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Metabolic flexibility: A valid concept or a catchy term?

We always have a small amount of glucose circulating throughout our blood stream, but the body strictly manages and ensures the proper amount(2).

Our blood sugar, and thus insulin, increases anytime we consume carbs or protein (1).

Insulin is a hormone made in the pancreas that helps remove excess glucose from the blood stream(2).

Excess glucose is stored away in the liver and muscles.

Once those stores are full though, the remainder is converted and stored as fat(2).

Did you know the body has a limited capacity to store excess glucose?

The storage form of glucose is called glycogen. We can store about 100 grams in the liver and about 400 grams in our muscles(2).

This equates to roughly 2000 calories total. Anything beyond that, is then converted and stored as fat.

On the flip side, we have a hormone called glucagon. Glucagon is also a hormone made in the pancreas, but this hormone helps liberate fat and glucose to be used for energy(2).

Insulin must be low in order for Glucagon to take action, allowing fat to be used for fuel.

Think of Glucagon as the complete opposite of Insulin.

If you’re looking to lose weight, metabolic flexibility is key.

That means, keeping insulin low, which requires long lasting satiety.

Here are some simple tips for improving your metabolic flexibility:

  • Adjust the amount of fat, protein, and carbs you consume at each meal until you’re achieve fullness and satisfaction that lasts 3 to 5 hours

  • Strive for 3 square meals a day

  • Avoid snacking in between meals

  • Avoid consuming food after dinner to extend the time you fast between dinner & breakfast

  • Move your body in a way that feels good to improve your insulin sensitivity

  • Get ample good quality sleep

  • Keep stress in check



(1) Bikman, Ben PhD (2020) . Why we Get Sick. Dallas, TX: BenBella Books, Inc.

(2) Nutritional Therapy Association.  Blood Sugar Regulation Student Guide.  Olympia, WA.

PNOE Article: Key points

  • The body’s ability to rapidly and efficiently switch between oxidations of different energy substrates, namely fat and carbohydrates, depending on their availability, is known as metabolic flexibility.
  • Long-term caloric excess and ectopic fat accumulation are central mechanisms of impaired metabolic flexibility.
  • Insulin resistance is the link among a cluster of metabolic disturbances that are all characterized by impaired metabolic flexibility.
  • Mitochondrial dysfunction is a principal component of impaired metabolic flexibility.
  • Regular exercise and a healthy, low-calorie diet can significantly improve metabolic flexibility.
  • RER fluctuations measured through breath analysis when alternating between fasted and fed states can be used as an index of metabolic flexibility.

Human physiology has evolved during dramatic fluctuations in energy supply and demand. Coping with these challenges has enabled the human body to manage energy metabolism for optimal substrate storage and utilization during either food surplus or shortage and of either rest or increased calorie burn. This ability to efficiently adjust metabolism to fluctuations in energy demand by rapidly and efficiently switching between oxidations of different energy substrates, namely fat and carbohydrates, depending on their availability, is known as metabolic flexibility. More specifically, metabolic flexibility is our body’s ability to switch from high levels of fat oxidation during fasted states to increased carbohydrate utilization during feeding states. The greater our ability to burn the food we consume instead of storing it, the more metabolically flexible we are. 

Humans constantly cycle from fasting to postprandial (post-meal) conditions and vice versa. The primary purpose of this substrate shift is to move from catabolic (the metabolic process of breaking down fuels for energy production) to anabolic (the metabolic process of synthesizing molecules such as glycogen and triglycerides for energy storage) activities in which energy can be effectively stored in skeletal muscle, fat, and liver tissues.

Metabolic flexibility is not an ‘’on-off’’ phenomenon. It involves constant, tightly regulated adaptive responses of human metabolism to maintain energy homeostasis by matching fuel availability and demand to various conditions such as periodic fasting, varying meal composition, physical activity, and environmental fluctuations. However, nowadays, when the food supply overflows and there is a plethora of calorically dense processed foods combined with low levels of physical activity, metabolic flexibility is directly obstructed. 

In this article, we will review the principle mechanisms that control metabolic flexibility, its implications for health, and the prominent role diet and exercise play in maintaining it. 

Physiologic mechanisms leading to metabolic inflexibility

Healthy cells of metabolically active organs such as the liver, skeletal muscle, and fat tissue are metabolically flexible and communicate to organize the utilization of available fuels best. The inability to adapt to fuel availability may result in an abnormal mobilization and utilization of fat and glucose, leading to increased fatty acids and glucose concentration. After fat cells reach a threshold of calorie and lipid capacity, lipids also start to accumulate in other locations other than fat tissue, including skeletal muscle and the liver. This process, known as ectopic fat deposition, leads to lipotoxicity and eventually metabolic abnormalities and disrupted metabolic flexibility. Therefore, the previously healthy cells have now turned into dysfunctional cells.

Metabolic inflexibility is characterized by reduced skeletal muscle glucose transport, increased suppression of fat tissue lipolysis, reduced suppression of hepatic glucose production, and skeletal muscle mitochondrial dysfunction. All these defects result in increased glucose production by the liver, reduced glucose utilization for energy by the muscles, and decreased fat burn. At the core of these processes lies long-term caloric excess and ectopic fat accumulation. As a result, metabolic inflexibility and ectopic fat accumulation reinforce each other in a vicious cycle, causing and further cultivating metabolic dysfunction.

Metabolic flexibility and its association with insulin resistance

Impaired metabolic flexibility is associated with an increased risk of obesity and obesity-related pathologies, such as metabolic syndrome, type 2 diabetes, systemic inflammation, cardiovascular disease, and cancer. Simultaneously, obesity, especially central obesity, where fat accumulates around the abdomen, is the leading cause of insulin resistance. Insulin resistance is the inability of muscle, liver, and fat cells to respond to insulin, thus taking up and utilizing ingested carbohydrates for energy. 

Insulin resistance is a vital component of the metabolically inflexible state, which is typically characterized by decreased fat oxidation during fasting and a reduced ability to upregulate carbohydrate oxidation during feeding. Therefore, the ingested carbohydrates are stored as fat in the fat tissues and other organs (ectopic fat).

Insulin resistance is also the predominant factor leading to type 2 diabetes and the link among a constellation of cardiometabolic risk factors known as metabolic syndrome, linking obesity, type 2 diabetes, and cardiovascular disease. Consequently, it’s becoming clear that not only Impaired metabolic flexibility is associated with an increased risk of insulin resistance but that insulin resistance itself deteriorates metabolic flexibility as well; hence why most individuals with obesity and/or type 2 diabetes are metabolically inflexible.

Metabolic syndrome is defined as having at least three components: visceral obesity in terms of elevated waist circumference, insulin resistance in terms of elevated fasting glucose, high blood pressure, elevated triglycerides, and/or low HDL-cholesterol. One of the hallmarks of metabolic syndrome is chronic systemic inflammation. Along with obesity and insulin resistance, systemic inflammation can trigger and propagate metabolic inflexibility. Thus, metabolic inflexibility, inflammation, obesity, and insulin resistance are part of a vicious cycle where the one trigger and reinforces the other. While impaired metabolic flexibility is strongly associated with insulin resistance, which of the two precedes is still unresolved. 

Overall, metabolic health is defined as a comprehensive state of well-being, and metabolic flexibility is essential for metabolic health and the absence of metabolic diseases, such as the metabolic syndrome.

Mitochondrial dysfunction: The cause or the consequence of metabolic inflexibility?

Mitochondria are dynamic intracellular organelles that play a foundational role in energy metabolism. When energy supply exceeds energy demand across the mitochondria (chronic caloric surplus), their oxidative capacity is reduced, predisposing to adverse health outcomes, such as the development of type 2 diabetes and obesity. 

The concept of metabolic flexibility has particularly been associated with the mitochondria’s function and places mitochondrial function at its core. Mitochondria are crucial in determining whole-body metabolic flexibility, and the deregulation of mitochondrial function underlies the onset of metabolic inflexibility. More specifically, mitochondrial dysfunction, in terms of low skeletal muscle mitochondrial capacity, function, and/or density, is associated with reduced resting lipid oxidation and therefore increased muscle lipid accumulation (ectopic fat) and insulin resistance.

Although the hypothesis that such mitochondrial abnormalities may be a primary cause of metabolic inflexibility has been raised, definite conclusions regarding the causal relationship cannot be drawn based on current evidence. However, there is a substantial body of evidence to support the presence of impaired mitochondrial adaptation as a principal component of systemic metabolic inflexibility, particularly in conditions related to insulin resistance, such as metabolic syndrome. Therefore, the relationship between insulin resistance and altered mitochondrial function seems to be bidirectional and mutually amplifying.

 Metabolic flexibility and its relation to physical activity and diet

Several studies have highlighted the positive relationship between sedentary behaviors, such as time spent sitting, and the risk of developing obesity, type 2 diabetes, and cardiovascular disease. Indeed, regular physical exercise is a key determinant of metabolic flexibility, favoring metabolic and cardiovascular health while preventing weight gain and its related metabolic abnormalities. Particularly, exercise training increases metabolic flexibility by reducing insulin resistance and increasing muscle lipid oxidation.

Therefore, it’s becoming clear that exercise profoundly affects metabolic flexibility. This effect is also mediated by the impact of exercise on the mitochondria. Current evidence shows that exercise-trained skeletal muscles, especially of endurance athletes, present increased skeletal muscle mitochondrial biogenesis and have higher mitochondrial content, capacity, and function. In other words, exercise-enhanced mitochondrial performance is related to better metabolic flexibility. In contrast, skeletal muscle from individuals with obesity and insulin resistance is metabolically inflexible compared with skeletal muscle from healthy individuals. 

Besides physical activity, a chronic caloric surplus is another major factor impairing mitochondrial function and inducing metabolic flexibility. Therefore, weight loss through a suitably-applied caloric deficit is crucial in restoring metabolic flexibility and is the most common intervention for obesity and obesity-related metabolic comorbidities.

Taken together, physical activity, especially aerobic exercise, is an effective way to improve metabolic flexibility. Combined with a proper nutrition regime that will not be characterized by overconsumption of calories and nutrients from highly-processed caloric-dense foods that promote weight gain, thus dysregulation of metabolic health, it can comprise the best strategy to restore metabolic flexibility.

Can breath analysis be utilized as an index of metabolic flexibility?

Metabolic flexibility as individuals alternate between feeding and fasting can be assessed through changes in the respiratory exchange ratio (RER), calculated from the VCO2-to-VO2 ratio measured by breath analysis (AKA indirect calorimetry). RER is an index of the proportion of carbohydrates and fat being oxidized for energy. 

In humans, RER typically fluctuates between 0.7 and 1.0, depending on the fuel being oxidized. When fat or glucose is the unique energy source, the RER is 0.7 or 1.00, respectively. In fasted conditions, typically, RER is about 0.80 in subjects fed with mixed diets, while values lower than 0.75 are observed in individuals fed with low-carbohydrate diets (<30% of energy from carbohydrates). Individuals with negative energy balance or fed high-fat diets (>50% of energy from fat) tend to have even lower fasting RER values. However, in a state of increased visceral fat (central obesity) and insulin resistance, there is a higher preference for glucose relative to fat as an energy source in the fasting state (high fasting RER).

The extent to which RER increases from fasting to feeding conditions has been considered an index of metabolic flexibility. An impaired drop in RER during an overnight fast (high fasting RER→glucose oxidation predominance and inability to switch to fat oxidation), as well as an impaired rise in RER in response to feeding (baseline RER of ≈0.85, which fails to increase further), indicates a metabolically inflexible state. Several studies suggest this is the case for obese insulin-resistant and type 2 diabetic subjects.

However, indirect calorimetry should be used with caution and critical thinking to measure metabolic flexibility. Someone should always consider a subject’s energy balance and dietary macronutrient composition while interpreting the results since those factors affect the RER.

In summary, metabolic flexibility is not only a valid term regarding metabolic health. Still, it may actually underlie the epidemic changes in metabolic disease that affects all demographic groups and burden healthcare systems. It may also be an early condition that, if timely detected and appropriately handled, could prevent the onset of several serious metabolic disturbances, such as type 2 diabetes and cardiovascular disease. 

Source:  PNOE Metabolic Testing

Which functional lab tests correlate with insulin resistance?

  1. Fasting Blood Glucose (FBG): A simple test that measures your blood sugar levels after an overnight fast. Elevated fasting blood glucose levels (typically above 100 mg/dL) can indicate insulin resistance.
  2. Hemoglobin A1c (HbA1c): This test provides an average of your blood sugar levels over the past 2-3 months. Elevated HbA1c levels, usually above 5.7%, can be an indicator of insulin resistance and diabetes.
  3. Oral Glucose Tolerance Test (OGTT): This involves drinking a sugary solution and then measuring blood sugar levels at specific intervals. Insulin resistance can be indicated by higher-than-normal blood sugar levels during the test.
  4. Fasting Insulin Levels: Measuring fasting insulin levels alongside fasting blood glucose can help evaluate insulin resistance. Elevated fasting insulin levels can indicate reduced insulin sensitivity.
  5. Homeostatic Model Assessment of Insulin Resistance (HOMA-IR): This is a formula that calculates insulin resistance based on fasting glucose and fasting insulin levels. Higher HOMA-IR values suggest greater insulin resistance.
  6. C-peptide Levels: C-peptide is a marker of insulin production by the pancreas. High levels of C-peptide, especially in the presence of elevated blood sugar, can suggest insulin resistance.
  7. Triglyceride Levels: Elevated triglyceride levels often accompany insulin resistance and are part of the metabolic syndrome. A triglyceride-to-HDL ratio is sometimes used as an indicator.
  8. High-Density Lipoprotein (HDL) Cholesterol Levels: Low HDL cholesterol levels can be associated with insulin resistance.
  9. Fasting Serum Leptin Levels: Leptin is a hormone that regulates appetite and metabolism. Elevated leptin levels are often seen in individuals with insulin resistance.
  10. Adiponectin Levels: Adiponectin is a hormone that plays a role in insulin sensitivity. Lower levels of adiponectin are associated with insulin resistance.
  11. Liver Function Tests: Elevated liver enzymes and markers of non-alcoholic fatty liver disease (NAFLD) can be indicative of insulin resistance.
  12. Inflammatory Markers: Elevated levels of inflammatory markers like C-reactive protein (CRP) and interleukin-6 (IL-6) are often associated with insulin resistance and metabolic dysfunction.

It’s important to note that these tests provide a snapshot of your metabolic health, and a comprehensive evaluation should be conducted by a healthcare professional. Additionally, insulin resistance is often part of a larger picture of metabolic syndrome and can be influenced by genetics, lifestyle, and other factors.

How to reverse insulin resistance in functional medicine


  1. Dietary Changes:
    • Focus on a whole foods, nutrient-dense diet rich in vegetables, fruits, lean proteins, healthy fats, and complex carbohydrates with a low glycemic index.
    • Reduce or eliminate processed foods, sugary snacks, sugary beverages, and refined carbohydrates.
    • Consider incorporating anti-inflammatory foods like turmeric, ginger, omega-3 fatty acids, and green tea.
  2. Balancing Blood Sugar:
    • Eat regular meals and snacks to maintain stable blood sugar levels.
    • Avoid large meals that can lead to spikes in blood sugar.
    • Include protein and healthy fats with meals to slow down the absorption of carbohydrates.
  3. Exercise and Physical Activity:
    • Engage in regular physical activity, including both aerobic exercise and strength training.
    • Exercise helps improve insulin sensitivity and can lower blood sugar levels.
  4. Stress Management:
    • Chronic stress can contribute to insulin resistance. Practice stress-reduction techniques such as mindfulness, meditation, yoga, and deep breathing.
  5. Sleep Optimization:
    • Aim for 7-9 hours of quality sleep each night. Poor sleep can disrupt insulin sensitivity.
  6. Supplements and Nutritional Support:
    • Some supplements may help improve insulin sensitivity, such as chromium, magnesium, alpha-lipoic acid, and berberine. Consult a healthcare provider before adding supplements.
  7. Gut Health and Inflammation:
    • Address gut health issues as imbalances in gut bacteria can impact metabolism and inflammation.
    • Consider probiotics and a diet that supports a healthy gut.
  8. Detoxification Support:
    • Support the body’s natural detoxification processes by staying hydrated, consuming fiber-rich foods, and supporting liver health.
  9. Individualized Approach:
    • Functional medicine focuses on personalized care. Work with a healthcare provider experienced in functional medicine to create a tailored plan based on your unique health history and needs.
  10. Monitoring and Adjustments:
    • Regularly monitor your progress through lab tests, glucose monitoring, and other relevant assessments.
    • Adjust your approach based on your results and how your body responds.

Remember that reversing insulin resistance takes time and commitment. It’s advisable to work with a qualified healthcare provider, such as a functional medicine practitioner or a registered dietitian, to guide you through the process and ensure you’re making safe and effective choices. Functional medicine aims to treat the whole person, so lifestyle, nutrition, and other factors will be considered as part of your treatment plan.

What does Dr. Ben Bikman say to reverse insulin resistance


  1. Low-Carbohydrate Diet: Dr. Bikman has highlighted the benefits of a low-carbohydrate diet for improving insulin sensitivity. He suggests reducing the consumption of refined carbohydrates and sugars, which can lead to chronically elevated insulin levels.
  2. Healthy Fat Intake: He supports the consumption of healthy fats, such as those found in avocados, nuts, olive oil, and fatty fish. These fats can provide sustained energy and may help improve insulin sensitivity.
  3. Intermittent Fasting: Dr. Bikman has discussed how intermittent fasting and time-restricted eating can help regulate insulin levels and improve insulin sensitivity. These eating patterns can give the body more time to clear excess glucose from the bloodstream.
  4. Exercise: He emphasizes the importance of regular physical activity, both aerobic exercise and strength training, for improving insulin sensitivity and metabolic health.
  5. Avoiding Overeating: Dr. Bikman advocates for avoiding overeating, as excess calorie intake can contribute to insulin resistance and obesity.
  6. Reducing Inflammation: Addressing chronic inflammation through dietary choices and lifestyle changes is important for improving insulin sensitivity. Consuming anti-inflammatory foods and managing stress can play a role in this.
  7. Personalized Approach: Dr. Bikman often emphasizes that individuals may have different responses to dietary and lifestyle interventions. He encourages people to monitor their own responses to different foods and habits to find what works best for them.
  8. Metabolic Flexibility: He discusses the concept of “metabolic flexibility,” which is the body’s ability to switch between using glucose and fats for energy. Improving metabolic flexibility can be beneficial for insulin sensitivity.

It’s important to note that while Dr. Ben Bikman’s insights can provide valuable guidance, every individual’s situation is unique. If you’re interested in following his recommendations to reverse insulin resistance, consider consulting with a healthcare professional who can tailor a plan to your specific needs and medical history. Additionally, staying updated with his latest research and presentations will provide the most current information on his views and recommendations.

What is METABOLIC Flexibility as per Dr. Ben Bikman?


Here’s a more detailed explanation of metabolic flexibility:

  1. Glucose Utilization: When glucose is available, such as after consuming carbohydrates, a metabolically flexible individual can effectively take up and use glucose for energy. This is important to maintain stable blood sugar levels and provide energy to cells, especially those that rely on glucose as their primary fuel source, like certain parts of the brain.
  2. Fat Utilization: On the other hand, when glucose availability is low, such as during fasting or low-carbohydrate intake, a metabolically flexible individual can switch to using stored fat as a source of energy. This involves breaking down stored fats into fatty acids, which can then be utilized by various tissues and organs.
  3. Insulin Sensitivity: Metabolic flexibility is closely linked to insulin sensitivity. Insulin sensitivity refers to how responsive cells are to the effects of insulin, a hormone that regulates glucose uptake by cells. When cells are insulin sensitive, they are better able to take up glucose from the bloodstream, reducing the risk of high blood sugar levels.
  4. Benefits of Metabolic Flexibility: Metabolic flexibility is associated with improved metabolic health. It allows the body to adapt to different situations, such as variations in food availability and energy demands. It may also play a role in preventing insulin resistance, obesity, and type 2 diabetes. People with good metabolic flexibility are often better equipped to maintain stable energy levels and body weight.
  5. Factors Affecting Metabolic Flexibility: Various factors can influence metabolic flexibility, including diet, physical activity, genetics, and overall metabolic health. Regular exercise, a balanced diet that includes both carbohydrates and healthy fats, and maintaining a healthy body composition can contribute to better metabolic flexibility.

Dr. Ben Bikman, in his research and presentations, emphasizes the importance of metabolic flexibility as a marker of overall metabolic health. He often discusses how promoting metabolic flexibility through dietary strategies like reducing carbohydrate consumption and improving insulin sensitivity can have positive effects on various health markers, including insulin resistance.

As with any scientific concept, the understanding of metabolic flexibility is continually evolving, so it’s a good idea to refer to Dr. Bikman’s latest work or other reputable sources for the most current insights and research findings on this topic.

What is insulin resistance and how does it cause fat weight gain?

  1. Elevated Blood Sugar Levels: With insulin resistance, cells are less efficient at taking up glucose from the bloodstream. As a result, blood sugar levels remain elevated. To control high blood sugar, the body produces more insulin. Elevated insulin levels can promote the storage of excess glucose as fat in adipose tissue.
  2. Increased Fat Storage: Insulin plays a role in fat metabolism. When insulin resistance is present, the body’s ability to break down stored fat and use it for energy can be impaired. Instead, the body favors fat storage, especially in the abdominal area.
  3. Disrupted Appetite Regulation: Insulin resistance can disrupt the signals that regulate appetite and satiety. This can lead to overeating and a higher intake of calories, contributing to weight gain.
  4. Promotion of Lipogenesis: Insulin resistance can lead to an increased conversion of glucose into fatty acids in the liver, a process known as lipogenesis. These fatty acids are then transported and stored as fat in various tissues.
  5. Inflammation and Hormonal Imbalances: Insulin resistance is associated with chronic low-grade inflammation and hormonal imbalances. These factors can contribute to metabolic dysfunction, including the promotion of fat storage.
  6. Impaired Lipolysis: Lipolysis is the process by which fat is broken down to release fatty acids for energy. Insulin resistance can hinder this process, making it more difficult for the body to use stored fat as an energy source.
  7. Effect on Fat Cells: Insulin resistance can affect adipocytes (fat cells) directly, causing them to become larger and promoting the release of inflammatory substances. Larger fat cells can lead to increased fat storage.
  8. Metabolic Syndrome: Insulin resistance is often a component of metabolic syndrome, a cluster of conditions that include high blood pressure, high blood sugar, excess abdominal fat, and abnormal cholesterol levels. Metabolic syndrome can further contribute to weight gain and other health issues.

It’s important to note that while insulin resistance can contribute to weight gain and obesity, it’s not the sole factor. Genetics, diet, physical activity, and other lifestyle factors also play a significant role. Addressing insulin resistance through lifestyle changes, such as improving diet, increasing physical activity, and managing stress, can help mitigate its effects on weight gain and overall health. If you suspect you have insulin resistance, it’s advisable to consult a healthcare professional for proper diagnosis and guidance.

What is Insulin sensitivity and what impacts insulin to become insensitive?

On the other hand, insulin insensitivity (or insulin resistance) occurs when cells become less responsive to insulin’s signals. This means that even when insulin is present, cells don’t efficiently take up glucose, leading to elevated blood sugar levels. Insulin resistance can eventually lead to type 2 diabetes if not properly managed.

Several factors can impact insulin sensitivity and contribute to the development of insulin resistance:

  1. Obesity: Excess fat tissue, especially around the abdominal area, can promote inflammation and affect insulin signaling, leading to insulin resistance.
  2. Physical Inactivity: Lack of regular physical activity can reduce insulin sensitivity. Exercise helps improve glucose uptake by cells and can lower insulin resistance.
  3. Dietary Factors:
    • High Sugar and Refined Carbohydrate Intake: Consuming large amounts of sugary foods and beverages can lead to chronically elevated blood sugar levels, contributing to insulin resistance.
    • Low Fiber Intake: A diet low in fiber can lead to rapid spikes in blood sugar after meals, which can impact insulin sensitivity.
    • Unhealthy Fats: Diets high in unhealthy saturated and trans fats can contribute to inflammation and insulin resistance.
  4. Genetics: Genetic factors can play a role in determining an individual’s susceptibility to insulin resistance.
  5. Age: Insulin sensitivity tends to decrease with age, making older individuals more prone to developing insulin resistance.
  6. Sleep Disturbances: Poor sleep quality and insufficient sleep can negatively affect insulin sensitivity and glucose metabolism.
  7. Stress: Chronic stress can lead to hormonal imbalances and inflammation that affect insulin sensitivity.
  8. Inactivity: Prolonged periods of sitting and a sedentary lifestyle can contribute to insulin resistance.
  9. Hormonal Imbalances: Conditions such as polycystic ovary syndrome (PCOS) and hormonal disorders can impact insulin sensitivity.
  10. Inflammation: Chronic low-grade inflammation in the body can disrupt insulin signaling and promote insulin resistance.
  11. Medications: Some medications, such as certain antipsychotics and corticosteroids, can contribute to insulin resistance.
  12. Gut Health: Emerging research suggests that imbalances in gut bacteria (the microbiome) might influence insulin sensitivity.

It’s important to note that insulin sensitivity is a dynamic condition that can change based on lifestyle choices and health status. Lifestyle modifications, including a balanced diet, regular physical activity, stress management, and adequate sleep, can improve insulin sensitivity and help prevent or manage insulin resistance. If you suspect you have insulin resistance, consulting a healthcare professional for proper evaluation and guidance is recommended.

Does low estrogen impact insulin sensitivity?


Here’s how low estrogen levels can affect insulin sensitivity:

  1. Insulin Sensitivity and Menstrual Cycle: Throughout the menstrual cycle, estrogen levels fluctuate. Some research suggests that insulin sensitivity tends to be higher during the follicular phase (when estrogen levels are rising) compared to the luteal phase (after ovulation, when estrogen levels decrease). This could indicate that higher estrogen levels are associated with improved insulin sensitivity.
  2. Postmenopausal Women: In postmenopausal women, estrogen levels decline significantly. This decline in estrogen can contribute to changes in body composition, including an increase in visceral fat (fat stored around internal organs). Visceral fat is linked to insulin resistance and metabolic disturbances.
  3. Estrogen Replacement Therapy: Estrogen replacement therapy (ERT) or hormone replacement therapy (HRT) is sometimes prescribed to postmenopausal women to alleviate symptoms of menopause. Some studies suggest that ERT might have a positive effect on insulin sensitivity.
  4. PCOS: Polycystic ovary syndrome (PCOS) is a hormonal disorder that often involves insulin resistance. Women with PCOS typically have higher levels of androgens (male hormones) and lower levels of estrogen, which could contribute to insulin resistance.
  5. Pregnancy: During pregnancy, estrogen levels increase significantly. This hormonal shift can influence insulin sensitivity to accommodate the changes in glucose metabolism needed to support the growing fetus.

It’s important to note that estrogen’s impact on insulin sensitivity is complex and can be influenced by various factors, including the specific context (e.g., menstrual cycle, pregnancy, menopause), genetics, overall hormonal balance, and lifestyle factors. Estrogen is just one piece of the puzzle when it comes to insulin sensitivity, and individual responses can vary.

If you have concerns about insulin sensitivity, hormonal balance, or any related health issues, it’s recommended to consult with a healthcare provider who can evaluate your specific situation and provide appropriate guidance and recommendations.

How does exercise make us more insulin sensitive and nutritional therapy?



  1. Enhances Muscle Glucose Uptake: Physical activity, especially aerobic exercise and resistance training, increases the demand for energy by muscles. This stimulates glucose uptake by muscle cells, even in the absence of high insulin levels. This process improves insulin sensitivity over time.
  2. Reduces Body Fat: Regular exercise helps reduce body fat, especially visceral fat (fat stored around organs), which is strongly associated with insulin resistance. Lowering body fat levels can help improve insulin sensitivity.
  3. Muscle Adaptations: Exercise induces changes in muscle cells that improve their ability to take up glucose. It enhances the function of glucose transporters on cell membranes, allowing more efficient glucose uptake.
  4. Increases Insulin Receptor Sensitivity: Exercise helps sensitize insulin receptors on cells, making them more responsive to insulin’s signals and improving glucose uptake.
  5. Affects Hormone Regulation: Exercise can positively influence hormones related to metabolism, such as reducing cortisol (stress hormone) levels and increasing adiponectin (a hormone associated with improved insulin sensitivity).
  6. Enhances Overall Metabolic Health: Exercise improves overall cardiovascular health, lipid profiles, and inflammatory markers, which are all connected to insulin sensitivity.

Nutritional Therapy:

  1. Balanced Diet: A diet rich in whole, unprocessed foods provides essential nutrients for proper metabolic function. Avoiding excessive consumption of refined sugars and carbohydrates helps prevent blood sugar spikes that can lead to insulin resistance.
  2. Controlled Carbohydrate Intake: Managing the intake of carbohydrates, especially those with a high glycemic index, can help regulate blood sugar levels and reduce the demand for insulin secretion.
  3. Healthy Fats: Including healthy fats, such as omega-3 fatty acids from sources like fatty fish, and monounsaturated fats from sources like avocados and nuts, can support insulin sensitivity.
  4. Fiber-Rich Foods: Foods high in fiber, such as whole grains, legumes, vegetables, and fruits, help slow down the absorption of glucose and improve insulin sensitivity.
  5. Protein: Adequate protein intake supports muscle maintenance and growth, which in turn can enhance glucose uptake and utilization.
  6. Balanced Meals: Combining carbohydrates with protein and healthy fats in meals can help stabilize blood sugar levels and prevent rapid spikes.
  7. Hydration: Staying hydrated supports overall metabolic processes, including insulin sensitivity.
  8. Anti-Inflammatory Foods: Incorporating foods with anti-inflammatory properties, like turmeric, ginger, and green tea, can help manage inflammation and improve insulin sensitivity.

Exercise and nutritional therapy are complementary approaches. Combining regular physical activity with a balanced diet that supports metabolic health is an effective strategy to enhance insulin sensitivity. Consulting with a healthcare professional, such as a registered dietitian or a fitness expert, can help you create a personalized plan that takes into account your health goals, preferences, and any underlying conditions.

Does exercise work the same way as fasting to improve insulin sensitivity?


Exercise and Insulin Sensitivity:

  • Exercise increases glucose uptake by muscle cells even without the need for a large amount of insulin. This effect is partly due to the increased expression of glucose transporters on muscle cell membranes.
  • Physical activity stimulates the activation of certain cellular pathways that enhance insulin receptor sensitivity. This means that cells become more responsive to insulin’s signals, leading to improved glucose uptake and utilization.
  • Regular exercise helps lower body fat levels, especially visceral fat, which is linked to insulin resistance. Reduced body fat contributes to better insulin sensitivity.

Fasting and Insulin Sensitivity:

  • Fasting involves periods of not consuming calories, allowing insulin levels to decrease. When insulin levels are low, cells become more sensitive to insulin’s effects.
  • Fasting helps deplete glycogen stores (the stored form of glucose) in the liver and muscles. This makes room for the uptake of glucose during periods of refeeding, improving insulin sensitivity in response to carbohydrate consumption.
  • Fasting can promote metabolic adaptations that improve glucose utilization and insulin sensitivity.

Synergistic Effects: There is evidence to suggest that combining exercise with fasting might have synergistic effects on insulin sensitivity and metabolic health. For example, exercising in a fasted state can enhance the body’s ability to use fat for energy, preserve muscle mass, and further improve insulin sensitivity.

It’s important to note that individual responses to exercise and fasting can vary. Some people may find certain strategies more effective or sustainable than others. The key is to find an approach that works for you, supports your health goals, and aligns with your lifestyle.

Before making significant changes to your exercise routine or dietary habits, especially if you have underlying health conditions, it’s advisable to consult with a healthcare professional. They can provide personalized guidance based on your individual needs and circumstances.

Are you ready to test and not guess how you should fuel, train and perform your best each day?  

Schedule a call with Coach Debbie Potts today to get started on your fat loss, performance and longevity program here.

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