If you've read at all on the LC web you'll see that there's an almost grudging hatred (well that might be too strong a word, but ...) towards those who take "the easy way out" getting gastric bypass surgery. If not aimed at the person who has undergone surgery, a palpable feeling of animosity towards the WLS "industry" and the "pusher" doctors is in the air. At some point someone will chime in to remind everyone that "you know what kind of diet they eat don't you?", because it is low carb. The implications of which are that the weight loss is due to going LC so why not forego the surgery.
I tend to agree with this sentiment, somewhat, especially since most WLS candidates must follow a diet and lose a bit of weight before the surgery. Which begs the question of if one can do this before the surgery, why can't they just keep it going and lose weight w/o the surgery? It's a fair enough question, but one with no easy answer. But leaving aside this issue, the LC community seems to jump quickly to attribute the improvements in diabetes markers seen with GBP to the diet. Seems like a reasonable assumption, but wait .....
I came across this paper looking into the whole gut flora obesity thing which led me to GLP-1 and eventually to this paper popped up in a search.
Bariatric surgery is the most effective available treatment for obesity. The most frequently performed operation, Roux-en-Y gastric bypass (RYGB), causes profound weight loss and ameliorates obesity-related comorbid conditions, especially type 2 diabetes mellitus (T2DM). Approximately 84% of diabetic patients experience complete remission of T2DM after undergoing RYGB, often before significantweight reduction. The rapid time course and disproportional degree of T2DM improvement after RYGB compared with equivalent weight loss from other interventions suggest surgery-specific, weight-independent effects on glucose homeostasis. Potential mechanisms underlying the direct antidiabetic impact of RYGB include enhanced nutrient stimulation of lower intestinal hormones (e.g. glucagon-like peptide-1), altered physiology from excluding ingested nutrients from the upper intestine, compromised ghrelin secretion, modulations of intestinal nutrient sensing and regulation of insulin sensitivity, and other changes yet to be fully characterized. Research aimed at determining the relative importance of these effects and identifying additional mechanisms promises not only to improve surgical design but also to identify novel targets for diabetes medications.
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