Vitamin D3 could help heal or prevent cardiovascular damage

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Vitamin D3 could help heal or prevent cardiovascular


January 30, 2018


Ohio University


A new study shows that Vitamin D3 could help restore
damage to the cardiovascular system caused by diseases like hypertension and



A new study conducted by Ohio University scientists
suggests that a little more sunlight might help restore damage to your
cardiovascular system.


The study shows that Vitamin D3 — which is made by the
body naturally when skin is exposed to the sun — can significantly restore the
damage to the cardiovascular system caused by several diseases, including
hypertension, diabetes and atherosclerosis. Vitamin D3 supplements are also
available over-the-counter.


The study, by Marvin and Ann Dilley White Chair and
Distinguished Professor Dr. Tadeusz Malinski and two graduate students, Alamzeb
Khan and Hazem Dawoud, has been published in the International Journal of


“Generally, Vitamin D3 is associated with the bones.
However, in recent years, in clinical settings people recognize that many
patients who have a heart attack will have a deficiency of D3. It doesn’t mean
that the deficiency caused the heart attack, but it increased the risk of heart
attack,” Malinski said. “We use nanosensors to see why Vitamin D3 can
be beneficial, especially for the function and restoration of the
cardiovascular system.”


Malinski’s team has developed unique methods and systems
of measurements using nanosensors, which are about 1,000 times smaller in
diameter than a human hair, to track the impacts of Vitamin D3 on single
endothelial cells, a vital regulatory component of the cardiovascular system. A
major discovery from these studies is that vitamin D3 is a powerful stimulator
of nitric oxide (NO), which is a major signaling molecule in the regulation of
blood flow and the prevention of the formation of clots in the
cardiovasculature. Additionally, vitamin D3 significantly reduced the level of
oxidative stress in the cardiovascular system.


Most importantly, these studies show that treatment with
vitamin D3 can significantly restore the damage to the cardiovascular system
caused by several diseases, including hypertension, atherosclerosis, and
diabetes, while also reducing the risk of heart attack. These studies, performed
on cells from Caucasian Americans and African Americans, yielded similar
results for both ethnic groups.


“There are not many, if any, known systems which can
be used to restore cardiovascular endothelial cells which are already damaged,
and Vitamin D3 can do it,” Malinski said. “This is a very inexpensive
solution to repair the cardiovascular system. We don’t have to develop a new
drug. We already have it.”


These studies, performed at Ohio University, are the
first to identify the molecular mechanism of vitamin D3-triggered restoration
of the function of damaged endothelium in the cardiovasculature. While these
studies were performed using a cellular model of hypertension, the implication
of vitamin D3 on dysfunctional endothelium is much broader. The dysfunction of
endothelium is a common denominator of several cardiovascular diseases,
particularly those associated with ischemic events.


Therefore, the authors suggest that vitamin D3 may be of
clinical importance in the restoration of dysfunctional cardiac endothelium
after heart attack, capillary endothelium after brain ischemia (stroke),
hypovolemia, vasculopathy, diabetes and atherosclerosis. This suggestion is
strongly supported by several clinical studies which indicate that vitamin D3
at doses higher than those currently used for the treatment of bone diseases,
may be highly beneficial for the treatment of the dysfunctional cardiovascular


“Professor Malinksi has an international reputation
for outstanding and innovative research related to the cardiovascular
system,” Ohio University Dean of Arts and Sciences Robert Frank said.
“This latest work is yet another example of his impact on this


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Ohio University. “Vitamin D3 could help heal or
prevent cardiovascular damage.” ScienceDaily. ScienceDaily, 30 January
2018. <www.sciencedaily.com/releases/2018/01/180130140242.htm>.