First, the bad news.
Cardiovascular disease (CVD) is the No. 1 cause of death worldwide.
The World Health Organization estimates that 17.9 million deaths per year are due to CVD—31 percent of all deaths. In the United States, the Centers for Disease Control attributed 647,000 deaths to CVD in 2019, accounting for 1 in 4 deaths—one every 37 seconds.
The major risk factors for CVD are high blood pressure, high LDL cholesterol, and smoking. Almost half of all Americans have at least one of these risk factors.
Now the good news.
Exciting new discoveries indicate that vitamin D can protect against CVD, and, quite amazingly, even reverse the damage to diseased cardiovascular tissue.
Vitamin D is readily available, cheap, safe, and plentiful. In fact, all we have to do is go outside on a sunny summer’s day to allow our skin to manufacture all we need. Fortunately, when there’s no sun available, there are safe and inexpensive vitamin D supplements to fill the need.
The problem is that many of us don’t get enough sun or take enough vitamin D to compensate. Many cross-sectional studies of the population have shown that Americans are vitamin D deficient—some severely so.
Furthermore, the National Health and Nutritional Examination Survey III (NHANES) found that vitamin D deficiencies are related to increased risk for hypertension, diabetes, hyperglyceridemia, and obesity. Other studies have found greater risk of stroke, heart attack, and all-cause cardiovascular mortality linked to lower vitamin D levels.
To understand CVD, we need to understand endothelial dysfunction.
The endothelium is a single layer of cells that line the interior surface of blood vessels. These cells are in direct contact with circulating blood and have dramatic effects on cardiovascular function.
This single layer of cells is really where the rubber meets the road with respect to CVD.
Healthy endothelial cells provide a smooth surface over which blood flows freely. The loss of proper endothelial cell function, which can occur in a variety of situations—most notably under conditions of oxidative stress—can lead to those cells becoming inflamed, rough, and sticky. Blood-borne fats (LDL cholesterols) and/or calcium adhere to the inflamed endothelium causing the narrowing of the blood vessels (atherosclerosis).
Endothelial dysfunction is a common denominator in diseases such as hypertension, diabetes, obesity, and heart failure. Interestingly, these are the diseases associated with insufficient levels of vitamin D.
Because of a series of elegant experiments by Tadeusz Malinski and his colleagues at the Nanomedical Research Lab at Ohio University, we now know what constitutes healthy endothelial function at the level of the single endothelial cell. By using a nanosensor system, Malinski was able to record, in real-time, the molecular changes that occur in healthy and diseased endothelial cells.
Malinski found that healthy endothelial cells are characterized by a relatively greater production of nitric oxide (NO), a cytoprotective vasorelaxant, or substance that relaxes blood vessels and stimulates mucus production and enhanced blood flow. These healthy cells also produce relatively less of the cytotoxic vasoconstrictor, peroxynitrite, better known by its chemical formula ONOO. ONOO reduces blood flow by constricting blood vessels.
Cytotoxic substances cause cell damage or cell death.
In healthy blood vessels, concentrations of NO greatly outweigh those of ONOO. Dysfunctional endothelial cells demonstrate higher concentrations of ONOO.
This balance between the vasorelaxant nitric oxide (NO) and the vasoconstrictive peroxynitrite (ONOO) determines the health of the vascular endothelium. Not enough NO or too much ONOO spells trouble for cardiovascular health.
What determines the balance? You guessed it—vitamin D! Using the same nanosensor experimental setup, Malinski found that administering the active form of vitamin D (calcitriol) increased the concentrations of NO almost fourfold in the endothelial cell while keeping the concentration of cytotoxic ONOO at bay. NO is also a vasoprotectant, which means it protects blood vessels.
Remarkably, Malinski claims that his studies indicate that vitamin D treatment may be important in the “restoration of dysfunctional cardiac endothelium after heart ischemia, and capillary endothelium after brain ischemia.”
In other words, vitamin D could be a powerful agent to not only prevent various cardiovascular diseases from developing, but also in repairing the vascular damage following heart attack and stroke, as well as vascular damage caused by diabetes, hypertension, and atherosclerosis.
Researchers try to find ways to recreate diseases symptoms so they can test cures. Researchers can apply Angiotensin-II (A-II) to healthy endothelial cells, to create an experimental model of dysfunctional endothelium. This model is similar to that observed in hypertension.
The model enables researchers to study treatments that affect the diseased endothelium. When researchers apply A-II, it creates the unhealthy balance of too much ONOO and too little NO. When Malinski applied vitamin D to this dysfunctional endothelial cell preparation, the NO–ONOO balance reverted back to that of healthy cells.
In other words, treatment with vitamin D restored levels of vasoprotective NO and reduced levels of vasodestructive ONOO. The effect of the vitamin D on reversing this disease state was dose-dependent and occurred within a few seconds.
The takeaway message from these studies is that vitamin D plays an important role in maintaining vascular health and preventing and treating vascular disease.
Even though Malinski’s experiments were done in a Petri dish on isolated human endothelial cells, the results are immediately applicable for several reasons.
First, there is a long history of observational reports showing a relationship between adequate levels of vitamin D and cardiovascular health. Previous studies have shown that vitamin D improves NO, modulates vascular tone, and lowers blood pressure in those with hypertension. Malinski’s studies reveal a molecular mechanism that could explain these beneficial effects.
Second, many of the antihypertensive drugs used today operate by adjusting the balance between vasoprotective and vasodestructive substances in endothelial cells, conceptually similar to what Malinski has shown vitamin D to do. However, in contrast to these pharmaceuticals, vitamin D—which is generated by sunlight on the skin—has no harmful side effects.
“There are not many, if any, known systems which can be used to restore cardiovascular endothelial cells which are already damaged, and Vitamin D 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.”
What to Do
You can take immediate steps to maintain your health in a safe and inexpensive manner by making sure you’re getting enough life-saving vitamin D. Consult with your doctor. If your doctor is not recommending much higher levels of vitamin D, 5000 IU to 8000 IU per day, they are not up to date. This is not abnormal. Clinical practice usually lags years (or even decades) behind available research.
It is a good idea to get your vitamin D levels tested. For most people, 50–100 ng/ml is a healthy level and should be achieved with sensible exposure to sunlight and supplements. If you are vitamin D deficient, and getting sunlight is a problem, supplement with vitamin D3 (cholecalciferol) the most bioavailable form of vitamin D.
William F. Supple Jr. holds a doctorate in neuroscience from Dartmouth College. He is one of the founders of StarPower LifeSciences, a research and educational foundation in South Burlington, Vt., that serves to inform regarding the power and benefits of vitamin D in health, disease, and longevity. Learn more about the health benefits of vitamin D at StarPowerLifeSciences.org