5/06/2009 11:51pm, #151
Today's flimflam is "waxy maize starch", also known as amylopectin. I've been reading about amylopectin - it's a glucose polysaccharide (starch) which branches every twenty-four to thirty residues, and can incorporate up to a million molecules of glucose. The branches get split off by debranching enzyme, and then chopped up into glucose molecules by amylase. It's been fairly well-established that amylopectin is more rapidly broken down by the human digestive system than its linear brother, amylose.
But apparently that's not fast enough.
Marketing claims have been made about amylopectin:
WMS has a much higher molecular weight and a much lower osmolarity rate compared to dextrose or maltodextrin, so what does this mean… Mainly, WMS bypasses the stomach, is absorbed by the intestines and immediately is assimilated; this is all done at a much faster rate than dextrose or maltodextrin, almost double.
First off, unless you've got a really peculiar anatomy, there are only three ways to "bypass the stomach":
1) Sublingual absorption
2) Intravenous injection
So just how serious are you about getting your fast carbs?
And then, beyond that, we've previously established in this thread that amylopectin can't make it across the intestinal wall and into the portal vein until it's been broken right down. Into dextrose. You know, the stuff it's supposed to be twice as fast absorbing as?
The osmolarity stuff is technically true but largely irrelevant, mostly because of the above.
Anyways, it's not just me who smells something fishy here. See also David Barr's The Myth Of Waxy Maize Starch, which goes into more detail about the literature's support (or rather, rejection) of the waxy maize starch marketing material.
All that said, it's still going to get your blood glucose (and insulin) up, and it's certainly not a "slow" carb (if such a thing actually exists), so if you already have some, it'll do the job. But I fail to see a reason to pay more for it than dextrose or maltodextrin.
Speaking of which, has anyone priced out a big jug of corn syrup (not HFCS) lately? I keep forgetting to look for it when I go to the grocery store.
5/07/2009 9:43pm, #152
The "waxy maize starch" thing is hilarious. I hadn't seen that marketing spiel before.“Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
5/08/2009 12:24am, #153
Two weeks of high protein, high fat, negligible carbohydrate intake as of today. No carb loads as of yet. Haven't really decided on the next step. I could either continue as-is for another week or so, start a carb-load this weekend (dubious without physical activity to justify it), start the cutting phase (with attendant reduction in calories from fat), or start on caffeine. I'm leaning towards the latter, also because it might help me stay awake during work and class.
5/08/2009 9:58pm, #154
So I've been pondering nutrition (there's a shocker), pre-bed nutrition in particular. How does one sustain a meaningful inflow of amino acids for a prolonged period of time?
Well, the simplest way is to eat more often. Time for a graph!
(Figure 2 from Dangin, "The digestion rate of protein is an independent regulating factor of postprandial protein retention")
The takeaway is this: the dark circles on the right side are repeated feedings of whey (every 20 minutes for four hours) - the elevated level of serum amino acid is sustained and stable for the whole period of the feedings.
That's great news, except that I don't want to wake up every twenty minutes to eat. In fact, let's say I refuse to wake up until I'm good and ready.
That brings us back over to the graphs on the left side. Casein shows elevated serum amino acid levels for the full 420 minute period, which is a solid nap. But let's say I wanted to string it out for a bit longer. I can think of two things, and coincidence of all coincidences, they're both mentioned in this next study:
French, "Effect of guar gum on hunger and satiety after meals of differing fat content: relationship with gastric emptying"
Guar gum is soluble fiber, and dietary fat is... fat. Both slow the gastric emptying rate, and soluble fiber forms a gel that slows down the rate of diffusion (and consequently, absorption) of nutrients. There's no shortage of options for fat - in particular, olive oil's easy to come by and high in monounsaturated fat - but I'm having a tough time figuring out how to swing a cheap and relatively pure source of soluble fiber.
Purity is important because although soluble and insoluble fiber are often grouped together into "dietary fiber", they actually have opposing effects in this application. Insoluble fiber increases the speed of food's transit through the gastrointestinal tract, which means the transfer of nutrients will be both shorter in time and smaller in magnitude.
Note that I've seen a lot of unreliable information about which types of fiber are soluble and which are insoluble. This is especially frustrating because it's really easy to tell - pour it in water, and watch what happens. If it stays in solid pieces, it's insoluble. If it turns into a gel, it's soluble.
So... where can a brother get soluble fiber without any insoluble fiber mixed in?
5/09/2009 12:50am, #155
The subject of lectins came up tangentially during the discussion of the Paleo Diet. Here's something interesting I just stumbled across.
For a number of reasons protein absorption might be incomplete. Some proteins, because of their physical or chemical structure, are resistant to proteolytic attack and therefore pass through the small intestine relatively unmodified. Furthermore, the absorption of free amino acids and peptides may be less than 100%, particularly if gut function is impaired. This occurs in a number of clinical conditions, such as intestinal infections or injury, and when certain 'antinutritional' factors such as lectins or trypsin inhibitor proteins are present in the diet. This unabsorbed protein or amino acid then passes through into the colon. Metabolism by the colonic microflora then occurs, but the amino acids are no longer available to the body, and are excreted in the faeces mainly in the form of bacterial protein.
5/09/2009 12:48pm, #156
Insulin-Like Activity of Concanavalin A and Wheat Germ Agglutinin—Direct Interactions with Insulin Receptors
Concanavalin A and wheat germ agglutinin are as effective as insulin in enhancing the rate of glucose transport and in inhibiting epinephrine-stimulated lipolysis in isolated adipocytes. These lectins, also like insulin, inhibit basal as well as epinephrine-stimulated adenylate cyclase activity of membranes obtained from homogenates of fat cells.
... more arrows pointing in what I feel to be a very fruitful research direction, but -- obviously -- experimentation is required to figure out whether the metabolic disorder of the insulin system that only occurs in grain-eating cultures is related to the insulin-like activity of grain leptins.
Oats & Whey product, but not tried it.“Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
5/09/2009 3:04pm, #157
When blood glucose values before the fructose infusion were at or below normal fasting levels, fructose elicited only a small plasma insulin response. In contrast, the insulin response was strikingly augmented when preinfusion blood glucose and plasma insulin levels were moderately elevated. The insulinotropic action of fructose appears closely related to the preinfusion blood glucose level. Fructose has little or no insulinotropic action in the absence of glucose but potentiates glucose-mediated insulin release.
Regardless, though, it's crucial that - at least at some level - we know what makes a difference and what doesn't. I can afford to spend a few extra bucks covering all the bases, but when you take a new nutritional paradigm and multiply it out over six-plus billion people, you need to have, ahem, trimmed the fat.
1) That under normal (or defined abnormal) circumstances, the human digestive system will allow intact leptins to reach, at minimum, the hepatic portal system, and probably the bloodstream. (Remember my previous question about polysaccharides? The same question applies to polypeptides. Same caveat also goes for sublingual absorption, of course...)
2) Or that said leptins can have an effect on the factors in question from within the gastrointestinal tract.
By my own amateur-level reasoning, those would combine to be necessary (but not sufficient) conditions for the hypothesis.
(I'll be set for casein pretty soon... got sixteen pounds of milk protein isolate in transit from TrueProtein as we speak)
Best I can do for oat fiber right now is this, which doesn't seem especially unreasonable, but I really wish these guys would ship to Canada.
How do you know that oat fiber is soluble, though? I ask because I'm irritated with the ambiguous/conflicting information that's been coming out of the manufacturing and marketing folks, and my good friends at the CNF and USDA NND haven't yet started to break up "dietary fiber" into soluble/insoluble/resistant starch.... so if there's a way to figure out the breakdown (without actually doing the test one's self), I'd really like to learn it.
5/09/2009 8:00pm, #158
High rates of endocytosis by small intestinal cells appear to be characteristic for lectins of all types [ ... ]
... some of the ones in wheat -- concanavalin A and wheat germ agglutinin -- are known to damage the epithelium (disruption of the microvilli, &c), thus increasing gut permeability (more so in coeliac patients):
Morphological changes of rat small intestine after short-time exposure to concanavalin A or wheat germ agglutinin
Your continued laboring of "slow carb" makes me wonder what you find controversial about the hydrolysis index (HI). Care to enlighten me?
“Most people do not do, but take refuge in theory and talk, thinking that they will become good in this way” -- Aristotle, Nicomachean Ethics, II.4
5/09/2009 10:05pm, #159
All right, this is a promising start. Raises two follow-up questions, though:
1) Lots of evidence to show the effect of lectins on the intestine itself. Is gut damage a viable mechanism for lectins to hit the portal vein? (I'm not clear about how endocytosis would transfer the lectins across the intestine - gets them into the border cells, but out?)
2) On p. 111, he mentions the effects of heat-treating the kidney beans. Most grain products I encounter have been baked - is this sufficient to denature their lectin content?
An equivalent amount of potentially available starch from each product was chewed by subjects, expectorated into a beaker and incubated with pepsin. The incubate was thereafter transferred to a dialysis tubing and incubated with pancreatic alpha-amylase for 3 h. Samples were removed from the dialysate at time intervals and the degree of hydrolysis was calculated as the proportion of the potentially available starch degraded to maltose. A hydrolysis index (HI) was calculated as the area under the hydrolysis curve with the product as a percentage of the corresponding area with white wheat bread. The method was applied to 21 cereal and legume products, chosen to cover as wide a range as possible with respect to metabolic response, and to include several of the proposed mechanisms to differences in metabolic behaviour of starch. The accuracy of the in-vitro method was evaluated versus the metabolic responses obtained with the same products in healthy subjects. A significant correlation between HI and glycaemic index (GI) was obtained in cereal as well as in legume products. A significant correlation was also obtained between HI and insulin index (II) with pooled data from all products.
The school library doesn't have the EJCN online that far back, so I can't look at the actual study itself, but based on the abstract, it seems fairly reasonable, and it would probably have a better test-retest.
The bigger issue, though, is more philosophical. If one wanted to take the GI -> HI progression to its logical conclusion, we'd extract the carbohydrate content from the foods directly and then expose it to known quantities of amylase. This would tell us interesting and useful things, and would make for an important component of a blood sugar/insulin model for dietary design.
But beyond the rate at which an arbitrary polysaccharide is broken down into constituent sugars, and the effects of said sugars on the body's chemistry, there lies the confounding factors - namely, the environment surrounding said polysaccharide in the foods that are actually being judged.
We can say, quite firmly, that amylopectin is hydrolyzed more quickly (in terms of liberated glucose per total glucose per unit time) than amylose. But our statements about the absorption over time-since-ingestion curves of two different foods - rather than the polysaccharides they contain - are much less firm.
Ad absurdum illustration, just because I enjoy drawing it: Take a portion of glucose. Divide it in half. Dissolve one half into an isotonic solution of water. Take the other half and weld it inside hollow steel balls.
The first serving is almost assuredly a "fast carb", and the second is almost assuredly a "slow carb" (or rather, a "no carb"). But the "carb" is identical between them. In this sense, referring to "fast carbs vs. slow carbs" gives a false impression of what's actually relevant to the calculations - see this thread for a protein equivalent.
This, incidentally, is one area where I'm not irritated with the researchers. I'm impressed with the work they're doing to identify and quantify the confounds. It's just the nature of the beast - the system's complex, and the testing is often intrusive and expensive.
But as you'd alluded to, manufacturers don't label the carb composition of food items beyond fiber/sugar/sugar alcohol/other. I've been trying to beat information out of Google Scholar for the past day or two, with limited success. Just a few tables is all I ask - one correlating a few significant (as in, I can buy them) foodstuffs with their saccharide constituents, and another to say "polysaccharide X is soluble, Y is insoluble, Z is digestible". If these tables exist, I haven't been able to find them.
More pragmatically, though... does oat fiber have cellulose (which, IIRC, is insoluble and thus undesirable for this purpose) in it?
Aside: apparently "beta-glucan" has been picked up as a marketing term by the fiber supplement folks, which is frustrating because (by my reading) it doesn't narrow things down any more than "dietary fiber" already does.
5/10/2009 9:26am, #160
page 257 of this protein delivery textbook, the section on endocytosis as a transport mechanism begins at page 261.
... dietary lectins are specifically taken up into the systemic circulation of rats, either through the disrupted intestinal wall or by breaching the gut absorptive barrier.
... that some lectins transit to general circulation is not controversial. If you read forward from page 264 you'll get a brief history of the study of lectins, which begins with the discovery of ricin-B (the most toxic lectin known). Aside: as unpleasant as the toxins and antinutrients in grains can be, the ones in certain legumes are much, much worse.
Cooking of beans does not necessarily destroy their toxic properties.
... there's much that can be done during preparation to improve the nutritive qualities of grains and legumes, though heat is often not enough. Sprouting is good (lectin content in seeds drops as they sprout). Unsprouted beans should be soaked for 24-48 hours before they're cooked (the combination providing better results than either step in isolation).
Traditional Food-Processing and Preparation Practices to Enhance the Bioavailability of Micronutrients in Plant-Based Diets
In the case of unsprouted wheat, the most useful process is lacto-fermentation (i.e. sourdough lactic acid bacteria hydrolyse gliadin peptides and inhibit their lectin-like behaviour, plus break down mineral-chelating phytates).
Proteolysis by sourdough lactic acid bacteria: effects on wheat flour protein fractions and gliadin peptides involved in human cereal intolerance
Sourdough bread made from wheat and nontoxic flours and started with selected lactobacilli is tolerated in celiac sprue patients
Amusingly, most of the steps that have turned out to improve mineral availability and reduce toxicity are exactly what your great grandmother would have done by oral tradition.
Handbook of food science, technology, and engineering, Yui H, Hui, pg 77
... for a quick rundown on the hydrolysis index (HI), dextrose equivalent (DE), &c. The Glycemic Index (GI) for most persons turns out to track the HI via a predictable function.
The CRC handbook of dietary fiber in human nutrition