Don't worry, I am neither going to rant, nor am I suggesting that the whole idea about the importance of the gut microbiome is similarly flawed as the "eat fat and get fat"-hypothesis. The thing I do yet want to point out, before I tell you more about the latest scientific findings, is that our knowledge about the good and the bad guys in our intestines, about the ways they interact and about the short- and longterm effects of these interactions are so limited that my gut tells me (all puns intended) that everything that goes beyond the classics, i.e. the consumption of a diet rich in various types of fibers and a reasonable amount of fermented foods could well turn against us in a not very distant future.
Feeding the good guys: Does it work? And how does it work?
Based on the currently available evidence, it does however in fact look like the shift towards short-chain fatty acid producing bacteria, the scientists from the University of Minnesota and the scientist from the Fred Hutchinson Cancer Research Center initiated in their 20 study participants (ten men and ten women) who had been recruited via flyers around the University campus (that alone goes to tell you how "mainstream" the notion of beneficial gut bacteria has become). The subjects were health and aged between 18 and 60 years, they were non-smokers and were not taking any prescription meds and contrary to the average American (cf. "How Fat We Have Become") their BMIs were in the normal range.
Obviously the test breakfast, as well as the bars and beverages the dietary composition of which you can see in table 1 contained additional "functional" additives. As indicated by the titles above the respective columns in table 1, these were
"Participants consumed five treatments in a double-blind, cross-over design with treatment periods of 7 d followed by a 21 d washout period. On day 1 of the study, following a 12 h fast, participants arrived at the GCRC and consumed either a low-fibre control breakfast or one of four fibre-containing breakfasts. Meals consisted of a muffin, hot cereal, and fruit-flavoured beverage. For the next 6 d, participants consumed the study products at home. Treatments were provided as cereal bars and a beverage mix, which was pre-measured into 500 ml water bottles. Participants were instructed to consume four cereal bars and one beverage over the course of each day." (Klosterbuer. 2013)
Table 1: Macronutrient composition of the test meal on day 1 and the supplemental cereal bars and beverages the subjects consumed in the course of the 6-day study period on four occasions every day (Klosterbuer. 2013) Figure 1: Short-chain fatty acid content of the stools (top), number of stools and consistency (1=hard, 4=diarrhea, middle), gastrointestinal symptoms (bottom, Klosterbuer. 2013)
- for the beverages and bars in the treatment groups, 20g SCF or RS alone or in combination with 5 g pullulan (SCF+P and RS+P) for the beverages and bars and
- for the beverages and bars in the control group, fully digestible maltodextrin
- the short chain fatty acids (SCF) were produced via hydrolysis of maize starch, followed by
cooling to form a branched structure,
- the resistant starch (RS) was a type 3 (RS3) retrograded starch roduced from heat moisture-treated, high-amylose maize starch, and
- pullulan is a linear glucose homopolysaccharide that's formed during the fermentation of dextrin by the yeast Aureobasidium pullulans.
Astrology was yesterday, feceology (=poopology ;-) is the future!
Aside from the obligatory protocols on the state of their digestive health the subjects also had to collect stool samples, which were then analyzed by the researchers who were looking at the RNA and DNA content of the samples to identify any changes in the makeup of the gut microbiom, without exact quantification of individual strains. What they found was that ...
"[a]mong the treatments, the control was significantly different from the SCF (P<0.001) and SCFþP(P<0.0002) treatments. The SCF treatment was significantly different from the RS treatment (P<0.007), and the SCF+P treatment was significantly different from the RS+P treatment (P<0.002). The GMC [gut microbial community] following the consumption of the SCF and SCF+P treatments was not significantly different." (Klosterbuer. 2013)Now this certainly does not sound very informative, right? It in fact isn't but let's be honest, what's the additional value of me telling you that the scientists were able to associate a certain peak in the bacterial make up with either Anaero-coccus vaginalis or Parabacteroides goldsteinii and another one with either Parabacteroides distasonis or Parabacteroides merdaeusing anisilico? Not much, right.
"I know that we know nothing" An adequate description of the "state of the art"
My casual observation that knowing the funky names of the individual bacteria that felt specifically cosy in the acidified short-chain fatty acid loaden milieu that formed in response to the dietary intervention is about as useful to you as knowing all the names of the tiny insects in the Amazon Delta. In view of the fact that this is not much different for the scientists who were not even able to tell exactly which bugs they were looking at here. In fact, we have not even come so far to say "little do we know" - the current state of our "understanding" of the complexity of the gut microbiom is simply far from allowing any reliable prognosis statements on which bacteria we want in which ratios.
|Figure 2 (first published in "Waxy Maize Reloaded"): Changes in postprandial energy expenditure (left) and fatty acid oxidation (right) after the ingestion of regular and WM-HPD pancakes (data adapted from Shimotoyodome. 2011)|
There is yet an important "on the other hand" we must not forget
|GLP-1 is also partly responsible for the profound weight loss after bariatric surgery. In this case it is yet not the rise in short chain fatty acids, but as the scientists speculate the mechanical stretch and the influx of dietary fat that would otherwise have been absorbed earlier during the digestive process that triggers the release of the "satiety hormone" glucacgon-like peptide 1 (GLP-1, read more)|
As far as this part of the equation goes, we do therefore actually "know" something, what we do not know, but there are obviously a couple of my beloved "on the other hands" we still have to take into account. The most significant of these is unquestionably that impressive results as those that were observed in the very short run in the Shimotoyodome study will only arise in scenarios, in which the regular sugars and starches 90% of the Western population literally lives on are replaced with fermentable alternatives.
As long as you keep on the twinkies and dingdongs diet, the composition of your gut microbiome won't save you - no matter how good the critters are in turning fermentable starches into short chain fatty acids.
|Figure 3: Different resistant starch content of various foods (% dry matter; based on Goni. 1996)|
Remember: If A → B & A → C, this does not imply B → C
Epidemiological studies such as Layden et al.'s 2012 analysis of the body composition of young, obese women in which the researchers found a negative correlation between body fatness (esp. visceral obesity) and the SCFA production in the colon do therefore not necessarily tell us that having a certain gut microbiome protects you from obesity (Layden. 2012). Observational studies like these, but also all experiments in which the human or rodent "participants" had the chance to compensate for the intake of fermentable starches or other supplements by skipping on foods they'd otherwise consume, simply tell us that eating fermentable starches is better than eating sugary junk - not more, but also not less.
|Can saturated fat cause endotexemia? Learn the answer here!|
All the aforementioned benefits require the reguar ingestion of more than just trace amounts of fermentable starches. These pre-biotics will automatically have the "beneficial" bacteria in your gut get the better of the "bad guys" and it is a necessary prerequisite that any probiotics you are consuming either in pill form or from enriched foodstuff can take full effect. In other words:
Pre-biotics don't support probiotics, it's the other way around. Probiotics can support and accelerate the desired permanent change the regular consumption of prebiotics will bring about.
I know the product descriptions on the shiny websites of the snake oil industry will conceal that, but without a consequent and permanent change in your dietary habits, you can as well flush your super-potent 100 billion bacteria per serving probiotic directly down your toilette.
|Even the nicest subtenants can become a real problem, when they come over without being asked day by day. Unfortunately, all sorts of gut bacteria (even the "good" ones) have as imilarly nasty habit of translocating through a leaky gut wall into parts of your body, where you certainly don't wont them... read about the nasty consequences, here|
You are what you eat, not what your supplement! The same goes for the composition of the bugs in your gut and if you want them to produce short chain fatty acids for you you better make sure they get the raw materials on a consistent basis. That this works like a charm within no more than 6 days is evidenced by the study publication of which triggered this lengthy discussion.
Whether all the purported health benefits will become visible in the short, long or very long term will yet still have to be elucidated... and that this is probably not going to happen, when you try to get your fermentable starches from bread only (0.25g per slice vs. navy beans 10g per 1/2 cup and even bananas 5g per banana)
- Goñi I, García-Diz L, Mañas E, Saura-Calixto F. Analysis of resistant starch: a method for foods and food products Food Chemistry. 1996; 56(4):445–449.
- Layden BT, Yalamanchi SK, Wolever TM, Dunaif A, Lowe WL Jr. Negative association of acetate with visceral adipose tissue and insulin levels. Diabetes Metab Syndr Obes. 2012;5:49-55.
- Klosterbuer AS, Hullar AJH, Li F, Traylor E, Lampe JW, Thomas W, Slavin JL. Gastrointestinal effects of resistant starch, soluble maize fibre and pullulan in healthy adults. British Journal of Nutrition. 2013 [Epub ahead of print].
- Lin HV, Frassetto A, Kowalik EJ Jr, Nawrocki AR, Lu MM, Kosinski JR, Hubert JA, Szeto D, Yao X, Forrest G, Marsh DJ. Butyrate and propionate protect against diet-induced obesity and regulate gut hormones via free fatty acid receptor 3-independent mechanisms. PLoS One. 2012;7(4):e35240.
- Shimotoyodome A, Suzuki J, Kameo Y, Hase T. Dietary supplementation with hydroxypropyl-distarch phosphate from waxy maize starch increases resting energy expenditure by lowering the postprandial glucose-dependent insulinotropic polypeptide response in human subjects. Br J Nutr. 2011 Jul;106(1):96-104.
- Wroblewska M, Brzuzan L, Jaroslawska J, Zdunczyk Z. Effect of buckwheat sprouts and groats on the antioxidant potential of blood and caecal parameters in rats. Int J Vitam Nutr Res. 2011 Sep;81(5):286-94.