93% of Americans are not metabolically healthy.

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Although the precursors to metabolic disease are strongly associated with being overweight or obese, less than one-third of normal weight adults are metabolically healthy. Even individuals with a normal BMI can carry dangerous levels of visceral fat, challenging the assumption that being at a normal weight equates to being low-risk. We’ve compiled evidence-based insights about the surprising relationship between visceral fat, subcutaneous fat, and metabolic health as part of our mission to simplify the complexities of metabolic health.

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Exploring the Complexities of Visceral and Subcutaneous Fat

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Researchers from the Department of Family Practice at the University of British Columbia noted three components of this relationship that best “open the book” on the discussion. The normal-weight centrally obese phenotype refers to those with a normal BMI, but have visceral fat levels that are higher than what is considered healthy. For those that fall under this category of physical composition, the mortality risks are similar to or greater than those who are overweight or obese according to BMI. In fact, these researchers noted that higher levels of subcutaneous fat actually offer some protection against visceral fat dangers. This phenomenon helps underscore why it is so critical to understand the “obesity paradox” as it relates to bias surrounding weight in the medical community.

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The Obesity Paradox

While being overweight or obese is known to increase the risk of metabolic diseases, it doesn’t always translate into worse short-term survival rates. This is what is referred to as the “obesity paradox” by the American Heart Association. One explanation for this phenomenon provided by the AHA is the fact that individuals classified as overweight or obese often receive early screening and timely treatment. This results in the oversight of individuals at the early stages of risk, a major blind spot of metabolic disease prevention that ultimately leads to poorer health outcomes.

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Breaking the Sugar Cycle: Visceral Fat and Insulin Resistance

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Building upon the insights gained from the obesity paradox, we encounter another intriguing enigma: the chicken-or-egg question of visceral fat and insulin resistance. Consuming foods with sugar triggers the release of insulin. Insulin converts this sugar into usable energy, moving it out of the bloodstream to either be used or stored. Eating too much sugar puts a strain on our body as the pancreas struggles to produce enough insulin to keep our blood sugar at a healthy level. This puts our body in a state of hyperinsulinemia, which is simply when there is more insulin in the blood than what is considered healthy.

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This excess insulin also leads to the storage of fat in our bodies. As more fat accumulates, it makes the body more resistant to insulin, requiring even more insulin to control blood sugar levels. This state of insulin resistance accelerates the breakdown of fat and releases fatty acids into the bloodstream, which contributes to both insulin resistance and high blood sugar levels. The cycle continues as the pancreas continues to bump up insulin production to compensate for the body’s resistance to it, perpetuating the cycle.

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Our Active Role in Energy Storage

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We play an active (pun intended) role in this process by modulating how, or if, excess sugar is stored in the body. Think of it this way: our body has a certain amount of storage space for sugar after it has been converted into energy. Whether it is stored as glucose in the bloodstream, or as glycogen in the muscles and liver, when we exceed this storage space- the rest is stored as fat.

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How Exercise Boosts Insulin Sensitivity and Glucose Uptake

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Our activity level plays a significant role in modulating the size of our body’s glycogen storage space. When your muscles contract during activity, your cells are able to take up glucose and use it for energy whether insulin is available or not. When we engage in activities that are intensive relative to our fitness level, we deplete our muscles’ energy reserves. This depletion stimulates a rebuilding process, resulting in muscle growth and an increase in the storage capacity for glycogen. Consequently, larger muscles can store more energy in the form of glycogen, enhancing our ability to utilize glucose efficiently during physical activity (Sports Medicine).

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Exercise enhances insulin sensitivity, the opposite of insulin resistance. Being physically active increases the ability of muscle cells to utilize insulin, facilitating glucose uptake during and after activity. Here’s how exercise achieves this:

1. Exercise activates GLUT4, a protein that acts as a gateway for glucose to enter the muscle cells. It also increases the number of these glucose transporters on the muscle cell surface.
2. Exercise triggers a cascade of intracellular signaling pathways that promote glucose uptake from the bloodstream.
3. Chronic low-grade inflammation is associated with insulin resistance. Exercise helps reduce systemic inflammation by modulating the release of cytokines and other inflammatory markers. (Centre of Inflammation and Metabolism (CIM), University of Copenhagen)
4. Exercise stimulates the production of new mitochondria. The additional mitochondria enhance the capacity to convert glucose and fatty acids into energy, providing a greater energy supply to the muscles. (Harvard Health Publishing)

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Shifting the Focus: Prioritizing Behavior Change for Optimal Metabolic Health Outcomes

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To quote previously referenced research from the Department of Family Practice at the University of British Columbia in Vancouver: “It seems reasonable that interventions targeting visceral fat should focus on addressing causation, primarily the environment of processed, calorie-dense foods, and sedentary lifestyle. Weight loss need not be the primary objective.”

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Understanding the causation behind dysfunctional metabolic health, particularly its connection to behaviors like activity level and sugar intake, is crucial when attempting to emphasize the distinctions between metabolic health and measures such as BMI that fail to provide a comprehensive view. As discussed earlier, challenges such as the obesity paradox and the absence of systemic screening for hidden red flags, such as visceral fat levels, need to be addressed in order to facilitate preventive care. Additionally, it is crucial to recognize this distinction as it has implications for those on the opposite end of the spectrum: metabolically healthy patients that are categorized as overweight according to BMI. We acknowledge that an above normal BMI carries significance. However, if our focus remains solely on a population-wide goal of “losing weight,” we are essentially addressing a side effect of adopting healthy lifestyle behaviors. It is in the best interest of patients across the entire spectrum to prioritize identifying and treating patients in a way that targets the behaviors directly linked to metabolic health outcomes. Dr. Robert Lustig hit the nail on the head when he said, “Obesity is not the problem, it never was… Metabolic syndrome is the problem.”

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At PreventScripts, we believe that weight loss is a symptom of adopting healthier lifestyle behaviors. Our approach to healthy living is strikingly simple, yet effective. With our remote monitoring program, we’re getting patients to move more, reduce sugar consumption, increase their intake of vegetables and fruits, and drink more water. We go beyond conventional health measures to shift the focus away from weight loss and create transformative and lasting metabolic health improvement. Our enhanced care strategy includes systematic risk screening and research-backed patient behavior change tools that make it easy to identify and treat metabolic disease across your patient population.

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