Pete said:
"But the extent to which people have assigned it a role in disease ranging from obesity to autism is ridiculous."
Pete, I looked this up and found 14,600 scholarly papers on the topic of gut microbiome and obesity. Here are two abstracts from highly respected peer-reviewed journals:
Gut microflora as a target for energy and metabolic homeostasis Cani, Patrice D; Delzenne, Nathalie M Current Opinion in Clinical Nutrition & Metabolic Care: November 2007 - Volume 10 - Issue 6 - p 729-734 doi: 10.1097/MCO.0b013e3282efdebb
Purpose of review: Gut microbiota plays an important role in health and disease, but this ecosystem remains incompletely characterized and shows a wide diversity. This review discusses new findings that may explain how gut microbiota can be involved in the control of energy and metabolic homeostasis.
Recent findings: Over the past 5 years studies have highlighted some key aspects of the mammalian host-gut microbial relationship. Gut microbiota could now be considered a 'microbial organ' placed within a host organ. Recent data suggest that the modulation of gut microbiota affects host metabolism and has an impact on energy storage. Several mechanisms are proposed that link events occurring in the colon and the regulation of energy metabolism.
Summary: Gut microflora may play an even more important role in maintaining human health than previously thought. The literature provides new evidence that the increased prevalence of obesity and type 2 diabetes cannot be attributed solely to changes in the human genome, nutritional habits, or reduction of physical activity in our daily lives. One must also consider this important new environmental factor, namely gut microbiota. Scientists may take into consideration a key question: could we manipulate the microbiotic environment to treat or prevent obesity and type 2 diabetes? This opens up a new area in nutrition research.
Changes in Intestinal Microflora in Obesity: Cause or Consequence? Bäckhed, Fredrik Journal of Pediatric Gastroenterology & Nutrition: April 2009 - Volume 48 - Issue - p S56-S57 doi: 10.1097/MPG.0b013e3181a11851
Obesity and the associated metabolic disorders, such as diabetes and metabolic syndrome, have become major public health issues worldwide. Obesity results from a positive energy balance and is associated with decreased microbial diversity in the human gut with lower levels of Bacteroidetes. However, whether changes in the gut microbiota are a cause or consequence in obesity remains to be definitively proven. Experiments using germ-free mice have begun to reveal some mechanisms by which the gut microbiota may affect the development of obesity.
Regarding autism and intestinal microflora, there were over 1400 scholarly papers. Here are two examples:
Autistic enterocolitis: Fact or fiction? Polymnia Galiatsatos, MD FRCPC, Adrian Gologan, MD, and Esther Lamoureux, MD Can J Gastroenterol. 2009 February; 23(2): 95–98.
Autism spectrum disorder refers to syndromes of varying severity, typified by impaired social interactions, communicative delays and restricted, repetitive behaviours and interests. The prevalence of autism spectrum disorders has been on the rise, while the etiology remains unclear and most likely multifactorial. There have been several reports of a link between autism and chronic gastrointestinal symptoms. Endoscopy trials have demonstrated a higher prevalence of nonspecific colitis, lymphoid hyperplasia and focally enhanced gastritis compared with controls. Postulated mechanisms include aberrant immune responses to some dietary proteins, abnormal intestinal permeability and unfavourable gut microflora. Two autism spectrum disorder patients with chronic intestinal symptoms and abnormal endoscopic findings are described, followed by a review of this controversial topic.
Gastrointestinal Microflora Studies in Late-Onset Autism Sydney M. Finegold1,4,5, et al. Clin Infect Dis. (2002) 35 (Supplement 1): S6-S16. doi: 10.1086/341914
Some cases of late-onset (regressive) autism may involve abnormal flora because oral vancomycin, which is poorly absorbed, may lead to significant improvement in these children. Fecal flora of children with regressive autism was compared with that of control children, and clostridial counts were higher. The number of clostridial species found in the stools of children with autism was greater than in the stools of control children. Children with autism had 9 species of Clostridium not found in controls, whereas controls yielded only 3 species not found in children with autism. In all, there were 25 different clostridial species found. In gastric and duodenal specimens, the most striking finding was total absence of non—spore-forming anaerobes and microaerophilic bacteria from control children and significant numbers of such bacteria from children with autism. These studies demonstrate significant alterations in the upper and lower intestinal flora of children with late-onset autism and may provide insights into the nature of this disorder.
I would say, Pete, that many disagree with your claim that this issue is ridiculous.
Christina
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