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.

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 http://www.clker.com/clipart-tango-face-surprise.html

"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.

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

Here are some plots from the MRFIT study.

From http://sph.bu.edu/otlt/MPH-Modules/PH/PH709_Heart/PH709_Heart5.html

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.

Molested milk: there's more to it than bovine xanthine oxidase.

The idea for the title came from Molested fats, Op. 139. Thank you, Bill!

Image from http://suppversity.blogspot.co.uk/2012/08/mutant-milk-new-research-fuels-flames.html

Homogenising/homogenizing milk has certain advantages, as per Creaming and homogenization.
"No link has been found between atherosclerosis and milk consumption." Hurrah! Not so fast...

According to Mutant Milk!? New Research Fuels the Flames on Hushed Up Concerns About Ill Health Effects of Homogenized Milk, homogenised milk has a different effect in the body (and not in a good way, if you're over-fat) from non-homogenised milk.
"...mice who received the regular formula with small lipid droplets were fatter and had compromised lipid and blood glucose levels, as well as pathologically increased leptin levels." Yeah, mice.

I drink Tesco Finest Channel Island Milk (a.k.a. Gold Top Milk). It's "past your eyes" (by law, all shop-bought milk in the UK must be pasteurised) but unhomogenised milk from grass-fed (during the summer) cows. During the summer, the cream is much more yellow than during the winter. To distribute the fat throughout the milk, you have to shake the bottle. Does that smash the milk fat globules to buggery? I think not.

Raw (i.e. unpasteurised) milk is legal in the UK, but the nearest farm where I can buy it is Meadow Cottage Farm in Churt. I used to buy it from them at a Farmer's Market in Aldershot, but that closed.

EDIT: I just noticed something in Why Doesn’t Medical Care Get Better When Doctors Rest More? (hat-tip to Yoni Freedhoff).
"Take heart failure—the most common reason for admission to the hospital in the United States—and a problem that I, as a cardiologist, deal with often." In the US, heart failure is now more common than blocked coronary arteries. See Is Coenzyme Q10 a supplement or a drug? It all depends. Statins reduce Coenzyme Q10 synthesis. Just saying.