Hyperinsulinemia: the condition we are not looking for

Hyperinsulinemia is a condition characterised by elevated insulin levels in the blood. Insulin is a hormone produced by the pancreas that helps regulate blood sugar levels by facilitating the uptake of glucose into cells. When insulin levels are consistently high, it can indicate that the body is struggling to maintain proper blood sugar control, which can lead to insulin resistance and eventually, type 2 diabetes.

In a healthy individual, fasting insulin levels (measured after an overnight fast) typically range from 2 to 24 micro international units per milliliter (µIU/mL) or 12 to 140 picomoles per liter (pmol/L). However, optimal fasting insulin levels are generally considered to be below 10 µIU/mL or 60 pmol/L. Fasting insulin levels above this range could indicate hyperinsulinemia or insulin resistance.

After eating, insulin levels rise as the body responds to the influx of glucose from the consumed food. Postprandial (post-meal) insulin levels depend on various factors, including the type and amount of food consumed and an individual’s insulin sensitivity. Generally, insulin levels peak about 30 to 45 minutes after eating and return to baseline within 2 to 3 hours.

Hyperinsulinemia is characterized by consistently elevated insulin levels, both when fasting and after eating. As mentioned earlier, fasting insulin levels above 10 µIU/mL or 60 pmol/L can be indicative of hyperinsulinemia. For postprandial insulin levels, there isn’t a strict cutoff, but levels that remain substantially elevated or do not return to baseline within a few hours after eating can be a sign of hyperinsulinemia.

Unlike blood sugar or HbA1c tests, which measure glucose levels or the average blood sugar over a 2-3 month period, respectively, diagnosing hyperinsulinemia requires different testing methods. The most common test is the fasting insulin test, which measures insulin levels after an overnight fast. Another method is the oral glucose tolerance test (OGTT) with insulin measurements, which involves measuring insulin levels before and after consuming a glucose drink. These tests can help determine if someone has hyperinsulinemia, even if their blood sugar and HbA1c levels appear normal.

In some cases, hyperinsulinemia may be present even when blood glucose levels are within the normal range. This is because the body compensates for insulin resistance by producing more insulin to maintain blood sugar control. However, this compensation can only last for so long before it becomes unsustainable, leading to worsening insulin resistance and eventually type 2 diabetes. And that is where the problem lies – a ‘normal’ HbA1c or even fasting glucose may give a false sense of assurance to an individual, when the real problem is going unchecked.

When insulin levels are high, the body tends to store more fat and decrease the breakdown of stored fat. Insulin promotes the synthesis of fatty acids in the liver, which are then converted into triglycerides. High insulin levels also inhibit the activity of an enzyme called lipoprotein lipase, which is responsible for breaking down triglycerides in the bloodstream. As a result, triglyceride levels in the blood can increase*. This can be seen in a fasting blood test measuring cholesterol. As this advances, this can lead to metabolic associated fatty liver disease.

In its early stages, hyperinsulinemia may not present with obvious symptoms. As the condition progresses, however, individuals may experience symptoms such as weight gain, fatigue, and difficulty concentrating. Insulin plays a critical role in regulating glucose uptake into cells, including brain cells. When insulin levels are consistently high, as in hyperinsulinemia, the brain’s ability to effectively use glucose for energy may be impaired. This can lead to suboptimal brain function and difficulty concentrating. High insulin levels can impact the balance of neurotransmitters in the brain, which are essential for communication between neurons. For example, insulin resistance has been associated with altered levels of dopamine and serotonin, which are crucial for regulating mood, attention, and cognitive function. These imbalances may contribute to this difficulty concentrating. The low-grade inflammation caused by the condition can negatively affect brain function, including the ability to concentrate, by damaging brain cells and impairing the connections between them. Further, the reduced blood flow can contribute to vascular dysfunction and atherosclerosis, leading to reduced blood flow in the brain. This reduction in blood flow can impair the delivery of oxygen and nutrients to brain cells, negatively affecting cognitive function and concentration.

Underlying these concerns is the impact hyperinsulinemia has at the cellular level. There is reduced mitochondrial biogenesis, with a reduction in the formation of new mitochondria (mitochondrial biogenesis). This can result in a decrease in the overall number of mitochondria in cells, impairing their ability to produce energy efficiently.

There is also impaired mitochondrial function with existing mitochondria. Insulin resistance can lead to the accumulation of reactive oxygen species (ROS) within cells, which can damage mitochondrial DNA, proteins, and lipids. This damage can impair the electron transport chain, which is crucial for energy production, and may contribute to a reduction in overall mitochondrial efficiency. In addition to the rise in triglyceride levels, there is altered fatty acid metabolism. High insulin levels promote the storage of glucose and fatty acids, leading to a reduced availability of fatty acids for oxidation in the mitochondria. This can impact the production of adenosine triphosphate (ATP), the primary energy currency in cells. Additionally, high insulin levels can suppress the expression of genes involved in mitochondrial fatty acid oxidation, further impairing energy production, this may be one of the reasons that people feel fatigued. And there is increased inflammation. Insulin resistance and hyperinsulinemia have been linked to increased inflammation in the body. Inflammation can cause further mitochondrial dysfunction by impairing the electron transport chain, increasing oxidative stress, and inducing mitochondrial swelling.

Risk factors for hyperinsulinemia include a sedentary lifestyle and consuming excess calories (particularly carbohydrate calories which require insulin to be stored). However, a high fat diet in the presence of too many calories can also lead to dysregulated insulin. However, athletes are also at risk of this, as the high-carbohydrate diets that many endurance athletes consume can lead to increased insulin production, which, over time, can result in hyperinsulinemia. A recent study showed that athletes undertaking a higher carbohydrate diet had blood sugars in the ‘pre diabetic’ range, which, while not a direct measure of insulin, is suggestive of poor blood sugar management. Additionally, higher glucose levels (which is the next metabolic issue after high insulin) can impair performance and reduce adaptation over time. Intense training schedules can cause stress on the body, and overtraining can lead to hormonal imbalances, chronic inflammation, and immune system dysregulation, which may impair insulin sensitivity and contribute to the development of hyperinsulinemia. Additionally, inadequate rest and recovery between training sessions can lead to elevated stress hormones, such as cortisol, which can negatively impact insulin sensitivity and increase the risk of hyperinsulinemia.

While fasting insulin can provide valuable information about an individual’s insulin levels and risk of hyperinsulinemia, it’s important to note that it only reflects insulin levels in a fasted state. To obtain a more comprehensive assessment of an individual’s insulin dynamics and metabolic health, additional tests such as an oral glucose tolerance test (OGTT) with insulin measurements, or HOMA-IR (homeostatic model assessment of insulin resistance) may be performed.

Advice for addressing this issue would include the same advice given for someone with disregulated blood sugar, as it is all the same problem but at different ends of the spectrum.

  • A low carbohydrate diet that removes the overt carbohydrate sources (breads, cereals, pasta, rice, crackers, potatoes and kumara (unless cooked and cooled, as this would change their impact on blood sugar)).
  • Protein set higher to help buffer blood sugar responses and provide more stable blood sugar is important, and the inclusion of fats as appropriate to energy requirements is key.
  • Maintaining hydration status, while not directly impacting on insulin levels, are important for kidney function, blood circulation (and vascular function), and thermoregulation (important if an athlete)
  • Non-athletes need to engage in low level activity such as strength training and walking that allows for increased energy expenditure, building muscle as a reservoir for glucose, increased fat burning. The aim is for at least 8000 steps per day and 2-3 x a week of traditional weight training that gives a quick cortisol spike, but not the extended elevation that would be a consequence of cross fit or F45-style training. Walking post meal will reduce the post-prandial insulin requirement.
  • Reduce training load by focusing on zone 2- style training that helps reduce inflammation and encourage the body to burn more fat. This will help lower inflammation and improve mitochondrial efficiency. Ensure there is also activity during the day outside of structured training, as extended sedentary time also places an athlete at risk.
  • Managing stress: be it sleep management, work stress, or just life stress, this is crucial to improving metabolic health due to the impact high cortisol has on insulin regulation.

*It is important to note that There could be other factors contributing to high triglycerides, such as excessive alcohol consumption, obesity, excess carbohydrate intake or certain medications such as beta blockers, diuretics, some oral contraception medication, steroids and immunosuppressive drugs.

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