Pennington Biomedical Research Center in Baton Rouge
Pennington Biomedical Research Center in Baton Rouge
News Article | November 2, 2016
New national study raises questions about how to reduce unhealthy child weight gain during school breaks NEW ORLEANS, LA--(Marketwired - November 02, 2016) - Children are at greater risk of gaining unhealthy amounts of weight during summer vacation than during the school year, according to a new study published in the Obesity journal. Researchers studied more than 18,000 kindergartners over two years and found that obesity increased only during the two summer vacations, and not at all during the school years. The results are being unveiled at the Obesity journal symposium at ObesityWeek℠, the annual conference of The Obesity Society (TOS), Oct. 31 - Nov. 4, 2016. "Educators have long worried that summer break leads to knowledge loss, and now we know that it is also a time of excessive weight gain for our youngest school children," said Paul von Hippel of the LBJ School of Public Affairs at the University of Texas, Austin, who conducted the research with Joseph Workman of the University of Oxford. "Our findings raise questions for parents and policymakers about how to help children adopt healthy behaviors during the long summer vacation to stop unhealthy weight gain. Our results also suggest that we cannot reverse the obesity epidemic if we focus only on what children are doing and eating while they are in school." Between the start of kindergarten and the end of 2nd grade, obesity increased from 8.9 percent to 11.5 percent of children, and overweight increased from 23.3 percent to 28.7 percent. None of the increase happened during the school years; all of it happened during the two summer breaks. "Now that we have solid data pointing to summer vacation as a time for potential weight gain in young children, the next step is to work together to shape out-of-school behaviors," said Amanda Staiano, PhD spokesperson for The Obesity Society and Assistant Professor at LSU's Pennington Biomedical Research Center in Baton Rouge, Louisiana. "Parents can take some simple steps to help their children like sticking to a school-year sleep schedule and reducing screen time." But parents cannot solve the problem alone. The study authors suggest that to reduce the increase in childhood obesity and overweight, school-based programs should try to shape out-of-school behaviors as well as preserve improvements made to school meals and physical activity during the school year. They suggest testing additional interventions outside of school to see what works best, but could include: "We hope these findings galvanize efforts by parents, educators, public health advocates and officials to make sure that summer does not set back efforts made during the school year to not just teach our children, but to keep them healthy," said Dr. Staiano. Funded by the Russell Sage Foundation, this study used nationally representative data to objectively measure height and weight over a three-year period. Researchers used the Early Childhood Longitudinal Study to follow a national, complex random sample of 18,170 children from kindergarten in 2010 through second grade in 2013. Weight and height were measured in the schools each fall and spring, and the authors estimated growth in mean BMI, overweight prevalence and obesity prevalence during each summer and school year. The purpose of the study was to assess the importance of risk factors for weight gain both in and out of the school setting. Find additional information and the full abstract here. This press release can be published in full or in part with attribution to The Obesity Society. The Obesity Society (TOS) is the leading professional society dedicated to better understanding, preventing and treating obesity. Through research, education and advocacy, TOS is committed to improving the lives of those affected by the disease. For more information visit: www.Obesity.org. Connect with us on social media: Facebook, Twitter and LinkedIn. Find information about industry relationships here. ObesityWeek is the premier, international event focused on the basic science, clinical application, prevention and treatment of obesity. TOS and the American Society for Metabolic and Bariatric Surgery (ASMBS) host the world's pre-eminent conference on obesity, ObesityWeek 2016, Oct. 31 - Nov. 4, at the Ernest N. Morial Convention Center in New Orleans, Louisiana. For the fourth year, both organizations hold their respective annual scientific meetings under one roof to unveil exciting new research, discuss emerging treatment and prevention options, and network and present. Connect and share with ObesityWeek on Twitter and Facebook, or by using #OW2016.
News Article | February 15, 2017
Fasting is all the rage. Self-help books promise it will incinerate excess fat, spruce up your DNA, and prolong your life. A new scientific study has backed up some health claims about eating less. The clinical trial reveals that cutting back on food for just 5 days a month could help prevent or treat age-related illnesses like diabetes and cardiovascular disease. “It’s not trivial to do this kind of study,” says circadian biologist Satchidananda Panda of the Salk Institute for Biological Studies in San Diego, California, who wasn’t connected to the research. “What they have done is commendable.” Previous studies in rodents and humans have suggested that periodic fasting can reduce body fat, cut insulin levels, and provide other benefits. But there are many ways to fast. One of the best known programs, the 5:2 diet, allows you to eat normally for 5 days a week. On each of the other 2 days, you restrict yourself to 500 to 600 calories, about one-fourth of what the average American consumes. An alternative is the so-called fasting-mimicking diet, devised by biochemist Valter Longo of the University of Southern California in Los Angeles and colleagues. For most of the month, participants eat as much of whatever they want. Then for five consecutive days they stick to a menu that includes chips, energy bars, and soups, consuming about 700 to 1100 calories a day. The food, produced by a company that Longo helped found (but from which he receives no financial benefit), is high in unsaturated fats but low in carbohydrates and proteins, a combination that may spur the body to restore itself and burn stored fat. Two years ago, Longo’s team reported that mice on the rodent version of the diet lived longer and exhibited other positive effects, such as lowered blood sugar and fewer tumors. They also presented preliminary data suggesting health benefits in humans. Now, the researchers have completed a randomized clinical trial in which 71 people followed the fasting-mimicking diet for 3 months, while volunteers in the control group didn’t change their eating habits. Overall, the dieters lost an average of 2.6 kilograms (5.7 pounds), whereas the control group remained at the same weight, the scientists report online today in . The calorie cutters also saw reductions in blood pressure, body fat, and waist size. A 3-month trial can’t determine whether the diet increases longevity in people like it did in mice, which rarely survive beyond a couple years. But Longo notes that levels of insulin-like growth factor 1, a hormone that promotes aging in rodents and other lab animals, plunged in the low-cal group. And subjects who were at the highest risk for age-related illnesses also saw other indicators of malfunctioning metabolism go down, such as blood glucose levels and total cholesterol. Longo says that this diet “treats” aging, the most important risk factor for killers like diabetes and cardiovascular disease. “It looks like you can go at the underlying problem rather than just putting a Band-Aid on it,” he says. In a follow-up trial, the team hopes to determine whether the diet helps people who already have an age-related disease—probably diabetes—or are susceptible to one. Dieting is often hard, but 75% of the low-cal participants managed to complete the trial, notes gerontologist Rafael de Cabo of the U.S. National Institute on Aging in Baltimore, Maryland, who wasn’t involved with the work. The next step, says physiologist Eric Ravussin of the Pennington Biomedical Research Center in Baton Rouge, is to determine whether the diet also works in people “who are not as healthy as they used in this study.” Research dietitian Michelle Harvie of the University Hospital of South Manchester in the United Kingdom adds that she wants to see longer studies confirm that the benefits persist and that people remain on the regimen. “We need to help a lot of people, but what if only 2% of them are willing to do this?”
News Article | November 6, 2016
People who meet recommended weekly physical activity guidelines are still at risk of developing chronic disease if they spend too much non-exercising time sitting, new research suggests. Peter Katzmarzyk, associate executive director for population and public health sciences at Pennington Biomedical Research Center in Baton Rouge, La., will discuss epidemiological data and other current findings about the effects of sedentary behavior on long-term health at the American Physiological Society's Integrative Biology of Exercise 7 meeting in Phoenix. Studies show that spending excessive amounts of time sitting or watching television is linked with chronic health issues such as heart disease and type 2 diabetes. The American Heart Association recommends at least 150 minutes of moderate-intensity exercise each week. Habitual non-exercisers have an increased risk of premature death than people who are highly active. Data from the U.S. National Health and Nutrition Examination Survey show that women -- especially obese women -- spend more time sitting as they grow older. People of both genders with higher levels of education tend to be more sedentary, too. "It appears that there are independent health effects associated with excessive sitting, and that even in people who are meeting the physical activity guidelines of 150 minutes per week, there are ill health effects associated with sitting excessively during the rest of the day," Katzmarzyk said. Studies that explore the association between exercise and sedentary behavior consistently show that replacing sitting time with even light activity -- even though moderate-to-vigorous activity is preferred -- can have a positive effect on health in the long term.
News Article | September 14, 2016
Attendees at the 2015 Genitourinary Cancers Symposium in Orlando, Florida, were presented with a head scratcher. At a poster session on renal cancer, a team at the Dana-Farber Cancer Institute in Boston, Massachusetts, led by Laurence Albiges, now at Gustave Roussy near Paris, presented its findings from a study of 4,657 individuals with metastatic kidney cancer. Almost two-thirds were classified as overweight or obese on the basis of their body mass index (BMI)1. That breakdown made sense — it is well established that obesity puts people at greater risk of developing kidney cancer. But the researchers found something striking: the higher the patient's BMI, the longer their survival time. That counter-intuitive finding added to a growing body of evidence for an obesity paradox in kidney cancer. Similar results are found in obese people with other disorders, including heart disease, diabetes and even hip fractures. Kidney specialist Kamyar Kalantar-Zadeh at the University of California, Irvine, was one of the first to report these confounding results. He compares the situation to having the wrong sort of friend. It's like “that guy who led you to prison, becomes your friend in prison”, he says. This idea is controversial, however. Indeed, attendees at same session at the Orlando symposium could also find a poster purporting to discredit the obesity paradox. Researchers led by Kathryn Wilson from Brigham and Women's Hospital and the Harvard T. H. Chan School of Public Health, both in Boston, had combed through data from two longitudinal studies to identify 575 individuals who had gone on to develop kidney cancer. The people had been followed for three decades or more as part of two long-term epidemiological studies. When the researchers zoomed in on these patients' medical histories and looked at their BMI trajectories they found that obese participants were more likely not only to develop kidney cancer, but also to die from it. “The real question is whether the obesity paradox is a true biological phenomenon,” says Martin Lajous, an epidemiologist at Harvard T. H. Chan School of Public Health, who was not involved in the study. It is more likely, he contends, that the perplexing results are merely “the result of a poor analytic strategy”. Determining whether the obesity paradox is valid in kidney cancer matters for clinicians who treat and manage the disease. Do fat and thin people develop different types of kidney cancer, for instance? Should treatments take body weight into consideration? And should clinicians be advising overweight people who develop kidney cancer to refrain from dieting? “Since obesity is reaching these epidemic proportions,” says Helena Furberg, an epidemiologist at the Memorial Sloan Kettering Cancer Center in New York City, “we've got to figure out what's going on with this paradox. In the early 1980s, a team in France found that dialysis patients with advanced kidney disease had fewer cardiovascular complications and longer survival times if they were overweight. Research over the next few decades confirmed that finding. In 2012, researchers in South Korea found evidence that the paradox also applied to kidney cancer. The most common type of kidney cancer is renal-cell carcinoma. And the biggest risk factor for this disease is obesity, which accounts for 40% of all cases in the United States and 30% in Europe. Moreover, the rate of kidney cancer worldwide has been growing — there was a 2.6% annual increase between 1997 and 2007 in the United States. In South Korea, it grew by 6% a year between 1999 and 2007. To further investigate the role of obesity in kidney cancer, South Korean researchers identified 1,543 patients who had undergone surgery to remove a kidney tumour between 1994 and 2008. The team found that obese people with kidney cancer had a 53% lower risk of dying from renal-cell carcinoma than patients who were normal weight2. To see if their findings matched those of other labs around the world, the team scoured the literature and turned up 15 studies of cancer-specific survival from Europe, Asia and the United States. The researchers found that the 5-year survival rate of patients in the lowest BMI category was around 76% compared with almost 93% for those in the highest BMI category. But the study was purely observational. “We do not know the exact mechanism,” says co-author Jung Eun Lee, an epidemiologist at Sookmyung Women's University in Seoul. On the other side of the world, Furberg and kidney specialist Ari Hakimi, also at the Memorial Sloan Kettering Cancer Center, came across the obesity paradox in their research. But their team realized that it could take the analysis up a notch. In the mid-2000s, the US National Cancer Institute and the National Human Genome Research Institute began profiling the genomes of different cancers for the Cancer Genome Atlas. Cancer institutes around the United States and Canada began collecting genomic information on tumours — Memorial Sloan Kettering was one of them. When The Cancer Genome Atlas Research Network reported its genomic profiling of clear-cell kidney tumours, about one-quarter of participants (126 patients) had been operated on at Memorial Sloan Kettering3. Furberg, Hakimi and their colleagues pulled up the medical data from these 126 people and calculated each patient's BMI just before surgery4. They wanted to see if a person's BMI had any bearing on the tumours' gene expression. It did. They found lower expression of the gene FASN in people who were obese. FASN encodes the enzyme fatty acid synthase, which is responsible for making fatty acids — an essential source of energy. The altered gene expression may have led to slower-growing kidney tumours. Albiges's team followed up on Furberg and Hakimi's work by comparing survival rates of normal weight and obese individuals with kidney cancer that had metastasized. Not only did obese patients have better survival outcomes, but they also had lower expression of fatty acid synthase. By explaining a potential genetic mechanism, says Kalantar-Zadeh, the Memorial Sloan Kettering team has “brought this paradox to a higher level of understanding”. Obesity-paradox sceptics such as Lajous criticize the use of BMI as a proxy for fatness. Because muscle weighs more than fat, a bodybuilder could have the same BMI as someone who is obese. Smokers, who are typically thinner, are often included in analyses. And BMI does not account for conditions that cause muscle wasting, potentially giving an obese sick person a normal BMI measurement. People with cancer and sarcopenia are known to have poor outcomes. To understand the obesity paradox in kidney cancer, some researchers are now homing in on the fat that surrounds the kidneys. Besides providing protection, the fat around the body's organs may also serve a metabolic purpose. “If you stripped away all of that fat, more than likely the kidney wouldn't function optimally,” says Steven Heymsfield, a metabolism researcher at Pennington Biomedical Research Center in Baton Rouge, Louisiana. Molecular oncologist Ricardo Ribeiro at the University of Lisbon has been studying the fat around various organs by looking at its molecular characteristics and measuring its thickness using tools such as CT scanners. “We are looking at the relevance of specific fat depots,” says Ribeiro. Although Ribeiro's research into kidney fat is too new to have borne results, his earlier work on prostate cancer could hold some clues about the kidney-cancer obesity paradox. Fat in the body, including around the organs, is known to come in different colours, from brown to white. Babies are born with predominantly brown fat; as humans get older, more and more of the brown fat is replaced by white fat. Exercise, however, seems to transform white fat into beige fat — a middle ground between white and brown. Ribeiro has shown that the colour of fat around the prostate influences prostate-cancer aggressiveness5. Molecular analysis and microscopic observations revealed that the fat around the cancerous prostrate is mostly white. When Ribeiro studied the interaction between different-hued fat cells and prostate-tumour cells in the lab, he found that the tumours were more aggressive in the presence of white fat. This would suggest that fat offers no survival advantage — and that the obesity paradox does not exist in prostate cancer. The fat around kidneys seems to remain more brown-like regardless of weight. Ribeiro's team is now investigating the molecular composition of the fat around the kidneys, particularly tissue in close contact with tumours. It is also using CT scans from more than 200 patients with kidney cancer to see if the thickness and density of those renal fat deposits are a better measure of obesity than BMI. It's still too early to know exactly what's going on, Ribeiro says. But he thinks that both the colour of the fat around the kidneys and its thickness might provide some insight into why obesity seems to suppress kidney tumours. But even if researchers such as Ribeiro find more precise ways to measure fatness, critics of the obesity paradox contend that there is a more pervasive bias in how patients are selected for such studies. Take the Memorial Sloan Kettering study. When Hakimi, Furberg and colleagues started researching the obesity paradox in kidney cancer, they looked into all the ways that their approach might skew the results. “Our first question was: 'Is this a phenomenon that could be explained away by other potential confounding factors?'” Hakimi says. To find out, the researchers ran through several variables. They measured tumour size and found that people with normal weight and excess weight presented with similar-sized masses. They also measured albumin, a proxy for nutritional status, and found no differences between groups. (Low albumin can indicate that a person has begun to waste away from disease.) Whenever possible, they asked patients if they had lost weight before surgery. But that too did not change the results. “The findings persisted regardless of different adjustments,” Furberg says. The one piece of information that the study lacked was patients' weight trajectory over many years — the study included only a single weight measurement taken just a few weeks before surgery. But critics of the obesity paradox see that single BMI measurement as problematic, especially when it comes to cancer. Unlike other diseases that have an obesity paradox, such as diabetes and cardiovascular disease, cancer can trigger unexpected weight loss well before the disease's clinical symptoms appear, says Hailey Banack, an epidemiologist who recently completed her doctorate at McGill University in Montreal, Canada. So measuring a person's BMI just before surgery, and even asking about recent weight loss, might lump formerly obese people in with people who have had a normal BMI for many years. What's more, protracted weight loss can be a harbinger of more aggressive forms of cancer. This could explain the poor outcomes for normal weight individuals with kidney cancer. This line of reasoning is what made the findings presented by Wilson's group so striking. In that study, researchers had access to the medical histories of participants enrolled in the Nurses' Health Study, which began in 1976 to assess the health of US women, and the corresponding men-only Health Professionals Follow-up Study, which began in 1986. Participants had their BMI measured every two years. When viewed across many years, the benefits of obesity for people with kidney cancer disappeared. As researchers try to make sense of what is going on, doctors must work out how to advise people with a kidney-cancer diagnosis. “It comes right down to the bedside,” Heymsfield says. “Should you be telling someone, 'No, this isn't the right time to go on a diet?' Most people studying the obesity paradox in kidney cancer think that changing medical guidelines to endorse obesity or weight gain rather than weight reduction is misguided. Being fat does not suddenly become beneficial after diagnosis. Instead, Banack and Furberg both think that a plausible explanation for the difference between fat and thin people is that they develop different subtypes of kidney cancer. Although excess weight probably contributed to kidney cancer in an obese (or formerly obese) person, something else, such as environmental factors or genetic predisposition, is likely to have been the culprit for the cancer in a normal-weight person. Somehow, that 'thin-person' cancer is more aggressive. “Obesity appears to be protective,” Banack says, but that's an illusion. More likely, she says, is that the disease variants that come from other causes are so much worse. Furberg hopes that it will one day be possible to use an individual's BMI — or some other, more suitable, proxy for obesity — to develop treatments that are specific to a person's cancer subtype, as well as to provide better prognoses. “My colleagues and I are doing research to see whether we can better understand the types of kidney cancer that different body sizes impart,” Furberg says. Rather than ratchet up the competition, the various players investigating the obesity paradox in kidney cancer did something unusual in the cutthroat world of scientific research: they decided to collaborate. “It just makes more sense for us to work together on this,” says Mark Preston, a urologist at Brigham and Women's Hospital. The plan is for the Memorial Sloan Kettering team to evaluate the genetic profiles of tumours excised from patients in the two longitudinal cohorts used by Wilson, Preston and their colleagues. The various groups will also address shortcomings in the weight measurements by assessing both BMI and waist circumference, a better proxy for obesity (bodybuilders rarely sport a bulging belly). “Right now we seem to be getting these two diametrically opposed answers,” says Preston. “I think there's probably truth in both.”
News Article | September 20, 2016
Carefully counting steps, stairs and sprints might backfire for some people. At the end of a two-year weight-loss trial, people who used activity monitors had lost less weight than people without the device. The results, described in the Sept. 20 JAMA, are the exact opposite of what researchers expected to find. Going into the study, researchers thought that wearable technology would help people, particularly tech-savvy young adults, keep extra weight off. “It turns out that it actually worked against us,” says study coauthor John Jakicic, a weight-management researcher at the University of Pittsburgh. Jakicic and colleagues followed 470 overweight or obese young adults, ages 18 to 35, over two years as they completed a weight-loss program that focused on healthful eating, exercise and support through meetings, phone calls and texts. During the first six months, participants lost fairly comparable amounts of weight. The real challenge, though, is in keeping extra weight off. And that’s why researchers turned to an exercise monitor. At the six-month mark, half the participants received an armband device that monitored their activity levels, providing readouts to both participants and researchers. But unexpectedly, by the end of the study, people without the device had maintained a better weight loss — 5.9 kilograms on average, or about 13 pounds. People with the device lost only 3.5 kilograms on average, or about 7.7 pounds. Other factors, however, such as overall fitness, body fat and diet were similar for both groups at the study’s end. These factors “are just as, if not more, important than solely weight,” points out developmental psychologist Amanda Staiano of Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge. It’s puzzling why only weight seemed to be affected by the technology. “We’ve been scratching our heads,” Jakicic says of the finding. He and colleagues have a few possible explanations. Perhaps the device encourages people to lean too heavily on the technology and its emphasis on moving, and users let other aspects of weight loss slip. “Everyone is looking for a magic bullet,” he says, but weight loss is hard. Or, instead of getting motivated by a challenge, people trying to lose weight might be discouraged if their activity level readouts are low. What’s more, after a few months of using the gadget, people might become bored and stop using it as much. “Maybe these technologies lose their luster,” Jakicic says. “If you’re not wearing it, it won’t be helpful to you.” A lack of engagement could help explain the results, says physical activity epidemiologist Lisa Cadmus-Bertramof the University of Wisconsin‒Madison. “Technology can be helpful, but we should absolutely expect that it could backfire if the device isn't ideal,” she says. On days when people wore the armband monitor, they typically wore it for only about four hours — far less than people usually wear a wristband Fitbit, she adds. The good news is that a small number of people with the technology kept off more weight than the average of people with the device. Jakicic and colleagues are analyzing why those people seemed to benefit while others did not. A strength of the new study is its focus on young adults, about a quarter of whom were not white. Young people, and particularly young minorities, are “in need of creative, effective strategies to combat their historically high rate of obesity,” says Staiano, who is also a spokesperson for the Obesity Society. Because young adults spend much of their days using technology, scientists shouldn’t give up attempts to figure out how to enlist devices to help manage weight, she says. Today’s gadgets, which look like jewelry on the wrist and can track not just activity but also diet, sleep and mood, may still hold promise.
News Article | April 27, 2016
A drug company says economic sticks, not just carrots, are needed to fix the reproducibility crisis in science. If academic discoveries turn out to be wrong, one drug company wants its money back. That’s the tough-minded proposal floated today by the chief medical officer of Merck & Co., one of the world’s 10 largest drug companies, as a way to fix the “reproducibility crisis,” or how many, if not most, published scientific reports turn out to be incorrect. Michael Rosenblatt, Merck’s executive vice president and chief medical officer, said bad results from academic labs caused pharmaceutical companies to waste millions and “threatens the entire biomedical research enterprise.” The problem of irreproducible research has been getting attention thanks partly to the efforts of a group of psychologists who have been redoing scores of classic experiments and have found most don’t mean much. Wrong results are also a problem for translational research—the kind drug companies do when they try to turn biological discoveries into actual medicines. Since companies don’t want their cash draining down ratholes, they’re among the few organizations that have taken the trouble to doublecheck results. The results aren’t pretty. Back in 2012, the biotechnology company Amgen dropped a bomb on academic science when it said it found only six of 53 “landmark” cancer papers stood up to efforts to reproduce the results of promising new research. Other studies that drug companies say can’t be replicated include one that found a cancer drug might treat Alzheimer’s and another that showed a particular gene was linked to diabetes in mice. Rosenblatt says the costs of repeating wrong research are adding up. He says on average it takes “approximately two to six scientific personnel one to two years of work in an industry laboratory” to try to reproduce original experiments at an average cost of $500,000 to $2 million. In his editorial, published today in Science Translational Medicine, Merck’s medical chief paints a dire picture: As the public, government, and private funders of research comprehend the extent of the problem, trust in the scientific enterprise erodes, and confidence in the ability of the scientific community to address this problem wanes. In addition, there is considerable potential for reputational damage to scientists, universities, and entire fields (for example, cancer biology, genomics, and psychology). Why is science wrong so often? Merck lists the usual suspects: pressure to publish and win grants, careerism, poor training of students, and journals that don’t review reports rigorously enough. Instead of trying to fix cultural problems in labs or passing new regulations, Merck thinks some punitive economic incentives are in order, specifically, a “full or partial money-back guarantee.” That is, if research that drug companies pay for turns out to be wrong, universities would have to give back the funding they got. Merck thinks this will put the pressure right where it belongs, on the scientists. It’s unlikely that universities will jump at Merck’s offer for more accountability. That’s because they are set up to collect R&D money, not return it. “The issue is certainly serious—but if this became a requirement it would stop [university-industry] research in its tracks,” says David Winwood, a business development executive at the Pennington Biomedical Research Center in Baton Rouge, Louisiana. “Few if any public schools would have either the (financial) capacity or, I suspect, the legal authority, to enter into such an agreement.” Drug companies aren’t saints, either. Suppressing and massaging negative results from drug trials isn’t uncommon and it’s a lot more likely to harm patients than bungled academic research. Yet at least drug firms can pay an economic price for mistakes: in 2004, Merck had to recall the pain drug Vioxx and pay out billions in damages after it became clear that the pill posed a deadly risk the company knew all about. The other problem with Merck’s proposal to universities is it would open a kind of Pandora’s box of accountability. According to the Association of University Technology Managers, a trade body that Winwood is currently president of, companies paid for $4.6 billion in “sponsored” research at U.S. universities, hospitals, and research centers in 2014. The federal government, on the other hand, spent $37.9 billion. So is most taxpayer-funded research wrong, too? Maybe it’s taxpayers, not Merck, who should get a check in the mail.
Cefalu W.T.,Pennington Biomedical Research Center in Baton Rouge
The Journal of the American Osteopathic Association | Year: 2010
Treatment of patients with type 2 diabetes mellitus (T2DM) traditionally has involved a progression of phases, from conventional lifestyle interventions and monotherapy, to combination therapy involving oral agents, to insulin initiation and its use either alone or with oral pharmacotherapy. Currently, the need for antidiabetic therapies with fewer adverse effects (eg, weight gain, reduced rates of hypoglycemia) is unmet. In addition, most treatments fail to adequately control postprandial hyperglycemia. Traditional options have generally been directed at the "insulin demand" aspect and have targeted insulin secretion or insulin resistance in peripheral tissues. Only recently have agents been available to address the "glucose supply" aspect that leads to fasting hyperglycemia in patients with T2DM. Incretin-based therapies, however, address both aspects. Two classes of incretin-directed therapies are available and work by either increasing endogenous levels of glucagon-like peptide-1 (GLP-1) (ie, dipeptidyl peptidase-4 inhibitors) or by mimicking the activity of endogenous GLP-1 (ie, GLP-1 agonists). These therapies treat the key metabolic abnormalities associated with T2DM but do so with reduced rates of hypoglycemia and do not promote weight gain as compared with conventional therapies.
PubMed | Pennington Biomedical Research Center in Baton Rouge
Type: Journal Article | Journal: The Journal of the American Osteopathic Association | Year: 2010
Treatment of patients with type 2 diabetes mellitus (T2DM) traditionally has involved a progression of phases, from conventional lifestyle interventions and monotherapy, to combination therapy involving oral agents, to insulin initiation and its use either alone or with oral pharmacotherapy. Currently, the need for antidiabetic therapies with fewer adverse effects (eg, weight gain, reduced rates of hypoglycemia) is unmet. In addition, most treatments fail to adequately control postprandial hyperglycemia. Traditional options have generally been directed at the insulin demand aspect and have targeted insulin secretion or insulin resistance in peripheral tissues. Only recently have agents been available to address the glucose supply aspect that leads to fasting hyperglycemia in patients with T2DM. Incretin-based therapies, however, address both aspects. Two classes of incretin-directed therapies are available and work by either increasing endogenous levels of glucagon-like peptide-1 (GLP-1) (ie, dipeptidyl peptidase-4 inhibitors) or by mimicking the activity of endogenous GLP-1 (ie, GLP-1 agonists). These therapies treat the key metabolic abnormalities associated with T2DM but do so with reduced rates of hypoglycemia and do not promote weight gain as compared with conventional therapies.