Thursday, 5 September 2013

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 will result in a large glucose response that goes away rapidly, as the carbs 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 will result in a lower but longer sustained glucose & insulin response, as the carbs (are converted into glucose slowly and) 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 will result in an even lower glucose & insulin response that is sustained for even longer, as the carbs (are converted into glucose very slowly and) 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) will produce lower satiety than b) or c). Whether hunger is caused by a sudden drop in blood glucose level or by a sudden drop in the amount of nutrients in the gut, I don't know.

The reason for this post is A satiety index of common foods (full study) 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, which has 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 hot won't produce as much satiety, as they contain no resistant starch.

Has anyone compared the satiety of freshly-boiled potatoes with boiled & refrigerated potatoes?

Sunday, 1 September 2013

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

The lipoprotein "limousines" vary a lot in size.
(a) VLDL (b) chylomicrons (c) LDL (d) HDL. 

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.

Wednesday, 28 August 2013

Things that make you go "Struth!"

I was wading through my Facebook News Feed when I spotted THIS. That article led me to New approach to coeliac testing identifies more Australians at risk, which in turn led me to A novel serogenetic approach determines the community prevalence of celiac disease and informs improved diagnostic pathways (provisional pdf), where I saw: "HLA-DQ2.5, DQ8, or DQ2.2 was present in 56% of all women and men in the community cohorts."
HLA-DQ2.5, DQ8 & DQ2.2 are the alleles for Coeliac/Celiac Disease (CD).
Image from
"Transglutaminase (TG)-2 IgA and composite TG2/deamidated gliadin peptide (DGP) IgA/IgG were abnormal in 4.6% and 5.6%, respectively, of the community women and 6.9% and 6.9%, respectively, of the community men, but in the screen-positive group, only 71% and 75%, respectively, of women and 65% and 63%, respectively, of men possessed HLADQ2.5, DQ8, or DQ2.2."
There were abnormalities in ~5% of Australian women & ~7% of Australian men, even in those who didn't carry CD alleles.

"...but based on relative risk for HLA-DQ2.5, DQ8, or DQ2.2 in all TG2 IgA or TG2/DGP IgA/IgG screen-positive subjects, CD affected 1.3% or 1.9%, respectively, of females and 1.3% or 1.2%, respectively, of men."
~1.6% of Australian women & ~1.3% of Australian men have CD.

From the discussion: "The concept of a ‘celiac iceberg’ has been important in drawing attention to a large, unrecognized group of patients with CD who do report symptoms considered ‘typical’ of CD [29]. Investigators have proposed expansion of the ‘iceberg’ to encompass patients who are genetically susceptible to CD, but show only raised IEL counts or an isolated abnormal CDspecific serology and normal intestinal histology [30-32]. Consequently, there is considerable uncertainty regarding the true extent of gluten-mediated disease in the community.

Random thoughts: About 1 in 20 Australian women & about 1 in 15 Australian men have some kind of a gut problem (IBS?) due to gliadin, even in those who don't carry CD alleles. The following made me smile.
"Making a diagnosis based on a blood test alone or commencing a gluten-free diet without a confirmatory bowel biopsy is inappropriate and can impose an unnecessary and lifelong treatment."
'Cos life without wheat, rye, barley & oats is such an imposition (undue burden) and everyone just loves to be given a bowel biopsy. <- sarcasm alert.

From Ancestry of Australian population: "More than 92 percent of all Australians descend from Europeans. Anglo-Celtic Australians (English, Scottish, Welsh, Cornish or Irish ancestral origin) make up 74 percent of the Australian population."
Most Australians have genes that originate from Britain & Europe. Uh-oh!

Why do only a small percentage of people carrying the CD allele go on to develop CD? I believe that it's down to luck. During digestion, gliadins are snipped into fragments & amino acids by the peptidase enzymes pepsin, trypsin & chymotrypsin. Gliadin fragments that contain the wrong triplet of amino acids and that manage to slip through excessively-loose tight junctions may trigger CD. Once the "damage is done", it only takes a tiny amount of gliadin to provoke an immune response.

Monday, 26 August 2013

False dichotomies: serum cholesterol level vs all-cause mortality. Cause or effect?

Here are some plots from the MRFIT study.

Although the relative risk (RR) for coronary heart disease (CHD) and cardiovascular disease (CVD) mortalities increase with serum total cholesterol (TC) level, all-cause mortality follows a U-curve.

According to Low Serum Cholesterol and Mortality: Which Is the Cause and Which Is the Effect?, certain illnesses that increase mortality lower TC levels. This is the Iribarren hypothesis.

According to Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study, TC that's low and is still low 20 years later results in a 64% increase in the RR for mortality relative to TC that's intermediate and is still intermediate 20 years later.

Table 4 Relative risk for mortality based on change in cholesterol between examinations three and four
Is low TC level the cause of, or the effect of fatal illnesses? I think that it's both. Cholesterol is an important substance, as a severe lack of it is bad news, as per Smith–Lemli–Opitz syndrome. If certain illnesses result in a depletion of cholesterol and cholesterol synthesis is too low, there's insufficient cholesterol to allow recovery.

Interestingly, TC that's low but is intermediate 20 years later results in a 30% increase in the RR for mortality, whereas TC that's low but is high 20 years later results in a 5% increase in the RR for mortality.

P.S. There's a false dichotomy for vitamin D level vs illness. Ditto for carbohydrates vs calories.