Vitamin D Can Significantly Lower Your Risk of Metabolic Syndrome

By Dr. Mercola

Vitamin D is a steroid hormone that influences virtually every cell in your body, which is why maintaining a healthy level is important not just for your bones but also for heart and brain health, optimal immune function and general disease prevention. In fact, there’s an important connection between insufficient vitamin D and insulin resistance, metabolic syndrome and diabetes, both Type 1¹ (insulin-dependent diabetes) and Type 2.²

According to recent research,³ vitamin D may actually be key to addressing metabolic syndrome, a condition thought to affect about half of all women over the age of 50 in the U.S.

According to coauthor Eliana Aguiar Petri Nahas, professor of gynecology and obstetrics at São Paulo State University's Botucatu Medical School, "[T]he lower the level of blood vitamin D, the greater the occurrence of metabolic syndrome. The results suggest that supplementing and maintaining adequate levels of vitamin D in postmenopausal women can reduce the risk of disease."⁴

What Is Metabolic Syndrome?

Metabolic syndrome is characterized by a cluster of factors, including:

• Low high-density lipoprotein (HDL) cholesterol
• High triglycerides
• Large waist circumference (indicative of high levels of harmful visceral fat around your organs)
• High blood pressure
• High blood sugar and/or insulin resistance

Having three or more of these factors over a certain level is considered evidence of metabolic dysfunction that sets the stage for chronic disease, including Type 2 diabetes, heart disease, stroke, gout, cancer, Alzheimer's, nonalcoholic fatty liver disease (NAFLD) and more, and compelling evidence suggests low vitamin D plays an important role in the development of these risk factors.

Low Vitamin D Raises Your Risk of Metabolic Syndrome and Associated Diseases

Of the 463 women included in the featured study,⁵ nearly 33 percent had vitamin D insufficiency, characterized as a level between 20 and 29 nanograms per milliliter (ng/mL) and more than 35 percent were deficient (a vitamin D blood level below 20 ng/mL). Only 32 percent had “sufficient” levels of 30 ng/mL or higher.

I placed “sufficient” in quotation marks here, as there’s a compelling body of research suggesting 40 ng/mL is the lowest end of sufficiency, and that ideal levels for optimal health and disease prevention is actually between 60 and 80 ng/mL.

Of those with insufficient or deficient vitamin D levels, nearly 58 percent had risk factors qualifying them for a diagnosis of metabolic syndrome. Here, parameters for metabolic syndrome included a waist circumference greater than 88 centimeters, blood pressure above 130/85 mmHg, fasting glucose above 100 milligrams per deciliter (mg/dL), triglycerides above 150 mg/dL and high -density lipoprotein cholesterol below 50 mg/dL. A diagnosis of metabolic syndrome was issued if three or more of these criteria were present.

“[T]he most plausible explanation for the association is that vitamin D influences insulin secretion and sensitivity, which play a major role in [metabolic syndrome],” EurekAlert reports.⁶ “'The vitamin D receptor is expressed in insulin-secreting pancreatic beta cells and in peripheral target tissues such as skeletal muscle and adipose tissue. Vitamin D deficiency can compromise the capacity of beta cells to convert pro-insulin to insulin’ ...

According to Nahas, aging is a key factor in vitamin D deficiency. ‘Exposure to the sun activates a sort of pre-vitamin D in the adipose tissue under the skin… Aging leads not just to loss of muscle mass but also to changes in body composition, and this pre-vitamin D is lost. That's why older people produce less vitamin D even if they get plenty of sunlight.’

In her view, postmenopausal women deserve and require more specific care. They should seek medical advice on the need for vitamin D supplementation. ‘Hypovitaminosis can have repercussions, be it on breast cancer, vascular disease or metabolic syndrome,’ she said."

Other Studies Confirm Link Between Vitamin D and Metabolic Syndrome

A number of other studies have reached the same conclusions. For example, in 2015, researchers reviewing studies assessing effects of vitamin D insufficiency on outcomes associated with metabolic syndrome such as Type 2 diabetes, heart disease and NAFLD, also concluded that low levels are associated with a greater risk for these conditions. According to the authors:⁷

“[T]he finding that hypovitaminosis D is associated with impaired glucose homeostasis is of particular interest. A meta-analysis of 28 studies demonstrated that higher serum 25(OH)D levels were associated with a 55 percent reduction in diabetes, a 51 percent decreased risk of the metabolic syndrome and a 33 percent lower risk of cardiovascular disease (CVD).

Further, treatment with vitamin D supplements over two months improved fasting glucose levels and insulin resistance … in 100 patients with Type 2 diabetes. It is suggested that the mechanism for this latter finding involves improved sensitivity of target tissues such as the liver, muscle and bone to insulin as well as enhanced beta cell function.

Given that many risk factors for CVD are clustered in the highly prevalent metabolic syndrome, which is characterized by insulin resistance and abdominal obesity, it is reasonable to speculate a significant role for the vitamin in the development of the syndrome and its sequelae of diabetes and CVD.”

Another review published the following year noted that:⁸

“Vitamin D deficiency plays key role in the pathophysiology of risk factors of metabolic syndrome which affect cardiovascular system, increase insulin resistance and obesity, stimulate rennin–angiotensin–aldosterone system that cause hypertension.

The discovery of vitamin D receptor expressed ubiquitously in almost all body cells such as immune, vascular and myocardial cells, pancreatic beta cells, neurons and osteoblasts suggests an involvement of vitamin D mediated effects on metabolic syndrome. Moreover, vitamin D deficiency as well as cardiovascular diseases and related risk factors frequently co-occur. This underlines the importance of understanding the role of vitamin D in the context of metabolic syndrome.”

In 2017, research⁹ published in the journal Nutrition & Diabetes also concluded that vitamin D deficiency and metabolic syndrome were closely linked. Here, they also noted that vitamin D deficiency was prevalent in the Qatar population. Despite the country’s notoriously high level of sunshine, 64 percent of the population was found to have vitamin D levels below 20 ng/mL, and those with metabolic syndrome had, on average, 8 percent lower vitamin D levels than those who did not qualify for a diagnosis of metabolic syndrome.

Metabolic Syndrome Is Rooted in Insulin Resistance

Metabolic syndrome could perhaps be more aptly named insulin resistance syndrome, as insulin resistance is at the heart of all of the risk factors for metabolic syndrome. Moreover, since insulin secretion is the key measurement for insulin resistance, measuring your insulin level — particularly after a meal (post-prandial) — will give you the information you need without having to evaluate those other metabolic syndrome parameters.

The video above features the late Dr. Joseph Kraft, who wrote the book "Diabetes Epidemic and You: Should Everyone Be Tested?" Based on data from 14,000 patients, Kraft developed a test that is a powerful predictor of diabetes. He would have the patient drink 75 grams of glucose, and then measure their insulin response over time, at half-hour intervals for up to five hours. This is the most sensitive test for insulin resistance known, far more accurate than a fasting insulin level.

Kraft noticed five distinctive patterns suggesting that a vast majority of people were already diabetic, even though their fasting glucose was normal. In fact, 90 percent of patients with hyperinsulinemia (which is when you have an excess of insulin in your blood relative to your glucose level) passed the fasting glucose test, and 50 percent passed the glucose tolerance test.

Only 20 percent of patients had a pattern signaling healthy post-prandial insulin sensitivity, which means 80 percent were actually insulin resistant and at increased risk of Type 2 diabetes. One of the take-home messages here is that insulin resistance and hyperinsulinemia are two sides of the same coin, as they drive and promote each other.

In other words, if you have hyperinsulinemia, you are essentially insulin resistant and on your way toward developing full-blown diabetes lest you change your lifestyle, starting with your diet.

Insulin Resistance and Hyperinsulinemia Lead to the Same End

Hyperinsulinemia means that there’s more insulin at the fat cell, which means you’ll shunt more energy into those fat cells (because that’s what insulin does). Insulin resistance is clearly associated with weight gain, but while many believe insulin resistance is caused by excess weight, Dr. Robert Lustig has argued for the converse, i.e., that it’s the insulin that is driving the weight gain.

When your liver turns excess sugar into liver fat and becomes insulin resistant, that generates hyperinsulinemia, and hyperinsulinemia drives energy storage into body fat.

As liver fat increases, you end up with fatty liver, which in turn drives high blood insulin and associated mechanistic pathways that shuttle lipids (fats) into your vascular walls, which is a hallmark of atherosclerosis. It also leads to high blood glucose, particularly post-prandial blood glucose, and this too has mechanistic pathways that promote atherosclerosis.

High blood pressure is another side effect of insulin resistance that drives atherosclerosis by placing stress on your arteries. Most idiopathic hypertension (high blood pressure with no known cause) is thought to be caused by hyperinsulinemia.

Hyperinsulinemia/insulin resistance also promotes inflammation, causing your visceral fat to release inflammatory cytokines and systemic signaling molecules. Over time, your visceral fat becomes increasingly resistant to insulin as well, causing the systemic signaling to falter.

Taken as a whole, this cascade of events drives atherogenic dyslipidemia, characterized by high low-density lipoprotein (LDL) cholesterol, oxidized LDL and triglycerides, and low HDL. Ultimately, these factors lead to the development of heart disease, but they’re all predicated on insulin resistance, and therefore resolving the insulin resistance needs to be the aim of the treatment. This is where diet comes in.

The evidence is quite clear: Insulin resistance is the result of eating a diet that is high in sugar (especially processed fructose, which has more detrimental metabolic effects than glucose¹⁰).

For example, a paper¹¹ published in JAMA Internal Medicine in 2014 looked at consumption of added sugar over two decades, as a percentage of total calories, concluding that it significantly contributed to cardiovascular deaths. People who consumed 30 percent of their daily calories as added sugar had a fourfold greater risk of dying from heart disease.

Artificial Sweeteners Also Threaten Your Metabolic Health

In related news, researchers have linked regular consumption of the artificial sweetener sucralose with an increased risk of metabolic syndrome.¹² As reported by MedPage Today,¹³ “At a cellular level, those who consumed sucralose experienced increased glucose uptake, inflammation, and adipogenesis — all of which were most notable in people with obesity.” The findings were presented at the Endocrine Society's annual meeting in Chicago.

Overall, sucralose was “dose-dependently related to upregulation of genes related to adipogenesis,” and those with the highest exposure had the most prominent gene activation. GLUT4, a glucose transporter (i.e., a protein that helps get glucose into the cell), was upregulated by about 250 percent in obese participants, which results in the accumulation of body fat. Two taste-receptor genes were also upregulated by 150 to 180 percent.

Obese individuals who consumed sucralose also had increased insulin response and higher levels of triglycerides than obese individuals who did not consume artificial sweeteners. As noted by co-author Dr. Sabyasachi Sen, who recommends health care providers instruct their obese patients to avoid both sugar- and artificially-sweetened beverages:

“The only part [in artificially sweetened beverages] that's not there is the calories — it's not adding the calories, but it's doing everything else that glucose does. It shouldn't be the replacement from sweetened beverages because it's obviously causing inflammation, fat formation, and so on. But [are artificial sweeteners] causing some inflammation, some reactive oxygen species beyond what glucose does? I think there is some noise towards it, but I cannot say that for sure."

How to Reverse Insulin Resistance

In summary, metabolic syndrome is rooted in insulin resistance, and a vast majority of people — likely 8 in 10 Americans — have some level of insulin resistance that predisposes them to Type 2 diabetes and related health problems, including heart disease, cancer and Alzheimer’s. Based on these statistics, it’s a rare individual who does not need to address his or her diet and physical activity, as these are the two most important and most effective prevention and treatment strategies.

The good news is insulin resistance is simple to address, and is fully preventable and reversible. Ditto for full-blown Type 2 diabetes. I originally wrote my book “Fat for Fuel” for cancer patients, but it is even more effective for insulin resistance, metabolic syndrome and diabetes. Cancer is a complex and typically major challenge to treat, requiring more than diet. However, insulin resistance is easily resolved with the type of eating plan I discuss in “Fat for Fuel.”

Here is a quick summary of some of the most important guidelines. Taken together, this plan will lower your risk of diabetes and related chronic diseases and help you to avoid further deterioration of your health.