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Dr. Josh Trutt of New York discusses Vitamin E, Vitamin D3, Curcumin and other antioxidants such as Astaxanthin. One of the several interesting topics he discusses is that several studies show that the best levels of Vitamin D3 for all cause mortality reduction are around 40 ng/mL or 100 nmol/L.



More info at http://truttmd.com/who-the-heck-is-paul-offit/

Thanks NHE.

Great video. And to think, my vitamin D/hormone D level was found to be 38 ng/ml with the 25(OH)D blood test. This was when my spasticity was minimal. I had only been taking 1,000 IU - 2,000 IU per day. Then I got serious about dealing with my MS so I started taking 5,000 to 10,000 IU per day. Over the next few years my spasticity gradually grew worse and worse. Finally I realized that I had driven my magnesium level down, down, down. I am still struggling to this day to get my magnesium to a Healthy level and to finally get rid of the spasticity.

Magnesium is used in many of the steps in processing vitamin D3. See figure 1 in the following paper.


Magnesium, vitamin D status and mortality: results from US National Health and Nutrition Examination Survey (NHANES) 2001 to 2006 and NHANES III
BMC Medicine 2013, 11:187

http://www.biomedcentral.com/content/pd ... 11-187.pdf

Here's another paper linking low magnesium to low vitamin D3.


Relationship of Serum Magnesium and Vitamin D Levels in a Nationally-Representative Sample of Iranian Adolescents: The CASPIAN-III Study.
Int J Prev Med. 2014 Jan;5(1):99-103.

BACKGROUND: This study aims to assess the relationship of serum Mg and vitamin D levels in a nationally-representative sample of Iranian adolescents.

METHODS: The study participants consisted of 330 students, aged range from 10 to 18 years, consisting of an equal number of individuals with and without hypovitaminosis D. The correlation between serum 25 hydroxy vitamin D (25(OH) D) and magnesium (Mg) concentrations was determined.

RESULTS: The mean age of participants was 14.74 ± 2.587 years, without significant difference between those with hypovitaminosis D and those without it. The mean 25(OH) D level was 6.34 ± 1.47 ng/ml in the group with hypovitaminosis D and 39.27 ± 6.42 ng/ml in the group without it. The mean Mg level was 0.80 ± 0.23 mg/dl with lower level in the group with hypovitaminosis D than in others (0.73 ± 0.22 mg/dl vs. 0.87 ± 0.22 mg/dl, respectively) and according to t-test analysis, significant lower levels in the deficient group was observed (P = 0.0001). The linear regression analysis showed the meaningful relationship between Mg and 25(OH) D serum levels (P = 0.0001).

CONCLUSIONS: Our study revealed significant associations between serum Mg and 25(OH) D levels. This finding may be of use for further studies on the prevention and management of hypovitaminosis D in children and adolescents. Further longitudinal studies shall evaluate the underlying mechanisms and the clinical significance of the current findings.