Vitamin D Deficiency increases the risk of death, and increasing levels may even slightly reduce risk, researchers looking at data from the UK’s Biobank have found.
They used a Mendelian randomization approach that used genetic variation as a ‘surrogate’ for external factors that affect vitamin D levels, such as sun exposure and dietary intake. Relationships with outcomes such as mortality can be analyzed, but this cannot be done in randomized clinical trials for ethical reasons.
Using this method, Dr. Joshua P. Sutherland, a nutritionist at the Australian Center for Precision Health in Adelaide, and colleagues discovered genetically predicted associations between vitamin D levels. [25-(OH)D] A causal relationship has been demonstrated among people with measured concentrations below 50 nmol/L but not above 50 nmol/L. Here are the findings: publish online October 24th Annals of internal medicine.
“Unlike other types of observational studies, we overcame several methodological hurdles. Most randomized controlled trials don’t show much benefit because most people have sufficient concentrations. We cannot test people at very low levels without treatment. Medscape Medical News.
Data support 50 nmol/L cutoff approved A study by the US National Academy of Medicine is consistent with previous data suggesting that the benefits of vitamin D supplementation are primarily seen in people with deficiencies.
“Anyone with vitamin D levels below 50 nmol/L is recommended to raise their levels. Our results suggest that they do not need to be very high. A positive message. If you can get your levels up to the current US recommended levels, that’s fine.
Therefore, she said, “Supplements can clearly help, especially during the winter months, or where a person is not getting enough vitamin D from the sun, or where food is not fortified with vitamin D.
But the data don’t support an approach that uses large intermittent doses, she added.
“Physicians may wish to quickly correct the deficiency with a large ‘bolus’ dose, followed by a maintenance dose. growing evidence It is not beneficial and suggests that it may disrupt the body’s metabolism in such a way that we cannot get the amount we need. there is. ”
Rather, says Hippenen, “I feel the best way to go is to get a moderate daily dose of vitamin D when you need it.”
Genetic approach to unravel causality
Researchers analyzed data from 307,601 individuals in the UK Biobank, a prospective cohort of people recruited from England, Scotland and Wales between March 2006 and July 2010. Mostly of white European ancestry, at baseline he was 37–73 years old.
Genetically predicted vitamin D levels were estimated using 35 confirmed 25-(OH)D variants. Participants tracked their results through June 2020.
The mean baseline measured 25-(OH)D concentration was 45.2 nmol/L, with 11.7% of participants (n=36,009) having levels between 10.0 and 24.9 nmol/L. Higher levels were found in people living in southern regions, nonsmokers, and people with high levels of physical activity, low socioeconomic deprivation, and low body mass index.
During follow-up, 6.1% of participants died (n=18,700). After adjusting for variables, the odds ratios for all causes of death were highest in people with 25-(OH)D levels below her 25 nmol/L, plateaued between 50 and 75 nmol/L, and increased between 75 and 75 nmol/L. 125 nmol/L.
36% higher mortality in vitamin D deficient people
25-(OH)D 25 nmol/L participants had a significantly 36% higher risk of death compared with 50 nmol/L participants.
Mendelian randomization showed an L-shaped association between genetically predicted 25-(OH)D levels and all-cause mortality (P. non-linearity < .001) and cancer and cardiovascular mortality (P. for nonlinearity ≤ .033).
Again, the strongest association between these results and genetically predicted 25-(OH)D was seen at levels below 25 nmol/L, with a plateau at 50 nmol/L. .
The researchers estimated a 6-fold increase in genetically predicted all-cause mortality compared to a measured 25-(OH)D concentration of 50 nmol/L (odds ratio). [OR]6.00) in the 10 nmol/L participants and 25% (OR, 1.25) in the 25 nmol/L participants.
Also, compared with a measured 25-(OH)D concentration of 50 nmol/L, the genetic predictive odds ratios for patients with 10 nmol/L were 5.98 for cardiovascular mortality and 3.37 for cancer mortality. , with a respiratory mortality of 12.44.
Comparing measured 25-(OH)D concentrations of 25 nmol/L and 50 nmol/L, the odds ratios for these outcomes were 1.25, 1.16, and 1.96 (95% CI, 1.88–4.67), respectively. All were statistically significant.
Consistent results supporting a genetically predicted causal effect of 25-(OH)D on all-cause mortality in persons with low measured vitamin D levels were also found in a sensitivity analysis of 20,837 individuals of non-Caucasian ethnicity. was given.
This study was funded by the Australian National Health and Medical Research Council. Sutherland’s student funding is covered by an Australian Research Training Program scholarship.
An intern doctor. Published online on October 24, 2022. Overview
Miriam E. Tucker is a freelance journalist based in Washington, DC. She is a regular contributor to her Medscape, and her other work appears in her The Washington Post, her Shots blog on NPR, and Diabetes Forecast magazine. She uses @MiriamETucker on her Twitter.
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