Breaking news: Research shows a common vitamin may slam the breaks on one of America’s deadliest epidemics

I write about vitamin D more than any other nutrient…and for good reason.

In my view, September is a good time of year for a reminder. True, you may have spent time in the sun every day this summer (which is ideal for natural vitamin D production, as I often report). But within another month, the sun won’t be high enough in the sky to activate your body’s natural production of vitamin D in the skin.

Which is why it’s crucial to supplement with D year-round. And now, new research gives us yet another reason…

A brand-new study shows vitamin D may help prevent — and even reverse — one of the most deadly, chronic diseases affecting nearly 30 million Americans. Of course, I’m talking about Type II diabetes…

Vitamin D thwarts insulin resistance

Published in Cell, the respected molecular biology journal, scientists reported vitamin D protects beta cells in the pancreas — a key function in managing Type II diabetes.

Of course, pancreatic beta cells make and release insulin — an essential function for controlling blood sugar levels.

But when these beta cells in the pancreas don’t produce enough insulin, as is the case with Type I diabetes, sugar accumulates in the blood.

So, as I explained a few weeks ago, the discovery of insulin was a great breakthrough for the treatment of Type I diabetes for this reason.

However, with Type II diabetes, beta cells do actually produce insulin. It’s just that the cells of the body become resistant to it. And that’s why we call Type II diabetes insulin-resistant diabetes.

It’s also why just flooding the body with more insulin, or “insulin-like” drugs, isn’t a good solution for Type II diabetes treatment. It only pushes excess sugar from the blood into your cells, instead of addressing the underlying problem. And in this case, the underlying problem is too much sugar in the blood as a result of a diet filled with sugar and carbs.

But big pharma never gives up on repurposing a profitable solution for a different problem. So, they continue to push insulin and “insulin-like” drugs for the treatment of Type II insulin-resistant diabetes.

However, this new study looked at vitamin D’s role in improving the body’s natural blood sugar response.

Active vitamin D receptors lead to better blood sugar control

Type II diabetes progresses in part because of chronic inflammation and insulin resistance. This inflammation causes beta cell dysfunction. And preventing this action is a huge challenge.

For this new study, a compound called iBRD9 — a selective chemical probe that influences certain cells in the body — boosted the activity of vitamin D receptors in animal models. This action reduced blood sugar levels, bringing them back into a normal range.

Previous research links higher vitamin D blood levels with a reduced risk of developing Type II diabetes. And this study shows how and why it actually works.

Researchers even think increasing the activity of vitamin D receptors may help protect against pancreatic cancer, a possible complication of Type II diabetes.

Perhaps now, the scientific world can take vitamin D more seriously. And you should too.

As always, I recommend supplementing with 10,000 IU daily of vitamin D, which you can find in convenient liquid form, together with the potent marine carotenoid astaxanthin.

And while we’re on the topic of diabetes…I’ve also just finished putting the final touches on my new free report on one of the most stunning blood sugar discoveries of the century. We’ll be sending it out tomorrow morning, so keep your eyes open. If you’re looking to improve your fasting blood sugar, A1C, or insulin sensitivity, this is an absolute must-see!

In the meantime, to learn about all the natural steps you can take to reverse and prevent Type II diabetes, check out my Integrative Protocol for Defeating Diabetes. Click here to learn more about this online learning tool or to enroll today!


“Vitamin D switches BAF complexes to protect beta cells,” Cell May 17, 2018; 173(5): 1135-1149