Insulin resistance, also known as metabolic syndrome or Syndrome X, is a complex dysregulation of blood sugar and insulin that can lead to imbalances in hormones, immunity, digestion, metabolism, and cardiovascular health. Insulin is required to get glucose into most cells of the body. In insulin resistance, the insulin receptor sites do not respond to normal amounts of insulin, leading to higher blood glucose levels and increased production of insulin. When glucose can’t enter the cell, it stays in the bloodstream and gets oxidized, damaging many tissues, especially the eyes, kidneys, and nerves. Because the cells aren’t responding to a normal level of insulin, the pancreas will secrete even more in an attempt to get the cells to respond. However, high levels of insulin also directly lead to inflammatory damage, and higher insulin production can exhaust the pancreas’ ability to make both insulin and digestive enzymes. High levels of insulin also stimulate the adrenals to produce cortisol, which, in turn, creates more insulin resistance, and producing high levels of cortisol will eventually exhaust the adrenal glands. This cortisol-insulin cycle is key to many of the other imbalances that occur with insulin resistance.
High levels of insulin activate the aromatase enzyme that converts testosterone to estrogen in men, which creates more insulin resistance and more estrogen characteristics. High levels of insulin in women cause estrogen to be converted into testosterone, which can create polycystic ovary syndrome (PCOS), with hair loss, male pattern hair growth, voice deepening, acne, weight gain, fluid retention, menstrual irregularities, ovarian cysts, infertility, and further insulin resistance.
The immune effects of insulin resistance result primarily from the cortisol changes: elevated cortisol decreases the cellular immune response and increases the antibody response, which results in greater susceptibility to infections and greater difficulty recovering from infections, as well as more allergies. The digestive system is also affected by the cortisol elevation. High cortisol decreases the secretory IgA antibody that lines all the mucous membranes and acts like “glue” in the intestines to keep pathogens and large proteins from being absorbed. This decreased IgA creates a leaky gut, where things can pass through the intestines that normally would be blocked from entering. The leaky gut then creates a vicious allergy cycle with the higher antibody immune response.
The high cortisol also kills off the beneficial bacteria in the intestines, further impacting immunity. Pathogenic bacteria can then colonize the intestines, and components of these pathogens shut down the liver’s detoxification of hormones, including insulin, leading to further insulin resistance. Elevated levels of insulin also shut down enzyme pathways directly required for detoxification.
High insulin shuts down the hormone-sensitive lipase enzyme, which is required to convert break down fat. People with insulin resistance also experience fatigue because the glucose cannot enter the cells and provide fuel for energy production.
Insulin resistance increases the risk for cardiovascular disease via enzyme changes that elevate cholesterol, increase clotting and risk for stroke, and decrease HDL. In addition to producing cortisol, the adrenal glands produce aldosterone, which regulates sodium and potassium retention. As the adrenals produce more cortisol due to the high insulin, they also produce more aldosterone, increasing sodium retention and blood pressure.
Symptoms of insulin resistance include fatigue, sugar cravings, constant hunger, fatigue after meals, food cravings, and inability to lose weight. Early signs on blood tests include high glucose, cholesterol, and/or triglycerides. Later, glucose and triglycerides will be high, HDL will drop, and uric acid, LDL, total cholesterol, and hemoglobin A1C will rise. Many people with insulin resistance are overweight but atypical insulin resistance presents with many of the same signs and symptoms, but weight may be normal.
© Kimberly Hindman, 2007
Comments are closed, but trackbacks and pingbacks are open.