Gastric Bypass Surgery & Diabetes
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.
What is GLP-1? It stands for glucagon-like protein 1 and is secreted by distal (end of small intestine) intestinal cells in response to fats and carbs. Incretins stimulate insulin secretion and may be improve insulin sensitivity although I'm seeing some conflicting reports on the latter. Diabetes drugs like Byetta are GLP-1 analogs (mimic GLP-1) and there are more in the works. Something about GLP-1 seems to be involved in satiety.
The Swedish Obese Subjects study, a prospective, contemporaneously matched, multicenter trial of bariatric surgery vs. medical care for obesity, reported outcomes after 2 yr in4047 patients and 10 yr in 1703 patients (2). At 2 yr, no postsurgical patients had developed T2DM, whereas 5% of the medical group had. This protection persisted to 10 yr, at which time the risk of developing T2DM was more than three times lower for surgically treated patients, whereas recovery from T2DM was more than three times as common. In these studies, the few RYGB patients who remained diabetic after surgery had longer duration of disease, suggesting that they lacked sufficient residual β-cell mass to recover normal glucose regulation (17). Nevertheless, the vast majority of these patients enjoyed improvements in their glycemic control and reduced medication dependence. At least seven published reports show significantly decreased overall mortality after RYGB, most notably two large, multicenter studies recently published in the New England Journal of Medicine (20, 21). One described a remarkable 92% decrease in diabetes-related deaths after RYGB (21).
Although bariatric procedures have traditionally been reserved for patients with body mass index (BMI) higher than 40 kg/m2, or higher than 35 kg/m2 with significant comorbidities, the remarkable impact of these operations on diabetes raises the possibility of surgical therapy for less obese patients with T2DM. Trials of RYGB in people with BMI lower than 35 kg/m2 have reported similar or even higher diabetes remission rates than those conducted in severely obese patients (22, 23). Given that leaner individuals lose less total and percent body weightafter RYGB than do more obese persons, the similarity in T2DM response hints that the operation might exert antidiabetic effects unrelated to weight loss. Consistent with this concept, experimental studies indicate that variations of RYGB improve T2DM in both obese and nonobese diabetic animals (24, 25, 26, 27). Although there is growing interest in using RYGB specifically to target T2DM, the mechanisms mediating metabolic effects of this procedure remain poorly understood. The evidence that gastrointestinal (GI) surgery eliminates T2DM more effectively than do existing nonsurgical therapies and the rapidly increasing number of bariatric operations performed worldwide (28) mandate that elucidating the physiological mechanisms underlying these procedures be an important research priority. Such insights could provide guidance in proper patient selection for future diabetes surgery and, importantly, might lead to new pharmaceuticals that would obviate the need for surgery.I think this is definitely a reason for obese diabetics and perhaps even some not quite so obese ones to consider surgical intervention, particularly if they are unable to manage their blood sugars through diet and weight loss. And the sooner the better for curing diabetes! (No I'm not arguing pro or con on the surgery, just that there's far more than weight loss benefits of this surgery). The role of GLP-1 is interesting, and all of this happening days after surgery. It might also be reason to consider pharmaceutical intervention with drugs like Byetta as an alternative to surgery.
Interestingly enough, some long term patients end up hypoglycemic because their pancreas' have apparently lost something in the signalling and still pump out too much insulin.
As profit-driven as the WLS industry is, I do believe this article gives reason to reconsider views on this procedure given the myriad complications and health risks of T2.