Madam Reverie

Sarcasm? Yes. Teasing? Yes. Being down right offensive? Not yet, Laura

I personally think that although certain people espouse total and utter factually incorrect lunacy on occasion; I think people making personal attacks and being down right rude and offensive is a more of a wider issue on this website.... And it appears to go on with total impunity....

You'll get there, honey. One step at a time.

The absolute best of luck to you, Adam. You'll be fabulous and it will be fabulous! We'll all be thinking of you and see you on the other side

I've lived in a green-zone or two. Didn't stop us from getting rocketed, frag grenaded or car-bombed. AND we were compliant! Sheesh!

I would answer the door in something a little similar to this. Or something new and hideously expensive. I would not say a word, other than genteel greetings accompanied by an air of light, sparkling effervescence. I would serve the best Thanksgiving dinner in the history of the world - ever - being the consummate host as I went. Whilst oozing myself over the table to pass the various dishes and flashing an engaging smile; I would lift the mash potatoes, look your SIL straight in the eye and say; 'One lump, or two?' < I would then probably make an excuse to retire to the kitchen, where I would quietly shut the door and spend a quality 30 seconds getting down, doing the Carlton Banks dance> Oh yes, indeedy!

Holy cow, you're smokin'!!! Your stomach looks amazing. I am, officially, green with envy!!!!

i'm not a vet, nor am I particular sensitive about my appearance. I just like to keep my identity private and be evaluated on the content of my character in this here cyber-t'internet-world. That is all

I agree with you. Real world experience is entirely valid. I wouldn't be on this website, if I thought I could glean everything I'd like to know from research papers alone. That being said, they're often very handy in crystalizing chains of thought - which is often very much required on this website. I proffer in order for people to do their own analysis and deduce their own reality. And lo! How scary that reality can be sometimes!

Oi! Butter, I like academic studies and journals and all things cerebrally interesting!

Comparisons with other females? B'iatches, there aint no comparing! If there is someone in this world that wants to attempt to bring someone down with the 'my cats blacker'/'Jimmy two-sh*t routine - you have to question just how utterly SAD their lives are, don't you? If they have an innate need to feel 'superior' to someone, in any thematic area, it is usually born out of their own sense of inadequacy or just plain jealousy. When people attempt to do that to me, it actually makes me laugh. Which, invariably makes them seethe with frustration, as it is patently clear my 'give-a-shit-ometer' is broken and by laughing it off, I've made the 'aggressor' look like the doughnut they are. However, if I see that someone is genuinely desperate in their actions, my sympathy mode can often kick in and I'll either a) leave them be (after all, normally they are the architects of their own embarrassment/demise, so don't need me making them look any more desperate than they already are), or b ) I see where their sensitivities lie and I'll change tack and offer counsel and solace instead. I'm kinda like that. Blame my mother and my catholic guilt-laden upbringing. If, however, someone (despite receiving the obligatory 'shot across the bow') continually insists on attacking me, those who are defenseless, or those whom I respect and love?.....The gloves are f****ng off. Fact. Laura? Don't sweat it. You're better than that snidey rubbish, honey

Oh, do I hear this. Excellent agreement between the two of you. I have something similar and I, too, have days when I could rip my partners head off. Its calming down now, but its amazing how something so small as an enquiry 'Do you think this looks okay, or do you think this would look better?' (because I'm getting concerned about the excess skin I'm getting) to be responded to with 'Yeah' (subtext; 'I don't know what the hell to say and would prefer it if you left me the hell alone'). Cue rampant discussions about 'being there'... Its all rubbish and its entirely related to hormones, feelings of deprivation and, if I'm honest, food consumption jealousy. Its like the biggest flash of PMS and then its gone. I have taken now to walking outside (I live in far north of the UK and it's BLOOOMIN' cold at the moment), having a few seconds (and often a few cigarettes) and then coming back in with a fresh perspective. Although in saying that, I have oft felt moments where I felt I should come back in with an AK47..... Devising a red flag signal might be a good way to halt proceedings when the touch-paper is lit and allow you just a few minutes to calm down and see things objectively again. Hell, I've even managed to turn our 'ding-dongs' into a point of humour, which has in fact lead to carnal relations! Ha! Good way to get out the 'angst'! You know you don't really hate your husband - like I don't hate my partner. its just hard to control the inner beast sometimes. Consequently, I advocate 'abusing' him in the bedroom! Poor hubbies, don't they put up with enough of our crap as it is?!! Try getting some breathing space and I reckon you'll be fine. Best of luck, honey

You look fabulous. Congratulations

I would guess it depends on how bad a case you have and what kind of meds you have to take as a consequence. Whether you're on steroids or antibiotics and whether there might be a conflict? I can't imagine they would though... Weightloss, I would have thought, would only improve things?

lol MIA. There's also something wrong with the prefrontal lobe of one in particular.... That might be selective though, so I don't think they could claim diminished responsibility. Maybe they're just a total arse naturally.

Did you notice the sycophantic hypocrisy whilst you were there, too? I love a bit of double-standards, me

You're more than welcome, Susan, happy to help. If there's anything else you'd like to know, please just shout x

The system wouldn't accept the reference list attached to the rest of it - so here it is. References 1. . ↵ Chang J, Wittert G. Effects of bariatric surgery on morbidity and mortality in severe obesity. Int J Evid Based Healthc 2009;7:43–48 CrossRefMedline 2. . ↵ O'Brien PE. Bariatric surgery: mechanisms, indications and outcomes. J Gastroenterol Hepatol 2010;25:1358–65 CrossRefMedline 3. . ↵ Ashrafian H, Roux Carel W le, Ara D, Thanos A. Effects of bariatric surgery on cardiovascular function. Circulation 2008;118:2091–102 FREE Full Text 4. . ↵ Lakdawala M, Bhasker A. Report: Asian Consensus Meeting on Metabolic Surgery. Recommendations for the use of bariatric and gastrointestinal metabolic surgery for treatment of obesity and type ii diabetes mellitus in the Asian population. Obes Surg2010;20:929–36 CrossRefMedline 5. . ↵ Smith BR, Schauer P, Nguyen NT. Surgical approaches to the treatment of obesity: bariatric surgery. Endocrinol Metab Clin North Am 2008;37:943–64 CrossRefMedline 6. . ↵ Pories WJ. Bariatric surgery: risks and rewards. J Clin Endocrinol Metab 2008;93(11 Suppl 1)S89–96 CrossRefMedline 7. . ↵ Karra E, Yousseif A, Batterham RL. Mechanisms facilitating weight loss and resolution of type 2 diabetes following bariatric surgery. Trends Endocrinol Metab 2010;21:337–44CrossRefMedline 8. . ↵ Beard JH, Bell RL, Duffy AJ. Reproductive considerations and pregnancy after bariatric surgery: current evidence and recommendations. Obes Surg 2008;18:1023–7 CrossRefMedline 9. . ↵ Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA 2004;292:1724–37 CrossRefMedline 10. . ↵ Kokkinos P, Moutsatsos G. Obesity and cardiovascular disease: the role of diet and physical activity. J Cardiopulm Rehabil 2004;24:197–204 CrossRefMedline 11. . Jordan J, Schlaich M, Redon J, et al. European Society of Hypertension Working Group on Obesity: obesity drugs and cardiovascular outcomes. J Hypertens 2011;29:189–93 CrossRefMedline 12. . ↵ Elangbam CS. Review paper: current strategies in the development of anti-obesity drugs and their safety concerns. Vet Pathol 2009;46:10–24 Abstract/FREE Full Text 13. . ↵ Cannon-Diehl MR. Emerging issues for the postbariatric surgical patient. Critic Care Nurs Q 2010;33:361–70 Search Google Scholar 14. ↵ National Institute for Health and Clinical Excellence. Obesity: guidance on the prevention, identification, assessment and management of overweight and obesity in adults and children. Clinical guideline 43. London: NICE, 2006 15. . ↵ Christou NV, Sampalis JS, Liberman M, et al. Surgery decreases long-term mortality, morbidity, and health care use in morbidly obese patients. Ann Surg 2004;240:416–24CrossRefMedline 16. . ↵ Sjostrom L, Narbro K, Sjostrom D, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med 2007;357:741–52 CrossRefMedline 17. . ↵ Ochner CN, Gibson C, Shanik M, Goel V, Geliebter A. Changes in neurohormonal gut peptides following bariatric surgery. Int J Obes (London) 2011;35:153–66 CrossRefMedline 18. . ↵ Vetter ML, Cardillo S, Rickels MR, Iqbal N. Narrative review: effect of bariatric surgery on type 2 diabetes mellitus. Ann Intern Med 2009;150:94–103 CrossRefMedline 19. . ↵ Pinkney J. Bariatric surgery for diabetes: gastric banding is simple and safe. Br J Diabetes Vasc Dis 2010;10:139–42 Abstract/FREE Full Text 20. . ↵ Koch TM, Finelli FC. Postoperative metabolic and nutritional complications of bariatric surgery. Gastroenterol Clin North Am 2010;39:109–24 CrossRefMedline 21. ↵ British Obesity Surgery Patient Association2012. www.bospa.org [Accessed 9 March 2012] 22. ↵ Longitudinal Assessment of Bariatric Surgery (LABS) ConsortiumPerioperative safety in the longitudinal assessment of bariatric surgery. N Engl J Med 2009;361:445–54 CrossRefMedline 23. . ↵ Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med 2007;357:753–61 CrossRefMedline 24. . ↵ Buchwald H, Estok R, Fahrbach K, Banel D, Sledge I. Trends in mortality in bariatric surgery: a systematic review and meta-analysis. Surgery 2007;142:621–32 CrossRefMedline 25. . ↵ Monkhouse SJW, Morgan JDT, Norton SA. Complications of bariatric surgery: presentation and emergency management – a review. Ann R Coll Surg Engl 2009;91:280–6CrossRefMedline 26. . ↵ Schweitzer DH, Posthuma EF. Prevention of Vitamin and mineral deficiencies after bariatric surgery: evidence and algorithms. Obes Surg 2008;18:1485–8 CrossRefMedline 27. . ↵ von Drygalski A, Andris DA. Anemia after bariatric surgery: more than just Iron deficiency.Nutr Clin Pract 2009;24:217–26 Abstract/FREE Full Text 28. . ↵ Sjostrom L, Lindroos AK, Peltonen M, et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med 2004;351:2683–93 CrossRefMedline 29. . ↵ Welbourn P, Fiennes A, Kinsman R, Walton P, United Kingdom National Bariatric Surgery Registry: first registry report to March 2010. Henley-on-Thames: Dendrite Clinical Systems, 2010:1–215. Search Google Scholar 30. . ↵ Rubino F, Kaplan LM, Schauer PR, Cummings DE. The Diabetes Surgery Summit consensus conference: recommendations for the evaluation and use of gastrointestinal surgery to treat type 2 diabetes mellitus. Ann Surg 2010;251:399–405 CrossRefMedline 31. ↵ International Diabetes Federation. Bariatric surgical and procedural interventions in the treatment of obese patients with type 2 diabetes: a position statement from the International Diabetes Federation Taskforce on Epidemiology and Prevention. Brussels: IDF,2011. Available at: www.idf.org (accessed 30 July 2012). 32. . ↵ Borer KT. Nonhomeostatic control of human appetite and physical activity in regulation of energy balance. Exerc Sport Sci Rev 2010;38:114–21 CrossRefMedline 33. . ↵ Scerif M, Goldstone AP, Korbonits M. Ghrelin in obesity and endocrine diseases. Mol Cell Endocrinol 2011;340:15–25 CrossRefMedline 34. . ↵ Nguyen AD, Herzog H, Sainsbury A. Neuropeptide Y and peptide YY: important regulators of energy metabolism. Curr Opin Endocrinol Diabetes Obes 2011;18:56–60 CrossRefMedline 35. . ↵ Gersin KS, Keller JE, Stefanidis D, et al. Duodenal-jejunal bypass sleeve: a totally endoscopic device for the treatment of morbid obesity. Surg Innov 2007;14:275–8Abstract/FREE Full Text 36. . ↵ Szmitko PE, Teoh H, Stewart DJ, Verma S. Adiponectin and cardiovascular disease: state of the art. Am J Physiol Heart Circ Physiol 2007;292:H1655–63 Abstract/FREE Full Text 37. . ↵ Ziemke F, Mantzoros CS. Adiponectin in insulin resistance: lessons from translational research. Am J Clin Nutrition 2010;9:258S–61S CrossRef 38. . ↵ Morton GJ. Hypothalamic leptin regulation of energy homeostasis and glucose metabolism. J Physiol 2007;583:437–43 Abstract/FREE Full Text 39. . ↵ Miyawaki K, Yamada Y, Ban N, et al. Inhibition of gastric inhibitory polypeptide signaling prevents obesity. Nat Med 2002;8:738–42 CrossRefMedline 40. . ↵ Victor AG, Irwin N, Green BD, et al. Chemical ablation of gastric inhibitory polypeptide receptor action by daily (Pro3) GIP administration improves glucose tolerance and ameliorates insulin resistance and abnormalities of islet structure in obesity-related diabetes.Diabetes 2005;54:2436–46 Abstract/FREE Full Text 41. . ↵ Flatt PR, Day C, Bailey CJ. Bariatric surgery: to treat diabesity. Br J Diabetes Vasc Dis2009;9:103–7 Abstract/FREE Full Text 42. . ↵ Merhi Z, Jindal S, Pollack SE, Lieman HJ. Pregnancy following bariatric surgery. Expert Rev Obstet Gynecol 2011;6:57–67 CrossRef 43. . ↵ Guelinckx I, Devlieger R, Vansant G. Reproductive outcome after bariatric surgery: a critical review. Hum Reprod Update 2009;15:189–201 Abstract/FREE Full Text 44.

Here is an academic overview of the various bariatric procedures with a bit of excess 'science stuff' thrown in. No opinion. No bias. Published 2012 by the UK Royal College of Physicians. If anyone requires further clarification to the sources contained (hopefully its been copied successfully), please see the reference list at the end. This will provide you (licensing permitting) with a link to those original source documents so you can do your own further research/analysis. Any questions or queries, please do not hesitate to ask. Revs x Overview of bariatric surgery for the physician Keng Ngee Hng, Specialty registrar in gastroenterology1⇓ and Yeng S Ang, Consultant gastroenterologist and honorary lecturer2 + Author Affiliations 1Salford Royal NHS Foundation Trust 2Faculty of Medicine, University of Manchester, Oxford Road, Manchester Address for correspondence: Dr KN Hng, 4 Fern Close, Shevington, Wigan WN6 8BL. Email:keng_ngee@hotmail.com Abstract The worldwide pandemic of obesity carries alarming health and socioeconomic implications. Bariatric surgery is currently the only effective treatment for severe obesity. It is safe, with mortality comparable to that of cholecystectomy, and effective in producing substantial and sustainable weight loss, along with high rates of resolution of associated comorbidities, including type 2 diabetes. For this reason, indications for bariatric surgery are being widened. In addition to volume restriction and malabsorption, bariatric surgery brings about neurohormonal changes that affect satiety and glucose homeostasis. Increased understanding of these mechanisms will help realise therapeutic benefits by pharmacological means. Bariatric surgery improves long-term mortality but can cause long-term nutritional deficiencies. The safety of pregnancy after bariatric surgery is still being elucidated. Introduction Obesity is a worldwide pandemic,1–4 with the number of obese children and adolescents increasing alarmingly.5 This has serious health and socioeconomic implications due to the attendant increase in related comorbidities.1,2,4,6 Obesity causes type 2 diabetes, hypertension, dyslipidaemia, cardiovascular disease, obstructive sleep apnoea, obesity hypoventilation syndrome, cancer, steatohepatitis, gastro-oesophageal reflux, gallstones, pseudotumour cerebri, osteoarthritis, infertility and urinary incontinence.1–6 Severe obesity reduces life expectancy by 5–20 years.1 Diet, exercise and drug treatments for severe obesity have been disappointing.1–3,5–12 At the present time, bariatric surgery is the only treatment that reliably produces substantial and sustainable weight loss.1–7,9,13 It is indicated in people with BMI >40 kg/m2 or with BMI >35 kg/m2 in the presence of significant comorbidity.3,5,7,14 Bariatric surgery is cost effective,3,6,15 achieving weight loss, as well as improvement or resolution of associated comorbidities.1,2,5,6,9,15,16 In the past decade, the development of centres of excellence,5,6laparoscopic techniques,2,5,6 improved safety profiles2,6,9 and better documentation of clinical effectiveness2,6,15 have fuelled an increase in the number of procedures performed. Types of surgery Bariatric surgical procedures are traditionally classified as restrictive, malabsorptive or combined according to their mechanism of action. The procedures most commonly performed are laparoscopic adjustable gastric banding and roux-en-y gastric bypass.3,13 Sleeve gastrectomy is increasingly performed.2,6,7 Biliopancreatic diversion and biliopancreatic diversion with duodenal switch are much more complex and performed infrequently.2,5,17,22 Other historical procedures are no longer in common use. In addition to restriction and malabsorption, recent evidence suggests that neurohormonal changes are an important effect of bariatric surgery.2,6,7,17,18 Bariatric surgery is only part of the management of severe obesity. Careful patient selection and preparation are extremely important, as are long-term compliance with diet, nutritional supplementation and follow up.2,5,6,19 Laparoscopic adjustable gastric banding2 A purely restrictive procedure, laparoscopic adjustable gastric banding (LABG) is the least invasive procedure, is completely reversible and has the lowest mortality.19 A silicone inflatable band is placed around the stomach cardia immediately below the gastrooesophageal junction (Fig 1). This is connected to a subcutaneous port that is used for band adjustment.5,6 The band compresses the cardia to generate a sense of satiety and reduced appetite, which is thought to be mediated via vagal afferents.2 Roux-en-Y gastric bypass (RYGB) is a combined procedure that is also performed laparoscopically. A 20–30-ml gastric pouch connected to the jejunum forms the Roux limb (Fig 2). The disconnected duodenal limb is anastomosed 75–150 cm along the Roux limb, forming a Y configuration. The distal stomach, duodenum and part of the proximal jejunum are thus bypassed.5–7,20 Despite the traditional classification of the this procedure, malabsorption is not significant with the standard RYGB surgery.7 In an extended gastric bypass, the Roux limb is lengthened to increase the malabsorptive component.6,20 In sleeve gastrectomy, 60–80% of the stomach is removed along the greater curvature to leave a restricting ‘sleeve’ of stomach along the lesser curve (Fig 3).5,20,21 Originally the first step of the biliopancreatic diversion with duodenal switch (see below), sleeve gastrectomy has evolved into a staging procedure for super obese or high-risk patients.2,5–7,20 It is also increasingly used as a standalone procedure.2,6,7 Biliopancreatic diversion (BPD) and biliopancreatic diversion with duodenal switch (BPD/DS) are malabsorptive operations that result in bypass of most of the small intestine. With BPD/DS, a sleeve gastrectomy is performed, leaving the pylorus intact. The duodenum is then disconnected and the stomach anastomosed to the distal small bowel (the ‘duodenal switch’), creating a short alimentary limb. The long biliopancreatic limb is then anastomosed to the ileum 75–100 cm proximal to the ileocaecal valve, so digestion and absorption occurs only in the short common channel.5,6,20 With BPD, a partial gastrectomy leaves a 400 ml gastric pouch and the common channel is shortened to just 50 cm.5 Safety profile and complications Bariatric surgery is safe.2,5,6,9,22–24 High-volume centres of excellence deliver bariatric surgery with inhospital mortality of 0.14% and 90-day mortality of 0.35%, which is comparable to that for cholecystectomy.6 Acute complications, including haemorrhage, obstruction, anastomotic leak, wound infection, cardiac arrhythmias, pulmonary emboli, respiratory failure and rhabdomyolysis, occur in 5–10% of patients.5,6,9,10,25 Long-term complications include internal hernias, anastomotic stenoses, marginal ulceration, fistulae, diarrhoea, dumping syndrome, gallstones, emotional disorders and nutritional deficiencies.5,6,13,15,20,25–27 Patients with LAGB can experience port problems, stomal obstruction, band slippage/erosion, pouch dilation, gastro-oesophageal reflux and oesophageal dilation.5,13,19,25 Malnutrition is a concern with BPD with or without DS.1,17 Long-term risks for sleeve gastrectomy are unknown.5 The Longitudinal Assessment of Bariatric Surgery22 reported overall 30-day mortality of 0.3% for 4,610 patients having LAGB or RYGB for the first time, with 4.3% of patients having a major adverse outcome within 30 days. This was most frequent among patients having open RYGB (7.8%). A meta-analysis involving 85,048 patients reported a total 30-day mortality of 0.28% and a two-year mortality of a further 0.35%.24 The most complex malabsorptive procedures had the highest perioperative mortality at 1.11%. Mortality for gastric banding is between one in 2,000 and one in 5,700.2 Effects on weight, comorbidities and long-term mortality After RYGB, patients lose 60–70% of their excess weight over two years, and this is largely durable.1,2,6,9,15,16,28 Weight loss is dependent on long-term compliance with dietary recommendations.2,5,6 Sugary, energy-dense foods and drinks can ‘bypass the bypass’. After gastric banding, patients lose about 50% (range 39%–59%) of their excess weight at a slower rate, often continuing into the fifth year.1,2,5,6,9,19 Regular band adjustment is necessary.16 The Swedish Obese Subjects (SOS) study reported a reoperation or conversion rate of 31% for gastric banding and 17% for gastric bypass among patients followed for ≥10 years, excluding operations for postoperative complications.16 However, at the centre in Melbourne, only about 10% of patients after LAGB need some revisional procedure, including band replacement, in the following 10 years.2 Biliopancreatic diversion with or without DS produces excess weight loss of 70.1%9sleeve gastrectomy produces initial excess weight loss of 55%, but this may not be durable.2 Bariatric surgery also produces significant improvement in obesity-related comorbidities, with the most remarkable effect being resolution of type 2 diabetes (T2DM). A meta-analysis encompassing 22,094 patients reported complete remission of T2DM in 76.8% of patients,9 and a registry from the UK with data on 8,710 patients reported resolution of T2DM in 85.5% of patients.29 Major improvement often occurs within days after RYGB, before significant weight loss is achieved.5–7,17,18 After LAGB, improvement in T2DM occurs more slowly as a result of weight loss.2,7,19 Combined or malabsorptive procedures produce greater improvement than purely restrictive procedures.1,2,5,9,18 Diabetes less than three years in duration, no insulin requirement, milder obesity with BMI <40 kg/m2 and weight loss ≥10% predict complete resolution of T2DM.18,19 Bariatric surgery is now advocated by some for the treatment of T2DM in patients with BMI <35 kg/m2.4,7,30,31 Bariatic surgery effectively treats all other associated comorbidities: from steatohepatitis and pseudotumour cerebri to urinary incontinence.1–3,5,6,15 Meta-analysis showed that hyperlipidaemia improved in ≥70% of patients, hypertension resolved in 61.7% (and resolved or improved in 78.5%) and obstructive sleep apnoea resolved in 83.6%.9 At five years, the risk of cardiovascular disease had decreased by 72%.3 The incidence of cancer also reduced markedly,6,15,16 as did the risk of developing new comorbid conditions.15 Long-term efficacy is well documented.5,6,28 At follow up after 10 years, the Swedish Obese Subjects (SOS) study showed a 29% reduction in adjusted all-cause mortality, primarily because of decreases in cancer and myocardial infarction.16A retrospective cohort study of 7,925 patients after RYGB reported a 40% reduction in all-cause mortality during mean follow up of 7.1 years.23 Specific mortality decreased by 56% for coronary artery disease, by 92% for diabetes and by 60% for cancer. A large observational study, in which the vast majority of patients had undergone RYGB, reported an 89% risk reduction in five-year mortality.15 Energy homeostasis and hormonal changes Weight loss after bariatric surgery is not explained by volume restriction and malabsorption alone.17 Indeed malabsorption is estimated to account for only 5% of the weight loss following standard RYGB.17 Bariatric surgery causes significant changes in the neurohormonal profile, which contributes to sustained weight loss through changes in appetite, satiety, food preferences and eating patterns and explains the remarkable effect on T2DM.2,5–7,17,18 The hypothalamus32 Hormonal signals provide information about energy status to the hypothalamus. Adipokines are secreted by adipose tissue and enterokines by the gut. Incretins are enterokines that stimulate release of insulin after food intake.18 Two hypothalamic circuits influence food intake, and both contribute to acquisition and storage of nutrient energy. The homeostatic circuit increases appetite and locomotion in response to energy shortage. The hedonic circuit is engaged at stable weight plateaus in association with increases in body fat. It heightens finickiness to taste of food. Obese animals overeat palatable food but undereat bland foods and lose weight. In our current obesogenic environment, the hedonic circuit facilitates the seeking of energy-dense foods uncoupled from energy status. Enterokines Ghrelin,33 which is mostly synthesised in the stomach, is a potent appetite stimulator involved in hunger and meal initiation. Circulating levels are inversely proportional to BMI and respond to changes in body weight. Ghrelin enhances gut motility and speeds gastric emptying.17 It promotes lipid accumulation and weight gain, favouring glucose utilisation. It also inhibits insulin secretion and impairs glucose tolerance.18 Levels of ghrelin reported after bariatric surgery have been variable, which may be due to differences in surgical techniques and research methods.7,18Overall, the trend is for a decrease in ghrelin levels after RYGB and an increase after gastric banding.7,17 Sleeve gastrectomy, which removes most of the ghrelin-producing stomach, reduces levels of ghrelin. Peptide YY (PYY)34 is secreted postprandially by L cells in the pancreas, small intestine and colon. It suppresses appetite and promotes satiety via signalling actions in the brain. It also delays gastric emptying (the ileal brake) and enhances insulin sensitivity.7 Secretion of PYY generally corresponds to the energy ingested, although it may vary depending on the macronutrient content.17Interestingly, levels also correlate positively with exercise intensity, with resulting decreases in food intake. Glucagon-like peptide 1 (GLP-1) is co-secreted postprandially with PYY in the distal intestine.17 A powerful incretin, GLP-1 potentiates glucose-stimulated insulin secretion, enhances β-cell growth and survival, inhibits glucagon release and enhances all steps of insulin biosynthesis.7,17 It also slows gastric emptying to produce greater gastric distension and helps regulate appetite and body weight.7,17 Obese individuals have lower levels of PYY and GLP-1, and levels are decreased further in patients with diabetes.5,17,18 Two hypotheses exist to explain the hormonal and metabolic effects of the RYGB: the hindgut hypothesis the foregut exclusion theory. The hindgut hypothesis postulates that after RYGB and malabsorptive procedures, rapid nutrient delivery to the distal gut L cells and their increased exposure to incompletely digested nutrients lead to an early and exaggerated PYY and GLP-1 response, contributing to early satiety, reduced meal size and early resolution of T2DM.7,17,18 Ileal transposition studies provide strong evidence for this. Interposition of an ileal segment into the proximal gut in rodents produced exaggerated PYY, GLP-1 and enteroglucagon responses, reduced food intake, weight loss, improved insulin sensitivity and overall improved glucose homeostasis.7 The foregut exclusion theory proposes that exclusion of the duodenum and proximal jejunum after RYGB is the mechanism that mediates the effects of bariatric surgery.7,18 However, duodenal–jejunal bypass experiments in rats supporting this theory are compounded by the accompanying pyloric disruption that results in accelerated gastric emptying and rapid nutrient delivery to the hindgut.7 The endoluminal duodenal–jejunal sleeve also accelerates gastric emptying by abolishing duodenal osmoreceptor control of pyloric contraction.7 This 60 cm-long sleeve prevents nutrient contact with the duodenum and proximal jejunum, while biliary and pancreatic secretions flow outside the sleeve, delaying digestion.35 A possible mediator of the foregut exclusion theory is the gastric inhibitory polypeptide or glucose-dependent insulinotropic polypeptide (GIP), which is secreted by K cells in the duodenum in response to nutrient absorption.18,39,40 In addition to its incretin action, GIP promotes lipogenesis,41 with GIP receptor knockout mice protected against diet-induced obesity and insulin resistance,39 while antagonism of the GIP receptor improves glucose tolerance and insulin sensitivity and partially corrects pancreatic islet hypertrophy and β-cell hyperplasia.40 Levels of GIP are suppressed after malabsorptive procedures.18,41 Adipokines Adiponectin17,36,37 is synthesised primarily in adipose tissue, with levels inversely correlated with BMI. It is an important insulin sensitiser, and hypoadiponectinaemia causes insulin resistance and T2DM. Adiponectin also possesses antiatherogenic, anti-inflammatory and cardioprotective properties and may act centrally to modulate food intake and energy expenditure. Weight loss following bariatic surgery increases levels of adiponectin. Leptin38,32 is secreted by adipose tissue and regulates body weight via its action on the hypothalamus. It increases nocturnally to stimulate lipolysis but also increases postprandially to induce anorexia. In addition, leptin plays an important role in glucose homeostasis. Levels of leptin are proportional to body fat, with starvation or energy shortage activating the homeostatic mechanism in the hypothalamus to restore energy balance. However, leptin resistance develops in obesity. Weight loss from bariatic surgery reduces leptin levels.17 Many other enterokines and adipokines exist, some of which may also play a part in producing and sustaining weight loss or diabetes remission after bariatric surgery.17,18 Understanding the mechanisms of action of bariatric surgery will help realise therapeutic benefits by pharmacological means.6,7,19 Nutritional deficiencies Nutritional deficiency is common after bariatric surgery and the risk increases from LAGB through SG and RYGB to BPD with or without DS.20,26,31 The problem is heightened by the fact that micronutrient deficiencies are already highly prevalent in obese patients before surgery.21 After surgery, patients are at particular risk of deficiencies in Vitamins B1, B12, C, A and D and folic acid, as well as Iron, Calcium and Protein.20,26 Lifelong prophylactic supplementation is often necessary, and regular monitoring is essential.26 Investigation of clinical syndromes resulting from malnutrition can be challenging. Anaemia20,27 After bariatric surgery, patients are prone to iron deficiency because of intestinal bypass, pouch hypoacidity and intolerance of red meat. Obesity creates a state of chronic inflammation that can contribute to anaemia. Anaemia can also be caused by deficiencies in folate, Vitamin B12, vitamin E (haemolytic anaemia), copper (anaemia and neutropenia), Vitamin A and zinc. In refractory anaemia, gastrointestinal blood loss must be considered. Bleeding in the excluded stomach, duodenum or biliopancreatic limb is problematic as the usual endoscopic access route is no longer available. Neurological problems6,20 Neurological symptoms can result from deficiencies in thiamine, vitamin B12, niacin, vitamin E and copper or from hypocalcaemia secondary to Vitamin D deficiency. Clinical syndromes includes Wernicke's encephalopathy, peripheral neuropathy, dry beriberi, neuropsychiatric beriberi, pellagra, ataxia, spasticity, myelopathy, muscle weakness, posterior column signs and ptosis. Oedema6,20 Patients with oedema may have underlying heart failure, which can also be due to wet beriberi (thiamine deficiency) or selenium deficiency. Hypoalbuminaemia may be caused by liver cirrhosis secondary to steatohepatitis; severe protein/calorie malnutrition; kwashiorkor; and diarrhoea secondary to bacterial overgrowth, malabsorption of bile salts and niacin deficiency. Eye, skin and hair problems20 Vitamin A deficiency causes difficulties with nocturnal vision and reduced visual acuity. Vitamin E deficiency can cause retinopathy. Thiamine deficiency can present with blurred or double vision. Dry skin, pruritus and rash can be caused by deficiencies in vitamin A, niacin, riboflavin, zinc and essential fatty acids. Hair changes can be due to zinc deficiency or protein malnutrition. Pregnancy after bariatric surgery About half of patients undergoing bariatric surgery are women of childbearing age,8 which introduces specific concerns. Obesity is strongly associated with infertility8 and increases the risk of obstetric complications.8 Yet the effects of rapid weight loss and potential malnutrition in pregnant patients are of concern. Bariatric surgery improves fertility42,43 and reduces the incidence of obesity-related complications such as gestational hypertension, gestational diabetes, pre-eclampsia and foetal macrosomia when compared with obese controls. The effect on premature delivery, miscarriage, intrauterine growth retardation, low birth weight and neural tube defects and the need for caesarean section are unclear.8,43 Maternal surgical weight loss reduces the prevalence of obesity and cardiometabolic risk factors in offspring until the adolescent years.42 Pregnancy seems to have little effect on the surgically induced weight loss.8 Patients are generally advised to delay pregnancy until after the period of maximal weight loss (12–18 months).8 Extra vigilance in preconception, antenatal and obstetric care is required. Conclusion In summary, bariatric surgery is a safe and effective treatment for severe obesity and its associated comorbidities. It is particularly effective in the treatment of T2DM. Neurohormonal changes that affect appetite, satiety, glucose homeostasis and long-term energy balance contribute to its long-term efficacy. Two hypotheses exist to explain how hormonal changes produce these effects, and both may contribute. Patient adherence to postsurgical aspects of management is very important. Pregnancy after bariatric surgery brings additional considerations. Finally, the indications for bariatric surgery are being widened. Acknowledgements Dr Keng Ngee Hng is a specialty registrar in gastroenterology and has previously submitted part of this work for her Master of Science in gastroenterology (Salford University). Dr Yeng S Ang is the educational supervisor for Dr Hng and has refined the ideas, concepts and layout of the previous work. Recent updates are also included within this paper. © 2012 Royal College of Physicians

I was sleeved, have PCOS (so on drugs and only have a cycle once every 3 months) and whoosh, there it was. One week out of surgery (and I should NOT have been having one, as I had another 2 months to go). Damn thing lasted 17 days. Allegedly, its a combination of shock of the surgery and also, fat cells allegedly store a lot of oestrogen (which is part of the reason why big women like myself struggle to conceive). When you start to lose weight, you body says 'Yo! Dude! Lets release some of this crazy stuff!' and your system goes into overdrive. I gave serious consideration to buying shares in Lilets during that time...

I am 8 weeks out and I am EXACTLY like you. 28lbs. I have also stalled for 4 weeks. It's starting to move now, but it is sloooooooow going. I think this is a very common phenomenon for us women - and I think men, too. Hang in there, honey

Aww, darlin', you're more than welcome. Any time. Any time at all x

I'm glad that what I said resonated with you. Clearly you have looked at all the angles objectively and have identified both his and your vulnerabilities - which is key. From what you've said - he doesn't know what he wants and has little left to risk. The risk would appear to be all yours with little identifiable benefit long-term. In this period of great emotional instability, you've been brave enough to admit your temporary lapse of judgement. That takes guts. No one is perfect. Everyone makes 'boo-boo's' from time to time, but on balance - this is not a deal-breaking 'boo-boo'. You have stopped it before it got out of hand. I have no doubt that from this point onwards, you will find the strength to maintain your professional integrity by continuing to 'get the job done' and outside of this, zone this chap out of your life in preference to working on you, your relationship with your husband and enjoying 'home'. Walking away with dignity takes strength and courage. Working towards a better future for you and your family takes a lot of the same, mixed up with big bubbles of love. Its going to take a fair amount of self control to walk away from this salacious, but temporary excitement. I just hope that when you do start to zone this guy out, he doesn't then do the age-old thing of suddenly becoming incredibly interested in pursuing you. I hope, he'll recognise that you're the one in the driving seat, you have more to lose and that you've decided to protect your own interests and leave you be. I hope he is decent enough to do that for you. If he doesn't, be strong enough to tell him straight - that the risk just isn't worth the reward. Which, by the sounds of it, it really isn't. Additionally, if he doesn't - it will be a fairly clear identifier as to his primary motives and his level of respect for you.... You're a good lady. I wish you much strength, courage and luck x

Welcome to the madness

I TOTALLY identify with this one. I would walk into my kitchen at midnight - particular if there had been drink taken, I was bored or we had guests. I would open every cupboard in some sort of rhythmic haze and in a show of culinary inspiration, could knock up a three course meal. Loaves and fishes? Hell, I've turned the most ordinary ingredients into a gourmet meal for 6 - and eaten enough for 3. I resented the sleeve sometimes, because I missed the sensation of gorging on something I like the taste of - like lasagne and goats cheese. However, as quickly as the feeling comes - it now goes away promptly with a camomile tea. I also don't hate myself in the morning when I don't have the huge carb-hangover or my clothes are uncomfortably tight. Swings and roundabouts. This time round, my swings and roundabouts look more like a beautifully painted carousel.