|
Potatoes! I don't suggest you eat them raw, but if you did they would make a good source of resistant starch. You don't eat potatoes at all? Read the Potato Manifesto and learn why regular potatoes are not as black as they are portrait! |
I guess, you will remember my
post on WM-HDP from back in the day. As usual you, as a
SuppVersity reader were in the know, way before the ThermiCarbs and its identical clones hit the supplement market. It has however gotten relatively quiet around these purported super starches, which bypass enzymatic breakdown in the small intestine and get converted to short-chain fatty acids (SFCA) in the colon. Why? Well, my best bet is that people expected some sweet junk of which they could eat as much as they wanted with the only side effect being increased muscularity and decreased body fat levels. I am well aware that you knew better than that, but you know how people are: Always on the look-out for the magc pill... or in this case, the magic starch ;-)
Cutting fat by eating more: The old adage of the "fat burning foods"
Be that as it may, a soon to be published study by researchers from the
Commonwealth Scientific & Industrial Research Organization in Australia confirms: If you
exchange a high enough amount of regular carbohydrates with resistant starches (even regular ones, lower resistance to enzymatic breakdown that WM-HPD), this can be a viable tool to shed some body fat.
Unfortunately, though, the results of the very this study do also suggest that the effectiveness of this regimen will largely depend on (a) your phenotype and (b) your willingness to follow your hopefully not totally messed up satiety response and decrease your caloric intake voluntarily, just as the male Sprague-Dawley, the 'subjects in this study by Belobrajdic, King, Christophersen and Bird.
|
Figure 1: Energy intake and final body weight (left) and relative changes in fat mass and total liver weight after 6 weeks on diets with different resistant starch content (based on data from Belobrajdic. 2012) |
Both (a) and (b) could however be major caveats when it comes to the practical realization of similar results in human beings, to whom I would not suggest that they follow a standardized diet with ~15%
fat, 19% protein and ~66% carbohydrate, either - regardless of whether they exchange 0%,
4%, 8%, 12% and 16% of the mostly high GI carbs in their diets by resistant starch or not (the values are relative
to the weight of the chow).
|
Just as raw potatoes, green bananas contain RS-2, the natural form of fermentable resistant starch. When you cook them, the RS2 content is continuously reduced. |
Note: The "2" in "RS2", indicates that RS2 is, contrary to WM-HDP, which belongs to the "RS4" variety of resistant starches, a
naturally occurring molecule. And though this is the case for WM-HDP vs. high amylase maize starch, the latter does not necessarily mean that one is more resistant to enzymatic breakdown than the other. You could for example think of special applications, where you want to have a starch that of which roughly 75% will be broken down into glucose in the small intestine, while the other 25% are fermented further down in the large intestine. This would be a synthetic molecule and therefore categorized as RS4, but still relatively easily "digested".
What I consider especially problematic, though is the fact that people who like to eat, let alone those, who use food as a, if not the only way to experience pleasure in their lives (eating for reward), are going to have a very hard time to satisfy their cravings with this blatant "food". I mean, we all know that "satiety" is not really an issue for most people with weight problems, so it remains questionable to which degree those who actually need a crouch like this will eventually benefit from a resistant starch which exerts its fat loss effect in rodent experiments at least partly via dose-dependent decreases in food intake -- 3%, 6%, 9% and 11% in the 4%, 8%, 12% and 16% resistant starch groups, respectively.
Ok, I have to admit there is more to it than just eating less
|
Figure 2: For the lean rodents, body weight gain and feed efficacy (weight gain per gram of chow) favor different "optimal" RS2 levels. |
Allegedly, the reduction in food intake alone cannot explain the decrease in weight gain in either the obese or lean rodents, but if you take a closer look at the data I plotted in
figure 2, it does still become obvious that the ameliorative effects weight gain in the obesity resistant (i.e. naturally lean) rodents don't obey the "more is more" rule, as the scientists would have it in their abstract:
"Obesity prone rats (OB) gained less weight with 4, 12 and 16% RS compared to 0% RS, but the effect in obesity resistant [lean] animals was significant only at 16% RS. Irrespective of phenotype, diets containing ≥8% RS reduced adiposity compared to 0% RS. Energy intake decreased by 9.8 kJ/d for every 4% increase in RS. [...] Insulin sensitivity was not affected by RS." (Belobrajdic. 2012)
In the naturally lean animals, the "optimal", i.e. the lowest feed efficacy would be achieved with 8% of RS2 in the chow and not as the "≥8% RS" implies with 16% of resistant starch in the diet.
Ok, I have to admit there is more to it than "minimal feed efficiency"
In the scientists defense, it must however be mentioned that the
plasma lipid and
gut / satiety regulating hormone levels they measured did in fact show an almost linear increase with the amount of fermentable resistant starch in the diets (see
figure 3). Since Belobrajdic et al. do not provide individual data from the two groups, but settle for a table that will tell you that there were no treatment x group interactions (this means that the outcome was not different for obesity resistant and prone animals) and a phenotype interaction with the overall outcome was only present for leptin, there is no way to tell for sure.
|
Figure 3: Inter-group comparison (not differentiated for lean vs. obese, because there were no significant interactions, except for leptin) of plasma lipid and gut derived hormone levels (data adapted from Belobrajdic. 2012) |
So, with all these "admission" (as in "I have to admit..."), I have to admit *lol* that using high-amyolse starch as a part of your contest prep, maybe to bake pancakes or use it in another food, where the "taste" does not matter that much is could in fact be a viable dietary tool. It won't get you stage ready on its own, though and has one major caveat I have not even mentioned yet:
You better make sure you always know where the next clean toilette is. Assuming that those 16% RS2 have the same effect on the volume of your feces as they had on that of the rodents in the study at hand, you may be spending 5-times more time on the loo thhan usually ;-)
|
If you can't remember what WM-HDP was, click on the image to go back to the article. Regardless of whether you pick up a natural or an artificial starch, this stuff is not "zero calories"! The high amylose maize starch in the study at hand has 10.45kJ (WM-HDP should be similar), i.e. 2.5kcal/g you will have to make up for by cutting out real foods. |
Bottom line: Assuming that the results from the study at hand translate to human beings the incorporation of resistant starches in your diet seems - at least to a degree at which your bowel can handle it - to entail a lot of health benefits. The problem I see, is that you will have to force down these empty calories instead of eating healthy foods if you want to benefit.
If you simply add resistant starches (natural or artificial) to your diet, without cutting back on calories, elsewhere, you will become fatter, not leaner.
You will also have to take into account that adding resistant starch to the high sucrose diet of the rodents in this study will necessarily entail greater benefits than exchanging some tubers, rice, fruit and other non-sugary carbohydrate sources from a healthy diet with resistant starch powder - not to speak of all the beneficial micro-nutrients you will be missing!
References:
- Belobrajdic DP, King RA, Christophersen CT, Bird AR. Dietary resistant starch dose-dependently reduces adiposity in obesity-prone and obesity-resistant male rats. Nutr Metab (Lond). 2012 Oct 25;9(1):93.