Morning all. Woke up early to the lovely sound of rain here in drought-stricken California.




Still thinking about gut bacteria and sugar craving.....I'm stuck on this: if yeast and other sugar-loving bacteria in our colon are driving us to eat sugar, how does the sugar get to those bacteria in the colon if sugar is rapidly absorbed into the bloodstream, presumably in the small intestine? I wouldn't think much sugar actually makes it to the lower intestinal tract where these beasties live.
I would like to see if anyone is actively researching these issues, including leaky gut syndrome. Seems doable to sample intestinal flora in a systematic way and also find direct physical evidence for leaky gut syndrome. Meanwhile, I'll hedge my bets and go buy some Bubbie's probiotic sauerkraut.
I tend to binge on sugary treats with some regularity, about once/week. No matter what else is going on in my life emotionally or even while sticking to Ideal Protein and losing weight as I'm currently doing. According to an acquaintance who reads up on this topic, sugar craving is caused by die-off of sugar-loving microbes as they run out of fuel. They signal the brain somehow to crave more. Maybe for me this process is a 7 day cycle. I'm skeptical but interested.
I just remembered a recent IP coaching video which linked to this:
http://www.ncbi.nlm.nih.gov/pubmed/22064556
J Clin Gastroenterol. 2012 Jan;46(1):16-24. doi: 10.1097/MCG.0b013e31823711fd.
The intestinal microbiota and obesity.
Kallus SJ1, Brandt LJ.
Author information
Abstract
Obesity has been and continues to be an epidemic in the United States. Obesity has been addressed in multiple health initiatives, including Healthy People 2010, with no state meeting the proposed goal of a prevalence of obesity < 15% of the adult population. In contrast, obesity rates have continued to increase, with the self-reported prevalence of obesity among adults increasing by 1.1% from 2007 to the present. Indeed, since 2009, 33 states reported obesity prevalences of 25% or more with only 1 state reporting prevalence < 20%. There have been multiple approaches for the treatment of obesity, including fad diets, incentive-based exercise programs, and gastric bypass surgery; none of which have been optimal. In a murine model, it was shown that the majority of the intestinal microbiome consists of two bacterial phyla, the Bacteroidetes and the Firmicutes, and that the relative abundance of these two phyla differs among lean and obese mice; the obese mouse had a higher proportion of Firmicutes to Bacteroidetes (50% greater) than the lean mouse. The same results were appreciated in obese humans compared to lean subjects. The postulated explanation for this finding is that Firmicutes produce more complete metabolism of a given energy source than do Bacteroidetes, thus promoting more efficient absorption of calories and subsequent weight gain. Researchers were able to demonstrate that colonizing germ-free mice with the intestinal microbiome from obese mice led to an increased total body fat in the recipient mice despite a lack of change in diet. The converse, that, colonizing germ-free obese mice with the intestinal microbiome of thin mice causing a decreased total body fat in the recipient mice, has not yet been done. Other possible mechanisms by which the intestinal microbiome affects host obesity include induction of low-grade inflammation with lipopolysaccharide, regulation of host genes responsible for energy expenditure and storage, and hormonal communication between the intestinal microbiome and the host. The following review discusses the microbiome-obesity relationship and proposed mechanisms by which the intestinal microbiota is hypothesized to influence weight gain.
and this:
http://www.ncbi.nlm.nih.gov/pubmed/23526699
Obesity (Silver Spring). 2013 Dec;21(12):E607-15. doi: 10.1002/oby.20466. Epub 2013 Jun 22.
Human intestinal microbiota composition is associated with local and systemic inflammation in obesity.
Verdam FJ1, Fuentes S, de Jonge C, Zoetendal EG, Erbil R, Greve JW, Buurman WA, de Vos WM, Rensen SS.
Author information
Abstract
OBJECTIVE:
Intestinal microbiota have been suggested to contribute to the development of obesity, but the mechanism remains elusive. The relationship between microbiota composition, intestinal permeability, and inflammation in nonobese and obese subjects was investigated.
DESIGN AND METHODS:
Fecal microbiota composition of 28 subjects (BMI 18.6-60.3 kg m(-2) ) was analyzed by a phylogenetic profiling microarray. Fecal calprotectin and plasma C-reactive protein levels were determined to evaluate intestinal and systemic inflammation. Furthermore, HbA1c , and plasma levels of transaminases and lipids were analyzed. Gastroduodenal, small intestinal, and colonic permeability were assessed by a multisaccharide test.
RESULTS:
Based on microbiota composition, the study population segregated into two clusters with predominantly obese (15/19) or exclusively nonobese (9/9) subjects. Whereas intestinal permeability did not differ between clusters, the obese cluster showed reduced bacterial diversity, a decreased Bacteroidetes/Firmicutes ratio, and an increased abundance of potential proinflammatory Proteobacteria. Interestingly, fecal calprotectin was only detectable in subjects within the obese microbiota cluster (n = 8/19, P = 0.02). Plasma C-reactive protein was also increased in these subjects (P = 0.0005), and correlated with the Bacteroidetes/Firmicutes ratio (rs = -0.41, P = 0.03).
CONCLUSIONS:
Intestinal microbiota alterations in obese subjects are associated with local and systemic inflammation, suggesting that the obesity-related microbiota composition has a proinflammatory effect.
Copyright © 2013 The Obesity Society.