In support of a novel hypothesis, data from the National Health and Nutrition Examination Survey (NHANES) revealed a statistically significant link between magnesium intake and vitamin D status.
Deng X, Song Y, Manson JE, et al. Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III. BMC Med. 2013;11(1):187.
Researchers found that people who took in the most magnesium from diet and supplements were at the lowest risk of vitamin D deficiency and insufficiency. The effect was most profound in those most at risk of having a low vitamin D level.
We know that vitamin D levels among people can vary significantly even when vitamin D intake is similar. While body weight and genetics can affect how you respond to sun or supplements, this phenomena remains largely unexplained.
After potassium, magnesium is the most abundant, positively-charged mineral inside our cells. Magnesium is required for the chemical reactions in the body that activate vitamin D in the liver and kidneys, break it down for excretion, and the reaction that determines how much vitamin D binding protein is in circulation. Because of this, researchers hypothesized that having more magnesium available in your body would make it easier for people to convert vitamin D into its active form, raising vitamin D serum levels.
The NHANES is a government-funded research project that studies the health and nutrition habits of Americans. The conclusions are considered reliable due to the large amount of participants and the in-depth nature of the data that is collected. Participants are interviewed in person and give blood samples.
Researchers looked at the dietary and supplement use data of 12,257 participants from the 2001-2006 NHANES data set and compared this information to their vitamin D serum levels. Those who were considered vitamin D sufficient had an intake of vitamin D and magnesium that was equal to or greater than government recommendations for those nutrients. Those who were considered vitamin D insufficient had a lower intake of these vitamins, and those considered vitamin D deficient had yet an even lower intake .
The inverse relationship between magnesium intake and vitamin D deficiency was only significant in those older than 50 with PTH levels in the highest or lowest tertile category.
The inverse relationship between magnesium intake and vitamin D insufficiency was only significant in those at high risk of vitamin D insufficiency. This group included those whose samples were collected in the winter, women, blacks, and obese individuals.
Furthermore, individuals with higher serum vitamin D levels were significantly less likely to die from cardiovascular disease, but only if they had a higher than average magnesium intake.
This study provides an exciting look into magnesium’s role in determining vitamin D levels, as well as how it may work in conjunction with vitamin D to lower the risk of heart disease.
Magnesium, along with vitamins A & K, boron, and zinc are cofactors for vitamin D metabolism and action in the body. Vitamin D does not act alone in the body, and understanding its relationship to its cofactors is one key to understanding just how vitamin D functions in the body to prevent disease. That being said, the relationship between vitamin D and its cofactors is still poorly understood and future research, like this present study, should elucidate just how essential they are to each other.
So, how important are these results for the various intervention studies around the world that are supplementing vitamin D to see an effect on Multiple Sclerosis?
If these subjects are not given magnesium along with the vitamin D then we might expect that their VDBP levels may not be sufficient for the conversion of 25(OH)D to 1,25(OH)D. It may be that there is enough to carry the cholecalciferol to the liver for conversion to 25(OH)D and so allow a measurable increase of 25(OH)D but not sufficient to bind the 25(OH)D for conversion to 1,25(OH)D.
The consequence of that could then be that the researchers measure a significant rise in serum 25(OH)D but have little treatment effect of MS. The conclusion would then be that vitamin D supplementation raised levels but no or low effect on MS. The results would then be invalid because magnesium was not tested or given along with the vitamin D supplement (cholecalciferol). Unless they measured 1,25(OH)D before and after.
It is good that the world is concern about global deficiency of vitamin D. But more serious questions are to be answered before the matter is solved. Guess work is no option to solving the problem. Being positive is the Supergun to resolve the matter which is outstanding. Magnesium a co-factor in 300 pathways in biochemical process. You can not avoid it. Be it stress control, cancer prevention or insomnia among others. It is the king of minerals. I am not surprised to read this. Alone we fall but being together we win. The complexity of biochemical process is not a one man show. Trials where vitamin D has not validated its value has always been used by sckceptist to grow wings. Be warned! it is an integral function. One of the readers one time advised that in all trials where vitamin D has not produce valid results. Can it be re-designed in combination with a co-factor?. I don’t know if who want’s to discredit vitamin D benefits have taken note of this..Just think of omega-3 as an anti-toxin to clear way for for vitamin D transformation and use by different anatomical structure of the body tissues in both endocrine and panacrine pathways. Add the like of magnesium, boron,zinc, selenium as co-factors and best still carriers like VDBP. this is molecular biology telling you what is missing and you are playing a blind eye. It is serious. But some of us who are Advanced practitioners would not wait for evidence from RCT. We shall move forward to gather evidence
that is needed waiting for time of consensus.One of the recent article talked about functional deficiency of Vitamin D, whereby there si less signalling by 1.25(OH)2 while vitamin D level was high enough,PTH elevated, VDBP high enough but 1,25(OH)2D low, probably caused by anti-HIV drug tenovir. Nothing was mentioned about co-factors?. Was this a forgotten issue?.