POST SUMMARY: What this means for you…
Be sure to get your insulin checked on your next wellness visit or check-up. If it’s above ~6-7 IU/ml, make the necessary dietary changes to lower your insulin. As always, remember that dietary fat is the one nutrient that does not increase insulin production in your body. Let natural fats become an increasingly prominent part of your diet, whether it’s from meat or fruit sources.
Of the various factors that can cause insulin resistance (and we’ll discuss them all in future posts), insulin is the most relevant.
To be precise about it, for every 1 µU change in blood insulin level, a person may experience an approximately 20% increase in insulin resistance . This might seem like a strange cause and effect, but it represents a fundamental feature of how the body works; when a process is excessively activated, the body will often dampen its response to the excess stimulus in order to reduce the activation.
This is similar to how bacteria become resistant to antibiotics. With insulin resistance, if a cell, such as muscle or liver, is inundated with insulin, it can do nothing to directly reduce the insulin being produced, which is happening at the pancreas, but it can alter itself to ensure that insulin has a smaller effect; it becomes resistant to insulin. As this occurs in countless cells in several tissues, the body as a whole becomes insulin resistant.
Convincing and Distinct Studies
The studies that have highlighted this phenomenon of hyperinsulinemia cause insulin resistance are few, but very convincing and distinct from one another. For example, certain pancreas tumors consist of overactive beta cells, the cells that create insulin. This beta cell-loaded tumor is often referred to as an insulinoma because of the high amount of insulin coming from the tumor. Thus, these patients have elevated blood insulin, which is entirely a result of the tumor. The patients with the highest degree of insulin production from the insulinoma become highly insulin resistant, whereas the patients with the lower insulin levels become mildly insulin resistant. But, in the end, they always develop insulin resistance [2, 3].
In perhaps the most rare case of insulin driving insulin resistance, hypothalamic obesity is a terrible condition in which a person has had a distinct section of the brain damaged. This section of the brain is responsible, in part, for controlling the degree to which the pancreas releases insulin. Once damaged, which can happen as a result of an unrelated brain operation, the pancreas is stimulated to release insulin constantly. In addition to developing insulin resistance, the person concurrently gains massive amounts of fat .
In another instance, scientists caused an artificial hyperinsulinemia (i.e., high blood insulin) by infusing healthy insulin-sensitive men with insulin . Even though the insulin dose was at a physiologic level (i.e., a level normally reached in the day), by keeping a steady infusion, the men become insulin resistant after just a few hours. While this scenario is somewhat unrealistic (after all, nobody normally sits in a chair while receiving an insulin infusion), the next scenario is unfortunately all too common.
On Its Surface, It Makes Sense, But…
A common method of treating type 2 diabetes is to give the patient insulin injections. On the surface, this seems like a logical and benign treatment—“everybody knows diabetics need insulin”. This paradigm is an unfortunate consequence of lumping type 1 and type 2 diabetes into one family of glucose-centric diseases.
All type 2 diabetics have too much glucose, which is how the disease is diagnosed. However, type 2 diabetics also have too much insulin, just not enough to bring blood glucose down to a normal range. Thus, a common course of treatment is to have the diabetic take insulin.
This creates an artificially high state of insulin (higher than the pancreas alone would produce), which is then sufficient to bring blood glucose under control. However, because insulin causes insulin resistance, by administering insulin injections, the person is steadily making themselves increasingly insulin resistant, which is evident in the fact that type 2 diabetics usually find themselves needing more and more insulin over time .
In the end, irrespective of where the hyperinsulinemia starts, insulin resistance is the result.
Critically, the hyperinsulinemia doesn’t just arise from an overt medical problem, but can occur simply from a person’s lifestyle. I am convinced that too much insulin is the most relevant of all the causes because it is so intimately connected to lifestyle.
Unfortunately, our current lifestyle is a perfect storm of hyperinsulinemia.
(In upcoming posts, we’ll highlight the second-tier causes, such as inflammation, thyroid hormone, stress, sleep, and more.)
1. Marchesini G, Brizi M, Morselli-Labate AM, Bianchi G, Bugianesi E, McCullough AJ, Forlani G, Melchionda N: Association of nonalcoholic fatty liver disease with insulin resistance. The American journal of medicine 1999, 107:450-455.
2. Pontiroli AE, Alberetto M, Pozza G: Patients with insulinoma show insulin resistance in the absence of arterial hypertension. Diabetologia 1992, 35:294-295.
3. Pontiroli AE, Alberetto M, Capra F, Pozza G: The glucose clamp technique for the study of patients with hypoglycemia: insulin resistance as a feature of insulinoma. Journal of endocrinological investigation 1990, 13:241-245.
4. Lustig RH, Rose SR, Burghen GA, Velasquez-Mieyer P, Broome DC, Smith K, Li H, Hudson MM, Heideman RL, Kun LE: Hypothalamic obesity caused by cranial insult in children: altered glucose and insulin dynamics and reversal by a somatostatin agonist. The Journal of pediatrics 1999, 135:162-168.
5. Del Prato S, Leonetti F, Simonson DC, Sheehan P, Matsuda M, DeFronzo RA: Effect of sustained physiologic hyperinsulinaemia and hyperglycaemia on insulin secretion and insulin sensitivity in man. Diabetologia 1994, 37:1025-1035.
6. Henry RR, Gumbiner B, Ditzler T, Wallace P, Lyon R, Glauber HS: Intensive conventional insulin therapy for type II diabetes. Metabolic effects during a 6-mo outpatient trial. Diabetes care 1993, 16:21-31.
This blog post (and all other posts and content on this website) is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of qualified health providers with questions you may have regarding medical conditions.
About Benjamin Bikman, Ph.D. – Ben earned his Ph.D. in Bioenergetics and was a postdoctoral fellow with the Duke-National University of Singapore in metabolic disorders. Currently, his professional focus as a scientist and professor (Brigham Young University) is to better understand chronic modern-day diseases, with special emphasis on the origins and consequences of obesity and diabetes. He frequently publishes his research in peer-reviewed journals and presents at international science meetings.