> Conclusions: Vitamin D supplementation might reduce the incidence of major cardiovascular events, although the absolute risk difference was small and the confidence interval was consistent with a null finding.
Low blood levels of Vitamin D is highly correlated with just about every disease known to mankind.
Yet, studies repeatedly have shown that Vitamin D supplementation has next to no benefit in curing those diseases.
So either there's a jointly correlated third factor like sun exposure or low Vitamin D levels are CAUSED by those diseases and in general just an indicator of overall poor health.
It probably correlates with reduced mortality, because people exposed to sunlight tend to get out of the house more often and actually do some physical activity (that happens to be under the sun, sometimes).
It would be a very poor study that didn't control for those factors!
The reduction in mortality remains after controlling for level of exercise. Also, using sunbeds and sunbathing while on holiday is associated with reduced mortality, at least in this large study in Sweden:
This has been known for a long time and is why bodybuilders use nitric oxide supplements before workout. Whether that does what they’re hoping is not proven, but it’s common and popular.
l-citrulline is better than L-arginine I believe. It's better absorbed, causes more nitric oxide production and doesn't cause the problems l-arginine does at higher doses (This is from my crappy memory but I am sure pubmed will be able to back this up. I am not in a space I can easily research sources again at the moment).
Or that population studies are not individual studies.
Vitamin D 100% cures a vitamin D deficiency. And Vitamin D deficiency 100% causes disease.
This study was only looking at how vitamin D supplementation affected a large swath of people, both those deficiency and those replete. So why is everyone surprised the results ar inconclusive?
I'm surprised so many comments miss this. For heart disease it was a small effect size and not a statistically significant result. I.e. neither clinically nor statistically significant.
Can't publish a paper with no findings so they add "might reduce". By the same logic it "Might" increase all cause mortality or might increase lung cancer incidence. Trash study.
As an aside, starting Vitamin K2 a few months ago has given me a noticeable increase in energy and focus, make of that what you will. Vitamin K2 is one of those somewhat hard to get vitamins in a typical American diet.
As a note: lots of sauerkraut sold in stores (at least in America) isn't actually fermented but just cabbage soaked in vinegar which is shelf stable. If you want the fermented kind, make sure you get it from the refrigerated section and check the ingredients and it should not have vinegar.
Or just make it yourself, it's dead simple to do, especially with all the silicone waterless airlocks for mason jars showing up on amazon under cheap chinesium brand names (the original masontops product was more expensive)
Looks like nori seaweed sheets, some herbs including parsley and basil, egg yolks, soybean and grapeseed oils, and cheeses contain K2 as well(in rough order of concentration).
In case anyone isn't sure about kimchi and natto every few days, but "for better cognitive ability" would be a nice excuse usable for occasional sushi rolls, stir-fries, just a bit of extra Parmesan, maybe even fries :p
OP article shows no clinical or statistical difference for heart disease.
Why not just take a multi vitamin and think not much of it.
Probably everyone is low on vitamin D atleast at some point in the year and it costs next to nothing to just have a few other vitamins along for the ride.
It could also be that the study amount isn't enough. 60000 IU in a "monthly oral dose" seems like a poor way of going about it. First, it would average out to only 2000 IU/day and second, if there are absorption issues with either taking such a high dose at once or the person didn't eat enough fat or something you're going to absorb even less of it.
These doses are kind of laughable compared to what you get from the sun:
>A minimum erythema dose (1 MED) amounts to about 30 minutes midsummer midday sun exposure in Oslo (=20 mJ/cm2). Such an exposure given to the whole skin surface is equivalent to taking between 10,000 and 20,000 IU vitamin D orally, i.e. as much as 250-500 μg vitamin D
Sure, you might not have your entire skin exposed, but I'm the past we didn't only get 30 minutes of sun exposure either. It might just be that they didn't see any significant effect because the vitamin D supplementation wasn't high enough.
Multivitamins probably aren't going to give you enough either. Maybe if you take take them with 8g of fat and no caffeine, but even then it would depend on the multivitamin.
2000ui/day is quite a lot. Most supplements are 10ug / 400iu. Especially as it's a 5 year study.
With 4000ui per day being the safe limit for someone who's not monitoring levels. (Too much vitamin D is pretty grim because of the effects on calcium levels).
Once you get into checking levels you lose all benefits of a simple intervention.
>Most supplements are 10ug / 400iu. Especially as it's a 5 year study.
That's because an error was made when the RDAs were initially assessed. 400 IU is going to have no effect. I believe in the above link if the sunlight study they even mention that interventions below 1500 IU/day have no effect.
>Too much vitamin D is pretty grim because of the effects on calcium levels
Sure, but I wonder about this 4000 IU limit. Experts also royally screwed up last time with their suggestions that have had an impact for years . This was such a monumental screw up that somehow took decades to address:
>A statistical error in the estimation of the Recommended Dietary Allowance (RDA) for Vitamin-D was recently discovered, indicating that 8895 IU/day are needed for 97.5% of individuals to achieve values ??50 nmol/l, analyzing correctly the same data used by the Institute of Medicine. [0]
>Since all-disease mortality is reduced to 1.0 with serum vitamin D levels ≥100 nmol/L, we call public health authorities to consider designating as the RDA at least three-fourths of the levels proposed by the Endocrine Society Expert Committee as safe upper tolerable daily intake doses. This could lead to a recommendation of 1000 IU for children <1 year on enriched formula and 1500 IU for breastfed children older than 6 months, 3000 IU for children >1 year of age, and around 8000 IU for young adults and thereafter. [0]
That being said, I'm unsure if I would supplement 8000 IU either, but 2000 a day for a study still seems low.
Apparently it's not that easy to get vitamin D toxicity:
>A total of 127,932 serum/plasma 25(OH)D measurements were performed on 73,779 unique patients. Of these patients, 780 (1.05%) had results that exceeded 80 ng per mL and 89 patients (0.12%) had results that exceeded 120 ng per mL. Only 4 patients showed symptoms of vitamin D toxicity. Three of these cases involved inadvertent misdosing of liquid formulations. [1]
Although, it's important to keep in mind that others could've had problems, but just not shown identifiable symptoms.
K2 also is notorious for not agreeing with many people. Just do a little searching and you will find many anecdotes of K2 causing heart palpitations, muscle pain, bone pain, insomnia. Personally K2 in either MK4 or MK7 form causes me /extreme/ insomnia and /extreme/ bone pain. My experiment with MK7 was particularly horrifying because of the long half life (2-3 days.)
Added K2 to my regimen a while back when I learned it and vitamin D are needed together for calcium absorption. Too much D w/o K2 appears to make bones more brittle.
As mentioned above, it's not abundant in the western diet. I wonder if places where there is more K2 in the diet have less osteoporosis?
any time i take a vitamin i chug a huge class of water with it, which i am generally bad at. it's hard for me to decide whether it's my vitamin or just getting hydrated for once...
Why does Vitamin D supplementation have to be conclusive for people to see it can be beneficial on a personal basis? Majority of science is tentative/inconclusive by nature.
Medicine is moving to become more personal and preventive rather than purely guess and scientific method driven, especially with the advancement of AI and modern medicine.
When I read this trial, I see good news for those who personally believe in Vitamin D and have experienced benefits from it. I see no news for those who do not care for Vitamin D and have not tried it.
This is an incremental study that helps push Vitamin D forward in my opinion, even if the findings are weak.
Vit D + K2 have so much potential upside and so little downside that I rank that first among the supplements that I should always take because they seem to serve me well and I actually had deficiency when I first tested for it. It took more than expected to balance out my levels but once you start ramping up dosage, it's easy to reach upper desired limit so it's important to do regular blood tests
I started at 2k, saw it didn't do much, eventually went through 4k all the way to 8k, where I was close to acceptable maximum, so I cut it to 4k and then had a few blood tests spread over a year and the results remained almost in the middle of the range.
Not sure what you meant with evaluating them. I checked what results came up and adjusted dosage accordingly. Can't speak for side effects, but I feel subjectively better than back when I had deficiency.
It’s worth noting that this was done in a sunny place, it would be better to test this in an a place with a darker winter, that being the reason so many people are deficient in D. What is the incidence of deficiency in the study population?
It would likely be unethical to conduct a study to determine whether CVD risk is affected by vitamin D supplementation in those with vitamin D deficiency, because if you determine that study participants are vitamin D deficient then it is indicated to treat them regardless of impact on CVD risk. Thus the trial does not attempt to do such a thing, focusing only on a general sample, excluding anyone in whom vitamin D supplementation would be contraindicated.
Ultimately while it would be interesting to know if CVD risk is reduced with vitamin D supplementation in those who are vitamin D deficient, it is largely an academic question as those individuals should be taking vitamin D supplements anyway.
Related only tangentially. Doctor recommended a vitamin D supplement. Couple years later after terrible acid reflux, I eliminate prescribed medication X which solves 80% of reflux symptoms and pain. After self testing the remaining 20% of symptoms were caused by the vitamin D gummy supplement, tomatoes, and onions.
So yeah vitamin d might help on one hand, but cause it’s own issues in different areas.
No more vitamins for me. Better to eat well and get the occasional bit of Sun.
the dosing was 60,000 IU per month? that's only 2000 IU per day - most vitamin D dosing for effective results i've seen needs to be 10,000 IU per day, implying that they are drastically under-dosing the participants. and i agree with the other commenters who say vitamin K is necessary for proper absorption, and also that vitamin D from sunlight is more effective. so imho more studies should be done with a 10,000 IU daily dose.
The findings are so weak that it is entirely possible that the basic idea that someone who takes Vitamin D is less likely to have a major heart issue migth even be connected to the idea that people who take supplements generally have more healthy habits. You would need to control every factor of a person's life to see if D makes the difference: food, culture, stressors, exercise, etc.
You would need to control every factor of a person's life to see if D makes the difference: food, culture, stressors, exercise, etc.
Since it’s not possible to do this should we give up studying these sorts of things? Scientists study theses types of things the best way they know how. They search for clues, evidence. Then more studies are done. Eventually, hopefully, enough evidence has been amassed to make a conclusion that has a very good chance of being correct. It’s not perfect but it’s much better than doing nothing.
The authors acknowledge the limitations of the conclusions that can be made. They write:
Vitamin D supplementation might reduce the incidence of major cardiovascular events, although the absolute risk difference was small and the confidence interval was consistent with a null finding. These findings could prompt further evaluation of the role of vitamin D supplementation, particularly in people taking drugs for prevention or treatment of cardiovascular disease.
They do this in the paper. They explain what they do and their conclusions. Any similarly trained expert will understand the proper implications of the paper.
They gave vitamin D to one group and gave a placebo to the other group. I don't see how participants' likelihood of taking supplements could have any effect.
No, the findings are weak because they are, one, assuming that all heart disease is caused by vitamin D deficiency, and two, they are not segregating the population based on genetics, and the genetic need for vitamin D.
Sometimes I think they do these studies to discredit the value of nutrition and health.
"assuming that all heart disease is caused by vitamin D deficiency" - where is this assumption being made?
I think the study is valuable in that it suggests blindly giving everyone vitamin D is not strongly correlated with reduced cardiovascular events. I often see it stated that "nearly everyone" in developed countries is vitamin D deficient and so the majority of us should be supplementing.
I think results like this make for a strong argument that it's more important to get your individual levels checked before you waste your money on supplements.
One thing that's really important to note here is that the participants are all based in Australia. That's pretty significant considering the amount of sun Australians are exposed to. By some measures, Australia is the "sunniest" place in the world. And since exposure to sun causes your body to produce vitamin D, it's likely Australians have naturally higher levels than most other populations.
There's at least two different lab tests for vitamin D, one that measures the level in its inactive form, and one that measures the level in its active form. The inactive level is what you'll get for a routine test. The other test takes a long time to process and is more expensive, and in my experience, health insurance really doesn't like having to pay for it. The active level is ultimately what's important because it's what's interacting with your bodily functions. The tricky bit is that the relationship between the two levels is fairly inconsistent from individual to individual, and variably determined by poorly understood mechanisms. A decent subset of the population has under-diagnosed inflammatory diseases, and for whatever reason inflammatory disease tends to increase the ratio of active to inactive vitamin D. Outside of rheumatology, this dynamic isn't really known about by most doctors. There's therefore a non-zero risk of vitamin D poisoning from supplementing based purely on low test results from a primary care provider. Regulating your inactive level to the "normal" range may unknowingly increase your active level to the point that it causes problems like hypercalcemia and eventual bone damage.
If they are not grouping people by genetic risk than any of these nutritional interventions will always show a low impact.
Of course vitamin D is going to help some people more than others based on their genetic heritage. I am one of these people, and I get most of my vitamin D needs from my diet, mainly fish. Sun exposure might not be the best route for people to get their vitamin D, and this is especially true for light skinned northern people.
I ignore these genetically diverse nutritional studies and just focus on the metabolic pathways and my own genetics.
Genetic risk also depends on locality, since there's significant interplay between skin pigment, light exposure and endogenous vitamin D production (and between locality and light exposure).
> The rate of major cardiovascular events was lower in the vitamin D group than in the placebo group (hazard ratio 0.91, 95% confidence interval 0.81 to 1.01)
I don’t think this is the right way of looking at the result. Imagine you have cardiovascular disease. If you take vitamin D, the study suggests that you will on average a 9% reduction in risk. There is a ~97% chance that it provides you some improvement, but there is a ~3% chance that your risk actually increases. This seems like an easy decision to me if you are a high risk individual.
Looked at another way, imagine the authors used a 94% confidence interval instead of 95%. Suddenly, the risk reduction from vitamin D becomes “statistically significant”. There is nothing magical about 95%, and use of p values to assess boolean effective/ineffective should have been done away with a long time ago.
The issue is that with this result we cannot say that anyone was helped. The results are consistent with a null finding—that any effect measured is likely due to chance alone.
-that any effect measured is likely due to chance alone.
But this is a stronger statement that is not.
The 95% confidence interval for the hazard ratio was 0.81 to 1.01 which means there is more than a 5% probability that the result was due to chance, but not that it's likely due to chance, which implies "more probable than not". The result is more like: if the measured effect is real, it's small enough that a significantly larger study would be needed to demonstrate it with sufficient confidence.
Fair enough, I phrased it inaccurately, although “likely” is subjective. I should say it’s reasonable to conclude that the results could be due to chance alone. At any rate the results do not tell us that anyone, in fact, benefited from vitamin D supplementation with respect to CVD risk.
And it's bigger than that. It's one of the few large and well controlled studies done on the subject. It invalidates most of what was known about it (even though AFAIK, it doesn't contradict them).
The more I learn about Vitamin D, the less it appears that supplementation is necessary. The observed improvement in cardiovascular health among individuals with higher Vitamin D levels seems to be coincidental, as those who engage in more physical exercise also tend to spend more time outdoors.
I think the study is valuable, any piece of knowledge can help complete the puzzle. Sure, there might be more insightful constructions of a study to get at a root value for vitamin D supplementation, but at least we know under this circumstance it did not make a meaningful difference.
Can someone point to a study or an article claiming that Vitamin D has a benefit for cardiovascular health? I am taking Vitamin D supplements in winter, but it never occured to me that I should do this to improve the health of my heart.
The challenge is that Vitamin D is the new egg debate. i.e. eggs are good for you, eggs are bad for you.
Many Vitamin D studies like this one talk about major events (i.e. things associated with sudden death), less so about the symptoms of cardiovascular health.
Other studies talking about cancer will say similar that higher Vitamin D is found in certain cancers or the opposite effect in other cancers.
Why's this on the front page? As far as I can see (from the abstract), they found a small beneficial effect on cardio events, and no effect on strokes. It's almost a null result.
Let’s say I have a population of 100 people, and let’s say two of them get heart disease from a genetic risk of heart disease from low vitamin D, and the other 98 of them get heart attacks from any of the other numerous causes of heart disease.
You could give vitamin D to all those 100 people and vitamin D would appear to do nothing. Unless of course she one of the two people that it did work for.
So can you see how these randomized controlled trials of nutritional supplementation’s are useless for any individual?
I don’t care how vitamin D affect a population, I care how it affects me.
TLDR: "Vitamin D supplementation might reduce the incidence of major cardiovascular events, although the absolute risk difference was small and the confidence interval was consistent with a null finding."
What I think would be interesting is looking at something like "time spent outside" to see whether Vitamin-D might be more significant on persons with too little sunlight exposure (physical activity would be an obvious confounder you have to control for).
Ultimately the study wasn't especially meaningful and weak effects aren't too surprising as a result.
The best comment from a vitamin D study I remember is "you can lay buck naked on a rook in January all day but won't get enough vitamin D". Referring to northern US and Canada in winter.
People get this idea that northern US must be at a high latitude just because it is cold in winter, and it simply isn't true. The 49th parallel roughly matches the latitude of Paris, London, Brussels, Munich, Prague or Vienna.
The problem isn't that you won't get enough sunlight if you lay down naked in the sun, the problem is that you can't because it is too cold.
No the problem is the sun has to hit the earth's atmosphere at a certain angle in order for the correct wavelengths of light to pass through the earth's atmosphere. The amount of Vitamin D your body can generate from sunlight is based on your skin tone, where you are, the time of day, the day of the year, and the angle of the sun at that time and place.
Above/Below a certain latitude (N/S) there is a window of time where the sun never hits that angle at any point during the day, so you could sit outside naked all day long and still get zero vitamin D.
If this seems counterintuitive consider if you keep going far enough away from the equator and get into the arctic/antarctic the winter has no sunlight at all, and you clearly can't produce Vitamin D from sunlight if the sun never rises.
Yes that study (I can't recall the name of it) also noted the angle of the sun and limited daylight hours. Plus winter clothing means most often the only exposed skin is your face or even just half your face if you have a scarf on.
My city in Canada about 46.2 degrees north and about 300km from the eastern Maine border. Here in winter it gets light at 8am and dark at 4pm if there are no clouds. So most people are at work they go to work in the dark and leave when it is dark.
It’s insanity to me that the only route people think you should get vitamin D is from the sun. In fact, most of us Caucasian Europeans should be getting it from our diet.
Cold water fish has the highest amount of vitamin D.
> It’s insanity to me that the only route people think you should get vitamin D is from the sun. In fact, most of us Caucasian Europeans should be getting it from our diet.
The fact that the skin of your ancestors rapidly evolved to become much lighter as they migrated to more polar latitudes tells you all you need to know about whether diet was an adequate source of vitamin D.
Light-skinned people are particularly well-suited to obtaining all the vitamin D they need from sunlight alone.
It is dark-skinned people currently living far from the equator who benefit the most from vitamin D supplementation, because the melanin in their skin reduces their ability to synthesize vitamin D from the meager amount of sunlight they get.
It wasn’t very rapid. In most of Europe white skin was introduced by famers migrating from the middle east who displaced the hunter gatherer populations at the beginning of the neolithic.
Maybe, but my point is that it initially appeared in the middle east (and probably in northern Eurasia at a similar time) but was likely first introduced throughout most of Europe by migrants/invaders from modern day Turkey.
The people who lived in Western Europe for likely longer that it took for white skin to evolve in the middle east/caucasus(?) region were much darker skinned.
Also given how long anatomically modern humans have existed several thousands years is not such a short period.
Why would that be interesting? Presuming the effect of limited sun exposure is posited as vitamin D deficiency, that is already an indication for supplementation, regardless of any effect on CVD risk reduction.
The purpose of a study like this would be to determine whether vitamin D supplementation is indicated for CVD prevention independent of vitamin D deficiency, which is why the study recruited from the general population, excluding only those in whom vitamin D supplementation would be contraindicated.
But does the skin always produce the same amount of vitamin D just depending on the light and regardless of the levels in the body or is there a control loop that makes the skin produce less?
