Chow on chow, Parkinson's Law, two ways of doing something, and love.

Another mixed bag of subjects. First, here is Mr Carson C. Chow.

From A Mathematical Challenge to Obesity

According to Mr. Chow, Americans are getting increasingly fat because they're eating increasingly large amounts of "chow", because there's increasingly large amounts of it being produced. That's classic Parkinson's law (consumption expands to absorb the available supply).

According to Armi Legge, over-fat people need to . . . . Eat Less (& Move More).

There are two ways to "Eat Less".

1) Measure everything that goes into your mouth, calculate the calories in it and stick to an average daily calorie limit. Weigh yourself daily and adjust your intake to achieve a certain rate of rolling-averaged weight loss i.e. you consciously create a caloric deficit.

2) Tweak your diet until you find one that you can live with, that results in your belt and/or clothes getting looser i.e. you unconsciously create a caloric deficit. If you can't unconsciously create a caloric deficit, there will have to be some conscious restriction.

1) suits athletes & body-builders, as they are highly-motivated people who have a specific target in mind, whether it be athletic performance or a specific body-fat percentage/muscle mass/appearance.

2) suits the general public, as they aren't generally highly-motivated and won't tolerate hunger pangs.

Unfortunately, "Move More" has to be done consciously. Unconscious "Move More" i.e. Non-Exercise Activity Thermogenesis (NEAT) a.k.a. Spontaneous Physical Activity (SPA) is genetically-determined.

Finally, I read Stretching out. I've been spending too much time on a blog full of fallacies & hate and it's been making me tetchy. I've now disengaged from that blog permanently. Breathe in. Breathe out. That's better!

Continued on Completing the trine: vive la différence!

Diet, Nutrition & Fitness: Whatever the question, the right answer is "It all depends".

The carbohydrate pendulum keeps on swinging! Bloggers keep on fighting!

Carbohydrates are good. No, they're bad. Wait, they're good again. Nope, bad again. Good again. Aargh!

So, are carbohydrates good or bad? See the title. Gluten? See the title.

As Everyone is Different, whether "X" is good, bad or indifferent all depends on genes (including gender), the expression of those genes, environment (i.e. birth weight, exposure to pollutants in the womb & after birth), general diet (i.e. nutrients, anutrients & anti-nutrients), lifestyle (i.e. sunlight exposure, stress, sleep etc) and type, level & volume of activity.

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.

Not exactly rocket science, is it? Part 2

If there's a deficiency in "X", taking supplement "X" will correct the deficiency in "X".
If problem "Y" is caused by a deficiency in "X", then taking supplement "X" will fix problem "Y".

If there's no deficiency in "X", taking supplement "X" won't do anything.
If problem "Y" isn't caused by a deficiency in "X", then taking supplement "X" won't fix problem "Y".

If a person spends a lot of time outdoors in skimpy clothing in sun that's higher than 45deg in the sky, it's highly probable that they will not be deficient in Vitamin D3. Therefore, supplementing with 5,000iu/day of Vitamin D3 will highly probably do nothing.

If the above person has type 2 diabetes, supplementing with 5,000iu/day of Vitamin D3 won't fix their type 2 diabetes.

Not exactly...

Rocket Science!

There will be some people for whom all of the supplements & exercise that I recommend don't help their type 2 diabetes. Sorry about that. A low-carb (but not very-low-carb) diet will minimise your serum glucose level fluctuations without increasing your serum NEFA level excessively. See The problem with Diabetes.

Can supplements & exercise cure Type 2 diabetes?

Definitely, maybe!

From http://health-in-hand.co.uk/2013/03/24/supplements-for-the-non-supplement-takers/

According to Hyppönen and Power, in a large sample of the white British population born in 1958, 60.9% of subjects had serum 25(OH)D (the active metabolite of Vitamin D) of less than 75nmol/L in Summer & Autumn, and 87.1% had serum 25(OH)D of less than 75nmol/L in Winter & Spring. 75nmol/L ≡ 30ng/mL.

 From Hypovitaminosis D is associated with insulin resistance and β cell dysfunction, 2-hour post-load blood glucose level in an oral glucose tolerance test (OGTT) has a negative correlation with 25(OH)D concentration (Fig 1C). 25(OH)D concentration has a positive correlation with insulin sensitivity (Fig 2A). Therefore, 2-hour post-load blood glucose level in a OGTT has a negative correlation with insulin sensitivity.

"Extrapolation from the observations in the current study suggests that increasing 25(OH)D from 10 to 30 ng/mL can improve insulin sensitivity by 60%, from 3.8128 to 6.1176 (umol/L)·m-2·min-1·(pmol/L)-1. This improvement in insulin resistance could potentially eliminate the burden on cells and reverse abnormal glucose tolerance. Furthermore, the 60% improvement in insulin sensitivity that results from vitamin D treatment indicates that that treatment is more potent than either troglitazone or metformin treatment (54% and 13% improvement in insulin sensitivity, respectively). The modest effect of vitamin D on insulin sensitivity in individual persons may translate into a dramatic effect in the population as a whole because of the high prevalence of hypovitaminosis D, which, in a large population, carries an attributable risk for type 2 diabetes and the metabolic syndrome. Although a review of the literature suggests non-calcium-mediated effects, the underlying molecular mechanism remains to be elucidated."

As my 2-hour post-load blood glucose level in a OGTT became low (3.7mmol/L, from 8.7mmol/L in 2003) after supplementing with 5,000iu/day of Vitamin D3, this means that my insulin sensitivity became high. Therefore, I cured my pre-type 2 diabetes using supplements.

My fasting blood glucose level also fell from 6.8 mmol/L (> 7.0mmol/L = type 2 diabetes diagnosis) to 5.0mmol/L. I achieved this without taking any drugs for type 2 diabetes - not even Metformin, which I consider to be a safe & effective insulin-sensitiser, though it can cause gastric distress and B12 absorption issues, long-term. The supplements that I took had zero side-effects and merely corrected deficiencies.

Diabetes drugs cannot cure type 2 diabetes. However, supplements & exercise can cure type 2 diabetes, if the type 2 diabetes is caused by nutrient deficiencies and/or sedentary behaviour and if all pancreatic beta cells haven't been destroyed. Insulin injections can preserve pancreatic beta cells, while insulin resistance is being tackled. See Dr. Richard K Bernstein on insulin for type 2 diabetics, and some definitions.

Sadly, if there are no nutrient deficiencies and/or all pancreatic beta cells have been destroyed, supplements & exercise will not help.

The most simple tip to lose weight EVER is “Eat less and move more”.

Said Gaz at Cycle Of Life - Fix You.
He went from this...

Not a happy bunny.

To this...

A happy bunny.

Now tell me that ELMM doesn't work!

Low-glycaemic diet seen to reverse diastolic dysfunction of diabetes.

From http://www.medscape.com/viewarticle/802947?nlid=30763_1301&src=wnl_edit_dail (Medscape log-in required):-

"Of 32 overweight or obese diabetic patients (mean body-mass index, 34) without cardiac disease who were engaged in a "rehabilitation program in order to lose weight" that included two hours of supervised aerobic exercise per day, half followed a low-glycemic diet (25% carbohydrate, 45% fat, 30% protein) and the other half a low-fat diet (55% carbohydrate, 25% fat, and 20% protein) for three weeks. The diets provided the same amount of calories. Those on the low-fat diet then switched to the low-glycemic diet for an additional two weeks"

"....the two diets led to about the same declines in weight and waist circumference..."

The diet was 25% carbohydrate, 45% fat, 30% protein.
It was a low-carbohydrate/low-glycaemic load diet.
It was not a very-low-carb diet.

Musings on the Paleo Diet.

Would you ask the man below for advice on how to give up alcohol?

I recently read Patients less likely to trust and listen to overweight doctors, which mentioned Mark Sisson. Sisson and Robb Wolf are good representatives for the Paleo Diet. Some are bad representatives for the Paleo Diet due to poor physical condition or abrasive personality.

The Paleo Diet gets flak from scientists like Marlene Zuk and Christina Warinner and it was criticised in The Paleo Diet (hat-tip to Melissa McEwen).

The thing is that people don't need to eat a Palaeolithic diet to be 90% free from degenerative diseases. A mere 150 years ago, Mid-Victorian Brits who didn't die in childhood managed to live to a ripe old age, as cheap sugar imports, junk food, labour-saving devices and horseless carriages hadn't yet been invented.

Just Eat Real Food.

Everyone is Different, Part 3.

Cont'd from Everyone is Different, Part 2.

Hat-tip to Bill Lagakos, whose article Missing: 300 kilocalories reminded me of the following graphic from Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study.

Lo and behold, even when subjects are bribed to stick to the diets that they are provided with, the effect of eating those diets varies hugely.

So, people like ItsTheWoo and Petro Dobromylskyj (yes, I have to copy and paste the name from his site every freakin' time!) rave about how awful carbs are, while people like Go Kaleo and Matt Stone rave about how awesome carbs are.

Everyone is different for a number of reasons, some of which are unchangeable and some of which are changeable. We can't change our birth weight, what our mums ate when we were in the womb or the chemicals that we were exposed to in the past. We can't change our genes, but we can change the expression of our genes by changing diet, activity and even supplementation. See Influence of Vitamin D Status and Vitamin D₃ Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial.

How the Mid-Victorians Worked, Ate and Died.

Hat-tip to Prof. Tim Noakes, who recently tweeted the above study.

See How the Mid-Victorians Worked, Ate and Died.

"The crude average figures often used to depict the brevity of Victorian lives mislead because they include infant mortality, which was tragically high. If we strip out peri-natal mortality, however, and look at the life expectancy of those who survived the first five years, a very different picture emerges. Victorian contemporary sources reveal that life expectancy for adults in the mid-Victorian period was almost exactly what it is today.
.
.
From 1875 on and especially after 1885, rising imports of cheap food basics were increasingly affecting the food chain at home. Imported North American wheat and new milling techniques reduced the prices of white flour and bread. Tinned meat arrived from the Argentine, Australia and New Zealand, which was cheaper than either home-produced or refrigerated fresh meat also arriving from these sources. Canned fruit and condensed milk became widely available.

This expansion in the range of foods was advertised by most contemporaries, and by subsequent historians, as representing a significant ‘improvement’ in the working class diet. The reality was very different. These changes undoubtedly increased the variety and quantity of the working class diet, but its quality deteriorated markedly. The imported canned meats were fatty and usually ‘corned’ or salted. Cheaper sugar promoted a huge increase in sugar consumption in confectionery, now mass-produced for the first time, and in the new processed foods such as sugar-laden condensed milk, and canned fruits bathed in heavy syrup. The increased sugar consumption caused such damage to the nation’s teeth that by 1900 it was commonly noted that people could no longer chew tough foods and were unable to eat many vegetables, fruits and nuts [26]. For all these reasons the late-Victorian diet actually damaged the health of the nation, and the health of the working classes in particular.

The decline was astonishingly rapid..."

See also Who Lives Longest? (h/t to Melissa McEwen)

Everyone is Different, Part 2.

Cont'd from We are not all the same.

A long, long time ago...


I learned that Everyone is Different, thanks to a study by Julia H. Goedecke, Alan St Clair Gibson, Liesl Grobler, Malcolm Collins, Timothy D. Noakes and Estelle V. Lambert.

Well, stone the flamin' crows! Timothy D. Noakes' name just popped up in Alan Aragon's article 2013 NSCA Personal Trainers Conference: Looking Back at my Debate with Dr. Jeff Volek. Dr. Noakes has had problems with his blood glucose level and has adopted a very-low-carb/ketogenic diet.

What also caught my eye in Alan Aragon's article was (Note: TTE = Time To Exhaustion):-
"However, the authors’ conclusion is misleading since 2 of the 5 subjects experienced substantial drops in endurance capacity (48 and 51-minute declines in TTE, to be exact). One of the subjects had a freakishly high 84-minute increase in TTE, while the other increases were 3 and 30 minutes."

I expect that the subjects with 84 and 30 minute increases in TTE would be praising ketogenic diets, whereas the subjects with 48 and 51 minute declines in TTE would be cursing them and the subject with 3 minutes increase would be "Meh". Vive la difference!

Also note that sprint capability...remained constrained during the period of carbohydrate restriction. As mentioned in It's all in a day's work (as measured in Joules), exercise above a certain intensity (~85%VO2max) burns significant amounts of carbs, no matter how fat-adapted someone is.

Cont'd on Everyone is Different, Part 3.

Exercise and Food Reward

Given all the current interest in the Food Reward theories of obesity (check out Richard's post with a phenomenal number of comments), I thought I'd just point to this study that popped across my screen this morning:

Aerobic exercise reduces neuronal responses in food reward brain regions

Exercise reduced neuronal responses in brain regions consistent with reduced pleasure of food, reduced incentive motivation to eat, and reduced anticipation and consumption of food. Reduced neuronal response in these food reward brain regions after exercise is in line with the paradigm that acute exercise suppresses subsequent energy intake.

If Food Reward is an issue and I think it obviously is then we also need to think about exercise.

Reasons to get moving...

First, a music video. What else but...?


Part 1. Get slimmer.
Insulin increases the amount of nutrients entering adipocytes, which makes us fat and hungry.

Er, just a minute!

If increasing the amount of nutrients entering cells makes us hungry, exercise (which increases the amount of nutrients entering muscle cells) would make us hungry. It doesn't. See Fig. 1. in Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males.

If going for a walk outdoors makes you hungry, you're doing it wrong. Wrap up warm, as feeling cold increases hunger. Low blood glucose level also increases hunger, so don't over-exercise while on a long-term ketogenic diet.

By the way, insulin also increases the amount of nutrients entering muscle cells.
Q. What determines the relative amounts of nutrients entering adipocytes vs muscle cells?
A. The relative insulin sensitivities of adipocytes vs muscle cells.

Adipocytes are sensitive to insulin until they become full. To reduce the amount of nutrients entering adipocytes, divert more nutrients to muscle cells by increasing their insulin sensitivity. Emptying muscle cells by doing low-intensity exercise increases their insulin sensitivity. High-intensity exercise increases their insulin sensitivity.


Part 2. Prevent/reverse age-related sarcopenia (muscle loss).
See Use 'em or lose 'em. As diverting more nutrients to muscle cells increases muscle mass, increasing their insulin sensitivity results in increased muscle mass, unless you're eating way below maintenance calories. High-intensity exercise results in more muscle mass gain than low-intensity exercise.


Part 3. Make your brain work properly.
Thanks to Chris Highcock, who gave me a complimentary copy of Hillfit, I found IL-6 and IL-10 Anti-Inflammatory Activity Links Exercise to Hypothalamic Insulin and Leptin Sensitivity through IKKβ and ER Stress Inhibition.

In plain English, this means that exercise increases both insulin and leptin sensitivity in the hypothalamus. As the hypothalamus controls appetite and both insulin & leptin are appetite-suppressing, the net result is less appetite.

Use 'em or lose 'em

Hello world. I'm back. The title is referring to our muscles. The following image is from Figure 1 of Chronic Exercise Preserves Lean Muscle Mass in Masters Athletes.




I'm not going to start doing chronic exercise, but the above is a great incentive to continue with the walking.

Exercise and Insulin Sensitivity

The role of exercise in promoting insulin sensitivity is something that I mention in my ebook (Hillfit: Strength) which I hope to launch in the next week.  The book presents a basic strength training routine for hikers, backpackers and hillwalkers explaining why strength is so important and its many health benefits.  I am sure I will promote the life out of the thing once it is available, but that is not the point of this post. 

I just wanted to point to this abstract of a study that I saw today:

The role of skeletal muscle glycogen breakdown for regulation of insulin sensitivity by exercise

Glycogen is the storage form of carbohydrates in mammals. In humans the majority of glycogen is stored in skeletal muscles (∼500 g) and the liver (∼100 g). Food is supplied in larger meals, but the blood glucose concentration has to be kept within narrow limits to survive and stay healthy. Therefore, the body has to cope with periods of excess carbohydrates and periods without supplementation. Healthy persons remove blood glucose rapidly when glucose is in excess, but insulin-stimulated glucose disposal is reduced in insulin resistant and type 2 diabetic subjects. During a hyperinsulinemic euglycemic clamp, 70-90% of glucose disposal will be stored as muscle glycogen in healthy subjects. The glycogen stores in skeletal muscles are limited because an efficient feedback-mediated inhibition of glycogen synthase prevents accumulation. De novo lipid synthesis can contribute to glucose disposal when glycogen stores are filled. Exercise physiologists normally consider glycogen's main function as energy substrate. Glycogen is the main energy substrate during exercise intensity above 70% of maximal oxygen uptake ([Formula: see text]) and fatigue develops when the glycogen stores are depleted in the active muscles. After exercise, the rate of glycogen synthesis is increased to replete glycogen stores, and blood glucose is the substrate. Indeed insulin-stimulated glucose uptake and glycogen synthesis is elevated after exercise, which, from an evolutional point of view, will favor glycogen repletion and preparation for new "fight or flight" events. In the modern society, the reduced glycogen stores in skeletal muscles after exercise allows carbohydrates to be stored as muscle glycogen and prevents that glucose is channeled to de novo lipid synthesis, which over time will causes ectopic fat accumulation and insulin resistance. The reduction of skeletal muscle glycogen after exercise allows a healthy storage of carbohydrates after meals and prevents development of type 2 diabetes.

None of that is particularly new or innovative of course - Google "insulin sensitivity exercise" and you will find a stack of papers - but this one came out today so I thought it worth highlighting.

Exercise and immunity

I saw this reported today in a couple of places - including on grough a UK outdoors website - anyway it is a report of recent research that looks at the impact of exercise on immunity, particularly as medated through natural killer cells (NK).

It is reported as saying that moderate exercise is good whereas chronic endurance exercise is a problem. It is not clear where strength training would fit in to this analysis:

The major players in this immune regulation are immune cells called Natural Killer (NK) cells which are important weapons in the fight against viral infections. NK cells recognise viral-infected cells as foreign invaders and force them to commit suicide." During moderate exercise the activity of NK cells is enhanced, whereas stressful endurance activities such as marathons can turn down NK cell activity. These changes are tightly regulated by stress hormones and other immune cells," explained Professor Gleeson.

There is a clear take-home message from our current understanding of the link between exercise and immune function. "Moderate exercise has a positive effect on the immune system. So to keep colds at bay, a brisk daily walk should help - it's all about finding a happy medium," said Professor Gleeson.

The research is reported here:  Couch potato or elite athlete? A happy medium keeps colds at bay!

Physical activity counteracts the effects of a toxic environment?

See what you make of this:  Comparison of urine toxic metals concentrations in athletes and in sedentary subjects

Cadmium (Cd), tungsten (W), tellurium (Te), beryllium (Be), and lead (Pb), are non-essential metals pervasive in the human environment. Studies on athletes during training periods compared to non-training control subjects, indicate increased loss of minerals through sweat and urine. The aim of this study was to compare the level of these trace elements, determined by inductively coupled plasma mass spectrometry (ICP-MS) in urine samples, between athletes and age-matched sedentary subjects living in the same geographical area, although anthropometric and cardiovascular measurements showed that athletes have significantly (P ≤ 0.001) lower BMI, body fat and heart rate, whereas the muscle and bone percentage was significantly (P ≤ 0.001) higher than in sedentary subjects. The validity of the methodology was checked by the biological certified reference material. Trace element analysis concentrations, expressed in μg/mg creatinine, of five toxic elements in urine from athletes (n = 21) versus sedentary subjects, (n = 26) were as follows: Cd (0.123 ± 0.075 vs. 0.069 ± 0.041, P ≤ 0.05); W (0.082 ± 0.053 vs. < limit of detection); Te (0.244 ± 0.193 vs. 0.066 ± 0.045, P ≤ 0.001), Be (0.536 ± 0.244 vs. 0.066 ± 0.035, P ≤ 0.001); Pb (0.938 ± 0.664 vs. 2.162 ± 1.444 P ≤ 0.001). With the exception of Pb, urine toxic metal concentrations from athletes were higher than from sedentary subjects. This fact suggests that physical activity counteracts, at least in part, the cumulative effect of toxic environment by increasing the urine excretion of toxic metals in trained people.

So sweating as a result of exercise helps the body to get rid of some of the crap that builds up in it from the environment.

Congruent Exercise - Part 1

It is rare that I am truly excited by a book, that writing will really stimulate me intellectually, with sets of ideas that connect and make sense.  I like it when that happens, when you find something "new" but which makes so much sense because it is not really new, it is obvious when you put the pieces together.  It is the logic of it I like, when things hold together in consistent ways.

Bill DeSimone's new book, Congruent Exercise, is exciting me!  I will put up a proper review in a few days, but I am really savouring it at the moment.  As I read each page there is a pencil in my hand and I am marking up key paragraphs.....then I find that I am marking the whole thing!

In this new book, Bill is covering much of the same material that was in his first book - Moment Arm Exercise - but he has refined his presentation and the whole argument is very clearly presented.

Moment Arm Exercise fascinated me and I used to study it like a text book, I still dig it out to check out the worth of different movements.  Congruent Exercise is more like a manifesto, a simple pulling together of premises to give a clear and logical prescription for exercise.  Safety is key to all this, designing movements that reflect proper joint and muscle function, informed not by "feel" or dogma, but anatomy and mechanics.

As I say, I'll put up a proper review in a few days, but for now suffice to say that this is the best book I've read this year.  You can get a copy at Bill's eBay store here, or read about the book on its Facebook Page.

I intereviewed Bill way back here and it is  interesting to see that some of the things we touched on in that interview are developed a bit in the new book - such as the role of postural muscles.


You can see some of his videos here.

Move More: Solutions to problems.

Continued from Eat Less, Move More: Solutions to problems.

Firstly, here's "On the rebound" by Floyd Cramer. This was a hit in 1961 and it was recently used in a Sainsbury's "Taste the Difference" advert on TV.


Move More: Problems and their solutions:
1) Exercise makes me eat too much afterwards. Wrap up warm before you go outdoors, as feeling cold stimulates appetite.

2) Exercise is boring. Take a camera with you when you go for a walk. Look around. There's lots of interesting stuff out there that you don't normally notice*. Vary your route so that you see new things each time. Zumba is fun!

3) It's too cold/wet/windy etc. Dress appropriately. Have a small treat when you get back, so that you have something to look forward to.

4) I hate doing "x". Don't do "x", then. Things that I will not do are swimming & team sports (really bad memories from school-days). I also won't do anything faster than a power walk (being 72" tall with 31" legs makes any exercise involving my feet hitting the ground uncomfortable and hard on my joints).

5) I don't have the time. Neither do I. I'm now on-line less than I used to be. I'm sure I'll survive!

*I spotted a large photovoltaic solar panel on the roof of a house the other day. I knocked on the door and asked the occupants about it. Apparently, you get about 1kW from 10 square metres of panel and the Electricity supplier pays you about 43p for every kWh you generate. A 35 square metre system costs about £20,000.

When I realised that I had to get some exercise, it was a blow. Any news that is bad & inevitable takes some getting used to. See Kübler-Ross model. I have now accepted it.

Here's a school photo from when I was about 10.


Can you guess which one's me?

Any more problems & solutions that I haven't thought of?

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.