The Insulin/Heart Connection

IS INSULIN RESISTANCE THE FIRST SIGN OF HEART DISEASE? A GROWING BODY OF EVIDENCE SAYS IT IS

BY JONNY BOWDEN, PHD, CNS, AKA THE NUTRITION MYTH BUSTER™

Back in 2012 when cardiologist Steven Sinatra, MD, and I wrote our book, The Great Cholesterol Myth, I was pretty certain that testing for “good” and “bad” cholesterol was out of date, and that our belief in its value was no longer justified. “Bad” cholesterol was a lousy predictor of heart disease, was inaccurately named, and was certainly not enough on which to base a prescription for a powerful drug.

But I confess, I wasn’t 100 percent sure what we should be looking for. Now I am. It’s insulin resistance. Let me explain.

Insulin resistance is to heart disease what smoking is to lung disease

Insulin resistance (IR) doesn’t account for all cases of heart disease any more than smoking accounts for all incidences of lung cancer. But it tracks with and predicts cardiovascular disease better than any other variable yet studied.

And it shows up earlier. As a predictive marker, it blows “bad” cholesterol out of the proverbial water.

In the new and revised edition of our book—due out in 2021—we painstakingly detail the research showing that IR predates cardiovascular disease with startling consistency. In fact, the connection is so obvious and demonstrable that we consider insulin resistance syndrome as one, if not the primary, cause of heart disease. It’s been hiding in plain sight for a very long time.

When you have IR, you have some degree of dysfunction in your body’s ability to metabolize carbohydrates. IR is the opposite of insulin sensitivity, which is a desirable metabolic state where your body metabolizes carbs just fine. So the best way to explain IR is to spend a minute looking at how insulin sensitivity works so we can see what goes wrong in IR (and why it matters so much to your health).

So what is insulin resistance?

Let’s take a look at the undamaged metabolism of a healthy 8-year-old kid back in the days before the internet and play dates. The kid comes home from third grade and eats an apple, which raises his blood sugar a little, causing his pancreas to react by releasing a little squirt of a hormone called insulin.

One of insulin’s main jobs is to round up the excess sugar in the bloodstream and deliver it into the muscle cells where it can be “burned” for energy. That’s just fine and dandy for our 8-year old, since he’s going to be climbing on monkey bars and playing tag, so his muscle cells eagerly welcome the fuel. Eventually, his muscles use up the sugar provided by the apple, so his blood sugar is now slightly lower than normal, which makes him hungry. He goes home and eats a healthy dinner, and all is right with the world. End of story.

In this case, our hypothetical boy’s insulin-sensitive metabolism is working as it ought to. But in at least half of today’s population, that’s no longer the case.

Let’s look at that same kid 30 years later. He wakes up late, stress hormones already coursing through his body. Those stress hormones send a message to his brain to fuel up for an anticipated emergency (read: stock up on fat!). He runs out the door and stops at the local coffee emporium for a pumpkin spice latte (380 calories, 49 grams of sugar) and a lowfat blueberry muffin (350 calories, 55 grams of carbs, 29 grams of sugar).

His blood sugar takes off like the Challenger. The pancreas says, “Code Red! Send out the big guns! This dude just ate the equivalent of ten packs of Ding Dongs!” The pancreas produces a bucketful of insulin in a desperate attempt to get all that sugar out of the bloodstream and deliver it to the muscles. The problem is, his muscle cells aren’t having it.

“What do we need all this sugar for?” they seem to be asking. “The only ‘exercise’ this guy’s gonna get all day is pushing a computer mouse, and when he goes home, he’s going to sit on the couch and play with the TV clicker. The last thing we need here is more fuel.”

So the muscle cells begin to resist the effects of insulin. “Thank you but no thank you. We don’t need it. Go somewhere else.” And insulin has no choice but to take its sugar payload to another location, and guess where that is? The fat cells. Which happily welcome the sugar in.

Fat, Inflammation, and Blood Sugar

Fat cells are actually endocrine organs, and they secrete a ton of inflammatory chemicals. Inflammation is one of the major causes and promoters of heart disease. And making your fat cells bigger makes them even more powerful inflammation factories.

For a while, your blood sugar levels may stay in the normal range, as the pancreas valiantly tries to pump out enough insulin to keep up with this massive dietary sugar influx. Your blood sugar may still be hanging on in the “normal” range, but the high levels of insulin—which your doc may not be testing for—tell you that the whole thing is about to come tumbling down. (You can think of chronically elevated insulin as the body’s way of shouting “Help!”)

Eventually, insulin won’t be able to keep blood sugar in the “normal” range anymore, and blood sugar will start to rise. Now your blood sugar is high (because all that sugar has nowhere else to go), your insulin is also high, and you’re well on your way to a diagnosis of full-blown diabetes.

In other words, insulin resistance syndrome is “pre-diabetes.” And prediabetes is “pre-heart disease.” According to the American Heart Association, at least 84 percent of diabetics die from cardiovascular disease, and that number is undoubtedly a low estimate, since at least 33 percent of people with diabetes are walking around undiagnosed.

“Emerging evidence shows that insulin resistance is the most important predictor of cardiovascular disease and type 2 diabetes,” says Robert Lustig, MD, pediatric endocrinologist, and professor in the Department of Endocrinology at the University of California, San Francisco.

Take the Test

There are ways you can test for IR right now, with nothing more than the numbers you already have on your basic blood test.

One good “surrogate measure” is to calculate the ratio between your triglycerides and your HDL (so-called “good cholesterol”). Divide triglycerides by HDL—so for example, if triglycerides are 150 and HDL is 50, your ratio is 3. A ratio of 2 (or less) is superb and shows low likelihood for IR and little risk for a heart attack. A ratio of 5 means it’s time to pay attention to your diet.

Second way: Stand a few feet in front of a wall, and walk straight toward it. If your belly hits the wall before your nose does, you are insulin-resistant.

Third way: Order an inexpensive lab test called fasting insulin. Take the result, together with your fasting glucose (available on practically every blood test your doctor ever ordered), and plug those two numbers into an online calculator called a HOMA-2 calculator. It will give you an IR score, just like a BMI calculator tells you your BMI based on height and weight. [Editor’s note: one site that features a HOMA-2 calculator is thebloodcode.com/homa-ir-calculator.)

The state-of-the-art way—the one I recommend if at all possible—is the LP-IR test given by LabCorp (labcorp. com). Ask your doctor to order it.

What to Do About It

The best news about IR is that if you identify it early, you can turn it around. And you can do that without drugs. It’s completely modifiable by diet—specifically, a low-carb, high-fat diet, which can (and usually does) reverse IR. You just need to find a low-carb eating plan that works for you. And stick with it. (Shameless plug: the recently released 4th edition of my book Living Low Carb can help.)

If you focus on lowering insulin resistance, you will be doing your heart a much bigger favor than if you focus on lowering your LDL cholesterol. Emerging evidence—and clinical experience— is showing that insulin resistance shows up well in advance of other markers for heart disease, including elevated blood sugar, A1C, triglycerides, and disordered blood lipids. So pay attention!

And do me a favor—when the link between IR and heart disease finally becomes accepted in the medical establishment, please just remember one thing: You heard it here first.