New research suggests that regular Vitamin D supplements lower the risk of auto-immune disease in older people. Should you start taking it?
A new NIH-funded study reports that long-term use of vitamin D supplements reduced the incidence of auto-immune diseases such as rheumatoid arthritis, psoriasis, and Hashimoto's thyroiditis in a large population of Americans 50 and older. The subjects in this study were taking 2000IU of Vitamin D3 a day, and those who took them for two years or longer saw the greatest reduction in risk.
Vitamin D is perhaps best known for its role in building strong bones, and the market for vitamin D supplements has grown to over a billion dollars a year. However, recent research has cast doubts on the value of vitamin D supplements in preventing bone loss and osteoporosis. So this latest finding on vitamin D and auto-immune disease is welcome news for people who sell vitamin D supplements.
But it's also a textbook illustration of how scientific research (and nutrition research, in particular) works to either prove or disprove a hypothesis. It's usually a multi-step process. And in today's information economy, each incremental step in that process gets the same degree of fanfare and publicity. But this is not always warranted. Recognizing where we are in that process can help you put headlines in context and keep the information in perspective. So let's break it down, using this latest finding as an example.
How nutrition research works
Step 1: Observe a correlation
As is so often the case, the case for vitamin D as a possible preventive for auto-immune disease started with an almost random observation. Somebody noticed that multiple sclerosis is much more common in areas of the globe that lie north of 40 degrees latitude. In fact, the further from the equator you live, the higher your risk.
Step 2: Propose a hypothesis
There are a number of possible explanations for this phenomenon. It could be something about the diet in more northern countries or other aspects of their lifestyle. It could have to do with a pathogen that is more common in colder temperatures. Another hypothesis was that vitamin D might be protective against multiple sclerosis.
Sunlight hitting our exposed skin is one of the primary ways we get vitamin D. When you live further from the equator, there's less sunlight in winter, and colder temperatures mean you're less likely to be outside with your skin exposed. As a result, people who live further from the equator are more likely to be deficient in vitamin D. And maybe that has something to do with why they are more likely to have multiple sclerosis.
Once you have formulated a hypothesis ("Vitamin D helps prevent multiple sclerosis"), the next step is to look for other information that will either support or disprove your theory.
Step 3: Review existing data
Collecting data is expensive and time-consuming, and there's already a ton of data out there. So it makes sense to look at data that's already been collected to see if it fits your hypothesis. For example, we have huge, publicly available datasets that include information on the food and nutrient intakes of large groups of people over long periods of time, as well as information about their health, including blood work and diagnoses.
In this case, we'd want to see whether any of that data shows a relationship between vitamin D status and the incidence of auto-immune disease. And in fact, it does. Several studies have found an association between lower blood levels of vitamin D and increased risk of multiple sclerosis and other auto-immune conditions.
This is consistent with our hypothesis. If it weren't, it would send us back to the drawing board to come up with a different hypothesis. But even though the data supports our theory, it's still only a correlation. We haven't proven our hypothesis that vitamin D prevents auto-immune disease.
Step 4: Identify a plausible mechanism
Does the hypothesis make sense given what we know about the systems involved? In this case, the answer is yes. Vitamin D plays several key roles in the function of the immune system in general, and specifically in the part of the immune system involved in auto-immunity. So it's completely plausible that a deficiency of this nutrient might increase the risk of developing auto-immune conditions.
When you have a plausible mechanism for how one thing might cause another (as opposed to simply being correlated to it), it makes it easier to design studies to test your hypothesis.
Step 5: Test your hypothesis
So far, we've been looking at data in the rearview mirror. The next step is a prospective trial where we see whether an intervention (in this case, vitamin D supplements) reduces the auto-immune disease in the future. Ideally, you'd have a control group that gets a placebo. This generally starts with animal studies and eventually progresses to human studies.
It wasn't until this stage—prospective trials in humans—that the case for vitamin D supplementation for preventing bone loss started to fall apart. Of course, vitamin D had already become a billion-dollar enterprise on the strength of correlation and plausible mechanism. It's a good example of why we can't stop there. We need to test our hypotheses.
This latest research does bear out the hypothesis that vitamin D supplementation may reduce the incidence of auto-immune disease. There are a few caveats and qualifications to that conclusion, which I'll get to in a moment. But, first I want to add that even this is not the final step.
Step 6: Rinse and repeat
In order to be really confident in a cause and effect, we'd want to see that it's reproducible. If a similar study were repeated on different subjects or by different researchers, would you get similar results? Once you have half a dozen or so studies on the same question, you can even pool the results to see if the findings hold up in a meta-analysis.
Every step in this evidential chain can increase your confidence in your conclusions, as well as add additional nuances to the story. But, in nutrition, an awful lot of headlines and hype (not to mention commerce) are generated by findings that are far earlier in this sequence. My purpose in walking through the steps is to help you be more discerning about which results are merely interesting and which are grounds for action.
What does this study mean for you?
So, is this latest study grounds for action? Should you start taking vitamin D to reduce your risk of auto-immune disease?
In this study, those who took 2000IU of vitamin D were 20% less likely to be diagnosed with an auto-immune disease. However, auto-immune disease was pretty rare, even in those who didn't take vitamin D, affecting only about 1% of the population. (The only reason that they were able to detect an effect in this study is that it was so large, involving about 25,000 people.)
Keep in mind, however, that all of the people in this study were over 50 and most auto-immune conditions are diagnosed when people are in their 30s and 40s. An interesting question for a future study would be to test the effects of vitamin D on younger subjects. Auto-immune conditions also have a genetic component and it would be interesting to see whether vitamin D would be more or less protective in those who are at increased risk.
On the other hand, vitamin D is relatively inexpensive and quite safe. Although its impact on bone loss and osteoporosis has been a little disappointing, we're obviously still learning what vitamin D does for us. And we know that a significant portion of the population is deficient in this nutrient, especially in winter.
Finally, this nutrient is somewhat unique in that food is not the primary source. So my usual advice to get your nutrition from food instead of supplements may not apply here. I think there's a good case to be made for taking a vitamin D supplement, particularly in winter.
It's always a good idea to run these things past your own doctor, who is familiar with your particular situation. But if she agrees that a vitamin D supplement is a good idea, be sure to look for one that provides the Vitamin D3 (cholecalciferol) form of the nutrient.