This article suggests that obesity is linked to the type of microbiome of an individual in which obese people and normal or thin people have a difference in the species of microbes that live in their digestive tract. Given that this is true, how do you address the claim that obesity is hereditary or the likelihood of one being obese increases if their parents are obese and how would that relate to the individuals microbiome?
The article states that notable differences of gut microbiota between urban and rural US populations were found during this study. Do you believe this is due to the genetic variance in each population or the types of foods and toxins they are exposed to within their individual environments?
In the paper, the authors attempt to link a 'low genetic count' (LGC) with obesity. In Figure 4b, they show a graphic comparing the BMI changes and describe it by stating that obese LGC individuals gain significantly more weight than HGC individuals. Is it problematic to their claim that they fail to acknowledge the fact that lean LGC individuals had the greatest negative BMI change of all individuals portrayed in the figure?
In the "Getting to the Core of the Gut Microbiome" review, the authors call the obesity epidemic "sudden." Indeed, the epidemic is quite modern. The authors state that it is "likely to be the result of changes upstream of the human gastrointestinal microbiome." What caused these changes? What is different in our modern day environment, eating habits, genetics etc that caused this change?
In the Le Chatelier 2013 article, the authors state that the gene counts of the LGC and HGC individuals showed significant associations with all anthropometric and biochemical variables besides BMI and weight (p.544). Do you agree with their assessment that this points to the heterogeneity of the obesity phenotype where some individuals develop "co-morbidities" of type-II diabetes, CVD, etc. while others do not?
Also, do you think it would have strengthened their argument that a person's "other genome" may have a stronger influence on their obesity phenotype if they had analyzed the identified obesity susceptibility genetic variants in these same individuals and showed a weaker correlation than those found for their gut microbiome?
In "Getting to the Core of the Gut Microbiome" review paper, it is noted that "The role of host genetics, for example, is underscored by the fact that monozygotic twins exhibit a higher degree of co-variation in body adiposity compared with dizygotic twins, despite the similar microbial community structures of monozygotic and dizygotic twins", however due to the high amounts of research on the host genome's relation to obesity and this newer gut-microbiome approach, is there a possibility that the two genomes interact in novel ways to result in an obese or lean phenotype? How, then, should drug treatments be directed to help treat obesity?
In the review article "Getting to the core of the microbiome" the authors states that obese individuals have a lower percentage of Bacteroidetes in their gut microbiome compared to lean individuals. However, the author also states that if the individuals lost weight this percentage discrepancy is corrected. This led me to ask whether the individuals gut microbiome is inherited and therefore some people are more susceptible to obesity, as parts of the original article implied, or whether these individuals started off with the same percentage as their lean counterparts and the discrepancy came about as a result of them becoming obese.
In the 2013 Le Chatelier article, the researcher noted that "antibiotic use in early childhood...led to an increased risk of overweight" since certain microbial species which protect against weight gain had been eliminated. Do you think the high prevalence of antibiotic use in our society could be a contributing factor to the growing obesity problem in light of the information from this article?
The paper by Le Chatelier indicated that there were significant differences in microbiota diversity in urban and rural populations, as well as between populations from different countries. Since stress can impact the the gut microbiota, do you think it is likely that this may also be correlated with the stress levels of each group of individuals? Additionally, could stress have been a significant factor in patterns seen mouse model data?
In the methods and summary section of the research paper "Richness of human gut microbiome correlates with metabolic markers", they state that before each participant underwent blood sampling and anthropometric
measurements that they had fasted overnight. We each have our distinct gut microbiome whether we are obese or lean, which changes with our diet and environment. I understand that fasting would minimize ones blood tests from variations of lipids, but wouldn't ones diet, and personal habits play a factor in the results regardless of fasting? The differences between ones gut microbiome could be from other factors and not just that of their weight. Could this be the reasoning for the need for a large number of samples and participants, whether human or mice testing studied, to be able to normalize the data to get the results they concluded?
In the Le Chatelier 2013 article, the idea that antibiotic use early in life may contribute to obesity due to the elimination of some microorganisms was discussed. Do you think that dietary changes or supplements could help those individuals with a low gene count, for either those individuals who are predisposed to LGC or who have been affected by antibiotic use?
In the LeChatelier et al. 2013 paper, the authors state on page 543 that avoiding the "separation of individuals into the LGC and HGC groups, may allow identifying additional species that explain variation of gene numbers."
This then made me wonder why they ever separated these groups --
it seems problematic to me to put people in these groups immediately, since grouping people may have precluded more parsimonious explanations of the microbiome diversity/obesity correlations the authors were seeking to address. For example, they do address the types of species present in LGC and HGC individuals, but I think it makes more sense to compare that data directly to an individual's BMI and health status.
In the paper “Richness of human gut micro biome correlates with metabolic markers” and review paper “Getting to the core of the gut microbiome”, it is shown that different number of microbial genes and gut bacteria is related to obesity. Specifically, with low gene count (LGC), it is more likely to be obese while with high gene count (HGC), it is more likely to be lean. Then based on these outcomes, if diseases are related to microbial genes or micro biome, could it be possible to transfer certain microbiome to the patient who did not have the microbiome? In this case, do you think it is gonna be successful treatment without any problem?
In "Getting to the core of the gut microbiome" by Tschöp, et al, they discuss the possibility that certain gut microbe populations could have been wiped out by "phage predation." Do you think this could be utilized as a feasible treatment for obesity or other digestive tract problems? Could engineered phages be used to target certain species of bacteria in the gut?
The LeChatelier paper had some cool findings, including that their LGC group had higher levels of obesity and adiposity. That would seem to suggest that certain individuals with LGC "could" be at risk for developing obesity. The researchers were able to narrow down the differences between being LGC and HGC to relatively few species.
What kinds of research would need to be done to demonstrate a specific contribution of these gut microbes to higher rates of obesity?
While I found the paper on the richness of the human microbiome to be very interesting and relevant I believe that through the employment of quantitative metagenomics on fecal DNA. The paper defines the quantitative metagenomics approach as a way of determining the profusion of known intestinal bacteria. With the incredible diversity of bacteria, how are we to know that all of the integral bacteria in the gut are recognized through this method? What if an integral bacterium is not currently known to localize within the intestines? And what are the potential repurcussions for missing these unknown bacteria within the human gut?
Le Chatelier's ariticle mentions, when studying the phenotypes of LGCs and HGCs that "the difference is significant for men and a trend is detected for women". Noting these different results, would studying men and women in separate studies result in more accuracy? Or is grouping them together more useful for this study?
The Le Chatelier paper suggests that childhood antibiotic use may decrease gut microbial richness leading to an increased likeliness of obesity and related diseases later in life. However, humans are also exposed to antibiotics in other ways. In modern agriculture, it has become a common practice to feed animals antibiotics in order to reduce disease in livestock. Humans later consume products from these animals and indirectly ingest the antibiotics. Could these antibiotics affect human gut microbial levels leading to an increased likeliness of obesity across much of the population?