Showing posts with label Rye. Show all posts
Showing posts with label Rye. Show all posts

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 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.

Friday, 14 June 2013

Grains & soyabeans: more bad news.

Jamie Scott (THAT PALEO GUY) has been doing some digging and found more dirt on...
From http://commons.wikimedia.org/wiki/File:Various_grains.jpg
See Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4.
"We identify the α-amylase/trypsin inhibitors (ATIs) CM3 and 0.19, pest resistance molecules in wheat, as strong activators of innate immune responses in monocytes, macrophages, and dendritic cells. ATIs engage the TLR4-MD2-CD14 complex and lead to up-regulation of maturation markers and elicit release of proinflammatory cytokines in cells from celiac and nonceliac patients and in celiac patients' biopsies. Mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. These findings define cereal ATIs as novel contributors to celiac disease. Moreover, ATIs may fuel inflammation and immune reactions in other intestinal and nonintestinal immune disorders."

See Impact of antinutritional factors in food proteins on the digestibility of protein and the bioavailability of amino acids and on protein quality.
"Examples of naturally occurring antinutritional factors include glucosinolates in mustard and canola protein products, trypsin inhibitors and haemagglutinins in legumes, tannins in legumes and cereals, gossypol in cottonseed protein products, and uricogenic nucleobases in yeast protein products."

"Among common food and feed protein products, soyabeans are the most concentrated source of trypsin inhibitors. The presence of high levels of dietary trypsin inhibitors from soyabeans, kidney beans or other grain legumes have been reported to cause substantial reductions in protein and amino acid digestibility (up to 50 %) and protein quality (up to 100 %) in rats and/or pigs."

"Normally encountered levels of phytates in cereals and legumes can reduce protein and amino acid digestibility by up to 10 %. D-amino acids and LAL formed during alkaline/heat treatment of lactalbumin, casein, soya protein or wheat protein are poorly digestible (less than 40 %), and their presence can reduce protein digestibility by up to 28 % in rats and pigs, and can cause a drastic reduction (100 %) in protein quality, as measured by rat growth methods. The adverse effects of antinutritional factors on protein digestibility and protein quality have been reported to be more pronounced in elderly rats (20-months old) compared to young (5-weeks old) rats, suggesting the use of old rats as a model for assessing the protein digestibility of products intended for the elderly."

I eat grains, also peas, beans & lentils, but not as a dietary staple. I make sure that they're thoroughly cooked at 100°C.

Friday, 20 April 2012

Fiber and Insulin Sensitivity.

Bluddy Americans. It's Fibre! But anyway....

Stabby the Raccoon posted the following study in a comment on CarbSane's blog. I thought that it was so interesting that I am linking to it here.

Fiber and Insulin Sensitivity.

This study has built-in cognitive dissonance.

The first Fig. suggests that cereal fibre is associated with a much lower RR for Type 2 Diabetes Mellitus (T2DM) and that fruit & veggie fibre aren't.

Schulze et al. 2007: Cereal Fiber RR = 0.6 - 0.7. Fruit Fiber RR = 0.9 - 1.05. Vegetable Fiber RR = 0.95 - 1.15 approx.

The next table suggests otherwise.

Andersson et al., 2007: Whole grain diet contained 112 g/d of whole grain, 18 g fiber. No effect of whole grains on insulin sensitivity.

Ebeling et al., 1988: 5 g/d granulated guar. No effect on insulin sensitivity.

Johnston et al., 2010: Resistant starch supplement -40g/d. Improved insulin sensitivity with resistant starch.

Landin et al., 1992: 30 g/d granulated guar, given in 3-10 g doses. Improved insulin sensitivity with guar diet.

Maki et al., 2011: High-resistant starch diet- 30 g/d, Low-resistant starch diet- 15 g/d. Improved insulin sensitivity with both resistant starch diets, but effect only reached statistical significance for men.

Nilsson et al., 2008: White bread enriched with barley fiber and 8g resistant starch, Barley kernel based bread. Improved glucose tolerance with resistant starch.

Pouteau et al., 2010: 28 g/d acetogenic fibers (acacia gum and pectin). No effect on insulin sensitivity.

Robertson et al., 2003: High-resistant starch diet- 60 g/d. Improved insulin sensitivity with resistant starch.

Weickert et al., 2006: Fiber-enriched with 31.2 g insoluble fiber. Improved insulin sensitivity with increased insoluble fiber.

In conclusion, the resistant starches found in high-amylose rices such as Basmati, refrigerated boiled rice & boiled potatoes, also rye & barley breads are beneficial in terms of reducing your RR for T2DM. Watch out, though. Too much dietary resistant starch can cause colic, flatulence & diarrhoea if your intestinal bacteria are knackered. You want fermentation to short-chain fatty acids to occur, not osmotic laxation! See Genetics of Food Intolerance.

Saturday, 13 February 2010

The problem with "Wholegrain" cereals etc.

As I mentioned in Carbohydrates: Dogs' Doodads or Spawn of Satan?, some breakfast cereals turn into blood glucose faster than table sugar (half glucose bonded with half fructose) even though they're "Wholegrain" cereals.

A whole (i.e. intact) grain consists of a protective outer shell (a.k.a. bran) and innards consisting of starchy/proteiny endosperm and nutritious germ. See Cereal germ.

To turn a grain into a breakfast cereal, it's milled into dust, mixed with water to form a paste and the paste is extruded through holes into whatever shape the manufacturer desires. Technically, everything that was in the whole grain is in the finished product. However, the form and function have completely changed. Here are a couple of analogies.

1) I want to sell my car. I take it to a scrap-yard and have it shredded into tiny pieces. All of the tiny pieces are put in a skip, which is delivered to my driveway. I place a sign on the skip stating "Whole Mazda MX-5 for sale. Enquire within. £5,000 O.N.O.". What would you offer for my "Whole Car"?

2) An insane person gives me £5,000 (in £50 notes) for my "Whole Car". As I'm on a roll, I take the notes and put them through a cross-cut shredder which turns them into thousands of 2mm x 2mm pieces. I empty the pieces into an attaché case. Who will accept my attaché case full of "Whole £50 notes" as payment for their second-hand car? Any more insane people out there?

Roller-milling grains into fine dust does four things.

1) It exposes the starchy endosperm.

2) It greatly increases the surface area to volume ratio of the grain, resulting in faster digestion and absorption. Surface area to volume ratio is inversely proportional to particle size. If 3mm grains are roller-milled into 0.1mm particles, the surface area to volume ratio is 30 times bigger. See Particle size, satiety and the glycaemic response. Therefore, "wholegrain" breads made from roller-milled flours are as bad as white breads, in terms of glucose and insulin response. Choose wholemeal breads made from stone-ground flours, as the particle size is bigger.

3) It makes the finished product much more likely to stick to your teeth, resulting in the rapid formation of plaque that damages your teeth and gums.

4) It makes the finished product more energy-dense.

Rolled grains are grains that have been steamed (to cook and make them soft), then put through what's effectively a mangle. They're still intact, if somewhat flat. Puffed grains are grains that have been heated to make the water within boil. As steam takes up a much larger volume than water, the grains are inflated to a much larger size. They're still intact, if somewhat funky-looking!

Don't be conned by breakfast cereal labels. If they look like "O"s or Brillo pads or brake pads, they're not intact grains.

Oats are O.K. even when turned into oatmeal, probably due to their high beta-glucan content, which forms a wallpaper paste-like goo when wet. See Particle size of wheat, maize, and oat test meals: effects on plasma glucose and insulin responses and on the rate of starch digestion in vitro.

See also Anthony Colpo's The Wholegrain Scam.