Insulin Resistance and High Blood Pressure

It’s been well established that there is a strong correlation between insulin resistance (diabetes) and high blood pressure. This blog will aim to explain the mechanism behind that. Most cells of the body have insulin receptors, and insulin plays many roles other than just regulating blood sugar. Therefore staying insulin sensitive is extremely important for health. 

Quick review; after you eat carbohydrates, blood sugar rises and the pancreas recognizes that. It’s vital to have the right amount of sugar in the blood so it secretes insulin to usher the sugar into the skeletal muscle and liver. By the way, there is way more storage in the muscle than the liver, so the more muscle you have, the more of a buffer you have from elevated sugars. 

When you become insulin resistant, some tissues stop responding as well to insulin. Your pancreas often compensates by simply producing more insulin. This is important because you can have insulin resistance and elevated insulin for years while your fasting glucose and A1C still look relatively normal. Your pancreas is essentially working overtime to keep your blood sugar under control.

Meanwhile, those higher insulin levels and altered insulin signaling can affect other parts of your physiology, including your blood pressure. Healthy insulin signaling actually helps your blood vessels relax. When insulin interacts with the cells lining your blood vessels, it activates a pathway that eventually increases the production of nitric oxide. Nitric oxide tells the smooth muscle surrounding your blood vessels to relax, allowing the vessel to widen.

So under normal circumstances, insulin can actually promote vasodilation. With insulin resistance, this nitric-oxide pathway doesn't work as effectively. You produce less of that vasodilatory signal, meaning the blood vessels may not relax as readily. At the same time, another insulin-signaling pathway involved in producing endothelin-1, a powerful vasoconstrictor, can remain relatively intact.

So you can end up with an interesting imbalance: less signaling telling the blood vessels to relax while vasoconstrictive signaling remains active. That matters because the narrower the blood vessel, the greater the resistance the heart has to pump against.

Think about putting your thumb over the end of a garden hose. The smaller you make the opening, the more pressure you create. Your cardiovascular system is obviously much more complicated than a garden hose, but the basic idea is similar. More vascular resistance can mean more blood pressure.

Insulin resistance is also associated with increased activity of the sympathetic nervous system, essentially the "gas pedal" side of your autonomic nervous system. That's useful when you need it. If you're running from a bear or exercising hard, you want your heart pumping harder and your circulation adjusting to meet the demand.

Chronically elevated sympathetic activity is a different story. It can increase heart rate, increase the force of contraction of the heart and increase vascular tone. All of those things can push blood pressure higher. That’s the connection between stress and high blood pressure. 

This is another reason I don't like thinking about blood pressure as simply a plumbing problem. Your nervous system is constantly helping regulate the pressure inside that plumbing.

Your kidneys are one of the body's main long-term regulators of blood pressure because they determine how much sodium and water you retain versus excrete. Here's where insulin resistance gets especially interesting. Being "insulin resistant" doesn't necessarily mean that every effect of insulin stops working. Some insulin-signaling pathways become resistant while others can remain relatively responsive.

Insulin can encourage the kidneys to retain sodium. So if someone is insulin resistant and producing larger amounts of insulin to compensate, some of that sodium-retaining effect can remain. More retained sodium generally means more retained water. More fluid in the circulation can contribute to higher blood pressure.

This is where the vicious circle enters. You have insulin resistance, so the pancreas produces more insulin. The blood vessels aren't getting the same nitric-oxide-mediated relaxation they once did. Vasoconstrictive signaling can remain relatively active. Sympathetic nervous-system activity may increase. The kidneys may retain more sodium and water. Other blood-pressure-regulating systems, including the renin-angiotensin-aldosterone system, can also become involved.

Then add something that frequently travels alongside insulin resistance: visceral fat. Visceral fat isn't just passive storage sitting around your organs. It's metabolically active tissue that can influence inflammation, insulin sensitivity, vascular function and hormonal signaling. This is why insulin resistance, abdominal obesity, type 2 diabetes and hypertension so often show up together.

They aren't necessarily separate problems that just happen to occur in the same person. They share some of the same underlying physiology. This can all silently worsen without any symptoms. You don't necessarily have to have diabetes for insulin resistance to be contributing to your blood pressure.

Early on, the pancreas may be perfectly capable of producing enough insulin to compensate for insulin resistance. Blood sugar stays relatively controlled, so fasting glucose and A1C may not look particularly alarming. But that doesn't necessarily mean insulin sensitivity is optimal. The body may simply be using more insulin to accomplish the same job.

The nice thing about this connection is that many of the strategies we use to improve insulin sensitivity are also some of the best lifestyle interventions we have for improving blood pressure.

Exercise is a great example. Contracting skeletal muscle increases its demand for glucose, and regular physical activity improves insulin sensitivity. Exercise also improves vascular function and can reduce resting blood pressure.

Strength training is particularly interesting because skeletal muscle is one of the body's major destinations for glucose. Building and maintaining muscle gives you more metabolically useful tissue while also improving physical capacity. Even something as simple as walking after meals can help. You're giving the glucose entering your bloodstream somewhere to go.

Improving sleep matters too. Chronic sleep deprivation and sleep apnea can worsen insulin sensitivity while simultaneously increasing sympathetic activity and blood pressure.

High blood pressure is complicated. There isn't one mechanism that explains every case, and insulin resistance certainly isn't responsible for everyone's hypertension. However, if someone has high blood pressure along with abdominal weight gain, elevated triglycerides, low HDL, elevated glucose, sleep apnea, fatty liver, or other signs of metabolic dysfunction, it makes sense to look at the bigger picture.

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This article is for educational purposes and is not intended to diagnose or treat hypertension or replace medical care. Do not stop or change prescribed blood-pressure medication without discussing it with your healthcare provider.