear to consistently prevent progression of calcification, atherosclerosis, or arterial stiffness.
For example, artery calcification is particularly common in patients with chronic kidney disease, which can lead to increased artery stiffness, which is an important risk factor for heart attacks and strokes. An earlier trial didn’t find any benefit on coronary artery calcification between the vitamin K and placebo groups, but they were using kind of a small dose. So, these trials used a whopping dose daily for a year and…nada. Vitamin K supplementation did not improve vascular stiffness or other measures of artery health. In fact, one study on the effect of vitamin K supplementation on artery calcification in patients with diabetes found that calcification tended to increase after supplementation with a type of vitamin K found in a slimy fermented soy food called natto.
Now, those with higher levels of vitamin K circulating in their bloodstreams do tend to have lower levels of inflammation, but it’s no wonder. Where is vitamin K found? The predominant dietary form of vitamin K in the human diet comes from dark green leafy vegetables and cruciferous vegetables. So, how did people get high levels in their blood? Eating broccoli. Those with higher levels of vitamin K in their blood were eating more vegetables and less meat. No wonder they had lower levels of inflammation.
The recommended adequate daily intake for vitamin K is set at 70 micrograms a day in Europe, and between 90 and 120 micrograms a day here in the United States. Just two leaves of kale has over 70 micrograms. And a quarter cup of cooked kale will get anyone all the vitamin K they need for the day.
Now, there is vitamin K found in meat, dairy, eggs, averaging about 5 to 10 micrograms per serving. In other words, they are even beaten out by iceberg lettuce, which is mostly water, but still contains like two to three times more vitamin K. Ah, but that’s vitamin K1, and what is found in animal products is mostly vitamin K2. Do you need vitamin K2? Apparently not. Once you get enough plant-based vitamin K1, there’s no established requirement for vitamin K2, because it hasn’t been proven that vitamin K2 has effects that are different from vitamin K1. They both act the same way in the body; thus, there’s not even enough data to take vitamin K2 into account at all. So, when the recommended adequate daily intakes are set, they’re only talking about getting enough vitamin K1 from plants––mostly green vegetables.
In fact, most of the bone trials that flopped used the vitamin K2 found in animal products, and most of the failed heart studies used vitamin K2 as well. Okay, even though there is presently a lack of randomized trial evidence to support a beneficial role for vitamin K in preventing the worsening of cardiovascular disease, or bone health, what if that were to change? What if all the sudden vitamin K2 was shown to have some unique benefits? Well, guess what? The bacteria in your gut make vitamin K2. That’s why fermented foods have vitamin K2. Bacteria make it. And the bacteria in your gut not only make it, but it gets absorbed from your colon up into your system, contributing a significant amount of the human vitamin K requirement just in case you miss a couple days of greens.
Vitamin K1 is made by plants and is the primary dietary form. Then, there are a dozen or so types of vitamin K2, which are synthesized by bacteria, including several types in the human gut. The exception, though, is a type of vitamin K2 called menaquinone 4––MK4––which is endogenously synthesized in mammals, and therefore is found in animal products. Now, I don’t know if any of you noticed, but we’re mammals too. It has consistently been shown that vitamin K1 from greens is endogenously converted inside your body to the vitamin K2 in animal products. You’re made out of meat too, though it took until 2010 before we discovered the human biosynthetic enzyme that does it. So, there’s no reason at all to take any sort of vitamin K supplement. Eat your greens. In fact, when vitamin K2 supplements were looked at, researchers found significant problems in terms of contaminants and mislabeling. Eat your greens.
Now, vitamin K2 appears in higher concentrations in certain tissues, including the brain. Again, we make vitamin K2 from the vitamin K1 we eat in greens, but maybe extra vitamin K2 might help? If you measure vitamin K levels in the blood and brains of centenarians (those who live over 100), concentrations of circulating vitamin K1 from vegetables, but not cerebral vitamin K2—not the vitamin K2 in the brain—was positively correlated with a wide range of cognitive measures. Why? Likely because they were eating green vegetables, and green vegetables don’t just have vitamin K. Green leafy vegetables are the most concentrated source of lutein, the eye health nutrient that’s taken up into the brain, and is associated with cognitive performance across the lifespan. And so, in these centenarians, circulating vitamin K1 and lutein concentrations were highly correlated. So, it’s hard to tease out exactly what in greens was so beneficial. It’s like when you see data showing lower circulating vitamin K1 levels in the blood stream are associated with increased risk of all-cause mortality, meaning lower vitamin K1 levels were correlated with a shorter lifespan. Well duh; vitamin K1 is found in greens, and of all the dietary components correlating with all-cause mortality, the best evidence appears to support the intake of green leafy vegetables and salads to reduce all-cause mortality. In other words, eat your greens.
In our final story, we look at how might we replicate one of our greatest public health victories of all time—the reduction of smoking rates—in the field of nutrition?
What we learned from the tobacco experience, wrote two preeminent public health scholars, is how powerfully profits can motivate, “even at the cost of millions of lives and unspeakable suffering.” “Big Tobacco Played Dirty and Millions Died.” How similar is Big Food? I’ve talked about how Big Food has used the same tobacco industry playbook. What about using the anti-tobacco playbook to counter the obesity crisis?
Tobacco is one of our great public health victories. The share of adults who smoke declined from 42 percent in 1965 down to just 15 percent by 2016. That’s about 5 out of 12 down to less than 2 out of 12. Thanks to the decline, cigarettes now only kill about a half million Americans every year, whereas our diet now kills tens of thousands more. Currently, the leading cause of death in America is the American diet.
Might we be able to use the same strategies that were so successful in the battle against Big Tobacco? It may be no coincidence that three of the most cost-effective policy interventions against obesity seem to be taken straight from the tobacco wars: (1) taxes on unhealthy products; (2) front-of-pack labeling; and (3) a restriction of advertising to children.
Excise taxes on cigarettes has been cited as the single most effective weapon in slashing smoking rates. A 25 cents-per-pack tax to help deal with some of the societal costs of smoking was associated with as much as a nine percent decrease in smoking rates. The World Health Organization has estimated that a 70 percent global increase in the price could prevent up to a quarter of all tobacco-related deaths worldwide.
Extending taxes on alcohol and tobacco to foodstuffs was proposed by none other than Adam Smith in his 1776 Wealth of Nations: “Sugar, rum, and tobacco, are commodities which are nowhere necessities of life, which have become objects of almost universal consumption, and which are, therefore, extremely proper subjects of taxation.” People have the right to smoke and drink and eat fattening foods, the logic goes, but perhaps they should help defray some of the publicly-funded medical costs that result. Well, if that’s the case, why not tax obese people directly?
Taxing people based on their weight was proposed at least as far back as 1904 in the British Medical Journal, a kind of pounds-for-pounds strategy (actually only up to seven shillings and six pence per pound). This was not only to recompense public coffers, but nudge behavioral change. “A tax on fat,” read the proposal, “would also have an excellent effect on the health of the nation by bringing about a reform of unwholesome habits of eating and drinking.”
Even a penny-per-ounce tax on sugar-sweetened beverages could bring in more than a billion dollars a year in states like Texas and California. A 10 percent tax on fattening foods on a national level could yield a half a trillion dollars over 10 years. Even if it was combined with a subsidy that lowered the cost of fruits and vegetables by 10 percent, it would be expected to net hundreds of billions of dollars. But would it actually change people’s eating habits?
Even a small price differential (about 10 percent) between leaded and unleaded gas was able to shift the entire auto industry away from lead. Could it also shift Americans to apples from apple pie? A systematic review of the available evidence suggests that dietary financial incentives and disincentives work. The cheaper you make fruits and vegetables, the more people say they’d buy. And the more you tax unhealthy foods, the lower consumption drops. Based on this kind of modeling, a tax on saturated fat—found mostly in fatty meat, dairy, and junk—could potentially save thousands of lives a year.
But wouldn’t such a tax disproportionately affect the poor? Yes, in that we would expect them to benefit the most! It’s like cigarette taxes. The classic tobacco industry argument is that cigarette taxes are “unfair” and “regressive,” burdening the poor the most, to which the public health community responded, “Cancer is unfair.” Cancer disproportionately burdens the poor. So, taxes would be expected to affect the greatest health gains for the least well-off.
The fact that the tobacco industry fought tooth and nail against cigarette taxes—everything from inventing front groups to overtly buying off politicians—suggests that taxes can indeed shift consumption patterns. But much of the evidence on changing food behaviors has not been based on real-life data. You can put people through fancy 3D supermarket simulators and discover that a 25 percent discount on fruits and veggies appears to boost produce purchasing by the same amount—up to about two pounds a week. But virtual vegetables don’t actually do you any good. Does this work out in the real world? Apparently so.
South Africa’s largest private health insurer started offering up to 25 percent cash back on healthy food purchases to hundreds of thousands of households, up to the U.S. equivalent of $799 per month. Why would they give money away? Because it apparently works—increasing consumption of fruits and vegetables and whole grains, while at the same time decreasing the consumption of foods high in added salt, sugar, and fat, including processed meats and fast food.
Why not just pay people to lose weight directly? A systematic review found that 11 out of 12 studies on financial incentives for weight loss described positive results. The one that failed to find a benefit of direct monetary inducements was only offering $2.80 a day. With kids, you can get away with just a nickel or a sticker to get them to choose dried fruit over a cookie as an after-school snack––though as soon as the enticements ended, so did the change in behavior.
Even if the incentives have to be made permanent, they might still pay for themselves. In the U.S., every dollar spent taxing processed foods or milk might net an estimated $2 in healthcare cost savings. Every dollar spent making vegetables cheaper could net $3, and subsidizing whole grains might offer more than a thousand percent return on our investment. Even a one percent decrease in the average price of all fruits and vegetables might prevent nearly 10,000 heart attacks and strokes every year.
What about taxes, though, which tend to be less popular than subsidies? In Europe, a number of countries have instituted taxes on sugary or salty foods, but Denmark was the first to introduce a tax on saturated fat. It only took agribusiness about a year to squash it, demonstrating how weak public health professionals can be when trying to tackle corporate power. This was chalked up to the “enormous imbalance” between the political influence exerted by the public health community, compared to the industry’s lobbying might.