Managed a NEW goal

Today, I weighed less than I have any other time in my adult life…I weighed in at 143 today. YEAH ME!!!

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“Revisions – Does the Patient Fail the Procedure or Does the Procedure Fail the Patient?”



Hi, I’m Dr Mitchell Roslin, Chief of Bariatric Surgery at Lenox Hill Hospital in NY and Northern Westchester Hospital in Mt Kisco, NY. The title of this talk is, “Revisions – Does the Patient Fail the Procedure or Does the Procedure Fail the Patient?” This is a copy of a talk that I gave at the ASMBS in Orlando in 2011 and I was asked by many of the attendees at the session to see if I could record the talk and place it online.

The purpose of the talk is to try to explain some of the physiology behind bariatric procedures and weight regain or inadequate weight loss following bariatric surgery.

When I started doing bariatric surgery 17 years ago I really thought it was simple. I thought when we did a gastric bypass what we did is that we made the stomach smaller so that people were forced to eat less. Then we added an intestinal bypass so that some of what was eaten was passed into the fecal stream. I now know that bariatric surgery is far more complex. The stomach is far more than just a storage organ, it actually produces certain hormones that regulate hunger and satiety. As a result I think concepts like restriction (making the stomach small) or malabsorption (bypassing part of the intestine) are rather simplistic and instead we need to think of bariatric surgery as gastric and intestinal. What I’ve learned is that one of the major aspects of the gastric part of the operation is suppression of hunger, especially through the reduction of the hormone gherlin. In addition, instead of a malabsorptive component probably what the intestinal component of the operation does is it increases the work of digestion therefore increasing the metabolic rate.

Frequently, patients who haven’t done well with the various bariatric procedures have been labeled as non compliant, or not following directions. One of the things we have to realize is that if it were simple to follow eating directions nobody would have ever required bariatric surgery. Another thing that we have to realize is that obesity is not a single disease. Obesity occurs where there is inadequate regulation or inadequate balance between the amount of energy taken in and the amount of energy that is expended. As a result, the defect can be anywhere in the process, so that any no two patients that we see may have the same defect, yet we all treat them similarly. So when somebody doesn’t do well with an operation we tend to say that it’s because they haven’t followed the directions, or they’re noncompliant. An alternative explanation is that the operation doesn’t change or alter the physiology that caused their obesity and is not effective in their particular case. I think that if we’re going to take credit for bariatric surgery causing weight loss and being the most effective treatment of obesity, when patients regain weight the operation also has to be a part of the burden. We have to realize that there may be a physiological reason for weight regain, not just behavioral changes and lack of compliance. The purpose of this talk is to try to explain what we’ve seen in the two most common procedures performed in bariatric surgery – laparoscopic adjustable gastric banding and gastric bypass.

As mentioned, obesity occurs when there is any breakdown in the negative feedback system that controls energy balance. Human energy intake is mainly controlled by hormonal factors There are several key hormones that control hungry, satiety, as well as early energy and long term energy requirements. Ghrelin which is produced primarily in the stomach is considered the hunger hormone. PYY which is produced mainly in the intestine is considered the satiety or fullness hormone. Insulin is the short term energy hormone and it works along with GLP. Leptin is the long term energy hormone and is mainly produced in fat cells. But even this is relatively simplistic and leptin and insulin actually complete sometimes for binding in the hypothalamus of the brain. As a result a lot of patients who are insulin resistant also have excess leptin but leptin cant tell the brain that you already have too much fat tissue. So there is a breakdown in that regulation. As opposed to the input for energy intake which is mainly hormonal, the output is mainly through the nervous system. When the body wants to conserve energy it increases the tone of the parasympathetic system, reducing the heart rate and the metabolic rate. And this is what occurs when people try to reduce their caloric intake. When the body wants to produce more energy it activates the sympathetic system. The bottom line is that energy balance is a rather complex process and a deficit anywhere either in the input or the output or the afferent or efferent system or as well as in the brain or central nervous system and the hypothalamus can cause obesity because of the energy imbalance.

**Video clip of Jassira, an OH’er talking about her LapBand and DS revision

After watching the previous video of the patient who struggled with the Lap Adjustable Gastric Band, and has done so well with the Duodenal Switch, it’s obvious that there different physiologic factors that occur following the bariatric surgical procedures As mentioned the input for human energy intake is mainly hormonal. Laparoscopic adjustable bands don’t reduce ghrelin or increase PYY thus its not surprising that a number of patients are still hungry following lap adjustible banding. Thus instead of giving patients labels like noncompliant, or suggesting that the patient failed the operation because they didn’t work hard enough we need to understand the physiologic differences that our operations cause. And in addition we need to begin to gain insight into why the particular patient is obese and what their particular deficit is in energy imbalance. Unfortunately we’re not able to do that at the present time and we continue to treat patients with these broad operations. But it’s really important to realize that failing one bariatric procedure doesn’t mean that you’re going to fail another bariatric procedure, and there is a lot more than just restriction and malabsorption. The most important thing that we can offer our patients in bariatric surgery is hunger suppression.

While Lap Band appears to be an attractive alternative for many patients it also has many limitations. The advantage of banding is the fact that the operation is relatively simple. The complications and the risk of serious early complications are lower than other bariatric or stapling procedures. The disadvantage of lap adjustable banding is the results are more variable and approximately 20-25% of patients, if not higher, will be dissatisfied with their weight loss. A major reason is because that while can always increase the work of eating, making you chew more and eat slower, it frequently doesn’t make patients less hungry. I often say a lapband is a diet with a seatbelt, and what I mean by this is that the band doesn’t affect ghrelin levels, doesn’t increase PYY hormone or PYY levels, and as a result really functions similar to a diet accompanied by a restrictive device. Many patients do well with the band and patients who are most likely to do well are also those that are most likely to do reasonably well on a diet. They’re younger, they’re more active, and they have lower BMI’s, or are in the lower part of the morbid obesity scale. Patients that seem to do less well with LapBands include older patients, patients that have a BMI that approaches or above super morbid obesity, and there is now a suggestion from George Washington University that there may be ethnic differences, and African Americans seem to have lower overall weight loss as well as a higher failure rate. Thus patients that are determining what bariatric procedure they want to undergo need to understand the probability that they have a higher chance of having inadequate weight loss with a Lapband or a realize band, as well as a higher chance of requiring reoperation and extraction of the band. This is offset by a lower early serious complication rate. But people have to understand that not all patients that have a Lapband have hunger suppression and in fact a significant amount never ever have any reduction in hunger, or for that matter, satiety.

Thus the major issue with Lap Adjustable Banding is inadequate weight loss. Another thing that frequently occurs is that we make the band tighter hoping to achieve restriction and force a smaller amount to be eaten and patients to be less hungry. And what we’re successful in doing is creating a high pressure zone where patients don’t get hunger suppression and they continue to eat and we see dilation in the esophagus and changes in the motility of the esophagus itself. So when you look at the Xray on the left side of this diagram you see tremendous dilatation of the esophagus above the level of the band. When fluid is removed you can see that the esophagus becomes smaller and the band wide open but there are still these scalloping figures in the esophagus which is a signal of a motility disservice. What you realize is that when you make the band tighter you make it harder to eat, you also make the esophagus work harder and you take the risk of having permanent motility disorders to the esophagus, but you don’t necessarily make patients less hungry. The patient in this picture here actually came to me with the picture on the left because he started to regain weight because he was storing food in that large esophagus. So it’s very, very important to understand the role of fills in Lap Adjustable Banding. The role of fills is to create some level of restriction but if that pressure gets greater than what the esophagus can pump, then there can only be harmful side effects to the esophagus. And just making bands tighter does not make all patients less hungry. Frequently on the internet we see something called the Green Zone, which is a place where people who have bands eat less and are less hungry. Unfortunately, on diagrams the Green Zone always exists, but clinically it’s often very, very difficult tot find a therapeutic window where patients eat less, are less hungry, and where we don’t create a high pressure system that has an adverse effect on the esophagus.

Whereas inadequate weight loss or extraction are the main problems of Lap Adjustable Banding, gastric bypass is an outstanding weight loss operation. What I’m not convinced of is that it’s a great operation for the maintenance of weight loss. An increasing problem in bariatric surgery is the number of gastric bypass patients that have regained weight 3-10 years following the operation. We’ve done an awful lot of research on this topic and are beginning to form an understanding of why we believe this occurs. Over the course of time what we see happening is food, or in this case contrast as shown in this diagram, passing immediately from the esophagus into the small gastric pouch, and then going straight into the intestines. The food doesn’t remain in the pouch long because there is no restriction left between the gastric attachment and the intestinal bypass that was created. As a result as soon as the patient eats the food goes into the intestine. With this you get a rise in satiety factors followed by a rapid fall. Thus what we believe happens following gastric bypass is there’s a return of inter-meal hunger so that when you actually question patients what you find is that while they can still eat less than they did prior to the operation but the problem is that they’re hungry one to two hours after eating. If they eat foods that are higher in the glycemic index, or simple carbohyrdrates what happens is they have a very rapid insulin response followed by a low sugar, and this makes patients develop a maladaptive eating pattern. So what we are seeing is numerous patients with gastric bypass that have lost a considerable amount of weight, but approximately 30% of our post bypass patients we’re seeing regain a significant amount of the weight that was originally lost.

Thus we believe the major problem in gastric bypass surgery is weight regain with a return of inter-meal hunger. As a result it’s been our hypotheses that better bariatric procedures would have a valve at the end of the gastric pouch. And we believe that the best vale is the pyloric valve which is the normal valve of the stomach which controls emptying of food in the normal stomach. There are two operations that now exist that allow us to preserve the pyloric valve. They’re the Sleeve gastrectomy and the Duodenal Switch. In order to test this hypothesis we have designed a prospective trial that we received grant for that examines the weight loss as well as response to glucose challenge in sleeve gastrectomy, gastric bypass, and duodenal switch. This is the first 6 month data from that perspective trial. And you can see that all of the operations cause effective weight loss, with duodenal switch causing the most weigh loss in the first six months.

The purpose of the study though, was to compare the effects of a glucose challenge on the various operations that we perform. This shows data when glucose is given both preoperatively, as well as 6 months following from surgery. And what we do following the glucose challenge is we measure the insulin levels. What we can see is a vast difference between the different operations. With gastric bypass what happens at six months is that the insulin level goes down, but when challenged with glucose the insulin level actually goes up so high that it exceeds its preoperative value at six months. We don’t see this in sleeve gastrectomy and duodenal switch. When you get such a rapid rise in insulin what happens next is a rapid fall in the sugar. And we believe this rapid rise in insulin followed by the rapid reduction in sugar glucose level leads to inter-meal hunger. Because we know when people become hypoglycemic in order to relieve the symptoms of the low sugar they become hungry and forced to eat. So we believe what is happening in gastric bypass is that since there is no valve there’s rapid emptying and when there is rapid emptying there s rapid rise in the factors that determine fullness such as insulin as well as the other gut hormones, followed by a rapid fall. And when that rapid fall occurs patients become hungry. What is really fascinating is that we don’t see the same response in duodenal switch which also has an intestinal bypass.

This diagram shows the 6 month results for insulin levels. You can see that all the operations cause a reduction in fasting insulin level, which is very important and demonstrates an improvement in metabolic function. However, gastric bypass causes a rapid rise when stimulated with glucose, much greater than sleeve gastrectomy or duodenal switch. We believe that this rapid rise in insulin is a hallmark of a rapid emptying of food as well as the rapid distribution of nutrients to the intestine, and that this rapid emptying then leads to a rapid fall in glucose level and causes the inter-meal hunger that we think is responsible for a significant amount of weight regain following gastric bypass.

This diagram shows results that were determined in the RESTORE trial. The RESTORE trial was the first multi-center trial to look at endoscopic treatment for weight regain following gastric bypass. The idea was to try to reduce the anastomatic size so that patients could regain restriction. Unfortunately to date none of the endoscopic trials have been shown to be effective to provide long term weight loss. There are some suggestions that short term weight loss could be achieved. When we went back and looked at all of the data from patients that were eligible for the trial, and this means by definition that they have to have normal pouch following gastic bypass, no evidence of fistula, and an anastomatic size that was >2CM, which we estimated approximately 70% of post bypass patients would have. We found that the most significant factor that would determine weight regain was the time from surgery.. Thus we felt that this was evident that the weight regain was physiologic, and was steady and progressive over time, especially in patients that have an anastomatic size >2CM. When surgery is first done the anastomosis is made approximately 1.5CM, or slightly less. Unfortunately what we’re finding in time is that in time the anastomosis spreads to a greater size. What we found looking at the data from the RESTORE trial is that once it got to 2CM, it didn’t make a difference if it was 2CM or 3CM, there was already a loss of restriction and weight gain was steady and progressive. We believe that means that this is going to be very, very difficult to treat by an endoscopic procedure.

While weight regain following gastric bypass is becoming a much more common clinical problem, with the average patient regaining approximately 30% of the weight they lost and approximately 20-30% regaining a significant amount more, the options for patients remain limited.

They include
1) obviously dietary adjustments but many patients feel that we’re kind of like Indian Givers, because at one point in time they had no hunger, they had early satiety and now they’re hungry all the time.
2) An increasingly investigated option is endoscopic suturing but there is no long term data
3) Band over bypass works for certain patients, but has many of the same problems that primary banding has
4) the most aggressive option is to convert the operation to a Duodenal Switch but this is a rather large operation, requires multiple anastomosis, and is an option that we reserve to patients that have considerable problems because of their weight regain.

Thus it’s important to realize that…

  • Our operations have limitations and that inadequate weight loss and weight regain cant just be blamed on the patient.
  • Bands have no effect on Ghrelin, PYY, or GLP.
  • Gastric bypass has no valve and this can lead to inter-meal hunger.
  • The fact that the weight gain is steady and progressive over time I think is indicative that it is physiologic
  • We believe that increased insulin secretions after glucose challenge in bypass is indicative of the rapid emptying that occurs and the cause of inter-meal hunger.
  • Additionally, failing one operation should not preclude consideration for another bariatric procedure.
  • Obesity is a chronic disease and therefore we’re going to have to be prepared to treat our patients on a long term basis and realize that bariatric surgery is not a cure for obesity but merely a control mechanism.
  • We need to critically analyze our procedures
  • My opinion is that pyloric preserving procedures such as the sleeve gastrectomy and especially the duodenal switch, and maybe future varations of these procedures will replace gastric bypass as standard.
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    Diabetes Risk Rises as Statin Dose Increases

    Diabetes Risk Rises as Statin Dose Increases

    By: MARY ANN MOON, Internal Medicine News Digital Network
    Diabetes Risk Rises as Statin Dose Increases
    The risk of developing type 2 diabetes rises with increasing doses of statin therapy, according to the findings of a large meta-analysis in the June 22/29 issue of JAMA.

    “Our findings suggest that clinicians should be vigilant for the development of diabetes in patients receiving intensive statin therapy,” said Dr. David Preiss of the BHF Glasgow (Scotland) Cardiovascular Research Centre at the University of Glasgow, and his associates.

    Several recent studies have suggested that statin therapy may raise the risk of diabetes, and some have indicated that the risk is higher at higher doses of the drugs.

    Dr. Preiss and his colleagues conducted a meta-analysis of five large (at least 1,000 subjects each) randomized clinical trials that compared moderate-dose with intensive-dose statin therapy and followed patients for a minimum of 1 year. These trials were intended to compare cardiovascular outcomes, but they also tracked adverse events, blood glucose levels, and the use of diabetes medications, so cases of new-onset diabetes could be identified.

    Overall, 32,752 subjects who did not have diabetes at baseline were followed for a mean of 5 years. During that time 2,749 subjects (8%) developed diabetes.

    There were 149 more cases of diabetes among subjects taking intensive statin therapy than in those taking moderate statin therapy, for an odds ratio of 1.1.

    “In absolute terms, there were two additional cases of diabetes per 1,000 patient-years among those receiving intensive-dose therapy (mean 18.9 cases per 1,000 patient-years with high-dose statin treatment vs. 16.9 cases per 1,000 patient-years with moderate-dose therapy), corresponding to a number needed to harm of 498 per year,” the investigators said.

    This dose-response relationship persisted across several subgroups of patients, regardless of age, HDL cholesterol level, body mass index, and fasting plasma glucose level at baseline. The dose-response relationship also was comparable between subjects receiving simvastatin and those receiving atorvastatin, Dr. Preiss and his associates said (JAMA 2011;305:2556-64).

    However, more intensive statin therapy also provided clear cardiovascular benefits compared with less intensive statin therapy. “When expressed in absolute terms, there was one additional case of diabetes for every 498 patients treated for 1 year, compared with one fewer patient experiencing a cardiovascular event for every 155 patients treated for 1 year,” they noted.

    “We hypothesize that given that cardiovascular risk from diabetes is modest in the first decade after diagnosis, and as the benefit of statin therapy increases over time and in absolute terms with increasing age, net cardiovascular benefit in high-risk individuals will still strongly favor statin therapy,” the investigators said.

    The mechanism by which statins raise diabetes risk is not known. The data on subgroups in this meta-analysis do not shed light on the issue since all subgroups were at comparable risk.

    Future research should examine “the impact of statin therapy on glycemic control, and treatment requirements in patients with established diabetes,” they added.

    Dr. Preiss’s associates reported ties to numerous industry sources.

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    Cut down on “carbs” to reduce body fat, study authors say

    A paper from the 93rd Endo Meeting & Expo

    P2-459: Cut down on “carbs” to reduce body fat, study authors say

    A modest reduction in consumption of carbohydrate foods may promote loss of deep belly fat, even with little or no change in weight, a new study finds. Presentation of the study results will be Sunday at The Endocrine Society’s 93rd Annual Meeting in Boston. When paired with weight loss, consumption of a moderately reduced carbohydrate diet can help achieve a reduction of total body fat, according to principal author Barbara Gower, PhD, a professor of nutrition sciences at the University of Alabama at Birmingham.

    “These changes could help reduce the risk of developing Type 2 diabetes, stroke and coronary artery disease,” Gower said, noting that excess visceral, or intra-abdominal, fat raises the risk of these diseases. Gower and her colleagues conducted the study, with funding from the National Institutes of Health, in 69 overweight but healthy men and women. Subjects received food for two consecutive eight-week periods: first a weight maintenance intervention, and then a weight loss intervention, which cut the number of calories that each person ate by 1,000 each day.

    Subjects received either a standard lower-fat diet or a diet with a modest reduction in carbohydrates, or “carbs,” but slightly higher in fat than the standard diet. The moderately carb-restricted diet contained foods that had a relatively low glycemic index, a measure of the extent to which the food raises blood glucose levels. This diet consisted of 43 percent calories from carbohydrates and 39 percent calories from fat, whereas the standard diet contained 55 percent of calories from carbohydrates and 27 percent from fat. Protein made up the other 18 percent of each diet.

    At the beginning and end of each study phase, the researchers measured the subjects’ fat deep inside the abdomen and their total body fat using computed tomography (CT) and dual-energy x-ray absorptiometry (DXA) scans. After the weight maintenance phase, subjects who consumed the moderately carb-restricted diet had 11 percent less deep abdominal fat than those who ate the standard diet. However, when the researchers analyzed results by race, they found it was exclusive to whites. Whites have more deep abdominal fat than Blacks even when matched for body weight or percent body fat, and may benefit from loss of this metabolically harmful depot, Gower said.

    During the weight loss phase, subjects on both diets lost weight. However, the moderately carb-restricted diet promoted a 4 percent greater loss of total body fat, Gower said. “For individuals willing to go on a weight-loss diet, a modest reduction in carbohydrate-containing foods may help them preferentially lose fat, rather than lean tissue,”she said. “The moderately reduced carbohydrate diet allows a variety of foods to meet personal preferences.”

    P2-459: Effects of Dietary Macronutrient Composition on Total and Intra-abdominal Adipose Tissue During Weight Maintenance and Weight Loss
    Laura Lee Goree. The University of Alabama at Birmingham
    Laura Lee Goree,MS,RD,LD,1, Amy Ellis,MPH,RD,LD,1, Paula Chandler-Laney,PhD,1, Krista Casazza,PhD,1 and Barbara Gower, PhD,1. 1Nutrition Sciences, The University of Alabama at Birmingham, Birmingham, AL, United States.

    Body: BACKGROUND: Reduced dietary carbohydrate (CHO) and glycemic load (GL) may reduce insulin secretion and thereby facilitate loss of adipose tissue. OBJECTIVE: We tested the hypothesis that a consumption of a reduced CHO (RedCHO)/higher fat diet vs a standard (STD) diet would reduce insulin secretion, thus resulting in less intraabdominal adipose tissue (IAAT) during weight maintenance and less total body adiposity during weight loss.

    METHODS: Sixty-nine healthy overweight men and women (36 European Americans (EA), 33 African Americans) were provided food for two consecutive 8 week diet intervention phases: eucaloric and hypocaloric (1000 kcal/day deficit). Participants received either a RedCHO/higher fat diet (N=40; 43% CHO, 18% protein, 39% fat) or STD diet (N=29; 55% CHO, 18% protein, 27% fat). The RedCHO/higher fat diet contained foods with a relatively low GL ( 45 points/1000 calories). Body composition and fat distribution (IAAT) were assessed before and after each phase by DXA and CT, respectively. Before and after completion of the eucaloric phase, insulin secretion was assessed in response to a standardized liquid meal (59% CHO, 17% protein, 24% fat) and during one solid breakfast meal (RedCHO/higher
    fat or STD). RESULTS: After completion of the eucaloric phase, both acute and chronic insulin secretion were lower with the RedCHO/higher fat diet (P<0.05 for both). Participants who consumed the RedCHO/higher fat diet had 11% less IAAT than those who consumed the STD diet (P<0.05, adjusted for total fat mass and baseline IAAT) after the eucaloric phase. In subgroup analysis, we found this loss of IAAT was specifi c to EA (P<0.05). After the hypocaloric phase, participants who consumed the RedCHO/higher fat diet had 4% less total fat mass than those who consumed the STD diet (P<0.05, adjusted for lean mass and baseline fat mass). No diff erences were found in IAAT (P=0.158) nor lean mass (P=0.367) at completion of the hypocaloric phase. CONCLUSION: Consumption of a /higher fat
    diet, relative to a STD diet, promoted loss of IAAT during weight maintenance and augmented loss of total body fat during weight loss.

    Sources of Support: This work was supported by the National Institute of Health and National Institute of Diabetes and Digestive and Kidney Disease (R01DK67538). Core laboratory support, nursing, and inpatient/outpatient facilities were provided by M01-RR-00032 (GCRC), UL1RR025777 (CTSA), P30-DK56336 (NORC), and P60DK079626 (DRTC).

    Presentation Date: Sunday, June 5, 2011
    Presentation Time: 1:30-3:30 PM

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    Vitamin D Insufficiency is Associated with Decreased Bisphosphonate Response

    A paper from the 93rd Endo Meeting & Expo

    P1-228: Vitamin D Insufficiency is Associated with Decreased Bisphosphonate Response
    Albert Shieh. New York-Presbyterian Hospital/Weill Cornell Albert Shieh,MD,1, Amanda Carmel,MD,1 and Richard Bockman,MD,PhD,2. 1Internal Medicine, New York-Presbyterian Hospital/Weill Cornell, New York, NY, United States, 10021 and 2Medicine/Endocrinology, Hospital for Special Surgery, New York, NY, United States, 10021.

    Background: Randomized clinical trials have shown bisphosphonates to increase bone mineral density (BMD) and prevent fractures. It is unclear, however, why patients outside of these settings do not respond to bisphosphonates at comparable rates. The aim of this study was to explore the association between vitamin D status and response to bisphosphonates.

    Methods: A retrospective chart review of patients from a specialty osteoporosis practice was completed to identify subjects who were female; post-menopausal; had been taking alendronate, risedronate, ibandronate or zolendronate for >18 months; and had undergone >2 DXA scans separated by 18 to 60 months. Patients were excluded for chronic steroid use; metabolic bone disease; chronic kidney disease; or non-adherence to bisphosphonates. Data collected were age; BMI; bisphosphonate taken/treatment duration; concurrent calcium supplementation; fracture prior to/ during bisphosphonate therapy; BMD and T-score at the lumbar spine/femoral neck/trochanter/total hip from the two most recent DXA scans; bone markers and 25-hydroxyvitamin D (25OHD) measurements obtained with/between the two most recent DXA scans. Patients were categorized as responders or non-responders (defined as 1) >3.0% decrease in BMD at any site between initial/follow-up DXA scans; 2) incident low-trauma fracture despite >12 months of bisphosphonate use; or 3) T-score <-3.0 at any site despite >24 months of bisphosphonate use). Rates of vitamin D insufficiency (mean 25OHD <33 ng/mL) were compared between responders and non-responders. Patients were also stratified into quartiles by 25OHD level and rates of non-response were determined for each quartile.

    Results: 160 patients met criteria, of whom 89 were responders, and 71 were non-responders (decreased BMD: 42; incident fracture: 17; persistently low T-score: 12). 16.8% of responders were vitamin D insufficient compared to 54.9% of non-responders (p<0.0001). Patients with 25OHD concentrations of <20 ng/mL, 20-30 ng/mL, 30-40 ng/mL, and >40 ng/mL had non-response rates of 83.3% (10/12), 77.8% (21/27), 42.3% (22/52) and 24.6% (17/69) respectively. 25OHD levels >33 ng/mL was associated with an increased odds of response (OR=7.24, 95% CI 3.44-14.82, p<0.0001).

    Conclusions: Serum 25OHD >33 ng/mL was associated with a significant >7-fold increased odds of adequate response to bisphosphonates. Vitamin D status should be optimized to achieve maximal benefi t from bisphosphonate therapy.

    Presentation Date: Saturday, June 4, 2011
    Presentation Time: 1:30-3:30 PM

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    Low vitamin D levels are related to decreased response to osteoporosis medicine

    A paper from the 93rd Endo Meeting & Expo

    P1-228: Low vitamin D levels are related to decreased response to osteoporosis medicine

    Women with low bone density are seven times more likely to benefi t from a bisphosphonate drug when their vitamin D blood levels are above recent recommendations from the Institute of Medicine (IOM) as adequate for bone health. These new study results will be presented Saturday at The Endocrine Society’s 93rd Annual Meeting in Boston. “Maintaining adequate vitamin D levels above those recently recommended by the IOM is important for optimizing a standard therapy for osteoporosis: bisphosphonates,” said coauthor Richard Bockman, MD, PhD, chief of the endocrine service at Hospital for Special Surgery and professor of medicine at Weill Cornell Medical College, both in New York City.

    Last November the Institute of Medicine (IOM) issued its recommendations on vitamin D intake, reporting that most adults up to age 70 need no more than 600 International Units, or IU, a day to maintain bone health. According to the IOM, this intake, along with adequate calcium, is enough to achieve the minimum adequate vitamin D blood level, measured as serum 25-hydroxyvitamin D, which is 20 nanograms per milliliter (ng/mL). However, in Bockman’s study of 160 postmenopausal women with osteoporosis, an average 25-hydroxyvitamin D level of 20 to 30 ng/mL was associated with a high likelihood of not responding to at least 18 months of bisphosphonate treatment. Patients took alendronate, risedronate, ibandronate or zolendronate. The rate of women who were “nonresponders” at this serum vitamin D level was 77.8 percent, compared with 42.3 percent when serum vitamin D was in the range of 30 to 40 ng/mL. Only 24.6 percent were “nonresponders” for a level above 40 ng/mL, the authors reported.

    Patients with a hydroxyvitamin D level of 33 ng/mL and above had a sevenfold greater likelihood of having a favorable response to bisphosphonate therapy than below that level, they found. “This value of at least 33 ng/mL is higher than the level considered as “adequate” by the Institute of Medicine report for the general population and most likely requires a vitamin D intake higher than 600 IU for this therapeutic outcome,” Bockman said. “In the future, I think we’re going to see vitamin D recommendations based on specific conditions.”

    The researchers categorized patients as nonresponders if they had a new fracture while receiving a bisphosphonate or if their low bone density worsened by more than 3 percent as shown on dual-energy x-ray absorptiometry (DEXA) bone density scans obtained 18 to 60 months apart. Also counted as a nonresponder was any woman with a persistently low DEXA T-score worse than -3 (3 standard deviations below normal).

    A typical nonresponse rate to bisphosphonate treatment, according to Bockman, is about 30 percent in an osteoporosis specialty clinic, such as the one from which participants in this study were recruited. Doctors do not generally measure a patient’s serum vitamin D level before beginning bisphosphonate treatment, he said.

    This study received funding through a fellowship from the New York Academy of Medicine and a center grant from the National Institutes of Health.

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