2 MILLION ELIGIBLE TO HAVE GASTRIC BYPASS SURGERY ON THE NHS

No Gas No Gain:  “virtually all gastric bypass patients have increased intestinal gas production”

No Joke Bottom line: Increased dietary fiber better diabetes solution than gastric bypass surgery

Alternative headline:
NHS TO TREAT NATIONWIDE DIETARY FIBRE DEFICIENCY WITH GASTRIC BYPASS SURGERY

“NICE” guidelines recommend all diabetics with a body mass index over 35 should be evaluated for gastric bypass surgery. A bariatric surgeons’ spokesperson interviewed on BBC Radio 4 said the procedure produces remission of diabetes within days after surgery independent of any weight loss but the reasons for this improvement are unknown. 10% of the NHS budget goes to treating diabetes and its complications, for example she stated 100 amputations take place every week in NHS hospitals and argued that gastric bypass surgery is a more economical way for the NHS to treat diabetes—now enter the laws of unintended consequences:  COST & COMPLICATIONS.

In my past life as an anesthesiologist I know full well the seriousness of obese patients undergoing any type of surgery and gastric bypass surgery comes with a long list of serious and life threatening complications but among the less serious, virtually everyone has increased gas/flatus production and this is likely the key to its remarkable cure of diabetes.

Contrary to the statement by the bariatric surgeons’ spokesperson, much more is known about the mechanisms whereby gastric bypass but not gastric banding improves diabetes (1) and is likely related to dramatically increased production of certain hormones from intestinal cells in response to undigested food and/or products of fermentation such as short chain fatty acids(SCFA). One of the reasons for assuming fermentation and SCFA’s are important is that virtually all gastric bypass patients have increased intestinal gas production i.e. flatulence, bloating, rumbling feelings and noises, etc. (2). Food consumed by those who have had gastric bypass enters the small intestine downstream avoiding our own digestive enzymes secreted by the pancreas and is therefore available for fermentation by the bacteria which inhabit the gut. These bacteria produce hydrogen, organic gases and carbon dioxide along with SCFA’s which are important intestinal nutrients and signalling compounds that interact with SCFA receptors present at the surface of numerous cell types and organs of the body including immune cells regulating inflammation (3) (4) (5) (6) (7) (8) (9). SCFA’s stimulate receptors in intestinal cells to produce hormones (GLP1) that regulate glucose metabolism and appetite (10) (11) (12) (13) (14).

Conclusions:
Urgent reappraisal of farting as a social stigma is required as one way or another if you want avoid diabetes you take your choice— gastric bypass surgery or up your fibre but either way  avoiding the indiscretion of letting one rip at an embarrassing moment is not an option.

Works Cited
1. Madsbad S, Dirksen C, Holst JJ. Mechanisms of changes in glucose metabolism and bodyweight after bariatric surgery.  Lancet Diabetes Endocrinol 2014;2:152–164.
2. Potoczna N1, Harfmann S, Steffen R, Briggs R, Bieri N, Horber FF. Bowel habits after bariatric surgery. Obes Surg. 2008 Oct;18(10):1287-96. doi: 10.1007/s11695-008-9456-4. Epub 2008 Mar 8.
3. Andrew J. Brown, Susan M. Goldsworthy, Ashley A. Barnes, et al. The Orphan G Protein-coupled Receptors GPR41 and GPR43 Are Activated by Propionate and Other Short Chain Carboxylic Acids.  THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 278, No. 13, Issue of March 28, pp. 11312–11319, 2003.
4. Canani RB, Costanzo MD, Leone L, Pedata M, Meli R, Calignano A. Potential beneficial effects of butyrate in intestinal and extraintestinal diseases.  World J Gastroenterol. 2011 Mar 28;17(12):1519-28. doi: 10.3748/wjg.v17.i12. 1519..
5. D. Zapolska-Downar, M. Naruszewicz. Propionate Reduces The Cytokine-Induced Vcam-1 And Icam-1 Expression By Inhibiting Nuclear Factor-K B (Nf-Kb) Activation.  Journal Of Physiology And Pharmacology 2009, 60, 2, 123-131. http://www.jpp.krakow.pl.
6. Patrick M. Smith, Michael R. Howitt, Nicolai Panikov, Monia Michaud, Carey Ann Gallini, Mohammad Bohlooly-Y, Jonathan N. Glickman, Wendy S. Garrett. The Microbial Metabolites, Short-Chain Fatty Acids, Regulate Colonic Treg Cell Homeostasis. Science 341, 569 (2013). DOI: 10.1126/science.1241165.
7. Vinolo, Rodrigues, Nachbar, Curi. Regulation of inflammation by short chain fatty acids. Nutrients 2011, 3, 858-876. doi: 10.3390/nu3100858.
8. Xiao, et al. A gut microbiota-targeted dietary intervention for amelioration of chronic inflammation underlying metabolic syndrome. FEMS Microbiology Ecology, Volume 87, Issue 2, pages 357–367, February 2014.
9. Sebely Pal, Alireza Khossousi, Colin Binns, Satvinder Dhaliwal and Vanessa Ellis. The effect of a fibre supplement compared to a healthy diet on body composition, lipids, glucose, insulin and other metabolic syndrome risk factors in overweight and obese individuals.  British Journal of Nutrition (2011), 105, 90–100.
10. Gwen Tolhurst, Helen Heffron, Yu Shan Lam, Helen E. Parker, Abdella M. Habib, Eleftheria Diakogiannaki, Jennifer Cameron, Johannes Grosse,2 Frank Reimann, Fiona M. Gribble. Short-Chain Fatty Acids Stimulate Glucagon-Like Peptide-1 Secretion via the G-Protein–Coupled Receptor FFAR2. Diabetes 61:364–371, 2012.
11. Holst, JJ. Incretin hormones and the satiation signal. s.l. : International Journal of Obesity (2013) 37, 1161–1168.
12. Ji Hee Yu, Min-Seon Kim. Molecular Mechanisms of Appetite Regulation. Diabetes Metab J 2012;36:391-398.
13. L. Geurts, A.M. Neyrinck, N.M. Delzenne, C. Knauf, P.D. Cani. Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics. Beneficial Microbes, December 2013; 4(4): 1-15. ISSN 1876-2833 print, ISSN 1876-2891 online, DOI 10.3920/BM2012.0065 1 .
14. Slavin, Joanne. Fiber and Prebiotics: Mechanisms and Health Benefits.  Nutrients 2013, 5, 1417-1435; doi:10.3390/nu5041417 .