The latest headlines are claiming that a new study shows vitamin D can slow aging.
But is that actually what the study shows? What Vitamin D dose should we take? And should we get a Vitamin D blood test? Let’s take a look.
Table of Contents
The Study
The study examined a subset of participants in the massive VITAL trial. This was a study of the impact of vitamin D and omega-3 fatty acids in a group of over 25,000 older adults [1].
There were 4 groups. One took vitamin D3 at 2,000 IU a day. Another took omega-3 at 1 g a day. One group took both. And there was also a placebo group. Researchers measured the length of telomeres in participants’ white blood cells (called leukocytes) at baseline. Then they checked again after 2 and 4 years [1].
And here was the key finding. Omega-3s had no effect. But vitamin D supplementation reduced the rate of telomere loss by 140 base pairs. So the researchers concluded daily vitamin D supplementation might have a role in counteracting telomere loss and cell senescence [1].
So what’s the connection between these findings and aging? Think of telomeres as caps that protect the ends of our chromosomes from fraying [2].
Each time a cell divides, telomeres get a bit shorter. Eventually, they get too short and the cell stops dividing. This state is called cellular senescence [2].
And these aged cells don’t just quietly retire. They remain active, pumping out substances that can promote inflammation in surrounding cells and tissues. This can even push nearby cells into a senescent state, too [2].
It appears this is an important driver of the problems we associate with aging [2].
And all this means preventing the shortening of telomeres may hold a lot of promise when it comes to countering the aging process.
This is the big idea behind the book The Telomere Effect. It was written by the Nobel Prize-winning researcher Elizabeth Blackburn, along with co-author Elissa Epel. Blackburn won the prize for helping to uncover some of the key dynamics affecting telomere length. And she argues there are lifestyle choices we can make that translate into longer telomeres and healthier aging.
The Implications
That’s the theory. So what about these study results? Do they show us that vitamin D is one of the tools we can use to slow aging? And am I rethinking the dose of vitamin D I take in light of this new research?
First we need to talk about the impact found. Is 140 base pairs over 4 years a big deal? [1]
Well, leukocyte telomeres shorten by about 20–40 base pairs per year [3].
Given that average decline, 140 sounds like a big number. That equates to between 3.5 to 7 years of telomere shortening.
But we need to add some crucial context. The method used in the study to measure telomere length is the qPCR method. Like any measuring methodology, there are limits to its accuracy. A key question is this: when the qPCR test gives us a result of 140, how confident can we be that this reflects the actual number?
One way we can approach this question is to repeat a test on the same sample. If one time we get 140, but get 120 and 190 on the second and third attempts, we know the test isn’t super accurate. The answers are in the same ballpark, but the spread is fairly wide.
Researchers undertook exactly this kind of experiment to see how accurate the qPCR test is. It was actually an international effort, involving 10 different labs. They all used the same DNA samples [4].
What they found is that measurements of telomere length varied by more than 20% between labs. Within a lab — so here we’re testing the same sample in the same place again — the variation ranged from 1.4% to 9.5% [4].
So, best case scenario, variation in measurements within the same lab were 1.4%. The typical adult leukocyte telomere length is in the ballpark of 6–7,000 base pairs. A 1.4% variation would translate into a variation of 84 to 98 base pairs. Worst case scenario? The variation is over 650 base pairs between measurements of the same sample [5].
So let’s return to our figure of 140 base pairs. This is within the range of measurement error. So it’s hard to know if we’re seeing a real difference or if this is just noise.
But let’s lay aside this worry for the moment. Suppose that figure of 140 base pairs is 100% accurate. Is this difference biologically meaningful? In other words, will that 140 difference translate into reduced heart attack rates? Improved muscle performance? Lower cancer rates?
It’s important to note that individual variation in leukocyte telomeres is immense. The typical difference between two people at the same age is roughly 700 base pairs [6].
In comparison to these figures, 140 is quite modest. Plus, several large cohort studies have examined how leukocyte telomere length relates to mortality. A UK Biobank analysis of 472,000 participants found that mortality risk rose by 8% for each standard deviation decrease in telomere length [7].
They also explored linkages between telomere length and specific mortality causes. Sometimes, they noticed a relationship — shorter telomeres were associated with increased deaths from respiratory and digestive disorders [7].
In other cases, there didn’t appear to be a connection — for example, cancer-related and neurological disease-related mortality [7].
But, based on the data they provide, we can’t say how the associations they did find — like the 8% mortality risk boost — translate into base pairs. So we have suggestive evidence here that telomere length makes a difference, but we’re still unsure about how significant a change of 140 base pairs might be.
And it’s important to bear in mind that cohort studies like these just give us associations. It’s not possible to say from these studies alone whether the shorter telomeres drive the disease states. Shorter leukocyte telomeres might indicate stressed bone marrow, which is where these cells are made. And it may be that whatever is causing this stress is driving mortality increases, as opposed to the shorter telomeres being the primary cause [7].
Overall, the study authors conclude the prognostic relevance of telomere length is limited. The observed change in mortality risk with shorter telomeres is modest. When looking at any particular individual, other factors like BMI or blood pressure are much more relevant when trying to predict health outcomes [7].
And this reinforces a point that often gets lost in the excitement over new findings like the one we’re discussing. The traditional, boring metrics like BMI, LDL-c/ApoB, blood pressure, and exercise performance metrics are the ones that move the needle most when it comes to long-term health outcomes.
But, returning to the impact of a 140 base pair change in telomere length, what about within the VITAL study itself? After all, its primary purpose was to look at outcomes like cancer, heart disease, and strokes. Do we see differences in health outcomes that mirror the differences in telomere length?
In the main findings, vitamin D supplementation did not significantly reduce heart attacks, strokes, or all-cause mortality. The reduction in cancer mortality also failed to reach statistical significance [8].
If the modest telomere-shortening effect is real, it didn’t translate into tangible improvements in outcomes.
So here’s the takeaway with this new study. We’re not 100% sure there is a real impact on leukocyte telomere length with vitamin D supplementation. And if there is a real impact, we’re not sure this translates into meaningful differences in terms of health outcomes. So what about those headlines proclaiming this study shows vitamin D slows aging? It’s fair to say this is more about getting clicks than accurately reflecting the findings.
It’s also a helpful reminder in a time when there’s a push to test everything, especially in the dreaded “longevity clinics”. Not all tests give us information that’s useful and can be used to improve our health.
Current Approach
There’s been tremendous controversy when it comes to vitamin D supplements. And our understanding has shifted in some significant ways over the past decade or so.
If we back up to the early 2000s, 2 things were happening at once. Researchers were uncovering associations between low vitamin D and many important health problems through population studies [9].
And they were also raising alarm bells that huge numbers of people were deficient in vitamin D [10].
In this context, the Endocrine Society published a set of influential guidelines about vitamin D supplements. It included the recommendation of up to 2,000 IU a day of vitamin D to get levels in the blood to a sufficient threshold [11].
It also included support for pretty broad use of screening for low vitamin D levels through a blood test [11].
These recommendations and others like them helped boost the use of vitamin D supplements dramatically.
But in the years since those guidelines, we’ve learned a lot. And it’s caused a significant revision in recommendations.
For one thing, we’ve investigated the findings of those observational studies with trials looking at vitamin D’s causal impact. As with the VITAL trial, the findings have mostly been underwhelming. Vitamin D supplements haven’t made a big impact on problems like cancer or heart disease.
And we’ve learned that taking too much vitamin D can lead to problems. For instance, a 3-year clinical trial in Canada tested the impact of several daily doses of vitamin D. One group took 400 IU, another 4,000, and a third 10,000. Researchers were looking specifically at how this affected bone density. What they found was shocking. Those higher doses didn’t improve outcomes. In fact, they made things worse. Bone density in the wrist decreased by about 2.4% in the 4,000 IU group and 3.5% in the 10,000 IU group [12].
This is related to a known risk with excessive vitamin D: hypercalcemia. This is when the level of calcium in the blood is too high. This happens because vitamin D regulates calcium in the body. We need adequate amounts for healthy bones. But too much throws things out of balance. It can even start to pull calcium from our bones, which the trial we just looked at demonstrates.
We’ve also had to dial back our worries about a pandemic of vitamin D deficiency. This is reflected in a newer set of guidelines from the Endocrine Society. They acknowledge we aren’t sure about optimal vitamin D blood levels [13].
And so they also advise against routine screening for vitamin D levels, unless there are risk factors that point toward checking [13].
The guidelines do highlight certain groups where vitamin D supplementation is particularly recommended. These groups include children up to 18, pregnant women, prediabetics, and people over 75.
So what about the rest of us? The latest Endocrine Society guidelines suggest following the recommended daily intake — 600 IU for younger adults, increasing to 800 IU as you hit 70 and above [13].
Personally, I take 1,000 IU of vitamin D3 as part of MicroVitamin. This level lets me ensure I’m locking in the benefits without getting anywhere near the high doses that might lead to problems. But just because I take a supplement, that in no way means you also need to.
Reference List
1. https://www.sciencedirect.com/science/article/abs/pii/S0002916525002552
2. https://www.nature.com/articles/s41556-022-00842-x
3. https://pmc.ncbi.nlm.nih.gov/articles/PMC4112289
4. https://academic.oup.com/ije/article/44/5/1673/2594545
5. https://www.frontiersin.org/journals/genetics/articles/10.3389/fgene.2020.630186/full
6. https://pmc.ncbi.nlm.nih.gov/articles/PMC11896355
7. https://pmc.ncbi.nlm.nih.gov/articles/PMC8767489
8. https://pmc.ncbi.nlm.nih.gov/articles/PMC7089819/
9. https://academic.oup.com/jcem/article/109/8/1961/7686350
10. https://pubmed.ncbi.nlm.nih.gov/16529140/
11. https://academic.oup.com/jcem/article/96/7/1911/2833671
12. https://pubmed.ncbi.nlm.nih.gov/31454046/
13. https://academic.oup.com/jcem/article/109/8/1907/7685305
