Insulin Resistance (IR) is a major problem for a significant percentage of the population in the developed world. If left untreated, it can deteriorate into type 2 diabetes. See Type 2 diabetes in the UK.
IR can cause:-
High fasting & postprandial serum glucose, which increases the risk factor for Coronary Heart Disease, Retinopathy, Neuropathy & Nephropathy (Kidney failure), amongst other things.
High fasting & postprandial serum triglycerides, which increases the risk factor for Coronary Heart Disease. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
High serum cholesterol, which increases the risk factor for Coronary Heart Disease.
High serum Free Fatty Acids (a.k.a. FFAs a.k.a. NEFAs) from IR fat cells, which increases the risk factor for Sudden cardiac death and also worsens IR in liver & muscle cells.
High serum uric acid, which increases the risk factor for Gout & Uric acid Kidney stones.
Hypertension, which raises the risk factor for Coronary Heart Disease, Strokes & Kidney failure.
Excessive appetite after eating high-GL carbohydrates, leading to overeating & obesity.
Lethargy/sleepiness after eating almost anything, but especially after eating high-GL carbohydrates, due to postprandial hyperinsulinaemia.
Possible causes (IR is multi-factorial) and solutions:
1. "Bad" genes. My genes aren't particularly good, but it is possible to change the expression of genes. See below.
2. Full cells. A full cell is an IR cell. Consider Liver, Muscle and Fat cells:-
a) Liver cells: Liver cells are a 2-way street. "Stuff" (e.g. NEFAs, Glucose & Fructose) goes in and "stuff" (e.g. Ketones & Glucose) comes out. Glucose normally comes out of the liver at a rate of ~5g/hour to fuel the brain, but this can increase a lot under the control of Insulin, Glucagon & Cortisol. If more stuff goes in than comes out, liver glycogen stores fill up and vice-versa. When liver glycogen stores become full, liver cells down-regulate processes that produce liver glycogen e.g. hexokinase & Glu-T2 transporters. Liver cells effectively become IR, to stop more stuff from going in.
However, fructose is transported by Glu-T5 transporters which are insulin-independent & taken up by fructokinase which has a high affinity for fructose, so fructose effectively "barges its way in" to the liver. This is why fructose is a problem for people who have permanently full liver glycogen stores.
The Protein-Sparing Modified Fast (PSMF) depletes liver glycogen and liver & pancreatic fat rapidly. See also Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.
b) Muscle cells: Muscle cells are a 1-way street as far as Glucose is concerned, though Amino Acids can go in & come out. Muscle glycogen cannot be used to produce blood glucose - it can only be used by muscles. When muscle glycogen stores become full, muscle cells down-regulate processes that produce muscle glycogen e.g. hexokinase & Glu-T4 transporters. Muscle cells effectively become IR to stop more stuff from going in.
As per It's all in a day's work (as measured in Joules), muscle cells use mostly fat at rest & lowish-intensity exercise. Glycogen usage increases rapidly as exercise intensity increases. Now do you see the significance of the music video above? Intense exercise (e.g. Running, Sprinting, Resistance training with weights, parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your muscle cells and makes them Insulin Sensitive.
This means that activity is compulsory. See Physiological and health implications of a sedentary lifestyle.
See also Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects ,
Improvement in Glucose Tolerance After 1 Wk of Exercise in Patients With Mild NIDDM (hat-tip to Go Kaleo) and
Move More: Solutions to problems. Excessive sedentariness was a secondary contributor to my IR.
However, don't overdo it! You may have a funny turn, keel over & hurt yourself. See "Funny turns": What they aren't and what they might be.
c) Fat cells: Fat cells are a 2-way street. Fat cells are a bit like balloons that are full of holes. As stuff (e.g. NEFAs & glucose) goes in, the balloon expands to accommodate it. As more stuff goes in and the balloon gets bigger, the internal pressure increases and the holes get bigger, so stuff (e.g. NEFAs & glycerol) comes out at a faster rate. At some level of fullness, stuff comes out as fast as it goes in. At that point, fat cells are effectively IR. So, don't overstuff your fat cells by getting too fat. If you are already too fat, medium intensity exercise (e.g. Walking, Power Walking, Jogging, "Aerobics", parts of High-Intensity Interval Training a.k.a. HIIT, parts of Tabata & parts of Zumba) depletes your fat cells and makes them Insulin Sensitive.
Dress appropriately so that you don't feel cold. Feeling cold is what stimulates your appetite, not exercise. See Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.
3. Empty (of glycogen) cells.
If carbohydrate intake is too low (say, less than 50g/day), physiological Insulin Resistance develops in order to spare glucose for the brain (as parts of the brain run on glucose only) and red blood cells. This is reversible on increasing carbohydrate intake. People who are on ketogenic diets are advised to increase their carbohydrate intake for a few days prior to taking an Oral Glucose Tolerance Test. See HIGH CARBOHYDRATE DIETS AND INSULIN EFFICIENCY.
4. Deficiency in Vitamin D3.
See Hypovitaminosis D is associated with insulin resistance and ß cell dysfunction.
The effects of calcium and vitamin D supplementation on blood glucose and markers of inflammation in nondiabetic adults.
The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis.
A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men.
Plasma 25-hydroxyvitamin D concentration and metabolic syndrome among middle-aged and elderly Chinese individuals.
Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial.
In January 2003, I had Impaired Glucose Tolerance/Metabolic Syndrome/Prediabetes (fasting serum glucose = 5.8mmol/L & 2 hours post-75g glucose load serum glucose = 8.7mmol/L). A sandwich used to send me to sleep.
By September 2008, I had Normal Glucose Tolerance (fasting serum glucose = 5.0mmol/L & 2 hours post-75g glucose load serum glucose = 3.7mmol/L). I also no longer suffered from carbohydrate-induced comas. I was also about the same weight that I was in 2003, so the improvement wasn't due to weight loss. Hypovitaminosis D was the primary contributor to my IR.
So, either use a UVB sun-lamp as per instructions to receive a sub-erythemal dose (not quite going pink) or get tested by your GP and supplement with Vitamin D3 accordingly. I take 5,000iu of Vitamin D3/day.
5. Deficiency in Magnesium.
See Magnesium and type 2 diabetes. For the top 999 foods highest in Magnesium per 200kcal serving, see HERE. I take ~4g of Epsom Salts/day (~400mg Mg/day), dissolved in the 2 litres of fluids that I drink each day, to avoid laxative effects.
6. Deficiency in Vitamin K2.
See Vitamin K₂ prevents hyperglycemia and cancellous osteopenia in rats with streptozotocin-induced type 1 diabetes. Good sources of Vitamin K2 can be found HERE. I take a
Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective.
7. Deficiency in Manganese.
See Manganese supplementation protects against diet-induced diabetes in wild type mice by enhancing insulin secretion. For the top 999 foods highest in Manganese per 100g serving, see HERE.
8. Deficiency in, or excess of Copper w.r.t. Zinc. See Dietary copper supplementation restores β-cell function of Cohen diabetic rats: a link between mitochondrial function and glucose stimulated insulin secretion. For the top 468 foods highest in Copper per 100g serving, see HERE.
9. Deficiency in, or excess of Zinc w.r.t. Copper. See Zinc, pancreatic islet cell function and diabetes: new insights into an old story. For the top 999 foods highest in Zinc per 100g serving, see HERE.
10. Excessive intake of man-made trans-fats.
Base your diet on minimally refined produce rather than over-refined &/or moreish food products.
11. Excessive intake of chemicals.
Don't swallow toothpaste (fluoride) or disclosing tablets (as they may contain iodine). Don't hold till receipts between your lips (may be coated in BPA). Don't slather too many chemicals on your skin.
12. More than one of the above. See A tale of the unexpected & an analogy.
Any other ideas?
Finally, the obligatory picture. Hannah Spearritt is rather nice. :-p
I nearly forgot! Today, when I arrived at mum's nursing home, I found her reading a book. She hasn't done that for over a year. She even knew that it was Wednesday. Ketogenic diet for the win. Mum now has a dual-fuel brain. EDIT: Mum passed away in April 2013, so although it's possible to slow the progression of Lewy Body Dementia and reduce the symptoms of it, it wasn't possible to cure it.