Research Supports Causative Role For Reduced Vitamin D Levels In High Blood Pressure

Research supports causative role for reduced vitamin D levels in high blood pressure

Research supports causative role for reduced vitamin D levels in high blood pressure

Friday, June 21, 2013. The annual conference of the European Society of Human Genetics was the site of a presentation on June 11 by Dr Karani S. Vimaleswaran of the finding of a causative role for vitamin D in the development of hypertension. "We knew from earlier observational studies that low 25(OH)D concentrations were likely to be associated with increases in blood pressure and hypertension, but correlation is not causality", remarked Dr Vimaleswaran, of University College London.

Dr. Vimaleswaran reported the findings of the D-CarDia collaboration that included over 35 studies involving up to 108,173 participants which associated higher serum 25-hydroxyvitamin D levels with lower blood pressure. To validate causation, a team of researchers examined the association of four vitamin D-related genetic variants known as single nucleotide polymorphisms (SNPs) with 25-hyroxyvitamin D levels and with hypertension.

An association with serum 25-hydroxyvitamin D levels was confirmed for all SNPs. The researchers uncovered an association between one SNP (CYP2R1) and diastolic blood pressure and hypertension. Following further analysis, they concluded that reduced vitamin D levels have a modest causal association with hypertension, with a 0.24 mmHg decrease in diastolic blood pressure and a 7% decrease in the risk of hypertension associated with each 10% increase in serum 25-hydroxyvitamin D. "Even with the likely presence of unobserved confounding factors, the approach we followed, known as Mendelian randomization, allows us to draw conclusions about causality because the genetic influence on disease is not affected by confounding," Dr Vimaleswaran stated. "To put it in simple terms, by using this approach we can determine the cause and effect and be pretty sure that we've come to the right conclusion on the subject."

"Our study strongly suggests that some cases of cardiovascular disease could be prevented through vitamin D supplements or food fortification," he noted. "Our new data provide further support for the important non-skeletal effects of vitamin D. We now intend to continue this work by examining the causal relationship between vitamin D status and other cardiovascular disease-related outcomes such as lipid-related phenotypes, for example, cholesterol, inflammatory markers such as C-reactive protein, and type 2 diabetes and markers of glucose metabolism. We believe that we still have a lot to find out about the effect of vitamin D deficiency on health, and we now know that we have the tools to do so."

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Preventing vitamin D deficiency may help delay early puberty

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A presentation on June 17, 2013 at The Endocrine Society's 95th Annual Meeting held in San Francisco revealed a greater risk of precocious puberty in girls with deficient levels of vitamin D in comparison with girls who entered puberty at a normal age. Early puberty in girls is defined as the onset of sexual development before the age of 8. The incidence of precocious puberty has increased over the past several decades, and girls affected by the condition may have a higher risk of breast cancer or other conditions later in life.

The current research, led by Min Sun Kim, MD, PhD who is an assistant professor at Chonbuk National University Medical School in Jeonju, South Korea, included 110 girls aged 7 to 10 years, among whom 35 were categorized as having experienced precocious puberty according to the Tanner Scale. Blood samples collected from the subjects were analyzed for serum 25-hydroxyvitamin D levels and other factors.

Vitamin D levels were lower on average among girls with early puberty in comparison with girls who entered puberty at a normal age. Forty-four percent of the girls who underwent precocious puberty had serum 25-hydroxyvitamin D levels were classified as severely deficient at less than 10 nanograms per milliliter (ng/mL) in comparison with 21% of the normal group. In additional experimentation, the researchers found that the administration of vitamin D suppressed the ability of N-methyl-D-aspartate (NMDA) to release gonadotropin-releasing hormone (GnRH, which triggers the ovulation process) from neurons.

"If we understand more about the action mechanism of vitamin D on GnRH neuronal activities, we can find a clue to control of precocious puberty using vitamin D or related molecules," Dr Kim explained. "Our results suggest that vitamin D may inhibit early pubertal onset and/or the rapid progression of puberty, at least in part, through the suppression of NMDA-mediated GnRH neuronal excitation in humans."

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