I think this was a good post, but it didn't swing for the fences.
click to view larger... I am not going to waste my time further here. I've looked back at enough animal studies that were discussed previously here testing some other hypothesis and pointed out several, now, where the mineral imbalance notion doesn't fit. You cherry pick what you can make fit, you ignore the rest.I hope you'll read my post on hypothalamic damage when it comes out. ...
I'm hopeful the whole point of the article(s) won't be to just sweep this under the rug in some quick dismissal so that you can go about sticking to comfortable theories.
I took it upon myself to read your take of the microbiome—a burgeoning area of interest in the world of obesity and metabolic issues.
OK so I later had to ask what these were, and as it turns out, Duck has found his way back almost 5 years of blogging to the following:For the few times you've ever mentioned the microbiome on this blog, it felt like you basically took it upon yourself to sweep the entire microbiome under the rug with a two-part post.
- Of Mice, Men & Microflora I: The microflora transplant study
- Of Mice, Men & Microflora II: Microflora & Energy Balance
Dismissing new perspectives seems to be the name of the game here. I thought that seemed rather hasty and I personally think it shows a lack of interest in challenging your own ideas. (I wouldn't have engaged in a conversation here if I wasn't interested in getting outside of my own comfort zone).
And?There is so little we still know about the microbiome, but it's importance has already shown to be quite bigger than anyone ever previously imagined. And, whattaya know, our microflora influence the way we absorb micronutrients, like iron.
On the other hand, many major scientific discoveries are often ridiculed and dismissed when they are first examined by the established science. You certainly wouldn't be the first to dismiss something important—happens all the time.
|"Our results indicate that the obese microbiome has an |
increased capacity to harvest energy from the diet."
- Virtually no changes after six weeks in either group for pretty much everything.
- To stress: NO CHANGE IN WEIGHT (or anything else for that matter)
- No changes in intake, REE, etc.
- Changes in some strains of bacteria, increasing butyrate producing bacteria in those receiving the lean FMT.
- Improvement in peripheral insulin sensitivity as measured by hyperinsulinemic-euglycemic clamp.
Before moving on, Duck must have missed where the same day as Mice II, I posted a short post of links, one of which was to the "state of the knowledge" circa 2010. You will note that the "obese microbiome" is in and of itself a controversial issue. The same patterns aren't always seen. Despite discussing numerous other avenues vis a vis insulin sensitivity and overall metabolism, etc., the paper concludes as follows:
Intestinal microbiota may play a pivotal role in converting nutrients into energy. Variations in the composition of microbiota are found in obese humans and mice. Increased energy yield from diet in obese mice and humans could be a contributing factor to obesity, although the pathophysiological processes driving this bidirectional relationship have not been fully elucidated.
Nah nah na na nah naaaahhhhh ... Vindication!!!
In both humans and animals there are characteristic changes in the gut microbiota associated with obesity. In animals but not in humans altering the microbiota can result in weight loss and weight gain which does not occur in humans.
This suggests that in humans the changes in gut microbiota are an association with rather than the cause of obesity.
It is highly unlikely that fecal transplantation would be used in humans to treat a chronic non-life-threatening condition such as obesity. The one and only significant fecal transplant study which addressed only insulin resistance was first presented at the European Association for the Study of Diabetes meeting in Stockholm in 2010 and 2 years later was published in Gastroenterology.
Ref. 31: Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. (does not appear much different from thesis at first glance)
The study involved 18 insulin-resistant nondiabetic men who without a change in diet or activity and who after bowel cleansing received by nasogastric tube either an autologous fecal transplant or a fecal transplant from a lean male donor. This study showed a decrease in the median rate of glucose disappearance in those who received a fecal transplant from a lean donor compared with those who received an autologous fecal transplant (26.2–45.3 dmol/kg·min) without significant weight loss.The improvement in insulin sensitivity was only temporary since when retested 12 weeks later the rate of glucose disposal had returned to the baseline level which was similar to the glucose disposal rate in the autologous fecal transplant group.
- Transplantation of Microbes for Treatment of Metabolic Syndrome & NAFLD (FMT). Just submitted July 2015! Looks to be a longer term (6 months) repeat of the 2010 study, 9 autologous, 12 FMT from lean. They are not yet recruiting, starting in January though. Estimated completion data collection Sept. 2017, study Dec. 2017. If you don't see another blog post on this until 2018 if I'm still blogging, you'll know why ;-) If the effect didn't last for 12 weeks in the prior study ....
- Fecal Microbiota Transplantation on Type 2 Diabetes Mellitus. This one was initiated in 2012 and today's status is "this study is enrolling participants by invitation only". It was scheduled to end earlier this year. Not holding breath. It appears to be an uncontrolled study utilizing transplant via endoscopy.
Summary and conclusions
There is clearly in both animals and humans changes in the gut microbiota that are associated with obesity. In animals the transfer of these obese microbiota to germ-free animals causes the development of obesity. However, in humans the available evidence would suggest that the differences in the gut microbiota that are associated with obesity probably result from the utilization of a high-calorie, high-fat and high-carbohydrate Western diet.
Therefore, it is most likely that the typical obesity microbiota is an association with dietary intake rather than being a cause of obesity.
In both humans and animals environmental changes such as changes in diet, utilization of artificial sweeteners, decreased exercise and disrupted diurnal rhythm will quickly convert the microbiota to that of an obese pattern. In addition, dietary changes that occur following a gastric bypass most likely account for the changes in the microbiota from an obese to a lean gut microbiota pattern that occur with this surgery. However, the possibility that because of gastric bypass surgery, FXR is downregulated resulting in decreased bile acid production which allows for regrowth of bacteria which facilitate weight loss should also be considered.
If it is believed that obesity occurs as a result of an obese microbiota pattern rather than the obese microbiota being a marker for the obese state, large studies utilizing either probiotics or prebiotics should be performed since for ethical and practical reasons a study of fecal transplantation would be difficult to perform in humans who are neither acutely ill nor have a “life-threatening” illness. However, now that a fecal capsule which can be swallowed is available fecal transplant could in the future become more acceptable and could be tested in the obese human.
Currently, the outcomes of prebiotic and probiotic utilization in the treatment of human obesity are less than convincing and certainly do not match the studies performed in animals.
A large, blinded, randomized study could and should be performed utilizing either prebiotics or probiotics. If any of these studies showed positive results utilization of prebiotics or probiotics or even fecal transplantation or bacterial components of a healthy stool could be utilized to avoid or reduce the number of bariatric surgeries being performed which would result in substantial savings to the health-care system and decreased morbidity and mortality.
My Concluding Thoughts
I had a hunch in 2010 that this would not go anywhere. That wasn't some quick dismissal. I read way more than I ever link to or discuss in a blog posts, etc. I don't add much of late, but I have a Library Blog where I used to share some of the stuff I came across, just to give a glimpse of what I'm talking about. I use a service known as Mendeley (when I can remember) and have a folder on this topic in Mendeley that contains many more citations than I've ever shared.
I don't have a particular interest in digestive illness. Sue me. When this became a hot topic for obesity and metabolic disorders, I did look, probably in far greater depth than critics like Duck Dodgers, and no doubt with a deeper understanding of the process and meaning of what I'd read.
Rodents use bacteria to extract SIGNIFICANT energy from their food, humans do not.
- Rodents have substantial metabolically active brown fat.
- Rodents expend a much higher proportion of total energy on maintaining body temperature.
- Rodents can dial this down or ramp it up to maintain homeostasis to a greater extent.
- Human brains require a much higher proportion of total energy expenditure.
- Human white fat depots differ in size, location and proportion from rodents and there is great variability across the species on a gender, age, race and individual basis.
- Did I mention humans don't have a lot of brown fat?
- ... etc. etc. etc.
Together, these findings support the notion that the gut microbiota can influence both sides of the energy balance equation, and underscore the importance of considering our metabolome in a supraorganismal context.