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Insulin Resistance Information
Introduction
There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't. The diseases caused by our incorrect and unnatural diets are those featured on these pages.
Dietary causes:
carbohydrate-rich, 'healthy' diet.Part 1: Introduction
We have about 5 litres of blood travelling around our bodies at any given moment. And in these 5 litres we need only about 5 grams of glucose to supply the energy for all the body's processes that need it. Too much glucose is harmful to our health: it makes our blood thicker and more difficult for our hearts to pump round; it gets incorporated in red blood cells making their job of conveying oxygen around more difficult; and it also tends to clog up the tiny capillaries which can ultimately lead to the complete shut-off of blood to parts of the body with disastrous results.
Our bodies recognise the dangers of too high a glucose level and have evolved a system to confine the level within safe limits. Glucose is metered in the brain by the hypothalamus. When blood sugar levels get too high, the hypothalamus stimulates the pancreas to produce insulin. Insulin helps the body utilise the blood sugar, glucose, by binding with receptors on cells like a key would fit into a lock. This stimulates glucose uptake from the blood into body tissues. Once the insulin key has unlocked the door, the glucose can pass from the blood into the cell. Inside the cell, glucose is either used for energy or stored for future use in the form of a starch called glycogen in liver or muscle cells, or as fat in the body's fat cells (adipocytes). This latter process is the way we put on weight.
But overweight is only one consequence of eating a carbohydrate-rich diet. There comes a point where cells get fed up of continually taking in glucose they can't use. It then takes more and more insulin to achieve the same reduction of blood glucose. Insulin resistance occurs when the normal amount of insulin secreted by the pancreas is not able to unlock the doors to cells, and tissues have a diminished ability to respond to the action of insulin. To compensate for this and maintain normal glucose levels, the pancreas secretes more insulin. Insulin-resistant persons normally have high blood insulin levels (hyperinsulinaemia). Many people who are insulin resistant produce large enough quantities of insulin to maintain near normal blood glucose levels. If you continue to eat the ?healthy' recommended diet for long enough, your pancreas will be continually producing insulin and, as well as having high levels of blood glucose, you will also have high levels of insulin. And that isn't healthy either. In about one-third of the people with insulin resistance, when the body cells resist or do not respond even to high levels of insulin, glucose builds up in the blood resulting in chronic high blood glucose. This is the progression to type 2 diabetes.
A high blood insulin level also has many adverse effects: It increases risk of thrombosis, increases arterial plaque formation, prevents plaque regression, stimulates connective tissue synthesis and stimulates the production of insulin-like growth factor 1 (IGF-1),[i] [ii] all of which increase the risk of a heart attack. It also serves to make the kidneys retain sodium, and enhances the flow of sodium and calcium into the smooth muscle cells in artery walls which have been shown to increase blood pressure. If that weren't enough, insulin increases the risk of prostate, endometrial and breast cancers, and makes all cancers more likely to metastasise (spread).[iii] [iv] It also increases the risk of polycystic ovarian syndrome (PCOS),[v] and is suspected in relation to gestational hypertension, preeclampsia and osteoporosis.
References
[i]. Meigs JB, Mieeleman MA, Nathan DM, et al. Hyperinsulinemia, hyperglyceima, and impaired hemostasis. The Framingham offspring study. JAMA 2000; 283: 221-229.
[ii]. DeFronzo RA, Eleuterio F. Insulin resistance: a multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease. Diabetes Care 1991; 14: 173-91.
[iii]. Goodwin PJ, Ennis M, Pritchard KI, et al. Fasting insulin and outcome in early-stage breast cancer: results of a prospective cohort study. J Clin Oncol 2002; 20: 42-51.
[iv]. Rosen Q. Serum insulin-like growth factors and insulin-like growth factor-binding proteins: clinical implications. Clin Chem 1999; 45: 1384-90.
[v]. Amowitz LL, Sobel BE. Cardiovascular consequences of polycystic ovary syndrome. Endocrinol Metab Clin North Am 1999; 28: 438-58.
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