The Elephant in the Room.

On Twitter about two weeks ago, Max Roser tweeted the following graphic:

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

The plots of low & stable BMI's until ~1945 made me think.

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 BMI began to increase significantly are ~1945 (slow rate of increase) and ~1990 (rapid rate of increase). ∴ The 1980 "low-fat" dietary guidelines didn't cause obesity.

So, what happened in the US in ~1945? From my comment HERE:
"After World War 2, the economy was in a slump and something had to be done to get people to buy more stuff, to stimulate economic growth. Corporations changed the way that they marketed to people. Instead of appealing to people’s logic, they began to appeal to people’s emotions. It worked.

Edward Bernays pioneered all of the dirty tricks used by the Food Product Industry to get people to over-consume. Ref: http://www.dailymotion.com/video/x2d29tf_the-century-of-the-self-part-1-of-4-happiness-machines_school

One of Bernays' dirty 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 even more public confusion and even more mistrust of researchers & science. This is exactly what the Food Product Industry wants."

The Tobacco Industry used Bernays' dirty 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 focusing on foods/macronutrients/micronutrients etc, people like Taubes, Teicholz, Malhotra et al are helping the Food Product Industry to manipulate the masses to over-consume their products.


So, what happened in the US in ~1990? Which dirty trick used by the Food Product Industry caused the rapid rate of increase in BMI from ~1990?

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

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 http://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 http://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 http://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 a "Cherry-picking" fallacy.

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:-
In a meta-study (a study of studies), to make something that's bad (e.g. some 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 effects (due to them looking at different types of saturated fats/fatty acids, say), so that the overall result is null.

In a study, use a different type of the thing being studied (but bury this fact somewhere obscure so that it's easily missed) to get the opposite result. E.g. To make "carbs" look bad, use a test "carb" that comprises 50% simple carbs (sugars) and 50% complex carbs (high-GI starches, preferably), thus guaranteeing a bad result.

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 and 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 reversing a condition is better than 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 for the throat, criticising Jennifer Elliot, as the article she wrote 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:-

"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! 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 Health Professional/Fitness Trainer becomes one. Cognitive bias and a refusal to accept contradictory evidence are not good traits for someone who's supposed to be practising evidence-based health/fitness.

How we lose weight: Oxidation of carbohydrate & fat in the body.

1. Oxidation of Carbohydrate in the body.

Glucose is C6H12O6, or 6(CH2O)

6(CH2O)+ 6(O2) → 6(CO2) + 6(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 6 molecules of Oxygen produce 6 molecules of Carbon Dioxide, the Respiratory Exchange Ratio (RER) is 6/6 = 1

Converting molecular weights into their gram equivalents, 180g of Glucose combines with 192g of Oxygen to produce 264g of Carbon Dioxide plus 108g of water plus ~3,012kJ of energy. I'm using kJ rather than kcal, as the human body expends energy as mechanical energy (force x distance) and heat energy.

2. Oxidation of Fat in the body.

Fat is three fatty acids (Stearic Acid, say) attached to a Glycerol backbone. As ~95% of the energy released from a fat is from the three fatty acids, I'm ignoring the Glycerol backbone, to keep the maths as easy as possible.  Stearic Acid is CH3(CH2)16COOH. I'm approximating it to 18(CH2), to keep the maths as easy as possible.

54(CH2) + 81(O2) → 54(CO2) + 54(H2O) + energy

Oxygen is inhaled. Carbon Dioxide is exhaled. Water is lost in breath, wee, poo, sweat & other bodily fluids.

As 81 molecules of Oxygen produce 54 molecules of Carbon Dioxide, the RER is 54/81 = 0.67

Note: The RER for fats is actually 0.7, as the Glycerol backbone is converted into Glucose by the liver. As the RER for  Glucose is 1, this raises the RER of my approximated fat by ~5%.

Converting molecular weights into their gram equivalents, 756g of approximated fat combines with 2,592g of Oxygen to produce 2,376g of Carbon Dioxide plus 972g of water plus ~28,468kJ of energy.

We lose weight by breathing, weeing, pooing, sweating etc. See also Majority of weight loss occurs 'via breathing'.

This doesn't invalidate Energy Balance, as the kcal/kJ values for foods merely represents the amount of chemical energy that can be released by oxidation of the various fuels in the foods. See Why Calories count (where weight change is concerned).

We gain weight by consuming fuels & water.

Another penny drops: Why severe hyperinsulinamia can occur with a small increase in exogenous carbohydrate intake.

This blog post is a result of Vim's comments in the previous blog post. A penny suddenly dropped!

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

Insulin has a Chalonic (inhibitory) action on blood glucose level (via the liver, muscle mass & fat mass), blood FFA level (via fat mass) and blood ketone body level (via the liver).

As mentioned in the comments, GHB has a stimulant effect - up to a certain level of blood GHB. Beyond that level, there's a powerful sedative effect. This is because at low levels of exogenous ketone body input, insulin secretion increases slightly to reduce hepatic ketogenesis.

At a certain level of exogenous ketone body input, hepatic ketogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous ketone body input, results in a large increase in insulin secretion, as the pancreas increases Ketone body-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood ketone body level.

Exactly the same thing happens with exogenous carbohydrate or BHB input.

At a certain level of exogenous carbohydrate input, hepatic glucogenesis falls to zero and cannot be reduced any further. Any slight increase beyond this point in exogenous carbohydrate input, results in a large increase in insulin secretion, as the pancreas increases Glucose-Stimulated Insulin Secretion to maximum in a (failed) attempt to reduce blood glucose level.

Dry carbohydrates, wet carbohydrates & energy density.

Karen N Davids thought of it first!

From http://www.amazon.co.uk/Carbs-Weight-Manage-Nutritional-Carbohydrates-ebook/dp/B00DJF2GKU

Here's a list of commonly-eaten carbohydrates and their Energy Density, in kcals/100g. From http://nutritiondata.self.com/

Dry Carbohydrates:-
Bread, White_________________________________________________266
Bread, Multi-grain___________________________________________265
Bread, Rye___________________________________________________258
Bread, Pumpernickel__________________________________________250
Bread, Whole-wheat___________________________________________247
Bread, reduced-calorie, white________________________________207
Bread, reduced-calorie, wheat________________________________198

Wet Carbohydrates:-
Pasta, fresh-refrigerated, plain, cooked_____________________131
Rice, white, long-grain, regular, cooked_____________________130
Rice, brown, long-grain, cooked______________________________111
Peas, green, frozen, cooked, boiled, drained, with salt_______78
Beans, kidney, red, mature seeds, cooked, boiled, with salt__127
Lentils, mature seeds, cooked, boiled, with salt_____________114
Vegetables, mixed, frozen, cooked, boiled, drained, with salt_60
Broccoli, frozen, spears, cooked, boiled, drained, with salt__28
Sweet potato, cooked, baked in skin, with salt________________92
Potatoes, boiled, cooked in skin, flesh, with salt____________87
Grapes, red or green (European type), raw_____________________69
Cherries, sweet, raw__________________________________________63
Pears, raw [Includes USDA commodity food A435]________________58
Apples, raw, with skin________________________________________52


If a diet is high in carbohydrates:-
Which of the above foods are most likely to result in weight gain?
Which of the above foods are most likely to result in weight loss?
Answers on a postcard, please!

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

From http://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet → ↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So?

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleading. Siri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat → ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

Some thoughts on the essentiality of dietary carbohydrates.

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

From https://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 very precise. See http://nigeepoo.blogspot.co.uk/2012/04/how-eating-sugar-starch-can-lower-your.html

2) It's not enough to fuel high-intensity exercise. See http://nigeepoo.blogspot.co.uk/2011/02/funny-turns-what-they-arent-and-what.html

3) 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 only consumed Essential Fatty Acids, Essential Amino Acids, Vitamins, Minerals, Fibre/Fiber, Water & Anutrients, there wouldn't be much to eat. Also, there wouldn'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.

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.

A *very* special dual-fuel car analogy for the human body that I just invented.

The human body is like a very special dual-fuel car.

From http://www.aa1car.com/library/alternative_fuels.htm

In this very special dual-fuel car:-

Glucose is represented by Ethanol, 'cos Ethanol is a carbohydrate, according to Robert Lustig ;-)
Glucose is C₆H₁₂O₆. Ethanol is C₂H₆O. 3(C₂H₆O) = C₆H₁₈O₃. It's not very close, but it'll do!

Caprylic acid is represented by Octane, 'cos fatty acids are hydrocarbons, don'tcha know? ;-)
Caprylic acid is CH₃(CH₂)₆COOH and Octane is CH₃(CH₂)₆CH₃, which is actually pretty close.

Storage depots:

 

Carbohydrates:

For Ethanol, there's a large storage tank (≡ muscle glycogen) and a small storage tank (≡ liver glycogen). The contents of the large storage tank cannot be used to top-up the small storage tank, but the contents of the small storage tank can be used to top-up the large storage tank. The contents of the small storage tank are used to fuel a generator (≡ Hepatic Glucose Production) to keep the ECU (≡ brain) working at all times. The contents of the large storage tank are used to fuel the engine.

Fats:

For Octane, there's a large storage tank (≡ subcutaneous adipose tissue) and a small storage tank (≡ visceral adipose tissue). The contents of the small storage tank are used to produce hormones etc. The contents of the large storage tank are used to fuel the engine.

Substrate Utilisation:

When the car is driven at low speed, the engine burns mostly Octane (≡ RQ=0.7).
When the car is rapidly accelerating or driven at high speed, the engine burns mostly Ethanol (≡ RQ=1).
When the car is being driven intermediately, the engine burns a mixture of Octane & Ethanol.

Overeating/Undereating:

 

Carbohydrates:

If the large Ethanol storage tank becomes full, excess Ethanol overspills to the small storage tank.
If the small storage tank becomes full, a gizmo kicks-in and converts excess Ethanol into Octane (≡ De-Novo Lipogenesis).
It also shifts fuel usage of the engine towards Ethanol, to deplete Ethanol as quickly as possible.
If the small storage tank becomes full, the car malfunctions (≡ fatty liver).

Conversely, if the small storage tank becomes nearly empty, it shifts fuel usage of the engine towards Octane, to conserve Ethanol.

Fats:

If the large Octane storage tank becomes full, excess Octane overspills to the small storage tank.
If the small storage tank becomes full, the car malfunctions (≡ insulin resistance/metabolic syndrome/type 2 diabetes).

Jumping through hoops, and my Blog List.

I'm seeing a curious thing. The VLC "camp" seems to be "jumping through hoops" to prove a point.

From http://davidbressler.com/2013/08/26/easier-harder/

From Neuron fuel and function (emphasis & formatting, mine):-
"Ketones and lactate do not drive reverse electron flow through complex I. Glucose can. Palmitate certainly can. What you want from a metabolic fuel depends on the remit of your cell types. Neurons within the brain preserve information by their continued existence.

This is best done by burning lactate or ketones. NOT glucose and, of course, not FFAs.

Anyone who claims that glucose is the preferred metabolic fuel of the brain has not though (sic) about what a neuron has to do and what an astrocyte actually does do. Or much about the electron transport chain."

Basically, glucose is bad mmm-kay. Also, anyone who claims that glucose is the preferred metabolic fuel of the brain is a dumb-ass. Damn our livers & kidneys churning out glucose! Are they trying to kill us?

∴ Carbohydrates are bad and must be avoided at all cost! This, of course, is utter nonsense.

Glucose can drive reverse electron flow through complex I. Can means that it's possible. Is it probable?

On a hypercaloric Western diet of excessive crap-in-a-bag/box/bottle, yes.

On a Kitavan diet of ~70%E from tubers, no.

On a diet of Basmati rice & beans, no.

On a diet of whole fruits, no.

See also Another crash and burn on low carb paleo and CrossFit. Enough of the 'carbs are evil' nonsense. Carbphobia is hurting a lot of people.

I have a list of blogs that I read on a regular basis. As a result of the bad science & cherry-picking displayed in various VLC blogs, I have deleted them from my Blog List.

See also Guest post: Denialism as Pseudoscientific Thinking.

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.

Why Calories count (where weight change is concerned).

I have to add the words "where weight change is concerned", as calories have little to do with body composition or general health (unless somebody becomes morbidly obese).

From https://docs.google.com/file/d/0Bz4TDaehOqMKSXZHUUVxWnl5VTQ/edit?usp=sharing

Arguments used by Calorie Denialists include:-

1) Calories don't count because the human body isn't a Bomb Calorimeter and treats different macronutrients differently.
 
100g of liquid paraffin burns in a Bomb Calorimeter, yielding 900kcals. In a human, it passes through completely undigested. Ah-ha!, I hear you saying. This proves that the Energy Balance Equation is invalid. Uh, nope!

Calories in = Calories entering mouth - Calories exiting anus

As 100% of liquid paraffin calories entering the mouth exit the anus, Calories in = 0

This is why Sam Feltham's "Smash the Fat" "experiment" is nonsense. A high percentage of the large amount of raw almonds he ate would have exited his anus incompletely chewed, undigested & unabsorbed.

See the picture above? In the late 1800's, W.O. Atwater established Atwater Factors (3.75kcals/g for digestible Carbohydrates, 4kcals/g for Proteins, 5kcals/g for Ketones, 7kcals/g for Alcohols & 9kcals/g for Fats*) using Human Calorimeters, not Bomb Calorimeters. Atwater Factors are pretty accurate.

*Fats containing different fatty acids have slightly different kcals/g. Fats containing long-chain fatty acids are 9kcals/g. Fats containing medium-chain fatty acids e.g. coconut oil are ~8kcals/g.

For more information, see Calories ...


2) Calories don't count because Dietary Efficiency varies for different macronutrients.

Uh, nope! The Heat Power generated by the body is regulated by a NFB loop involving the Hypothalamus, Pituitary, Thyroid Axis, also Uncoupling Proteins (UCP's), also shivering, so as to maintain a body temperature of 37°C ±3°C. If this wasn't the case, different amounts & types of foods (also, changes in ambient temperature & clothing) would cause large variations in body temperature resulting in death, as the enzymes in our bodies function correctly over a limited range of temperatures.

Heat Power generated by the body (W) = Temperature difference between the body & ambient (°C) divided by Thermal resistance between the body & ambient (°C/W)

∴ Dietary Efficiency is irrelevant.

Lies, damned lies and statistics, part n+1. Riera-Crichton et al.

In Macronutrients and obesity: Revisiting the calories in, calories out framework, the conclusion is:-
"Our structural VAR results suggest that, on the margin, a 1% increase in carbohydrates intake yields a 1.01 point increase in obesity prevalence over 5 years while an equal percent increase in fat intake decreases obesity prevalence by 0.24 points."

So, carbohydrates are fattening but fat is slimming, eh? I declare shenanigans! Two can play at that game.

In Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating, Bray et al increased kcals by 40% by adding Fat grams. Carb grams didn't change. Protein grams changed a bit. ∴ Protein %E & Carb %E decreased by ~29%. %E means "as a percentage of total Energy".

Weight (lean body mass + body fat) increased as Fat kcals increased ± some interpersonal variation.

From Fig. 6.

_
 _Decreased P %E & C %E result in increased weight.
∴ Increased P %E & C %E result in decreased weight.

∴ Fat is fattening, but Protein & Carbohydrate is slimming! Q.E.D.

Do you see what's going on? Here's a summary:-

Diet contains A, B and C.
The amount of A increases, but the amounts of B and C remain constant.
A%E increases, but B%E and C%E decrease.  

In Riera-Crichton et al, A = Carbohydrate, B = Fat and C = Protein.
In Bray et al, A = Fat, B = Carbohydrate and C = Protein.

How 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 get more weight loss on low-carbohydrate diets than on high-carbohydrate diets, and insulin sensitive people get more weight loss on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes' carbohydrate/insulin hypothesis of obesity was correct, everyone would get more weight loss on low-carbohydrate diets. This isn't the case, therefore Gary Taubes' 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 Bodily 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. Trust me, I'm a retired Electronic Engineer. I've observed this (too) many times!

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 massive 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. ∴ Bodily stores increase. There are also accusations of sloth & gluttony!

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. ∴ Bodily 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

P.S. 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.

P.P.S. Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions.

P.P.P.S. Insulin Resistance can be fixed in the long-term. See Insulin Resistance: Solutions to problems.

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

Aim to fix the problem in the long-term. If a long-term fix isn't possible (due to excessive destruction of pancreatic beta cells), use a low-carbohydrate diet as an adjunct to medication.

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.

The Conflation Game.

Li-i-ife, is the name of the game, and I wanna play the game with you.....


People have been "grinding my gears" by conflating carbohydrates with sugars. All sugars are carbohydrates, but not all carbohydrates are sugars. See Carbs Carbs Carbs. to find out about the five basic different types of carbohydrates.

Krauss et al has done it again. In Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia, at the bottom of Table 1 is "carbohydrate, 50% simple and 50% complex". The carbohydrates consisted of half sugars and half starches.

The effect of such a sugary diet is as follows:-

The percentage of pattern B (small, dense) LDL particles increases significantly in proportion to the percentage of Dietary "carbohydrate". The implication of this study (also A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins ) is that high-carb, low-fat diets are atherogenic.

This is not on.

A high sugar diet is atherogenic, but carbs from new potatoes (especially if eaten cold), Basmati rice (especially if eaten cold), sweet potatoes, beans & whole fruits aren't.

Another tasty analogy.

Here's a tasty analogy.

From http://grannychoe.com/recipe3_Soup.php

In Ultra-high-fat (~80%) diets: Fat storage, and a delicious analogy, I analogised the effect of carbohydrate consumption on mean serum glucose level with the effect of fat consumption on mean serum triglyceride level. Here's another one.

Chronic excessive consumption of carbohydrates relative to what are being burned results in excessive fat synthesis in the liver, resulting in excessively-high fasting serum triglyceride level, which is harmful.

Chronic excessive consumption of fats relative to what are being burned results in excessive cholesterol synthesis in the liver, resulting in excessively-high fasting VLDL, LDL & IDL level, which is harmful.

Seems legit.

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.

Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Julianne Taylor of Paleo & Zone Nutrition posted the following excellent lecture on Facebook:-

Eating Through The Myths: Food, Health and Happiness - Taylor, Prof. R., Berlin, 28-Sep-12

Salient points:

1) It's a chronic calorie excess (of carbohydrates and/or fats) that causes problems.
2) Motivation, motivation, motivation!
3) Both diet and exercise are important. See Move More: Solutions to problems.
4) You can't outrun your fork. See The 5th Myth of Modern Day Dieting: You Can Outrun Your Fork.
5) Underlying Insulin Resistance needs to be addressed. See Insulin Resistance: Solutions to problems.

See also Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol, and Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.

For more information on Prof. Taylor's work, see Reversing Type 2 Diabetes.

Carbs, Carbs, Carbs, Carbs and Carbs.

Carbohydrates seem to get the blame for everything nowadays. "Carbohydrates made me fat". "Carbohydrates burned-out my pancreas". "Carbohydrates raised my blood glucose". "Carbohydrates raised my blood triglycerides". "Carbohydrates stole mer jerb!". O.K, I made the last one up!
If carbohydrates are responsible for all of these bad things, then how come a diet of only potatoes had the opposite effect? See 20 Potatoes a day.

Also, Blue Zone populations eat a diet with a high percentage of total energy (%E) from carbohydrates. See Low serum insulin in traditional Pacific Islanders--the Kitava Study and The Kitava Study. The Kitavans eat ~70%E from carbohydrates, ~20%E from fats and ~10%E from proteins. They don't eat a significant amount of Western crap-in-a-bag/box/bottle.

Maybe it has something to do with the type of carbohydrates and with what they're eaten. In A very-low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins , (emphasis, mine) "The very-low-fat, high-carbohydrate experimental diet was designed to supply less than 10% of energy from fat (2.7% saturated, 3.7% monounsaturated, and 2.6% polyunsaturated), with 75% from carbohydrate (with equal amounts of naturally occurring and added simple and complex carbohydrate) and 15% from protein." Simple carbohydrates are sugars.

The experimental diet which did bad things contained 37.5%E from sugars. I declare shenanigans!

1. There are simple carbs, there are simple carbs and there are simple carbs. In the previous post, the graph of plasma triglycerides after an OGTT showed that 100g of glucose had no significant effect on plasma triglycerides over a 6 hour period. If it had been 100g of fructose, there would have been a significant increase in plasma triglycerides. Galactose is taken-up by the liver and has minimal effect on blood glucose, but I don't know its effect on plasma triglycerides.

2. There are complex carbs, there are complex carbs and there are complex carbs. Overcooked starch is high in amylopectin which is highly-branched, which means that it hydrolyses rapidly into glucose which gives it a very high glycaemic index. Raw & refrigerated potato starches have very low glycaemic indices, due to the presence of amylose, or other resistant starches. Rice contains a mixture of starches which varies with rice type, cooking time and subsequent refrigeration.

3. There are oligosachharides e.g. FOS.

4. There are polysaccharides e.g. inulin.

5. There is soluble fibre/fiber e.g. cellulose.

Although overeating sugars containing fructose & starches that rapidly hydrolyse into glucose makes the liver fatty, overeating fats also makes the liver fatty. See Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause.

It's the chronic over-consumption of crap-in-a-bag/box/bottle (high in sugars and/or starches and/or fats), not just carbohydrates, that causes over-fatness and other health problems.