A little moderate to vigorous physical activity does more than you think.

There are others!

Hat-tip to Bill Lagakos for tweeting this:- The Influence Of Physical Activity On Vascular Complications And Mortality In Patients With Type 2 Diabetes Mellitus.

"RESULTS: Forty-six percent of participants reported undertaking moderate to vigorous physical activity for >15 minutes at least once in the previous week. During a median of 5 years of follow up, 1,031 patients died, 1,147 experienced a major cardiovascular event and 1,136 a microvascular event. Compared to patients who undertook no or mild physical activity, those reporting moderate to vigorous activity had a decreased risk of cardiovascular events (HR 0.78, 95% CI 0.69-0.88, p < 0.0001), microvascular events (HR 0.85, 95% CI 0.76-0.96, p0.010) and all-cause mortality (HR 0.83, 95% CI 0.73-0.94, p0.0044)."

A HR of 0.83 is a reduction of 17%. That's quite impressive, for at least 15 minutes of moderate to vigorous physical activity at least once a week. Must. Get. Off. This. Sofa. More. Often.

Insulin Resistance: Solutions to problems.

Before I start on what may be the most important thing that I've ever written, here's "Don't Stop Movin" by S Club 7. It's a clue to what's coming.


The problem:
Insulin Resistance (IR) is a major problem for a significant percentage of the population in the developed world. It can cause:-

High fasting serum glucose, which increases the risk factor for Coronary Heart Disease.
High post-prandial serum glucose, which increases the risk factor for Coronary Heart Disease, Retinopathy, Neuropathy & Nephropathy (Kidney failure) amongst other things.
High serum cholesterol.
High serum triglycerides, which in conjunction with high serum cholesterol 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 & urate Kidney stones.
Hypertension, which raises the risk factor for Coronary Heart Disease, Strokes & Kidney failure.
Excessive appetite after eating high-GL carbohydrates, due to rebound low serum blood glucose, leading to overeating & obesity.
Lethargy after eating almost anything, but especially after eating high-GL carbohydrates, due to compensatory hyperinsulinaemia.
If IR is left untreated, it can deteriorate into type 2 diabetes. See Type 2 diabetes in the UK.

The cause and solutions:
1) "Bad" genes. My genes aren't particularly good, but it is possible to change the expression of your genes.

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 uses Glu-T5 transporters which are insulin-independent & 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.

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 serum 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 exercise is compulsory. I have been in denial for years. Then, Uh-oh! There may be trouble ahead... happened. See Increased Glucose Transport–Phosphorylation and Muscle Glycogen Synthesis after Exercise Training in Insulin-Resistant Subjects and Improvement in Glucose Tolerance After 1 Wk of Exercise in Patients With Mild NIDDM (hat-tip to Go Kaleo). See also Move More: Solutions to problems.

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. I go for a 30 minute walk each evening.

3) 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 (fasting serum glucose = 6.8mmol/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 hyperinsulinaemic drowsiness. I was also about the same weight that I was in 2003, so the improvement was not due to weight loss.

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.

4) Deficiency in Magnesium.
For the top 999 foods highest in Magnesium per 100g serving, see HERE. I take ~4g of Epsom Salts/day (~400mg Mg/day). 

5) 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 Vitacost Ultra Vitamin K with Advanced K2 Complex/day. Note: Warfarin/Coumadin works by depleting Vitamin K, so lots of Vitamin K2 makes Warfarin/Coumadin ineffective. 

6) 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.

7) 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.

8) 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.

9) Excessive intake of man-made trans-fats.
Base your diet on Real Food rather than manufactured food products.

10) Excessive intake of chemicals.
Don't swallow toothpaste (fluoride) or disclosing tablets (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.

Any other ideas for normalising insulin sensitivity?

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.

Why exercise may or may not help you to lose weight.

Exercise. I hate it. I'm about as active as a Brazilian 2-toed Sloth. The problem that I have with exercise is that it makes me feel really hungry and I end up eating more Calories than I burned by exercising. This is due to the effect of AMPk on my brain.

The thing about exercise in moderation is that it's good for health and fitness. The problem is that some people think that lots more is better. That ain't necessarily so. The 38 year old lady sitting near me at karaoke last night used to run a lot when she was at school. She now needs a replacement knee joint due to damaged cartilage and she had her knee wired up to a TENS machine.

Too much early morning exercise can also make you ill, by raising serum Cortisol levels. Excessive Cortisol is immunosuppressive. See Early morning exercise could make you ill. Excessive Cortisol also causes water retention, so people who over-exercise can gain (water) weight. Excessive Cortisol can also cause muscle loss, thin skin and osteoporosis.

Starving yourself and over-exercising just makes things even worse. From WHY is the combination of high intensity and/or long duration activity a mistake when calories are being severely restricted?

"Water retention: cortisol binds to the mineralocorticoid receptor (the receptor involved in water retention, well one of them). And although cortisol has 1/100th of the effect on water balance of the primary hormones (aldosterone and a couple of others), since there is like 8000 times as much of it, it can cause a major effect." and

"Excessive cortisol, especially chronic elevations cause other problems not the least of which is leptin resistance. Which only magnifies the drop in leptin from dieting. This could be another mechanism behind the greater drop in metabolic rate for the study I mentioned above."

So, what's the best thing to do for maximum fat loss with minimal muscle loss? A mixture of high-intensity exercise (resistance training with weights, or sprinting) and medium-intensity exercise (jogging) is better than just medium-intensity exercise. See Resistance Weight Training With Endurance Training Enhances Fat Loss, Impact of Exercise Intensity on Body Fatness and Skeletal Muscle Metabolism and HIIT & Run.

One theory to try and explain the improved fat loss is that Calories are burned after the high-intensity exercise is finished. However, the Excess Post-exercise Oxygen Consumption (EPOC) only amounts to about 35kcals so it isn't significant. What is significant is the appetite reduction produced by high-intensity exercise, the opposite effect from low and medium-intensity exercise.