The Elephant in the Room.

On Twitter, Max Roser tweeted the following plots:-

From Health and the Economy in the United States from 1750 to the Present

The low & stable men's BMI's until some time between 1945 & 1960 was thought-provoking.

1. Over-refined sugars & starches entered the US food supply in ~1880. Ref: How the Mid-Victorians Worked, Ate and Died. ∴ Over-refined sugars & starches don't cause obesity.

2. Americans ate more carbohydrate per day from 1909 to 1929 than they do now. Ref: 3rd Fig. from More Thoughts on Macronutrient Trends. ∴ Carbohydrates don't cause obesity.

3. The "low-fat" dietary guidelines were issued in 1980. The two dates at which men's BMI began to increase significantly are some time between 1945 & 1960 and after 1990. ∴ The 1980 "low-fat" dietary guidelines didn't cause obesity.

What happened in the US some time between 1945 & 1960 to make men's BMI increase? After World War 2, the economy was in a slump and something had to be done to get people to consume more, to stimulate economic growth. Corporations changed the way that they marketed to people. Instead of telling people facts about their products, they began to connect with people emotionally. It worked.

Edward Bernays pioneered the psychological tricks used by the Food Product Industry to get people to want things they didn't need and consume more. For more information about Edward Bernays, watch The Century Of The Self Part 1 of 4 Happiness Machines. The first 2 minutes summarise the rest of the documentary.

Watch also Unreported World: Obesity in Paradise. At 6:50, a Samoan explains why they prefer imported "crap-in-a-bag/box/bottle" instead of their own local food - local food is often seen as inferior to imported food. I wonder how that belief got into their heads? At 19:40, you can see an example of the inefficacy of healthy eating guidelines.

Young Asian Indians also prefer imported foods, as they are perceived to be of 'high quality' in comparison to locally produced products. That innate tendency is exploited by the food product industry. From Page 4 of the full version of Abdominal obesity and type 2 diabetes in Asian Indians: dietary strategies including edible oils, cooking practices and sugar intake :-

See How Big Business Got Brazil Hooked on Junk Food , Former advertising executive reveals junk food-pushing tactics & How big companies are targeting middle income countries to boost ultra-processed food sales.

Once a child has adopted poor dietary habits, it's difficult to reverse them. As children are easier to manipulate than adults, there are regulations aimed at restricting marketing to children, regulations which the Food Product Industry finds ways to bypass.
A systematic review of persuasive marketing techniques to promote food to children on television.
Persuasive food marketing to children: use of cartoons and competitions in Australian commercial television advertisements.
Persuasive techniques used in television advertisements to market foods to UK children.
Weekday and weekend food advertising varies on children's television in the USA but persuasive techniques and unhealthy items still dominate.
Influence of food companies' brand mascots and entertainment companies' cartoon media characters on children's diet and health: a systematic review and research needs
Beyond Food Promotion: A Systematic Review on the Influence of the Food Industry on Obesity-Related Dietary Behaviour among Children
Children’s everyday exposure to food marketing: an objective analysis using wearable cameras
The effect of screen advertising on children's dietary intake: A systematic review and meta‐analysis 
Exposure to Child-Directed TV Advertising and Preschoolers’ Intake of Advertised Cereals

See also Strategies and motives for resistance to persuasion: an integrative framework and A typology of consumer strategies for resisting advertising, and a review of mechanisms for countering them

EDIT: As facts are ineffective at countering food product marketing which connects with people emotionally, psychologists have found that an effective way to counter such marketing is anti-food product marketing which connects with people emotionally. See How to get teens to give up junk food: Tell them they’re victims of corporate manipulation & A values-alignment intervention protects adolescents from the effects of food marketing.


Chronic consumption of "crap-in-a-bag/box/bottle" products high in sugars and fats induces insulin resistance in the hypothalamus resulting in impaired satiety, increased hunger and an increase in food consumption. Ref: The role of fatty acids in insulin resistance.


One of Edward Bernays's psychological tricks is confusing the public by promulgating conflicting information. The Tobacco Industry paid health professionals to advertise cigarettes. On the one hand, you had researchers telling people that smoking was bad for them and on the other hand you had a doctor on TV saying that he preferred to smoke Camel cigarettes. This confused the public and made them mistrust researchers & science. Another dirty trick was setting-up organisations with scientific-sounding names to promulgate conflicting reports which the press published as “science”, saying that “X” was good for you, then some time later “X” was bad for you, then some time later “X” was good for you again and so on. The public mistrusted researchers & science even more.

The recent NOF report from Malhotra et al telling people to eat more fat is conflicting information, resulting in more public confusion and more mistrust of researchers & science.

The Tobacco Industry used Bernays's psychological tricks to encourage women to smoke in public by making smoking a women's rights issue. Cigarettes were marketed to women as "Torches of Freedom". From the 1920's, women became as free as men to greatly increase their risk of getting Emphysema a.k.a. Chronic Obstructive Pulmonary Disease, Lung Cancer & Coronary Heart Disease, while the Tobacco Industry's profits increased.

By wrongly focusing on foods/macronutrients/micronutrients/eating guidelines etc, people like Taubes, Teicholz, Malhotra, Noakes etc are helping the Food Product Industry to continue manipulating the masses to over-consume over-refined Food Products.

What happened in the US after 1990 to make men's BMI increase? As total kcals/day didn't start to increase significantly in 1990 (see 2.), it wasn't due to food intake starting to increase significantly. See https://twitter.com/KlausKblog/status/867772729264447488  Energy expenditure didn't decrease significantly. Maybe it was the Pharmaceutical Industry. See https://www.statista.com/statistics/184914/prescription-drug-expenditures-in-the-us-since-1960/

Some medications cause weight gain by increasing water retention, and they are heavily prescribed. See https://www.independent.co.uk/life-style/health-and-families/health-news/huge-weight-gains-reported-by-patients-on-prescription-drugs-5333581.html

See also The cause of America's rising obesity rate is irrelevant. The cure for it is what's important.

In starvation or ketosis, protein should have NO EFFECT on blood glucose level, not RAISE it.

From Blood Sugar is Stable:-

In a healthy person, BG (blood glucose) is held at a fairly constant value by a NFB (negative feed-back) loop. See Blood Glucose, Insulin & Diabetes.

When protein is eaten, this produces a glucagon response from pancreatic alpha cells, which tries to raise blood glucose level by stimulating the liver to convert liver glycogen plus water to glucose. Protein also produces an insulin response from pancreatic beta cells, which tries to lower blood glucose level by a) increasing glucose uptake from the blood and b) inhibiting HPG (hepatic glucose production). The net result is no change in BG level.

In extended fasting or on VLC (very low carbohydrate)/ketogenic diets, there's no liver glycogen left after ~1 day.
∴ The glucagon response has no effect on HGP.

The insulin response still has an effect, until the 1st phase insulin response is lost*.
∴ Blood glucose tries to decrease, but the HPAA keeps it steady by raising cortisol level.

RE How eating sugar & starch can lower your insulin needs: Blood glucose level on a VLC/ketogenic diet can be RAISED, due to the BG NFB HPAA (hypothalamic pituitary adrenal axis) loop not having a precise set point with the cortisol/adrenaline response (hyperglycaemia is not fatal, whereas hypoglycaemia can be fatal, as the brain always needs some glucose to function (~50%E from glucose)).

So, how come people on LCHF (low carbohydrate, high fat) diets can have normal or slightly low BG levels?

1. Luck. The BG NFB HPAA loop isn't very precise.

2. Excessive intake of Booze. Ethanol inhibits HGP (dunno about RGP (renal glucose production)).

3. Insufficient intake of Protein. This deprives the liver & kidneys of glucogenic amino acids (Alanine & Glutamine are the 2 main ones), forcing BG down and making the HPAA run open-loop and raise cortisol level. There's another source of Alanine & Glutamine available - Lean Body Mass. Uh-oh!


Consuming more protein on extended fasting or a VLC/ketogenic diet can result in higher BG level for three reasons.

1. It allows the HPAA to run closed-loop, as it's supposed to.

2. The lack of a 1st phase insulin response* in people with IR/IGT/Met Syn/T2D results in a temporary BG level spike with the intake of rapidly-absorbed proteins e.g. whey. There's an unopposed glucagon response, until the 2nd phase insulin response begins.

See http://care.diabetesjournals.org/content/early/2015/11/29/dc15-0750.abstract

*Long-term carbohydrate restriction causes loss of the 1st phase insulin response. See https://carbsanity.blogspot.co.uk/2013/10/insulin-secretion-in-progression-of.html

P.S. This only applies to people who have sufficient liver glycogen, due to them eating some (50 to 100g/day, say) carbohydrate.

3. Hepatic Insulin Resistance results in the insulin response inadequately suppressing Hepatic Glucose Production. As 50g of protein (an 8oz steak, say) yields ~25g of glucose from glucogenic amino acids, there's an increase in the amount of glucose entering circulation, which raises BG level.

See https://academic.oup.com/bja/article/85/1/69/263650

Doctor in the House – Watch Diabetes Not Being Reversed Using Low Carb on BBC, While LCHF'ers Freak Out.

This post is about Doctor in the House – Watch Diabetes Reversed Using Low Carb on BBC, While Old-School Dietitians Freak Out.

The YouTube videos may be gone, but the image lives on!
Available to view in the UK on iPlayer 'till 19.12.15 at https://www.bbc.co.uk/iplayer/episode/b06q6y95/doctor-in-the-house-episode-1

In Dr. Eenfeldt's blog post, he makes some schoolboy errors.

1. T2DM (type 2 diabetes mellitus) Reversed with LCHF (low-carb, high-fat) diet. Uh, nope!
a) Sandeep's HbA1c fell from 9.0 to 7.0, which is an improvement but by no means a reversal, as Dr. Chatterjee agrees in https://twitter.com/drchatterjeeuk/status/669875378568171520.
b) Sandeep has T2DM, not T1DM. See When the only tool in the box is a hammer...
Sandeep's BG (blood glucose) went down on LCHF, but what about his dyseverything elseaemia? *sound of crickets chirping*

2. Old-school dietitians freak out. Uh, nope!
In BDA alarmed by controversial and potentially dangerous advice in BBC’s ‘Doctor in the House’, Dr. Duane Mellor sounds pretty cool, calm & collected (though I expect that he sustained injuries from all of the eyeball rolling, as he had to refute for the umpteenth time yet another load of LCHF bullshit).

3. He plays the Shill Gambit card.

Oh, the comments! In typical echo-chamber fashion, LCHF commenters praise Eenfeldt's flawed points. I wonder how long my comment will stay up for?

My comments on the programme (c/p'ed from Facebook):-
"6 minutes in. I think that Priti is deficient in Magnesium (Mg), from her stress levels, anxiety, headaches and difficulty in getting to sleep. Blood tests are useless, as they don't correlate with Mg stores. Need CSF (cerebrospinal fluid) test (lumbar puncture - very painful).

12 minutes in. Priti's blood test results normal. Sandeep has hypovitaminosis D, which is a cause of IR (insulin resistance, it's what caused mine). This important fact is not mentioned. unsure emoticon See http://www.ajcn.org/content/79/5/820.full.pdf

16 minutes in. Talked about sugar in foods & drinks but ignored the large amount of cheese that Sandeep ate earlier. Cheese is *very* energy-dense. Sandeep has been in positive Energy Balance for *way* too long.

24 minutes in. Priti's getting sugar cravings in the morning. Lack of Magnesium also causes IR & poor BG regulation. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4549665/

29 minutes in. HIIT (high-intensity interval training) for Sandeep is good for increasing his IS, but little use for reducing his VAT (visceral adipose tissue). You can't out-run your fork.

33 minutes in. Walking for Priti to lose weight? You can't out-walk your fork. If 1,000 steps takes 10 minutes and burns an extra 40kcals, then 10,000 steps takes 100 minutes and burns an extra 400kcals = one chocolate bar.

33:47 minutes in. Sareena has had a full-time job working indoors for the last year. Less sun exposure = falling Vitamin D3 level = deteriorating immune system, deteriorating mood & deteriorating IS. See https://nigeepoo.blogspot.co.uk/2008/12/vitamin-d.html

I don't think that I can watch much more of this programme!"

followed by:-
"In conclusion:-
1. Anyone who suffers from chronic anxiety is probably deficient in Mg.

2. Anyone who lives in the UK (United Kingdom :-D) and has coloured skin and/or works indoors is probably deficient in Vitamin D3.

3. ~85% of people who have T2DM have excessive VAT. Asians who were skinny in early adulthood have limited SAT (sub-cutaneous adipose tissue) hyperplasia, resulting in small skin-folds but large bellies. A LCHF diet is not suitable for over-fat people with T2DM. It should be a LCLF diet i.e. a low-calorie diet, to deplete over-full cells. Calories count.

4. You can't out-walk/run your fork.

5. Dr Chatterjee has a strong bias. This is not a good trait for someone who's supposed to be practising Evidence Based Medicine."

It's interesting that Priti is fatter than Sandeep, yet Priti doesn't have T2DM and Sandeep does. Priti was most likely fatter than Sandeep in their respective childhoods, for whatever reasons. Priti had more SAT hyperplasia than Sandeep, so she has more storage capacity for dietary fat than Sandeep does. Priti can gain more SAT, which protects her from developing T2DM. Sandeep can't, so he gains VAT, which has limited storage capacity and is more metabolically-active than SAT.

See also Adipocyte Hyperplasia - Good or Bad? and A *very* special dual-fuel car analogy for the human body that I just invented.

Science and zealots: How to detect bad science and how to detect zealots.

Last night, I got banned from Zoë Harcombe's blog. More on that later. Meanwhile, this...

From http://capisho.blogspot.co.uk/2013/07/science-vs-faith.html

I re-read It's all about ME, baby! (1997 - present) and there's something important missing.

In 2005, I discovered Lyle McDonald. Before this happened, I had the following beliefs:-
1. If something works for me, it must work for everyone else.
2. If someone with qualifications states a fact, it must be true.
3. If someone without qualifications states a fact, it must be false.
4. If a study confirms my beliefs, it must be true.
5. If a study contradicts my beliefs, it must be false.

Sound familiar?
1. is a "Hasty generalisation" fallacy.
2. is an "Appeal to authority" fallacy.
3. is an "Ad hominem" fallacy.
4. & 5. are "Cherry-picking" fallacies.

Suffice it to say, Lyle bitch-slapped the fallacies out of me. Thank you so much! Read Lyle's site, if you want to learn.

How can studies conflict with each other so much?

Having read a number of conflicting studies, here are some of the tricks that bad studies use:-

1. Fudge the methodology:-
a) In a meta-study (a study of studies), to make something that's bad (e.g. some types of saturated fats/fatty acids) look harmless or to make something that's good (e.g. Vitamin D) look useless, fudge the inclusion criteria so that only studies using low intakes or a narrow range of intakes are used, so that the RRs are either close to 1 or have 95% CI values above & below 1. In addition, include studies that show both positive and negative results (due to them looking at different types of saturated fats/fatty acids, say), so that the overall result is null. See Siri-Tarino et al, Forests & Trees and "Eureka!" moments.

b) In a meta-study, set the Δintake to values that are much smaller than a typical portion. See Milk and dairy consumption and risk of cardiovascular diseases and all-cause mortality: dose–response meta-analysis of prospective cohort studies.

c) In a study, use a different type of the thing being studied (but bury this fact somewhere obscure so it's missed) to get the opposite result. e.g. To make "carbs" look bad, use a test "carb" that comprises 50% simple carbs (fructose) and 50% complex carbs (maltodextrin), thus guaranteeing a bad outcome (high % small LDL particles). See https://www.ncbi.nlm.nih.gov/pubmed/?term=Krauss%20RM[Author]%20AND%20Dreon%20DM[Author]%20AND%20(hasabstract[text]%20AND%20%22humans%22[MeSH%20Terms])

2. Fudge the statistics:- e.g. Regression toward the mean. I'm not a stats nerd, but there are many ways to lie with statistics.

3. Make the abstract have a different conclusion from the full study (which you hide behind a pay-wall), by excluding the methodology & results.


Back to Zoë Harcombe: I left some comments on Jennifer Elliott vs Dietitians Association of Australia.

My M.O. for detecting zealots is by using a slowly, slowly, catchee monkey approach. I left a comment supportive of low-carb diets, because:-

For people with Insulin Resistance, low-carb diets DO ameliorate obesity, postprandial sleepiness and postprandial hyperglycaemia.

Was that loud enough?

I added that I thought the first priority should be to tackle the causes of the Insulin Resistance, because permanently reversing a condition is better than merely ameliorating it.

My comments were helpful, with links to blog posts showing the above and how to reverse T2DM in 8 weeks.

I then "went in for the kill" and strongly criticised Jennifer Elliot's article, as it contained cherry-picked references. I included three more links to my blog as supportive evidence. This resulted in the removal of all but one of my comments (and the comment that remained had the link removed) and the addition of the following comment:-

"Zoë Harcombe says:

October 23, 2015 at 8:55 pm

Nigel – too many comments purely trying to get traffic to your site – link above removed; other comments spammed. You’re now spammed.
Best wishes – Zoe"

The correct word is "banned", Zoë! Spammers try to sell something. My information is free.
Low-carb zealot successfully detected.

It's not a problem if a lay person becomes a low-carb zealot, but it is a problem if a Doctor/Health Professional/Fitness Trainer becomes one. Cognitive bias and a refusal to accept contradictory evidence are not healthy traits for someone who's supposed to be practising evidence-based medicine/health/fitness.

Variations in weight change for a given Calorie change - An Engineer's Perspective.

Another techie post, inspired by Insulin Doesn't Regulate Fat Mass. Consider the inverting amplifier using an Op-Amp, below:-

From HERE

As the amplifier is inverting (i.e. a ↑ input on V_in results in a ↓ output on V_out), the feedback from V_out via R₂ opposes V_in via R₁ at the - terminal of the Op-Amp.

If R1 = R2 and V_in changes from 0V to 1V, the change in V_- (the voltage on the - terminal of the Op-Amp) varies with A (the magnitude of the Op-Amp gain) as follows*:-

A_____________Change in V_-(V)
∞_____________0
1,000,000_____~0.000001
1,000_________~0.001
100___________~0.01
10____________~0.08
8_____________0.1
5_____________~0.14
3_____________0.2
2_____________0.25
1_____________~0.33
0_____________0.5

As the body operates on biochemical principles, slopes of input/output transfer functions aren't steep at their steepest points. E.g.

From http://bja.oxfordjournals.org/content/85/1/69.long

Therefore, the gains in the various parts of the Leptin "adipostat" NFB loop are not very high. Therefore, there will be a significant variation in weight change vs Calorie change, and there will be significant variations in the variation due to loop gain variations from person to person.

Insulin Resistance makes the slopes of  the above input/output transfer functions shallower, reducing the gain in the system. This increases the variation in weight change vs Calorie change. For ways to reduce Insulin Resistance, see Insulin Resistance: Solutions to problems.

*In case anyone thinks that I've made the numbers up, here's the maths:-
Current in/out of the - terminal of the Op-Amp = 0.
∴ I_R1 = I_R2
I set R1 = R2 to keep the maths simple. By Ohm's Law, V = I * R.
∴ V_R1 = V_R2
With a 0V input:-
All currents & voltages = 0.

With a 1V input:-
V_R1 = 1 - V_-
V_R2 = V_- - V_out.  As V_out is negative, - V_out is positive.
- V_out = A * V_-
∴ V_R2 = V_- + (A * V_-)
∴ 1 - V_- = V_- + (A * V_-)
Rearranging:-
1 = (2 * V_-) + (A * V_-)
Dividing both sides by V_-:-
(1/V_-) = 2 + A
∴ V_- = 1/(2 + A)

Dear ItsTheWoo, how do you do?

This post is attacking what I consider to be faulty reasoning. It's not a personal attack on ItsTheWoo, who I like (even though she drives me up the wall, sometimes!).

From http://hypetrak.com/2011/10/mayer-hawthorne-how-do-you-do-full-album-stream/

See What I believe and what I don't.
The basic The Energy Balance Equation:- Change in body stores = E_in - E_out
For a detailed mathematical analysis of weight change, see Completing the trine: vive la différence!

From Back to black, CIAB, pharmaceutical drug deficiencies & nerds:-
Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.


The faulty reasoning is in Dear Nigel and other CICO zealots: you are ignorant. Charming!

I'll quote passages from it and refute them, one by one.

• "With a zero caloric deficit, there is zero weight change"

"FACT: Calories neither determine weight OR body composition with certainty. Nigel / some CICO zealots may agree body composition changes are privy to nutrition, but wt is 100% controlled by calories. This is something they pretty much made up and biological science does not at all support this idea. Calories neither control body composition OR body weight/mass with any certainty. The bulk consumed with fork and spoon does not need to stick on your body in the form of a mass laden tissue, ever."
Calories determine weight change. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned). It would have been nice if Fig. 6 had contained a plot of "Effect of energy intake on change in body weight", but it didn't.
LBM = Lean Body Mass
FM = Fat Mass = Body Fat
Weight change = LBM change + FM change
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36
∴ A calorie IS a calorie (where weight change is concerned).
∴ Insufficient protein can result in loss of LBM (bad).

The main thrust of ItsTheWoo's argument is that inter-personal variations in weight gain from subject to subject, invalidates Bray's conclusion. It doesn't.
Some subjects become more energetic on a 40% caloric surplus, which increases their NEAT & TEA, which increases their Eout, which reduces their weight gain.
Some subjects don't change their energy on a 40% caloric surplus, which doesn't change their NEAT & TEA, which results in intermediate weight gain.
Some subjects become less energetic on a 40% caloric surplus, which decreases their NEAT & TEA, which decreases their Eout, which increases their weight gain.

I believe that the Insulin Sensitivity (IS) of the subject determines which category they fall into and by how much. The higher the IS, the higher the energy, as high IS results in low serum insulin, which minimises sedation. Energy Balance always applies.

I've never stated that Calories exactly determine weight change. That's a strawman.
I've never stated that Calories determine body composition. That's a strawman.

•  " Every subject [in bray's overfeeding study] gained weight (mostly fat mass) during the 40% energy excess overfeeding period. "

"Again, making crap up. There is NO RULE IN BIOLOGY which states all consumed energy must be retained as body mass. Indeed most typical people gain fat during overfeeding (with great resistance/inefficiency of fat gain), but it is indeed possible to hardly gain any or none at all as in constitutional thinness. What happens during calorie consumption among different people (and perhaps, different DIETS and different TIMES and different ENDOCRINE situations...) is a wild card determined by the biology i.e. neuroendocrine functions of the animal in question. There is NOTHING about physics which reflects / informs physiology other than the basic fact the latter exists within the former (which, again, tells us NOTHING ultimately). How organisms process consumed nutrition is not a physics question. There is no freakin' law of physics or physiology for that matter which states nom nom time = thigh chub. You don't have to wear that pizza as a popeye's muscle or as a shelf butt."
Somewhere within all of the irrelevant waffle about rules & laws, ItsTheWoo raises an interesting point. Although a caloric surplus is always required for weight gain, eating more Calories can sometimes result in zero weight gain. How so? From ItsTheWoo's link:-
"Conclusion: This data is the first to demonstrate a resistance to weight gain in constitutional thinness (CT) population in response to 4-week fat overfeeding, associated with an increase in resting energy expenditure and an emphasised anorexigenic hormonal profile.
In CT people, their energy expenditure increases in line with their energy intake. Therefore, even though they're eating more Calories, there's no caloric surplus, therefore there's no weight gain. Energy Balance always applies.

• "Yes, kcals do get wasted. You don't understand things quantitatively i.e. how many kcals get wasted."

"I know anxious/obsessional people like the safe feeling of balancing calories. The fact reality is more complex and you can't just enter things in a phone app and be ASSURED of what is going on in your body, doesn't invalidate the truth of the fact metabolic reactions are more complex THAN CALORIES.

Just because it is *impossible* for a reasonable free living human to quantify all of the metabolic, endocrine, nervous system factors influencing adipocyte growth changes does not mean they don't fucking exist."
ItsTheWoo left out my calculations. Here they are:-"if I eat 2000 calories of a ketogenic diet in 3 hrs, most of it is wasted as heat, physical energy (I know, because I am EXTREMELY warm/energetic) and then the rest of time i am using a relatively greater percent of stored fat."
Do you know at what rate you're burning-off extra energy intake as heat energy output when you're "EXTREMELY warm/energetic"? Here's an estimate:-
If the mean TEF for your meal is 11% (assuming your meal is 50%E protein & 50%E fat), that's 220kcals (921kJ) "wasted" as heat energy. That'll make you feel EXTREMELY warm, as 220kcal raises the temperature of 57kg of water (your body) by 3.84°C.

A 2,000kcal meal (a whole day's worth of food) takes a lot longer than 3 hours to digest & absorb. I'll guesstimate it as 24 hours. 921kJ of extra heat power over the course of 24 hours = 10.7W, which is an increase of 17.7% over your normal Metabolic Rate of ~60W heat power (~1kcal/minute).
It's easy to "prove" something by being vague. That's PSEUDOSCIENCE. I do science. If you do the maths, you can see that, of the 2,000kcal ketogenic meal, most of it isn't wasted as heat, because if most of it is wasted as heat, ItsTheWoo would spontaneously combust!

• "Dr. Robert C. Atkins made the same fundamental cock-up when he said that humans pissed-out loads of kcals of ketones each day, giving a Metabolic Advantage to ketogenic diets."

"1) The advantage of a ketogenic diet (non-fasting) does exist, so it's not a 'cock up", even if his mechanism was wrong.
2) If atkins was wrong (you pee out all LCHF food) who cares? That was 30+ years ago. He was a cardiologist who observed a VLC diet made him slim. He used his medical education to hypothesize a reason why. His hypothesis was wrong, but his observations were right. This happens all the time in science or basic human reasoning; make observations, form hypothesis. The hypothesis may be wrong, the findings are STILL RIGHT (i.e. low carb diets DO make slim, just not via peeing away ketones)."
1) There is no Metabolic Advantage to ketogenic diets. See https://www.jbc.org/content/92/3/679.full.pdf
2) Atkins' observations were wrong. See The Battle of the Diets: Is Anyone Winning (At Losing?)
a) Low-Carb diets work better than High-Carb diets for people who are Insulin Resistant.
b) Low-Carb diets work worse than High-Carb diets for people who are Insulin Sensitive.
c) Low-Carb diets work the same as High-Carb diets for everybody in Metabolic Ward Studies.
If there's a Metabolic Advantage to ketogenic diets, they would work better than high-carb diets all the time. They don't. See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes for my hypothesis, which explains a), b) and c).

Some thoughts on the essentiality of dietary carbohydrates.

I didn't know that there's a watch strap called Essentiality. I do, now.

From http://svpply.com/item/3229602/Swatch_Skin_Collection_Silver_Essentiality

This is a book-marking post for thoughts I had in https://www.facebook.com/TheFatEmperor/posts/1442430506020812.

"The human body does not need carbohydrates from an external food source, because it is capable of very precisely and correctly assembling its own amounts of glucose that is needed in very small amounts for auxiliary and specialized functions." - Igor Butorski.

1) It's not precise. See How eating sugar & starch can lower your insulin needs.

2) It's not enough to fuel sustained medium-intensity exercise for everybody EDIT: if there's insufficient protein intake. See "Funny turns": What they aren't and what they might be and Everyone is Different.

From Blood Sugar is Stable:-

After liver glycogen has been depleted in starvation or on Nutritional Ketosis (Ketogenic Diets with less than 14% of total energy from Protein), total glucose production from liver & kidneys is ~100g/day.

From It's all in a day's work (as measured in Joules), the body oxidises carbohydrate at a rate exceeding ~4g/hour at exercise intensities exceeding ~25%, on a LCHF diet. This is unsustainable.

EDIT: If protein is consumed, total glucose production increases, up to a maximum of ~400g/day.

3) It's wasteful. Glucose production from protein converts ~50% of the most expensive macronutrient (protein) into the cheapest macronutrient (carbohydrate). It creates expensive urine, as the nitrogen part of amino acids is detoxified by being converted into urea by the liver and then wee'ed out by the kidneys.

4) Using the above argument, the human body does not need saturated fats & monounsaturated fats from an external food source, because it is capable of very precisely and correctly assembling its own amounts of saturated fats & monounsaturated fats (out of carbohydrate) that are needed in very small amounts for auxiliary and specialized functions.

If we consume only Essential Fatty Acids, Essential Amino Acids, Vitamins, Minerals, Fibre/Fiber, Water & Anutrients, there won't be much to eat. Also, there won't be a source of chemical energy to generate heat energy & mechanical energy. That's what dietary carbohydrates & fats are for!

Respiratory Exchange Ratio/Respiratory Quotient (RER/RQ) varies with carbohydrate & fat intake, as the body preferentially oxidises the fuel that's most readily available, when it's working properly. If it's not working properly, due to Insulin Resistance (IR), fix the IR rather than kludge the diet (by eating LCHF) to compensate for it. See Insulin Resistance: Solutions to problems for how to do this.

RER/RQ varies with Exercise Intensity.
Low-intensity exercise results in mostly fats being oxidised.
High-intensity exercise results in mostly carbohydrates being oxidised.
Medium-intensity exercise results in a mixture of fats & carbohydrates being oxidised.

Why you really can't outrun your fork.

Hat-tip to Yoni Freedhoff.

From http://www.blacksheepfitness.co.uk/you-cant-outrun-your-fork.html

See Effect of school-based physical activity interventions on body mass index in children: a meta-analysis.
"Meta-analysis showed that BMI did not improve with physical activity interventions (weighted mean difference -0.05 kg/m², 95% confidence interval -0.19 to 0.10). We found no consistent changes in other measures of body composition."

Some people believe that if going to the gym isn't making them lose weight, they're not exercising hard enough. Chronically over-exercising can chronically raise serum cortisol, which makes the kidneys retain water, causing a stall in weight-loss, as well as causing raised fasting blood glucose, irritability, poor memory and a slower metabolic rate, due to the reduced conversion of thyroxine into tri-iodothyronine.

Don't over-exercise!

A healthy body weight is made in the kitchen, not the gym. Buy produce, cook it and eat it!

Although I totally support the use of low-carbohydrate/calorie diets for people with insulin resistance or Type 2 diabetes, now that I'm no longer insulin resistant, I can eat natural carbohydrates, without any problems.

A medium-sized (orange-fleshed) Sweet Potato takes only 4 minutes to bake in its jacket in a 700W microwave oven. The flesh is moist & sweet, unlike that of a Yam or potato.

I eat the whole thing, including the jacket. It's very filling and I'm still able to lose weight. For active and insulin sensitive people, a Kitavan-style diet is absolutely fine.

How low & very low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people lose more weight on low-carbohydrate diets than on high-carbohydrate diets and insulin sensitive people lose more weight on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes's carbohydrate/insulin hypothesis of obesity is correct, everyone would lose more weight on low-carbohydrate diets than on high-carbohydrate diets. This isn't the case, therefore Gary Taubes's hypothesis is not correct.

Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies".

The Aragon Insulin Fairy

The Energy Balance Equation

Change in Body Stores = Energy in - Energy out, where... 

Energy in = Energy entering mouth - Energy exiting anus, and... 

Energy out = BMR/RMR + TEF + TEA + SPA/NEAT

See The Energy Balance Equation to find out what the above terms mean.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. See Control of overshoot for more information.

1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Body stores increase. There are also accusations of gluttony & sloth!

2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Body stores decrease.

In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.

There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587

In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.

Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Insulin Resistance can be fixed. See Insulin Resistance: Solutions to problems.

Type 2 Diabetes can also be fixed. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Aim to fix the problem. If it's impossible to fix the problem, a low-carbohydrate diet as an adjunct to medication is fine.

How a B.Sc.(Hons) in Electronic Engineering is relevant to Diet & Nutrition.

The human body regulates various processes using negative feedback loops. Here's blood glucose regulation.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Here's a generic Hypothalamus-Pituitary-X Axis loop, where X may be thyroid, adrenal, gonadal etc.

From http://www.studyblue.com/notes/note/n/ch-47-chemical-signals-in-animals/deck/3085387

Electronic Engineers understand how negative feedback systems work, such as phase-locked loops & amplifiers.

Negative feedback control systems can overshoot, especially if there's a delay in the feedback path that's longer than the rise time of the input step.

An example of this is the first-phase insulin response. Loss of the first-phase insulin response occurs in over-fat people who are hyperinsulinaemic. Without the first-phase insulin response, there's a delay between an increase in blood glucose and an increase in insulin secretion. A rapid upwards step in blood glucose (say, from eating a high-GL meal) causes a massive overshoot in insulin secretion, resulting in postprandial sleepiness, also down-regulation of insulin receptor activity in the appetite centres of the brain, causing ravenous hunger when the insulin level falls to normal.

See also Blood Glucose, Insulin & Diabetes.

People shouldn't be too quick to write-off the knowledge of an Electronic Engineer who's delving into the mysteries of the human body.

I'm NOT a lipophobe, I'm a very naughty boy!

First, postprandial triglycerides again. From Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, here's a plot of HR for future CHD vs TG's at various times after eating.

Hazard ratio (HR) and 95% confidence interval (CI) for highest vs lowest tertiles of triglyceride level (see Table 3 for values), adjusted for age, blood pressure, smoking, hormone use, levels of total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and high-sensitivity C-reactive protein level.

Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.

It's been suggested that IR might increase PP TG's in the 2 - 4 hour period due to impaired clearance. According to Fig. 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism, TG clearance in healthy men doesn't significantly start until after 4 hours has elapsed. Therefore, an impairment in TG clearance isn't going to make a significant difference to TG level in the 2 - 4 hour period.

Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.

What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.

FAO the over-fat and/or those with metabolic syndrome: Big breakfast, medium lunch & small dinner is beneficial.

Breakfast like a King/Queen.

Go to work on an egg.

According to High caloric intake at breakfast vs. dinner differentially influences weight loss of overweight and obese women.
"High-calorie breakfast with reduced intake at dinner is beneficial and might be a useful alternative for the management of obesity and metabolic syndrome." See the other PubMed studies listed in the above study, which corroborate it.

What about all the "artery-clogging" cholesterol in egg yolks? See Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism.

Resistance is useless!

...said the Vogon guard. If that means nothing to you, watch this...


You probably know all about Insulin Resistance (IR) if you've read my blog for some time, as I may have mentioned it once or twice ;-) There's also Leptin Resistance (LR) in the brain, which reduces the amount of appetite suppression that leptin is supposed to produce. Robb Wolf's just written about Adrenaline Resistance (AR?) and chronically-high serum cortisol seems to induce Cortisol Resistance (CR?) in the hippocampus, resulting in poor short-term memory.

When the level of "X" in the blood is low most of the time, "X" receptors in the body up-regulate, so when the level of "X" in the blood goes high, it has an effect. When the level of "X" in the blood is high all of the time, "X" receptors in the body down-regulate, so when the level of "X" in the blood goes higher, it has a reduced effect.

The above suggests that regularly "grazing" on food is not a good idea, as this results in a fairly constant slightly elevated serum insulin level. Eating a meal, not eating for a few hours then eating another meal results in high serum insulin while the meal is being absorbed and low serum insulin for the rest of the time.

Impaired Glucose Tolerance: also between a rock and a hard place.

A high percentage of people with excessive visceral adiposity (belly fat) have Impaired Glucose Tolerance (IGT). This post is about them.

Image from http://carbsanity.blogspot.co.uk/2013/03/insulinproinsulinetc-in-normal-igt-and.html

IGT is caused by excessive NEFAs spewing into the blood and/or deficiencies and/or sedentariness.

If nothing is done about it, IGT will progress to full-blown Type 2 Diabetes, which will get worse and worse as per the graphs to the right of the IGT one.

To do something about it, see http://nigeepoo.blogspot.com/2011/02/insulin-resistance-solutions-to.html

Type 2 diabetes: your good signalling's gonna go bad.

A little bit of Tammy Wynette.

 

Good signalling:

There's a famine. You've got nothing to eat. Your body's glycogen stores have just run out. What happens next? As food intake is zero, serum insulin level is minimised, so lipolysis (fat mobilisation) is maximised. Serum NEFAs are maximised. High serum NEFAs provides fuel for tissues that utilise NEFAs (e.g. skeletal muscle) and a "stop utilising glucose!" signal, in conjunction with low serum insulin.

High serum NEFAs and low serum insulin increase ketogenesis in the liver, to give the parts of the brain that can utilise ketones an alternative choice of fuel, to reduce glucose utilisation to a minimum. Ditto for nerves. Glucose utilisation must be minimised during a famine, as it's generated by the liver & kidneys from glucogenic amino acids, obtained from lean body mass (LBM) by hypercortisolaemia.

Gone bad:

You're a type 2 diabetic with a fat belly. For reasons that I don't fully understand (better blood supply? close proximity to liver?), belly fat deposits spew NEFAs into the blood at a much higher rate than arm, boobs, love-handles, bum & thigh fat deposits. On a very-low-carb diet (less than 50g/day carbs), serum insulin level is minimised, so lipolysis (fat mobilisation) is maximised. Serum NEFAs are maximised. High serum NEFAs provides fuel for tissues that utilise NEFAs (e.g. skeletal muscle) and a "stop utilising glucose!" signal, in conjunction with low serum insulin.

A type 2 diabetic with a fat belly has underlying insulin resistance, due to over-full muscle, adipose and/or liver cells (making the liver spew glucose into the blood at too fast a rate, and the muscles & adipocytes take it out of the blood at too slow a rate). The very-low-carb diet makes the underlying insulin resistance worse and high serum NEFAs in a milieu of caloric sufficiency or excess wreak havoc. Serum glucose level increases. Serum LDL-c level increases. Serum TG level increases. Serum just about everything level increases, except for serum HDL-c level, which decreases.

Type 2 diabetes: between a rock and a hard place.

About 85% of type 2 diabetics have excessive visceral adiposity (belly fat). This post is about them.

Which is better - the rock or the hard place?

 

1) The rock:

This is serum glucose. People with type 2 diabetes can measure their own serum glucose. Eating carbohydrates makes serum glucose increase, the rate of increase being proportional to the glycaemic index and the magnitude of the increase being proportional to the grams of carbs consumed. By limiting the intake of dietary carbohydrates, large spikes in serum glucose can be avoided. The occasional spike above 7.8mmol/L (140mg/dL) doesn't hurt. It's spending long periods of time above 7.8mmol/L that's harmful (by glycation).

A low-carb diet (~150g/day of carbohydrate) halves serum glucose fluctuations compared to a higher-carb diet (~300g/day of carbohydrate). A very-low-carb diet (~75g/day of carbohydrate) further halves serum glucose fluctuations compared to the low-carb diet. This seems like an improvement, at first glance.

2) The hard place:

This is the invisible "elephant in the room", as it's not measured by doctors and people with type 2 diabetes can't measure it themselves. It's serum Non-Esterified Fatty Acids, or NEFAs (a.k.a. Free Fatty Acids, or FFAs). Serum NEFAs are high when fasting and fall after eating foods that raise serum insulin (carbs & certain proteins). People with type 2 diabetes and excessive visceral fat (belly fat) have higher-than-normal serum NEFAs due to adipocyte insulin resistance (IR). See Insulin Resistance: Solutions to problems.

Just like with serum glucose, there's nothing wrong with serum NEFAs going up & down. It's chronically-high serum NEFAs that's harmful (except during periods of caloric restriction). See Showing posts sorted by relevance for query NEFA "type 2 diabetes" .

See Fig. 1 in Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet. On a very-low-carb (less than 50g/day carbs) diet that's not calorie-restricted, serum insulin remains low all of the time. To insulin-haters, that sounds like a good thing. Unfortunately, it means that there is no insulin spike to suppress serum NEFAs by shifting the balance of NEFAs going in/coming out of fat cells. Serum NEFAs stay high all of the time, which is harmful.

Therefore, people who have type 2 diabetes and excessive visceral fat and who are permanently on a very-low-carb diet that's not calorie-restricted are harming themselves.

Type 2 diabetes in the UK.

From Insulin usage in type 2 diabetes mellitus patients in UK clinical practice: a retrospective cohort-based analysis using the THIN database:-

"Importantly, this analysis has been conducted using routine data from UK clinical practice, which allows an insight into how patients are managed in current UK practice. In summary, this study demonstrates a persisting delay both in oral therapy escalation and insulin initiations in patients with type 2 diabetes, with a relative reduction in the effectiveness of oral therapy escalation. There is an apparent threshold HbA1C of > 8.5% beyond which additional oral therapy in routine practice appears unlikely to achieve an HbA1C target ≤ 7.0%.
This study thus highlights the need for more timely escalation of glucose-lowering therapy, including insulin initiation, in order to limit unnecessary patient exposure to hyperglycaemia and associated serious consequences, such as macro-vascular and micro-vascular complications."

An HbA1C of 7.0% still results in macro-vascular and micro-vascular complications. If someone develops type 2 diabetes in the UK, the NHS isn't going to save them. They have to save themselves.

See also Having Diabetes and Car Insurance and Applying for a Driving Licence and Informing the DVLA. Basically, developing type 2 diabetes in the UK sucks.

People who have Impaired Glucose Tolerance need to take action to prevent their condition from deteriorating into full-blown Type 2 diabetes. See http://nigeepoo.blogspot.co.uk/search/label/Diabetes.

Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

Another techie post.

From https://en.wikipedia.org/wiki/Negative_feedback_amplifier

There's been some arguing discussion over whether Hyperinsulinaemia (HI) causes Insulin Resistance (IR). My answer is...Yes and No.

HI increases IR, long-term. See Downregulation and upregulation: The Insulin Receptor and Insulin oscillation.

HI doesn't increase IR, short-term. How can I claim this? The above diagram represents a Negative Feedback (NFB) control system, which is how Blood Glucose is regulated.

"Input" represents Glucose from digested sugars and starches. The arrow pointing at AOL represents Blood Glucose (BG). The triangle containing AOL represents pancreatic beta cells. "Output" represents Insulin Secretion (ISec). More BG = More ISec.

The box containing ß represents three things that work in parallel to reduce Blood Glucose.
1) The Liver. More ISec = Hepatic Glucose Production rate decreased.
2) Muscle mass. More ISec = Glucose intake to Muscle mass rate increased, via Glu-T4.
3) Fat mass. More ISec = Glucose intake to Fat mass rate increased, via Glu-T4.
The three things aren't of equal strength, but they provide overall negative feedback.

If overall negative feedback is halved due to doubling of overall IR in the above three paths, ISec doubles. If you don't believe me, see Idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha. Double the value of resistance 2 (the negative feedback resistor R2). and the output voltage on the inverting amplifier doubles from -10V to -20V.

The idealised Negative Feedback Inverting Amplifier using an idealised op amp on WolframAlpha is interesting in that an idealised op amp (the triangle with + and - inputs) has infinity gain and ±infinity voltage on its power supplies. As a result, there is zero volts (output voltage divided by infinity) between the idealised op amp's + terminal and its - terminal. If the idealised op amp's + terminal is connected to 0V (a.k.a. "Earth"), its - terminal is at 0V (a.k.a. "Virtual Earth") and has zero variation, whatever the input voltage. An actual op amp has a voltage gain of ~140dB (~10,000,000), so an output voltage of -10V can be achieved with a voltage of 1uV (one millionth of a Volt) on its - terminal.

If pancreatic beta cells had a zero threshold and infinity gain like an idealised op amp, BG would be zero and have zero variation with varying Glucose input. Pancreatic beta cells actually have a positive threshold and low gain, so BG is positive and varies slightly with varying Glucose input.

If ISec becomes zero (as in type 1 diabetes), there is zero negative feedback and BG increases. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are 0V instead of ±infinity.

If ISec becomes insufficient (as in type 2 diabetes), there is insufficient negative feedback and BG increases. The same thing happens to the voltage on the idealised op amp's - terminal if its power supplies are limited to ±5V.

Having established that ISec is proportional to overall IR, what would happen if overall IR was proportional to ISec? If ISec doubled, overall IR would double, which would double ISec, which would double overall IR, ad infinitum. ISec would increase to maximum instantly. THIS DOESN'T HAPPEN. Therefore, IR doesn't increase in proportion to ISec, short term.

Long-term, increased ISec increases IR for a variety of reasons, one of them being that increased ISec increases the rate at which cells fill with glycogen. Once full of glycogen, cells must down-regulate their intake by down-regulating Glu-T4 and Glu-T2 (fat and liver cells also up-regulate their output of stuff) or burst.

Reduce your IR by addressing all of the factors in Insulin Resistance: Solutions to problems.

Chris Highcock emailed me a link to Muscular strength and markers of insulin resistance in European adolescents: the HELENA Study.