Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Continued from Everyone is Different, Part 3.

EDIT: I made an error in stating that all of the extra calories came from fat, in the fat overfeeding phase. Thanks to commenter CynicalEng for pointing that out. It doesn't change the conclusion at all.

At 01:17 on 6th June, during a Facebook discussion, Fred Hahn told me:-
"Nigel Kinbrum - read this please.
Bray, et al. Shows that a Calorie is Not a Calorie and that Dietary Carbohydrate Controls Fat Storage.
Perhaps you'll learn something from a real expert who teaches metabolism to medical students at the largest medical school in the country."

So I did.

At 02:22, I replied:-
"Thanks for that. I read Feinman's blog post about Bray et al http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/ some time ago.
There's a fundamental error in Feinman's analysis. As LeonRover pointed out in his comment http://feinmantheother.com/.../bray-et-al-shows-that.../...
In Diets:- "Absolute carbohydrate intake was kept constant throughout the study."
Also, in COMMENT:- "The extra calories in our study were fed as fat, as in several other studies, and were stored as fat..."
Oh, whoops! That may be why it was rejected by the editor."

Here's Figure 6 from Bray's study.

From http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3777747/

Some Definitions:-

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) ± some inter-personal variation.
∴ Insufficient protein can result in LBM loss (this is bad).
As LBM has a lower Energy Density (~400kcals/lb) than FM (~3,500kcals/lb),  LBM loss can increase weight loss, when in a Caloric Deficit.
See The Energy Balance Equation, for a simple explanation, and The Dynamics of Human Body Weight Change, for an incredibly complicated one!


I was rather chuffed when Alan Aragon left the following comment at 04:34:-
"Nigel is correct. From Bray et al's text:
"The extra calories in our study were fed as fat, as in several other studies [33,34], and stored as fat with the lower percentage of excess calories appearing as fat in the high (25%) protein diet group. The higher fat intake in the low protein group probably reduced nutrient absorption (metabolizable energy) relative to the other groups and this would have brought the intake and expenditure closer together in this group.""

Feinman has deleted his blog post. However, his post I Told George Bray How to do it Right is still there. I believe that Dr. George A. Bray M.D. sort-of did it right.

Dr. George A. Bray used a "weight maintenance formula" in all three groups for the weight maintenance phase. He then changed the formula in all three groups to low-P, med-P and high-P formulas, for the fat overfeeding phase. Carbohydrate grams remained constant in all three groups for all phases, but additional fat grams were fewer in the high-P group than in the low-P group, for the fat overfeeding phase.

I would have used the low-P, med-P and high-P formulas for the weight maintenance phase and for the fat overfeeding phase, to equalise the additional fat grams in all three groups.

Continued on Everyone is different Part 4, Fallacies and another rant!

Saturday silliness.

Now that I have resumed annoying people discussing diet & nutrition on the internet, the following chart should be used by non-English people, to allow them to understand what I write.

From http://www.thepoke.co.uk/2011/05/17/anglo-eu-translation-guide/

For a laugh, I created the superhero of Diet & Nutrition "The Nigeepoo".

Using http://www.heromachine.com/heromachine-2-5-character-portrait-creator/

Have a nice weekend!

False dichotomies: cot'd.

I'm talking about the "What causes Z, X or Y?" & "What is best, X or Y" type statements.

From http://johnbarban.com/fitness-vs-fatness-a-false-dichotomy/

Some people believe that hormonal disruption causes obesity, rather than energy excess. The vast majority of people who are overweight or obese weren't born with hormonal disruption. It's years of chronic energy excess (see Determinants of the Variability in Human Body-fat Percentage for the many reasons causing it) that make people too heavy/fat than is healthy. Once too heavy/fat than is healthy, various hormones become disrupted, causing even more energy excess. Therefore, the cause of obesity is not one thing or another, it's both (plus lots of others), which is why reversing it is so difficult.

On Peter D's blog, the title reads "You need to get calories from somewhere, should it be from carbohydrate or fat?" I say "Both. And some protein. And a bit of alcohol, too!" And I know that I shouldn't start sentences with And.

It's been a while since I posted a video of me singing. Here's one from February this year.

Bacon cures cancer. Wait, WHAT?

It probably didn't, but here's a heart-warming case study from Dr. Terry Simpson I spotted on Twitter.


From http://www.yourdoctorsorders.com/2013/02/bacon-cures-cancer

Mmm, bacon!

http://upload.wikimedia.org/wikipedia/commons/3/31/Made20bacon.png

I'm back with some miscellaneous ramblings.

I'm not dead! Who knew?


I saw https://twitter.com/JimJohnsonSci/status/468745252170248192 and read Modeling type 2 diabetes in rats using high fat diet and streptozotocin.

What I find a bit sad is the "cure > prevention" attitude. The cause of pre-diabetes & type 2 diabetes is pretty well known now, i.e. it's basically the inability of bodily stores (liver/muscle glycogen stores & fat masses) to accommodate any more, resulting in excessive amounts of various things (e.g. glucose, fat, cholesterol, NEFAs etc) in the blood, with varying degrees of beta cell dysfunction.

The degree of fatness at which bodily stores become full depends on the degree of adipocyte hyperplasia, so it's possible for slim people to become type 2 diabetic, though ~85% of type 2 diabetics are over-fat. Some slim people are misdiagnosed with type 2 diabetes, as they have LADA or signalling abnormalities. Some have acquired endocrine abnormalities.

I've been pre-diabetic twice to my knowledge, the most recent occasion being last year when I became slightly manic after mum died and got into a large number of arguments on various blogs. I "took my eye off the ball" diet-wise and ended up gaining too much body-fat, even though my belt didn't feel noticeably tight. I blogged about feeling too hot last year. When I had blood tests in September to find out why I was overheating so much, the results revealed hyper****aemia, where **** = glucose, total cholesterol & triglycerides. The doctor recommended that I take a statin. I declined, stating that I knew what had caused the problem and that I would deal with it. I was told to have repeat blood tests in 3 months time.

I subsequently "kept my eye on the ball" diet-wise (using bathroom scales to monitor progress), lost 8kg (some of it fat mass & some of it muscle mass) and when I was retested 3 months later, the previously abnormal blood test results were back to completely normal. That's twice I've gone from pre-diabetes to normal, which suggests that deterioration from pre-diabetes to type 2 diabetes is not inevitable, provided that the cause is dealt with before excessive irreversible beta cell dysfunction occurs.

The main reason why the incidence of over-fatness & type 2 diabetes is increasing is the overconsumption of "Crap in a bag/box/bottle" by increasing numbers of people. How to reverse this trend? Damned if I know!

Boiled potatoes & Area Under the Curve (AUC): some thoughts.

Here are three "curves"... a 4 x 1 rectangle, a 2 x 2 square and a 1 x 4 rectangle.

The AUC for all three "curves" = 4.

Imagine that the three curves are for blood glucose level increase above baseline vs time.

a) "X" grams of a high-Glycaemic Index (GI) carb e.g. glucose, maltodextrin or amylopectin result in a large glucose response that goes away rapidly, as the carbs leave the gut rapidly, pass into the blood rapidly and are cleared from the blood rapidly due to the large insulin response.

b) "X" grams of a 50:50 mixture of high & low-GI carbs result in a lower but longer sustained glucose & insulin response, as some carbs leave the gut rapidly but some carbs leave the gut slowly, pass into the blood slowly and are cleared from the blood slowly due to the small insulin response.

c) "X" grams of a low-GI carb e.g. amylose or resistant starch result in an even lower glucose & insulin response that is sustained for even longer, as the carbs leave the gut very slowly, pass into the blood very slowly and are cleared from the blood very slowly due to the very small insulin response.

Will a), b) & c) produce the same satiety? I think not. I think that a) results in lower satiation than b) and b) results in lower satiation than c). Whether returning hunger is caused by a sudden drop in blood insulin level or by a sudden drop in the amount of food in the gut, I don't know.

The reason for this post is A satiety index of common foods (scanned image of full study here) and the related study An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods.

In the first study, boiled potatoes produced the highest satiety, yet in the second study, boiled potatoes produced one of the highest glucose & insulin AUCs. How can this be? Consider the preparation method for the Russet potatoes:-
"Peeled, boiled for 20 min, and stored at 4 °C overnight; reheated in a microwave oven for 2 min immediately before serving."

Potato starch when refrigerated produces resistant starch RS3, which gives it a low GI (see item 605 in International table of glycemic index and glycemic load values: 2002). Therefore, refrigerated potatoes contain a mixture of high & low-GI starches. This, I believe, is why boiled, refrigerated & reheated potatoes produced the highest satiety. The combination of water, fibre & resistant starch kept hunger pangs away the longest. I suspect that boiled potatoes that are eaten without being refrigerated won't produce quite as much satiation, as they contain no resistant starch.

EDIT: From https://en.wikipedia.org/wiki/Resistant_starch#Definition_and_categorization :-
"RS3 Resistant starch that is formed when starch-containing foods are cooked and cooled, such as pasta. Occurs due to retrogradation, which refers to the collective processes of dissolved starch becoming less soluble after being heated and dissolved in water and then cooled."
RS3 forms a gel in the stomach, which delays stomach emptying. This is most likely the reason for the increased satiation.

Lipoproteins & apolipoproteins: E, by 'eck.

In December 2008, I wrote about Cholesterol And Coronary Heart Disease , where I used a limousine metaphor to describe how cholesterol & fat are transported around the body. Here's a diagram of a chylomicron lipoprotein "limousine". Chylomicrons transport dietary fat (triglycerides) & cholesterol from the gut to the liver & other tissues. As there's much more dietary fat than dietary cholesterol, the contents are mostly fat.

A chylomicron. T=Triglyceride C=Cholesterol. From http://en.wikipedia.org/wiki/Lipoprotein

The lipoprotein "limousines" vary a lot in size.

(a) VLDL (b) chylomicrons (c) LDL (d) HDL. 
From http://healthcorrelator.blogspot.co.uk/2011/11/triglycerides-vldl-and-industrial.html

Apolipoproteins are the "chauffeurs" which determine to where lipoproteins transport stuff.
Apo A is found mainly on HDL, which transports fat & cholesterol from tissues to the liver.
Apo B is found mainly on LDL, which transports cholesterol from the liver to tissues.
Apo C is found on HDL when fasted, but moves to chylomicrons & VLDL when fat is eaten.
Apo D is found mainly on HDL and is is associated with an enzyme involved in lipoprotein metabolism.
Apo E is found mainly on chylomicrons & IDL and transports lipoproteins, fat-soluble vitamins, and cholesterol into the lymph system and into the blood. In the CNS, Apo E transports cholesterol to neurons. Defects in Apo E result in hyperlipidaemia , cardiovascular & neurological diseases, and is the E referred to in the title.

There's also Apo H, which is a β-glycoprotein involved in the binding of cardiolipin. It has nothing to do with the above lipoproteins.