Tuesday, July 23, 2013

Fructose Toxicity or Bacteria Deficiency? 10 Billion CFU of Probiotics Ameliorate, But Don't Solve the Fat Problems That Are Brought About by a Crappy Diet + Fructose Water

The mere fact that probiotics can ameliorate some of the damage that's done by the way people eat this day, does not imply that they are the origin of the obesity epidemic; and the study at hand shows: They are not the solution either.
A recently published study from the Key Laboratory of Dairy Biotechnology and Engineering at the Inner Mongolia Agricultural University could hold a "solution" - or rather a way to ameliorate the damage that comes with the overconsumption of fructose.

Cause or solution!? I don't care if it works!

Based on previous observations the researchers speculated that the provision of  10,000,000,000 CFU/day Lactobacilli Casei Zhang bacteria  to male Sprague Dawley rats who were guzzling "rodent coke", i.e. 25 % fructose water, 24/7 for either
  • 9 weeks after the supplementation was initiated, or
  • 4 weeks after 9 weeks on fructose water
would ameliorate the weight negative side effects of the addition of fructose to an already 100% unhealthy diet comprising 50 % corn and wheat starch, 25 % wheat bran, 20 % soybean pieces, 2 % bone powder, 2 % fish powder, 0.9 % table salt and a 0.1 % vitamin mixture would have on the impaired glucose tolerance and the incidence and severity of the other typical side effects that occur, when you are chronically poisoning rodents with this type of dieting.

So, what did the scientists find?

While it appears to be self-evident, the first trivial, yet extremely important result of the study at hand is the observation that the bacteria did not just make it to the gut of the rodents, but actually settled and survived there. This lead to a significant increased numbers of Lactobacillus and Bifidobacterium (what we currently think are the "good guys") and a concomitant decrease in the number Clostridium bacteria in the intestine.
Figure 1: Liver gylcogen, serum insulin, osteocalcin, and MDA levels expressed relative to rodents on control diet after 9 and 13 weeks on different diet + supplementation regimen (Zhang. 2013)
These microbial changes went hand in hand with normalization of liver glycogen in all groups. Only the animals who had been pretreated with probiotics did yet show lower insulin and GLP-2 levels.
The improved response to the glucose tolerance test, on the other hand was observed in both the pre-treated group, in which the rodents received fructose and probiotic bacteria together for 9 weeks, and the "therapeutic" group, in which the probiotics were gavaged to already obese rodents for only four weeks.
Figure 2: Glucose response (AUC) in tolerance test and body weight development (Zhang. 2013)
And while there were no significant differences in body weight, the administration of L. casei Zhang could at least improve the compromised glucose tolerance, increase the dropping osteocalcin levels and restore the bile acid secretion in the "therapeutic group".

Bottom line: In conjunction with the decreased serum MDA and the upregulation of LXR-a, PPAR-gamme and AdipoR2 gene expression the overall picture that emerges is somewhat similar to that you would see with some of the "better" diabetic drugs. Yet while this may sound great, at first, it is in the end a total bummer.

Aside from the people whose businesses flourish, when people are sick enough to need medication, but not so sick that they would die away anytime soon, "solutions" like these don't help anyone. And let's face it - we all know that the root cause of the problem is not a messed up gut microbiome. That may be a consequence, yes. The root cause, on the other hand, is the way millions of people "eat".

References:
  • Zhang Y, Wang L, Zhang J, Li Y, He Q, Li H, Guo X, Guo J, Zhang H. Probiotic Lactobacillus casei Zhang ameliorates high-fructose-induced impaired glucose tolerance in hyperinsulinemia rats. Eur J Nutr. 2013 Jun 25.