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    The High Insulin Type

    When your blood sugar test is normal but your body is telling a different story

    The afternoon crash. The 3 PM brain fog. The midsection weight that will not move no matter how clean the diet. The doctor's lab work that comes back ‘normal’ but does not match how you feel. There is a reason these things show up together.

    The Pattern That Has a Name

    The High Insulin Type is the second of the five hormonal patterns identified in the Hormetics framework, co-developed by health researcher Elwin Robinson and Dr. Miriam Mikicki MD, an IFM-certified functional medicine physician.

    If you have noticed any of the following, insulin signaling may be a meaningful part of your situation:

    • Energy that crashes hard in the mid-afternoon
    • Fatigue and brain fog after meals, particularly carbohydrate-heavy ones
    • Weight that has crept up around the midsection specifically
    • Strong cravings for sweets and starches, especially in the evening
    • Difficulty going more than a few hours without eating
    • Skin tags, or darkened patches at the neck or under the arms
    • Family history of type 2 diabetes
    • Standard blood sugar tests that come back normal even though something feels off
    • Standard diet-and-exercise approaches no longer producing the expected results

    These are signs commonly associated with insulin resistance, a pattern that develops gradually over years before it ever shows up on a routine blood glucose test ¹.

    What Insulin Actually Does

    Insulin pathways infographic showing how insulin moves glucose, amino acids, and fatty acids from the bloodstream into cells

    Insulin is one of the most important regulatory hormones in the human body. It is produced by the beta cells of the pancreas in response to rising blood glucose, primarily after meals ². Its main job is to act as a key, opening cellular receptors so that glucose, amino acids, and fatty acids can move out of the bloodstream and into the cells that need them ³.

    Beyond that, insulin is a master regulator of fuel storage. When insulin is high, the body is in a fed and storing state. When insulin is low (between meals, during sleep, after fasting), the body is in a fasted and burning state. The healthy oscillation between these two states is the foundation of metabolic flexibility .

    This is what insulin is supposed to do.

    When the Signal Stops Landing

    Insulin resistance is the gradual loss of cellular sensitivity to insulin. The pancreas keeps producing insulin in response to meals. The cells stop opening their doors as readily. To compensate, the pancreas produces more insulin, then more, then more again .

    This is the part that conventional testing tends to miss.

    Standard blood sugar testing measures glucose, not insulin. In the early stages of insulin resistance, glucose levels often remain in the normal range because the pancreas is working overtime to keep them there . The cost (hyperinsulinemia, chronically elevated insulin) does not show up unless someone specifically tests fasting insulin or runs a HOMA-IR calculation .

    This means the pattern can develop for five, ten, even fifteen years before it triggers a ‘diabetic’ or ‘pre-diabetic’ diagnosis . By that point, the pancreas is exhausted, glucose has finally risen, and the standard interventions begin. But the underlying issue (the cellular insensitivity) has been driving symptoms the entire time.

    Joseph Kraft, a pathologist who tested the post-meal insulin response of more than 14,000 patients over several decades, found that elevated insulin nearly always preceded elevated glucose, often by a decade or more . His work suggests that insulin resistance is far more common than glucose-only testing reveals.

    How This Pattern Develops

    The drivers of insulin resistance are well established in the research and concentrate on a small number of root causes.

    • Refined carbohydrate exposure. Foods that trigger sharp glucose elevations require correspondingly sharp insulin responses. Repeated daily, this trains the system toward chronic hyperinsulinemia ¹⁰. White flour, refined sugar, fruit juice, and processed snack foods are the most concentrated sources.

    • Snacking patterns. Insulin levels do not return to baseline as long as food keeps arriving. Modern eating patterns (three meals plus several snacks daily) keep insulin elevated for most waking hours, denying cells the recovery period they need ¹¹. This is one of the most underappreciated drivers in the literature.

    • Visceral fat accumulation. Fat stored around the organs (rather than under the skin) is metabolically active and directly contributes to insulin resistance through inflammatory cytokine production ¹².

    • Sleep deprivation. Even a single night of restricted sleep measurably reduces insulin sensitivity in healthy individuals ¹³. Chronic sleep loss is consistently associated with elevated fasting insulin and HOMA-IR ¹⁴.

    • Sedentary lifestyle. Skeletal muscle is the largest insulin-sensitive tissue in the body. When muscles are not contracted regularly, their insulin sensitivity declines ¹⁵. Even brief post-meal walking has been shown to meaningfully blunt the insulin response ¹⁶.

    • Specific food triggers. Industrial seed oils and trans fats have been associated with worse insulin sensitivity in multiple studies ¹⁷. Coffee on an empty stomach has been shown to acutely impair glucose tolerance in some individuals ¹⁸.

    The Vicious Cycle

    Insulin resistance is a self-reinforcing pattern. As cells become less responsive to insulin, the pancreas produces more. As insulin levels rise, fat storage is favored over fat burning. As fat (particularly visceral fat) accumulates, inflammatory signals worsen insulin sensitivity further. As sensitivity worsens, more insulin is required. And so on ¹⁹.

    The downstream consequences extend well beyond weight. Hyperinsulinemia is associated with elevated blood pressure ²⁰, dyslipidemia ²¹, increased cardiovascular risk ²², cognitive concerns ²³, and the cluster of conditions known as metabolic syndrome.

    It is also a major contributor to cravings. Insulin's interaction with the satiety system, including its overlap with leptin signaling, means that high insulin states often coexist with disordered appetite ²⁴. People with insulin resistance frequently describe feeling hungry on a schedule, regardless of whether they have actually eaten enough.

    Why Conventional Approaches Often Fall Short

    Still life on a wooden table: a stack of well-worn paperback diet books, a ceramic mug of tea, reading glasses, and an open notebook with handwritten food rules — symbolizing years of trying every diet

    The standard advice for blood sugar concerns tends to focus on glucose, not insulin. This makes sense when treating diagnosed diabetes, but it can mask insulin resistance for years.

    Two common approaches deserve specific mention.

    Calorie-restricted, low-fat diets. These were the standard recommendation for metabolic concerns for several decades. The problem is that they often replace fat calories with refined carbohydrates, which can worsen insulin response ²⁵. These protocols often produce initial body composition changes, but insulin resistance frequently persists.

    Long-term ketogenic and very-low-carb approaches. These can produce striking short-term improvements in insulin sensitivity by directly reducing the carbohydrate load ²⁶. The concern in the longer-term literature is that very strict ketogenic protocols can elevate cortisol ²⁷, reduce thyroid output ²⁸, and produce a metabolic slowdown that creates new problems. The Hormetics view, supported by Dr. Mikicki's clinical observations, is that moderate carbohydrate intake combined with proper meal timing tends to be more sustainable than chronic restriction.

    Both approaches share a deeper limitation: they treat the input (carbohydrates) without addressing the upstream context (chronic snacking, poor sleep, sedentary patterns) that allows insulin resistance to develop in the first place.

    A Different Approach

    The High Insulin Type framework starts by reframing the problem: insulin resistance is not about how much glucose you ate at one meal, but about the cumulative pattern of insulin elevation across days, weeks, and years.

    This is what the Hormetics system addresses for this type. The Insulin Reset Protocol, co-developed by Elwin Robinson and Dr. Miriam Mikicki MD, works through the structural drivers of chronic hyperinsulinemia rather than focusing exclusively on macronutrient ratios. The specifics of the protocol are beyond the scope of this page, but the framework addresses meal timing and structure, food quality, post-meal physical activity, sleep optimization, and targeted nutritional support. It does not require ketogenic restriction, prolonged fasting, or any approach that would be unsustainable as a long-term way of eating.

    The first step is identifying which of the five Hormetics types applies to your specific situation.

    The Bigger Picture

    The High Insulin pattern frequently overlaps with other Hormetics types. Insulin resistance and leptin resistance share common inflammatory drivers and often appear together ²⁹. Cortisol elevation directly promotes insulin resistance through hepatic gluconeogenesis ³⁰. Estrogen imbalance can also affect insulin sensitivity in both men and women ³¹.

    This is why a single-mechanism approach often falls short for the people most affected.

    If the description on this page sounds like your experience, the next step is the Hormetics Assessment. It will tell you whether insulin signaling is your dominant pattern, a secondary factor, or not applicable to your situation.

    Already taken the assessment and know you're a Insulin Type? If so, the following could help:

    The Insulin Reset Protocol guide

    The Insulin Reset Protocol

    The complete protocol for the insulin type — meal structure that brings insulin back to baseline, the foods to prioritise, and the daily rhythms that get blood sugar working with you instead of against you.

    Learn More
    Insulin Balance Formula bottle

    Insulin Balance Formula

    Formulated to support healthy blood sugar balance and metabolic function.†

    Learn More

    Important: The Hormetics framework is an educational system designed to support hormonal and metabolic optimization. It is not a substitute for medical evaluation, diagnosis, or treatment. If you have a medical condition, are taking medication, or have specific health concerns, consult with your healthcare provider before making changes. Individual results vary.

    Scientific Citations

    1. Hurren SM, Dunbar KH. Insulin Resistance. StatPearls [Internet]. 2023. https://www.ncbi.nlm.nih.gov/books/NBK507839/
    2. Varghese J, Gupta PK, et al. Hyperinsulinemia: an early biomarker of metabolic dysfunction. Front Clin Diabetes Healthc. 2023;4:1159664. https://pmc.ncbi.nlm.nih.gov/articles/PMC10186728/
    3. Reaven GM. Early clinical expressions of insulin resistance. BMC Endocr Disord. 2013. https://d-nb.info/1151809861/34
    4. Hurren SM, Dunbar KH. Insulin Resistance. StatPearls. 2023. (insulin basics) https://www.ncbi.nlm.nih.gov/books/NBK507839/
    5. Fowler MJ. Physiology of insulin. Clin Diabetes. 2008;26(2):66–69. https://pubmed.ncbi.nlm.nih.gov/18286298/
    6. Galgani JE, Ravussin E. Metabolic flexibility and insulin resistance. Am J Physiol Endocrinol Metab. 2008;295(5):E1009–E1017. https://pubmed.ncbi.nlm.nih.gov/18285522/
    7. Hurren SM, Dunbar KH. Insulin Resistance. StatPearls. (insulin resistance preceding diabetes) https://www.ncbi.nlm.nih.gov/books/NBK507839/
    8. Varghese J, Gupta PK, et al. Hyperinsulinemia: an early biomarker of metabolic dysfunction. Front Clin Diabetes Healthc. 2023. https://pmc.ncbi.nlm.nih.gov/articles/PMC10186728/
    9. Varghese J, Gupta PK, et al. Hyperinsulinemia: an early biomarker of metabolic dysfunction. (summarising Kraft) https://pmc.ncbi.nlm.nih.gov/articles/PMC10186728/
    10. Gerber J. Kraft Prediabetes Profile: Patterns Overview. Meridian Valley Lab, 2018. https://meridianvalleylab.com/kraft-prediabetes-profile-patterns-overview/
    11. Jimenez-Cruz R, et al. Excessive refined carbohydrates and scarce micronutrients are associated with insulin resistance and low-grade inflammation in obese children. Int J Endocrinol. 2014;2014:163612. https://pmc.ncbi.nlm.nih.gov/articles/PMC4248360/
    12. Maffetone P, et al. Refined carbohydrates and the overfat pandemic: implications for brain health and public health policy. Front Public Health. 2025;13:1585680. https://www.frontiersin.org/articles/10.3389/fpubh.2025.1585680/full
    13. Smeets BS, Westerterp-Plantenga MS. The effect of feeding frequency on insulin and ghrelin responses in human subjects. Br J Nutr. 2008;99(6):1316–1321. https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/effect-of-feeding-frequency-on-insulin-and-ghrelin-responses-in-human-subjects/3BBA9395F8161CA950C5A5D346C7B938
    14. Carlson O, et al. Effect of meal frequency on glucose and insulin excursions over the course of a day. Metabolism. 2010;59(9):1241–1247. https://www.sciencedirect.com/science/article/pii/S1751499110000545
    15. Hurren SM, Dunbar KH. Insulin Resistance. StatPearls. (visceral fat and insulin resistance) https://www.ncbi.nlm.nih.gov/books/NBK507839/
    16. Després JP. Body fat distribution and risk of cardiovascular disease: an update. Circulation. 2012;126(10):1301–1313. https://pubmed.ncbi.nlm.nih.gov/22949540/
    17. Broussard JL, et al. A single night of partial sleep deprivation induces insulin resistance in multiple metabolic pathways in healthy subjects. J Clin Endocrinol Metab. 2012;97(9):E1180–E1185. https://pubmed.ncbi.nlm.nih.gov/20371664/
    18. Spiegel K, Tasali E, Penev P, Van Cauter E. Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med. 2004;141(11):846–850. https://pubmed.ncbi.nlm.nih.gov/15583226/
    19. Stanford KI, Goodyear LJ. Role of skeletal muscle in insulin resistance and glucose uptake. Compr Physiol. 2014;4(1):1–25. https://pmc.ncbi.nlm.nih.gov/articles/PMC8074531/
    20. Hawley JA, et al. A pathway to enhanced insulin sensitivity and skeletal muscle health. Exerc Sport Sci Rev. 2024;52(4):187–196. https://pmc.ncbi.nlm.nih.gov/articles/PMC11863266/
    21. Mozaffarian D, et al. Trans fatty acids and insulin resistance. Atheroscler Suppl. 2006;7(2):29–32. https://pubmed.ncbi.nlm.nih.gov/17392081/
    22. Lichtenstein AH. Trans fatty acids, blood lipids, and cardiovascular risk. Curr Atheroscler Rep. 2006;8(6):459–465. https://pubmed.ncbi.nlm.nih.gov/17045596/
    23. Rafi S, et al. A ketogenic diet is effective in improving insulin sensitivity in type 2 diabetics. Curr Diabetes Rev. 2023. https://www.benthamdirect.com/content/journals/cdr/10.2174/1573399818666220425093535
    24. Færch S, et al. A 3-week ketogenic diet increases skeletal muscle insulin sensitivity in individuals with obesity. Diabetes. 2024;73(10):1631–1642. https://diabetesjournals.org/diabetes/article/73/10/1631/157025/A-3-Week-Ketogenic-Diet-Increases-Skeletal-Muscle
    25. Barbosa MCG, et al. Ketogenic diet and thyroid function: a delicate metabolic balance. Nutrients. 2025;17(9):2150. https://pmc.ncbi.nlm.nih.gov/articles/PMC12468144/
    26. Lombardi G, et al. Ketogenic diet and endocrine function: focus on thyroid and adrenal axis. Rev Endocr Metab Disord. 2023. https://pubmed.ncbi.nlm.nih.gov/37368943/
    27. Carroll TA, Chrousos GP, et al. The hypothalamic-pituitary-adrenal-leptin axis and metabolic health. Philos Trans R Soc Lond B Biol Sci. 2014;369(1649):20130427. https://pmc.ncbi.nlm.nih.gov/articles/PMC4142017/
    28. Borodkina A, Orlova E. Leptin resistance: underlying mechanisms and diagnosis. Probl Endokrinol. 2019;65(1):16–24. https://pmc.ncbi.nlm.nih.gov/articles/PMC6354688/
    29. Varghese J, Gupta PK, et al. Hyperinsulinemia: an early biomarker of metabolic dysfunction. Front Clin Diabetes Healthc. 2023;4:1159664. (metabolic syndrome cluster) https://pmc.ncbi.nlm.nih.gov/articles/PMC10186728/
    30. Meli R, Clegg DJ. Cross-talk between estrogen and leptin signaling in the hypothalamus. Am J Physiol Endocrinol Metab. 2008;294(5):E817–E827. https://journals.physiology.org/doi/10.1152/ajpendo.00733.2007
    31. Meli R, Clegg DJ. Cross-talk between estrogen and leptin signaling in the hypothalamus. Am J Physiol Endocrinol Metab. 2008;294(5):E817–E827. https://journals.physiology.org/doi/10.1152/ajpendo.00733.2007

    Medical Disclaimer: The information provided on this website and in our materials is for educational and informational purposes only and is not intended as medical advice. These statements have not been evaluated by the Food and Drug Administration. Our protocols and any referenced products are not intended to diagnose, treat, cure, or prevent any disease. Always consult with a qualified healthcare professional before starting any new diet, exercise, or supplement program.

    Results Disclaimer: Individual results may vary. Any testimonials or examples used on this page are not intended to represent or guarantee that anyone will achieve the same or similar results. Your specific outcomes depend on your individual baseline health, effort, and compliance with the protocol.

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