Diana,
This is the main reason I got the DS. To get a cure for my diabetes. I am 5 months out. I am not taking any diabetes meds now. (was on 4 orals plus insulin pre-op). My morning blood sugars have gone from the 180's/190's at three months out to the 140's. My surgeon wasn't concerned at my 3 month appt. I know my pcp is starting to get concerned. He's only had a couple of patients that have had RnY, a lot with the band, and I am his only DS patient. He doesn't totally "get" the DS and all that goes with it. I get my 6 months labs at the end of Nov., and I am hoping that my numbers are on the downward trend.
Pre-operatively, I was on insulin and the 4 meds for about a year right before surgery. And I was on insulin in about 2008-2009 for a year before I lost 30lbs back then. So accumulatively I was only on insulin about 2 1/2 years. I am hoping that I have this diabetes thing GONE!!!

ANY pre-op that is diabetic needs to look at the DS. It is the best chance to get rid if this terrible disease. As you said, do it right the FIRST time.
Lisa

 My endo asked me to take the glucose test to see if my insulin levels are normal (My A1C is 3.9). I said no, bc its yuckyand I wasn't sure if I could drink it fast, I know my level are fine, do you think I should suck it up and check the insulin level for pcos?

 of course.....................

How are you? Any kittens pictures for a woman about to teach fire safety to 10 1st graders???????? Iz need cute.

BUMP

.....

Why?  Let's see, perhaps because the pharmaceutical companies don't want it to be acknowledged as such, or because the insurance companies don't want to pay for the surgery for that HUGE population of patients?

http://www.paclap.com/news/publication-diabetes-cure.cfm

Diabetes Cure with Duodenal Switch

Obesity is the leading cause of Type II diabetes mellitus (adult onset diabetes) in the United States. With sufficient weight loss, diabetes will in most cases improve or resolve. Walter Poires, M.D. published in 2004 a study outlining the improvement in Type II diabetes after Roux-En-Y gastric bypass. Since we began performing the Duodenal Switch (DS) in 1993, we have observed that the majority of our patients following their DS for their morbid obesity have had their diabetes cured immediately following the surgery. In fact, we have seen a remarkable 97% recovery rate for our patients with diabetes. Many of our patients discontinue their insulin and/or oral hypoglycemic medications prior to their hospital discharge.

This phenomenon of immediate cure of the diabetes following the DS is, in large part, due to the intestinal rearrangement that is a component of the procedure. We have found that the improvement in and cure of Type II diabetes mellitus following weight loss surgery is, by far, most dramatic following the Duodenal Switch. We routinely perform the DS laparoscopically (LapDS) since we pioneered this minimally invasive approach in 1999.

Below is a chart outlining the differences following weight loss surgery in the cure and or reduction of diabetes and other serious morbid obesity related diseases reported by Harvey Buchwald, M.D. in his meta analysis published in 2004. In this study over 20,000 postoperative bariatric patients were followed for up to 13 years.

Obesity Related Illnesses that Improved/Resolved Following Weight Loss Surgery:

  Gastric Band RNY DS Diabetes Mellitus Hyperlipidemia Hypertension Sleep Apnea

47.9%	83.7%	98.9%
58.9%	96.9%	99.1%
43.2%	67.5%	83.4%
95%	80.4%	92%

Buchwald, H. Bariatric Surgery, A Systematic Review and Meta-analysis. JAMA, October 13, 2004-Vol 292, No. 14

Please visit our website at www.paclap.com where you can join an informational seminar online with John Rabkin, MD, FACS. He will review bariatric surgical procedures available today and explain why the Laparoscopic Duodenal Switch (LapDS) is the best procedure to treat morbid obesity and its medical co-morbidities.


http://www.diabetes.ca/documents/for-professionals/CJD--May_ 2011--Pomp.pdf

Alfons Pomp, Department of Surgery, Weill Medical College of Cornell University, New York

Review

Biliopancreatic Diversion with Duodenal Switch in the

Treatment of Diabetes: An Argument that a Chance to

Cut is a Chance to Cure

Diabetes is an increasing global health problem. Current medical strategies have had limited effect in controlling and curtailing the complications of the disease. Morbidly obese patients with type 2 diabetes are at particular risk of the cardiovascular complications of diabetes. Bariatric surgery in these patients has been shown to induce glycemic control and even obviate the need for chronic medical therapy. Of all the bariatric procedures, biliopancreatic diversion with duodenal switch is the most effective in inducing diabetes remission. The mechanism for this is likely multifactorial and not limited to weight loss alone. Understanding how this and other bariatric procedures affect diabetes may help to elucidate a new paradigm in treating both   obese and nonobese patients with diabetes.

ABSTRACT

Address for correspondence:

Presbyterian Hospital, 525 East 68th Street, Box 294, New York, New York, 10065, United States. E-mail: apomp@med.cornell.edu

I'm trying to find it too.  I found a few other things.

http://www.hindawi.com/journals/jobes/2011/860169/

Abstract

Introduction. Type 2 diabetes mellitus (T2DM) is one of the most important obesity-related comorbidities. This study was undertaken to characterise the effect of the biliopancreatic diversion with duodenal switch (BPD-DS) in morbidly obese and nonmorbidly obese diabetic patients. Methods. Outcome of 74 obese diabetic patients after BPD-DS and 16 non-obese diabetic patients after BPD or gastric bypass surgery was evaluated. Insulin usage, HbA_1c-levels, and index of HOMA-IR (homeostasis model assessment of insulin resistence) were measured. Results. A substantial fraction of patients is free of insulin and shows an improved insulin sensitivity early after the operation, another fraction gets free of insulin in a 12-month period after the operation and a small fraction of long-term insulin users will not get free of insulin but nevertheless shows an improved metabolic status (less insulin needed, normal HbA_1c-levels). Conclusion. BPD-DS leads to an improvement of T2DM in obese and non-obese patients. Nevertheless, more data is needed to clarify indications and mechanisms of action and to adjust our operation techniques to the needs of non-obese diabetic patients.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3123702/?tool=pu bmed

Diabet Med. 2011 June; 28(6): 628–642. doi: 10.1111/j.1464-5491.2011.03306.x

PMCID: PMC3123702

Copyright Journal compilation © 2011 Diabetes U Abstract The International Diabetes Federation Taskforce on Epidemiology and Prevention of Diabetes convened a consensus working group of diabetologists, endocrinologists, surgeons and public health experts to review the appropriate role of surgery and other gastrointestinal interventions in the treatment and prevention of Type 2 diabetes. The specific goals were: to develop practical recommendations for clinicians on patient selection; to identify barriers to surgical access and suggest interventions for health policy changes that ensure equitable access to surgery when indicated; and to identify priorities for research. Bariatric surgery can significantly improve glycaemic control in severely obese patients with Type 2 diabetes. It is an effective, safe and cost-effective therapy for obese Type 2 diabetes. Surgery can be considered an appropriate treatment for people with Type 2 diabetes and obesity not achieving recommended treatment targets with medical therapies, especially in the presence of other major co-morbidities. The procedures must be performed within accepted guidelines and require appropriate multidisciplinary assessment for the procedure, comprehensive patient education and ongoing care, as well as safe and standardized surgical procedures. National guidelines for bariatric surgery need to be developed for people with Type 2 diabetes and a BMI of 35 kg/m² or more.


http://bariatrictimes.com/2010/04/06/diabetes-surgery-what-h ave-we-learned/
Diabetes Surgery: What Have We Learned?

April 2010

by Ricardo Cohen, MD

Dr. Cohen is from the Center of Excellence of Bariatric Surgery and Metabolic Disorders, Oswaldo Cruz Hospital, Sao Paulo, Brazil

Financial Disclosures:
Dr. Cohen has no financial disclosures relevant to the content of this article.

Bariatric Times. 2010;7(4):23–25

Abstract
There is a growing body of evidence that demonstrates gastrointestinal surgery may provide benefits in the control of type 2 diabetes and metabolic syndrome. This article provides a general overview of what the surgical community has learned that has become the foundation of a new discipline—metabolic surgery.

Introduction
A growing body of evidence demonstrates that weight loss surgery can provide remission of type 2 diabetes melitus (T2DM). Roux-en-Y gastric bypass (RYGB) and bileopancreatic diversions (BPD) can achieve 80 to 95 percent of long-term T2DM remission. Regarding excess weight loss (EWL), the numbers long term[1] are quite impressive, but EWL over time is less representative than T2DM resolution numbers.[2] And T2DM resolution in the patients who undergo RYGB and BPD occurs before any significant weight loss.[3]
Several animal and human studies[4,5] demonstrated that the anatomical rearrangement of the gastrointestinal (GI) anatomy may contribute to the amelioration of the components of metabolic syndrome. Those initial results, with return to euglycemia and normal insulin levels observed within days after surgery, suggest that weight loss alone cannot entirely explain why surgery improves diabetes. It is the foundation of a new discipline, GI surgery for T2DM, based on a provocative rationale, where rerouting food through the bowel may effectively contribute to those formidable results. The main goal of this article is to provide a general overview of what the surgical community has done to achieve the status of “diabetes/metabolic surgeons.” It is not intended to deeply discuss mechanisms of action, levels of incretins, or statistically significant decreases in A1c or any other metabolic parameter. It is a reflection of what is going on in the foundation of a new discipline—metabolic surgery.

What have we learned?
How the operations work. We learned the mechanisms of action, as the proximal and distal intestinal mechanisms,[6–8] intestinal gluconeogenesis,[9] and intestinal bowel glucose transportation secondary to duodenal exclusion.[10] Those important contributions started to build a strong basis to understand the mechanisms underlying the good results achieved.

Working as a team. T2DM is absolutely a medical disease and surgery will probably benefit only a very small fraction of this enormous universe. So, in order to understand a new idiom—“diabetolese”—we learned to work with basic scientists and endocrinologists/diabetoligists.

To reach the patients and the other professionals we started to learn some new vocabulary, e.g., incretin effect, insulin resistance, antidiabetics, and when and how to introduce/withdraw drugs and insulin. Without knowing that language, we would not be able to communicate with the endocrinologists. As stated by Mr. Al Gore, “If you want to go quickly, go alone. But if you want to go distant, go with a group.”

Learning “diabetolese” and patient behavior. After some time dealing with this devastating condition, we were taught that there may be several causes of diabetes, including autoimmune diabetes mellitus and latent autoimmune diabetes of adults (LADA). We also learned that in a considerable amount of patients, surgery is not magic. Drugs may have to continue being taken and titrated over time. We heard and understood the meaning of “gluco and lipotoxicity” and that one of the primary goals of controlling T2DM is to reduce long-term cardiovascular mortality.

And diving into the medical literature, we learned that we must aim at all three points of the metabolic syndrome—blood pressure, lipid control, and glycemia. After all, it is not only about sugars.11,12 And what did we demonstrate from our perspective? In 2007, two major papers reported decreased cardiovascular, diabetes-related, and overall mortality in a long-term follow up of surgical bariatric patients.[13,14] Sjostrom et al[14] showed a 24-percent decrease in mortality rate, mainly second to cardiovascular and cancer, and Adams et al[13] showed a 92-percent decrease in diabetes-related deaths in the surgical group. In 2003, Schauer et al[15] reported an efficient “three endpoints attack” after studying RYGB in patients with diabetes. Surgery can be a multifactorial approach to metabolic syndrome.

In the first papers and reports of GI surgery in patients with body mass indices (BMIs) below 30kg/m2,[5,16–18] we learned that these patients have a different pathophysiology compared to patients with BMIs greater than 30kg/m[2] and diabetes. In later papers and reports, we learned that insulin resistance plays a major role in patients with BMIs less than 30kg/m[2]. Insulin resistance has a secondary participation, indicating that these patients have an intense beta cell dysfunction as a major component of their disease. This means that theese patients are harder to manage and good results are achieved over time where there is indirect evidence of an improved beta cell function.

Is it all about weight?
Indications for surgical treatment of T2DM should not be solely based on BMI. In general terms, BMI has been adopted worldwide as the predominant measure to guide classification of obesity and to determine risk of morbidity and mortality due to obesity. While BMI does represent one conveniently calculated parameter of obesity, it is far from a fully inclusive measure of all risk. For instance, ethnicity plays a large role in obesity risk. For example, Asians do not correlate their BMI with their metabolic risk profile.[19] Several other parameters should be taken into account to properly assess the patient’s risk and selectively indicate the more suitable treatment. Waist circumference, fat distribution, and body composition are parameters that play a role in defining who bears “malignant obesity,” meaning that BMI alone is not an accurate predictor of the risk to develop diabetes and/or metabolic syndrome. BMI is even less adequate as a measure to define the overall risk of morbidity and mortality in patients with established diabetes.[20] Fabbrini et al[21] recently proved that there other parameters that should be taken into account to stratify metabolic risk in individuals. Fabbrini et al found that the intrahepatic fat and insulin resistance are more important than the body fat distribution itself. In fact, using the current arbitrary BMI cutoff may delay a potentially life-saving option for patients with lower BMI who are at similar risk from diabetes. Cohen et al[22] in 2006 and Chiellini et al[23] in 2009 reported excellent results in treating patients with T2DM with RYGB and BPD, respectively, in a group of patients with BMIs below 35kg/m[2]. It is unquestionable that the discriminatory BMI criteria must be revised soon.

What was achieved?
So far, it has not been an inglorious enterprise. For the first time, bariatric surgery is mentioned in the American Diabetes Association Guidelines (ADA) for T2DM control.[24] By December 2009, a consensus statement of the ADA was published defining T2DM cure,[25] based on decrease of A1c over time without any antidiabetic drug. In 2007, in Rome, Italy, a group of diabetologists, basic scientists, and surgeons met to define some guidelines to the approach of GI surgery for T2DM. The position statement that came from that meeting was recently published in the Annals of Surgery[.26]

Where are we going?
Although the preliminary data from studies on the efficacy of surgery on diabetes in patients with BMI less than 35kg/m[2] are encouraging, it would still be premature to consider a surgical approach generally indicated in these patients. In fact, due to the lack of well-controlled studies, it is not clear if a surgical approach would have satisfactory long-term efficacy and safety in patients with lesser degrees of obesity.
A large multicentered, randomized, clinical trial comparing surgery versus conventional medical treatment on patients with overweight or mild obesity and T2DM would help clinicians select the best approach and assist healthcare payers in their decision to cover specific treatment options. Clearly, a large-scale, randomized, controlled trial, as well as investigations aimed at identifying new parameters other than BMI to select appropriate candidates for surgical treatment of diabetes have become important research priorities.
In fact, the current BMI-centric paradigm of bariatric surgery is clearly obsolete and should be replaced by criteria based on metrics of diabetes and metabolic disease rather than BMI alone, consistent with the modern concept of “metabolic surgery.”

References
1. Pories WJ, Dohm GL. Full and durable remission of type 2 diabetes? Through surgery? Surg Obes Relat Dis. 2009;5(2):285–288.
2. Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med. 2009;122(3):248–256. e5.
3. Bikman BT, Zheng D, Pories WJ. Mechanism for improved insulin sensitivity after gastric bypass surgery. J Clin Endocrinol Metab. 2008;93(12):4656–4663.
4. Rubino F, Forgione A, *******s DE, et al. The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg. 2006;244(5):741–749.
5. Cohen RV, Schiavon CA, Pinheiro JS, et al. Duodenal-jejunal bypass for the treatment of type 2 diabetes in patients with body mass index of 22-34 kg/m2: a report of 2 cases. Surg Obes Relat Dis. 2007;3(2):195–197.
6. Rubino F, Marescaux J. Effect of duodenal-jejunal exclusion in a non-obese animal model of type 2 diabetes: a new perspective for an old disease. Ann Surg. 2004;239(1):1–11.
7. Patriti A, Facchiano E, Sanna A, et al. The enteroinsular axis and the recovery from type 2 diabetes after bariatric surgery. Obes Surg. 2004;14(6):840–848.
8. Strader AD, Clausen TR, Goodin SZ, Wendt D. Ileal interposition improves glucose tolerance in low dose streptozotocin-treated diabetic and euglycemic rats. Obes Surg. 2009;19(1):96–104.
9. Troy S, Soty M, Ribeiro L, et al. Intestinal gluconeogenesis is a key factor for early metabolic changes after gastric bypass but not after gastric lap-band in mice. Cell Metab. 2008;8(3):201–211.
10. Stearns AT, Balakrishnan A, Tavakkolizadeh A. Impact of Roux-en-Y gastric bypass surgery on rat intestinal glucose transport. Am J Physiol Gastrointest Liver Physiol. 2009 Sep 3. [Epub ahead of print]
11. Dluhy RG, McMahon GT. Intensive glycemic control in the ACCORD and ADVANCE trials. N Engl J Med. 2008;358(24):2630–2633.
12. Gaede P, Lund-Andersen H, Parving HH, Pedersen O. Effect of a multifactorial intervention on mortality in type 2 diabetes. N Engl J Med, 2008;358(6):580–591.
13. Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med. 2007;357(8):753–761.
14. Sjöström L, Gummesson A, Sjöström CD, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med. 2007;357(8):741–752.
15. Schauer PR, Burguera B, Ikramuddin S, et al. Effect of laparoscopic Roux-en Y gastric bypass on type 2 diabetes mellitus. Ann Surg. 2003;238(4):467–484; discussion 84–85.
16. DePaula AL, Macedo AL, Rassi N, et al. Laparoscopic treatment of type 2 diabetes mellitus for patients with a body mass index less than 35. Surg Endosc. 2008;22(3):706–716.
17. Geloneze B, Geloneze SR, Fiori C, et al. Surgery for nonobese type 2 diabetic patients: an interventional study with duodenal-jejunal exclusion. Obes Surg. 2009;19(8):1077–1083.
18. Ramos AC, Galvão Neto MP, de Souza YM, et al., Laparoscopic duodenal-jejunal exclusion in the treatment of type 2 diabetes mellitus in patients with BMI

This is such an important thread.  Timing is everything.  Many studies indicate that by the time we've become pre-diabetic (metabolic syndrome) we've already experienced up to 50% beta cell dysfunction.  The fewer beta cells we have the less insulin we produce.  This used to be considered an irreversible loss, but we now know that there is some degree of beta cell regeneration and alpha cells can even mutate into beta cells to produce insulin.  "Reserves" is the key.  If we wait too long to do something about it, then even the DS will not work.  We'll essentially not have enough insulin-producing cells and will be diabetic (possibly insulin-requiring) for life.  

The effects of WLS on diabetes are so far-reaching I think we're only beginning to scratch the surface.  They certainly supercede restriction and malabsorption.  Researchers are just scratcthing the surface of neuroendocrine pathways and gastrointestinal pathways relating to obesity.  I think the most important thing we can do to reduce our chances of diabetes relapse are to limit GLYCEMIC LOAD (i.e. restrict carbohydrates).  Insulin is released in response to glycemic load and the better job we do keeping this under control in the first place is our best chance of being diabetes-free.  Glycemic index is a farce because many liver-harming, diabetes-producing substances (namely FRUCTOSE) are low-glycemic-index in nature.  They do not stimulate insulin release yet they are metabolized by the liver and promote fatty liver which is a pre-diabetic condition.  The bottom line is it doesn't matter how much insulin release a food substance stimulates, in the end we still have to process all of that food.  Fructose is metabolized to pure fat in the liver and is as hard on our livers as ethanol.  Protein drink and protein bar manufacturers exploit fructose's low-glycemic-index properties in the name of "health" when they know better.  

The benefits of exercise cannot be overlooked here.  Anyone who exercises with the goal of losing tons of weight is fooling themselves.  It just won't happen without a lot of other factors, which is why WLS is such a powerful, viable option.  But exercise burns up glycogen stores and reverses fatty liver infiltration thereby increasing insulin sensitivity and glucose metabolism.  That, in turn, reduces the risk of diabetes progression.  So, when I exercise, I do it with the mindset of maintaining a healthy liver and reducing diabetes risk regardless of what the scale says.  

So, ultimately, whether I want to split hairs on a 96+% diabetes remission vs. 100% cure with DS is a moot point.  My main reason for getting DS was to rid myself of diabetes for good.  My long-term personal plan of action for this is as follows:

1.   Duodenal switch.
2.   Limit glucose load at any one time and understand the pitfalls of the glycemic index.
3.   Frequent exercise to reverse/prevent liver fatty infiltration; not necessarily for weight loss.
4.   Limit liver-toxic substances such as acetaminophen, certain rx meds, ethanol, and fructose (especially synthetic HFCS).

I have every confidence that I will live a life free from diabetes if I adhere to the above plan.  It is certainly the best plan of action I have found in my exhaustive research to rid myself of this horrible condition.  My hemoglobin A1C has gone from 12.6% preop to 4.3% just last month.  Something's working!   I almost waited too long, though, so my caveat to any new readers or lurkers would be exactly what Diana said - ACT NOW!    

don't miss this one