Health Research Report #170 14 DEC 2013

Health Research Report

#170

Latest Health Research Report Click Image for Report
 

14 DEC 2013 /  White paper draft

Compiled by Ralph Turchiano

 

Detailed research references and further affiliations on each article are posted at www.healthreserachreport.me .

 

In this Issue:

1.       Evidence suggests that “healthy and overweight” is a myth
2.       Vitamin D Decreases Pain in Women with Type 2 Diabetes and Depression
3.       Estrogen: Not just produced by the ovaries
4.       Eating healthy vs. unhealthy diet costs about $1.50 more per day
5.       Progesterone changes may cause cognitive impairment of Alzheimer’s disease patients
6.       Does zinc supplementation reduce aluminum-induced neurotoxicity?
7.       Researchers see added nutritional benefits in organic milk
8.       You are what your father eats
9.       Long-term use of common heartburn and ulcer medications linked to vitamin B12 deficiency
10.   Gut microbes affect MicroRNA response to bacterial infection
11.   Low vitamin B12 levels increase the risk of fractures in older men
12.   Dietary amino acids relieve sleep problems after traumatic brain injury in animals
13.   Personal care products are possible sources of potentially harmful parabens for babies
14.   New study shows link between perfluorinated compounds and diabetes Continue reading “Health Research Report #170 14 DEC 2013”

Vitamin D Decreases Pain in Women with Type 2 Diabetes and Depression

Continue reading “Vitamin D Decreases Pain in Women with Type 2 Diabetes and Depression”

Study is the first to show higher dietary acid load increases risk of diabetes ( Up to 56% Increased Risk )

Contact: Dr Guy Fagherazzi Guy.FAGHERAZZI@gustaveroussy.fr 33-142-116-140 Diabetologia

A study of more than 60 000 women has shown that higher overall acidity of the diet, regardless of the individual foods making up that diet, increases the risk of type 2 diabetes. The study, the first large prospective study to demonstrate these findings, is published in Diabetologia, the journal of the European Association for the Study of Diabetes (EASD), and is by Dr Guy Fagherazzi and Dr Françoise Clavel-Chapelon, Center for Research in Epidemiology and Population Health, INSERM, Paris, France, and colleagues.

A western diet rich in animal products and other acidogenic foods can induce an acid load that is not compensated for by fruit and vegetables; this can cause chronic metabolic acidosis and lead to metabolic complications. Most importantly from a blood-sugar control perspective, increasing acidosis can reduce the ability of insulin to bind at appropriate receptors in the body, and reduce insulin sensitivity. With this in mind, the authors decided to analyse whether increased acidosis caused by dietary acid loads increased the risk of type 2 diabetes.

A total of 66,485 women from the E3N study (the French Centre of the European Prospective Investigation into Cancer and Nutrition, a well-known ongoing epidemiological study) were followed for new diabetes cases over 14 years. Their dietary acid load was calculated from their potential renal acid load (PRAL) and their net endogenous acid production (NEAP) scores, both standard techniques for assessing dietary acid consumption from nutrient intake.

During follow-up, 1,372 new cases of incident type 2 diabetes occurred. In the overall population, those in the top 25% (quartile) for PRAL had a 56% increased risk of developing type 2 diabetes compared with the bottom quartile. Women of normal weight (BMI of 25 and under) had the highest increased risk (96% for top quartile versus bottom) while overweight women (BMI 25 and over) had only a 28% increased risk (top quartile versus bottom). NEAP scores showed a similar increased risk for higher acid load.

The authors say: “A diet rich in animal protein may favour net acid intake, while most fruits and vegetables form alkaline precursors that neutralise the acidity. Contrary to what is generally believed, most fruits such as peaches, apples, pears, bananas and even lemons and oranges actually reduce dietary acid load once the body has processed them. In our study, the fact that the association between both PRAL and NEAP scores and the risk of incident type 2 diabetes persisted after adjustment for dietary patterns, meat consumption and intake of fruit, vegetables, coffee and sweetened beverages suggests that dietary acids may play a specific role in promoting the development of type 2 diabetes, irrespective of the foods or drinks that provide the acidic or alkaline components.”

They conclude: “We have demonstrated for the first time in a large prospective study that dietary acid load was positively associated with type 2 diabetes risk, independently of other known risk factors for diabetes. Our results need to be validated in other populations, and may lead to promotion of diets with a low acid load for the prevention of diabetes. Further research is required on the underlying mechanisms.”

Added benefit of dapagliflozin is not proven

Manufacturer’s dossier did not contain suitable data for any therapeutic indication

Dapagliflozin (trade name: Forxiga) has been approved in Germany since November 2012 for the treatment of type 2 diabetes mellitus. In an early benefit assessment pursuant to the Act on the Reform of the Market for Medicinal Products (AMNOG) the German Institute for Quality and Efficiency in Health Care (IQWiG) examined whether this new drug offers an added benefit over the current standard therapy. No such added benefit can be derived from the dossier, however, because the drug manufacturer did not present any relevant data for any of the possible therapeutic indications of dapagliflozin.

Monotherapy or combination therapy possible

Dapagliflozin is approved both as monotherapy and in combination with other blood-glucose lowering drugs, including insulin. As monotherapy it is an option for patients who do not tolerate metformin. Dapagliflozin can also be used as combination therapy, either together with metformin or with sulfonylureas if either of these two drugs alone is insufficient to control blood sugar. Dapagliflozin can also be combined with insulin if the target blood sugar levels cannot be achieved with insulin alone. Other combinations with oral antidiabetics are possible, but these were not presented by the manufacturer in its dossier.

G-BA specified appropriate comparator therapy

The Federal Joint Committee (G-BA) specified a sulfonylurea (glibenclamide or glimepiride) as appropriate comparator therapy for the dapagliflozin monotherapy. The combination therapy of dapagliflozin and metformin was also to be compared with one of these two drugs (each supplemented with metformin). The combination of dapagliflozin with a sulfonylurea was to be tested against metformin in combination with one of the sulfonylureas glibenclamide or glimepiride. According to the G-BA‘s specifications, the combination of dapagliflozin and insulin was to be compared either with human insulin and metformin, or, if metformin was unsuitable, with human insulin alone.

Monotherapy: patients did not receive approval-compliant treatment

The manufacturer did not submit any direct comparative study between dapagliflozin and one of the sulfonylureas. Instead, it conducted an adjusted indirect comparison based on several studies. In principle, such indirect comparisons can be suitable to prove an added benefit. But the patients in the studies used by the manufacturer were not treated according to the approval status of dapagliflozin as monotherapy because the vast majority were not intolerant to metformin.

Combination with metformin: manufacturer compared with glipizide

Regarding the combination therapy with metformin, the pharmaceutical company did not submit any study that compared dapagliflozin with glibenclamide or glimepiride as the G-BA had specified. Instead, it cited a study that compared dapagliflozin plus metformin with glipizide plus metformin. However, this sulfonylurea has no longer been approved in Germany since 2007. In addition, the manufacturer did not provide sufficient proof in its dossier that glipizide is equivalent to the other two sulfonylureas.

Combination with sulfonylureas: studies were unsuitable

As to the combination therapy with sulfonylureas, the company did not draw on a direct comparative study, but on an adjusted indirect comparison. However, the studies it used were unsuitable: in one case, the glibenclamide dose exceeded the maximum dose approved in Germany, in another case, the drug glipizide, which is not approved in Germany, was used.

Combination with insulin: therapy could not be optimized for the individual patient

Regarding the indication dapagliflozin combined with insulin, the manufacturer used three studies. However, the results of these studies cannot be used for the assessment of the added benefit. The main reason for this is that the insulin therapy could not be tailored sufficiently to the individual patient: even though their current insulin therapy was insufficient, patients were neither supposed to change the insulin nor to adapt the dose. But to be able to draw conclusions about the added benefit, the combination with dapagliflozin would have to be compared with other strategies for optimizing treatment, for example optimizing insulin use.

Not tailoring treatment to the individual patient does not meet the current standard of diabetological practice anyway. In fact, insulin therapy is optimized for the individual patient so that hyperglycaemia and hypoglycaemia do not occur in the first place. So in the studies insulin was not used in a way that would be necessary and appropriate in this indication.

Hence the dossier did not contain study results for any of the four therapeutic indications that would be suitable to prove an added benefit.

G-BA decides on the extent of added benefit

The dossier assessment is part of the overall procedure for early benefit assessments supervised by the G-BA. After publication of the manufacturer’s dossier and IQWiG‘s assessment, the G-BA conducts a commenting procedure, which may provide further information and result in a change to the benefit assessment. The G-BA then decides on the extent of the added benefit, thus completing the early benefit assessment.

An overview of the results of IQWiG‘s benefit assessment is given by a German-language executive summary. In addition, the website gesundheitsinformation.de, published by IQWiG, provides easily understandable and brief German-language information on dapagliflozin.

The G-BA website contains both general English-language information on benefit assessments pursuant to §35a Social Code Book V and specific German-language information on the assessment of dapagliflozin.

Statins block the ability of exercise to improve fitness levels

Cholesterol-Lowering Drug May Reduce Exercise Benefits for Obese Adults, MU Study Finds

May 15, 2013

Story Contact(s):

Jesslyn  Chew, ChewJ@missouri.edu, (573) 882-8353

By Kate McIntyre

COLUMBIA, Mo. – Statins, the most widely prescribed drugs worldwide, are often suggested to lower cholesterol and prevent heart disease in individuals with obesity, diabetes and metabolic syndrome, which is a combination of medical disorders including excess body fat and/or high levels of blood pressure, blood sugar and/or cholesterol. However, University of Missouri researchers found that simvastatin, a generic type of statin previously sold under the brand name “Zocor,” hindered the positive effects of exercise for obese and overweight adults.

“Fitness has proven to be the most significant predictor of longevity and health because it protects people from a variety of chronic diseases,” said John Thyfault, an associate professor of nutrition and exercise physiology at MU. “Daily physical activity is needed to maintain or improve fitness, and thus improve health outcomes. However, if patients start exercising and taking statins at the same time, it seems that statins block the ability of exercise to improve their fitness levels.”

Thyfault says many cardiologists want to prescribe statins to all patients over a certain age regardless of whether they have metabolic syndrome; the drugs also are recommended for people with Type 2 diabetes. He recommends that cardiologists more closely weigh the benefits and risks of statins given this new data about their effect on exercise training.

“Statins have only been used for about 15-20 years, so we don’t know what the long-term effects of statins will be on aerobic fitness and overall health,” Thyfault said. “If the drugs cause complications with improving or maintaining fitness, not everyone should be prescribed statins.”

Thyfault and his colleagues measured cardiorespiratory fitness in 37 previously sedentary, obese individuals ages 25-59 with low fitness levels. The participants followed the same exercise regimen on the MU campus for 12 weeks; 18 of the 37 people also took 40 mg of simvastatin daily.

Statins significantly affected participants’ exercise outcomes. Participants in the exercise-only group increased their cardiorespiratory fitness by an average of 10 percent compared to a 1.5 percent increase among participants also prescribed statins. Additionally, skeletal muscle mitochondrial content, the site where muscle cells turn oxygen into energy, decreased by 4.5 percent in the group taking statins while the exercise-only group had a 13 percent increase, a normal response following exercise training.

Thyfault suggests that future research determine whether lower doses of simvastatin or other types of statins similarly affect people’s exercise outcomes and thus their risk for diseases such as Type 2 diabetes. Starting a statin regimen after exercising and obtaining a higher fitness level may reduce the drugs’ effects on fitness, he says.

The study, “Simvastatin impairs exercise training adaptations,” was published in the Journal of the American College of Cardiology. Co-authors included first author Catherine Mikus, who is now a postdoctoral fellow at Duke University, and MU researchers Leryn Boyle, Douglas Oberlin, Scott Naples, Justin Fletcher, Harold Laughlin, Kevin Dellsperger and Paul Fadel. Funding was provided by a grant from the MU Research Board, the Veterans Affairs’ Career Development Award, an American Heart Association Midwest Affiliate Clinical Research Award and the National Institutes of Health. The Department of Nutrition and Exercise Physiology is jointly administered by the College of Agriculture, Food and Natural Resources, the College of Human Environmental Sciences and the School of Medicine. Thyfault has a joint appointment in the Department of Internal Medicine in the Division of Gastroenterology and Hepatology in the MU School of Medicine.

Study shows drinking one 12oz sugar-sweetened soft drink a day can increase the risk of type 2 diabetes by 22 percent

Contact: Sam Wong Press Office sam.wong@imperial.ac.uk 44-020-759-42198 Diabetologia

Drinking one (or one extra)* 12oz serving size of sugar-sweetened soft drink a day can be enough to increase the risk of developing type 2 diabetes by 22%, a new study suggests. The research is published in  Diabetologia (the journal of the European Association for the Study of Diabetes) and comes from data in the InterAct consortium**. The research is by Dr Dora Romaguera, Dr Petra Wark and Dr Teresa Norat, Imperial College London, UK, and colleagues.

Since most research in this area has been conducted in North American populations, the authors wanted to establish if a link between sweet beverage consumption and type 2 diabetes existed in Europe. They used data on consumption of juices and nectars, sugar-sweetened soft drinks and artificially sweetened soft drinks collected across eight European cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC study; UK, Germany, Denmark, Italy, Spain, Sweden, France, Italy, Netherlands)***, covering some 350,000 participants.

As part of the InterAct project, the researchers did a study which included 12,403 type 2 diabetes cases and a random sub-cohort of 16,154 identified within EPIC. The researchers found that, after adjusting for confounding factors, consumption of one 12oz (336ml) serving size of sugar-sweetened soft drink per day increased the risk of type 2 diabetes by 22%. This increased risk fell slightly to 18% when total energy intake and body-mass index (BMI) were accounted for**** (both factors that are thought to mediate the association between sugar-sweetened soft drink consumption and diabetes incidence). This could indicate that the effect of sugar-sweetened soft drink on diabetes goes beyond its effect on body weight.

The authors also observed a statistically significant increase in type 2 diabetes incidence related to artificially sweetened soft drink consumption, however this significant association disappeared after taking into account the BMI of participants; this probably indicates that the association was not causal but driven by the weight of participants (i.e. participants with a higher body weight tend to report higher consumption of artificially sweetened drinks, and are also more likely to develop diabetes). Pure fruit juice and nectar***** consumption was not significantly associated with diabetes incidence, however it was not possible using the data available to study separately the effect of 100% pure juices from those with added sugars.

The authors say the increased risk of diabetes among sugar-sweetened soft drink consumers in Europe is similar to that found in a meta-analysis of previous studies conducted mostly in North America (that found a 25% increased risk of type 2 diabetes associated with one 12 oz daily increment of sugar-sweetened beverage consumption).

Dr Romaguera concludes: “Given the increase in sweet beverage consumption in Europe, clear messages on the unhealthy effect of these drinks should be given to the population.”

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Notes to editors:

*The increased risk of 22% is for each extra 12oz sugar sweetened drink, so would apply to someone who had 1 drink versus someone who had 0, or someone who had 2 drinks versus someone who had 1, etc.

**The InterACT consortium is investigating, among other things, nutritional factors and physical activity to study the association of nutritional, dietary and physical activity behaviours with incident diabetes in the nested case-cohort study and to contribute to the analysis of gene-lifestyle interaction. It is a sub-division of the EPIC study, which was designed to investigate the relationships between diet, nutritional status, lifestyle and environmental factors and the incidence of cancer and other chronic diseases.

***The centres involved were France, Italy, Spain, Denmark, UK (Oxford, Cambridge), Netherlands (Bilthoven, Utrecht), Germany (Heidelberg, Potsdam), Sweden (Umea, Malmo)

****Extra info from Dr Romaguera:  The 22% figure is used as the top line because it is widely accepted by the scientific community that these models should not be adjusted for BMI. In the meta-analysis comparison with other studies from the USA, the risk is those studies is NOT adjusted by BMI. That makes it possible to compare the two sets of results (25% increased risk in North American studies versus 22% in Europe).

*****nectars (UK and USA definition) are fruit juices that have been diluted to some extent and may contain additives (sugar or sweeteners)

Grape intake may protect against metabolic syndrome-related organ damage

April 22, 2013

   Media Contact: Justin Harris       734-764-2220 

Study shows grapes reduced inflammation and fat storage, improved antioxidant defense

    ANN ARBOR, MI

Consuming grapes may help protect against organ damage associated with the progression of metabolic syndrome, according to research presented Monday at the Experimental Biology conference in Boston. Natural components found in grapes, known as polyphenols, are thought to be responsible for these beneficial effects.

The study, led by investigator E. Mitchell Seymour, Ph.D., of the University of Michigan Health System, studied the effects of a high fat, American-style diet both with added grapes and without grapes (the control diet) on the heart, liver, kidneys, and fat tissue in obesity-prone rats. The grapes – a blend of red, green and black varieties – were provided as a freeze-dried grape powder and integrated into the animals’ diets for 90 days.

Specifically, the results showed that three months of a grape-enriched diet significantly reduced inflammatory markers throughout the body, but most significantly in the liver and in abdominal fat tissue.  Consuming grapes also reduced liver, kidney and abdominal fat weight, compared with those consuming the control diet.  Additionally, grape intake increased markers of antioxidant defense, particularly in the liver and kidneys.

Metabolic syndrome is a cluster of conditions that occur together – increased blood pressure, a high blood sugar level, excess body fat around the waist or low HDL (the good cholesterol) and increased blood triglycerides – significantly increasing the risk for heart disease, stroke and Type 2 diabetes. Intake of fruits and vegetables is thought to reduce these risks, and grapes have shown benefits in multiple studies.  Metabolic syndrome is a major public health concern, and is on the rise in the U.S.

“Our study suggests that a grape-enriched diet may play a critical role in protecting against metabolic syndrome and the toll it takes on the body and its organs,” said Seymour.  “Both inflammation and oxidative stress play a role in cardiovascular disease progression and organ dysfunction in Type 2 diabetes. Grape intake impacted both of these components in several tissues which is a very promising finding.”

This work extends and reinforces the findings of Seymour’s previously published research which demonstrated that a grape-enriched diet reduced risk factors for heart disease and diabetes in obesity-prone rats.

Experimental Biology is a multidisciplinary, scientific meeting focused on research and life sciences, covering general fields of study such as anatomy, biochemistry, nutrition, pathology and pharmacology.  The meeting is comprised of nearly 14,000 scientists and exhibitors

Research suggests popular diabetes drugs can cause abnormal pancreatic growth in humans

Contact: Enrique Rivero erivero@mednet.ucla.edu 310-794-2273 University of California – Los Angeles Health Sciences

Individuals who had taken a type of drug commonly used to treat Type 2 diabetes showed abnormalities in the pancreas, including cell proliferation, that may be associated with an increased risk of neuroendocrine tumors, according to a new study by researchers from UCLA and the University of Florida. Their findings were published online March 22 in the journal Diabetes.

The researchers, from the Larry L. Hillblom Islet Research Center at UCLA and the Diabetes Center at the University of Florida, found that cell mass was increased approximately 40 percent in the pancreases of deceased organ donors who had Type 2 diabetes and who had been treated with incretin therapy. This widely used type of treatment takes advantage of the action of a gut hormone known as glucagon-like peptide 1 (GLP-1) to lower blood sugar in the body.

Although there have been conflicting reports on the effects of the incretin class of drugs on the pancreas in animal studies, this is the first study to note such changes in the human pancreas. The research was made possible by a unique research consortium called nPOD (Network for Pancreatic Organ Donors with Diabetes), led by Dr. Mark Atkinson, a professor of pathology and pediatrics at the University of Florida. The network, which is funded by the Juvenile Diabetes Research Foundation, obtains pancreases from deceased organ donors, with permission of their next of kin, to better understand diabetes by investigating tissues of those with the disease.

“There is an increasing appreciation that animal studies do not always predict findings in humans,” said Dr. Peter Butler, director of UCLA’s Hillblom Islet Research Center and chief of the endocrinology, diabetes and hypertension unit. “The nPOD program is therefore a very precious resource.”  The researchers examined the pancreases of 20 deceased organ donors with Type 2 diabetes. Eight had been treated for at least a year with incretin therapy, while the other 12 had received therapies that didn’t include incretin-based drugs. The researchers also evaluated 14 pancreases from a control group of non-diabetic individuals of similar age.

The pancreases of the individuals who had been on incretin therapy were larger than those of patients on other types of diabetes therapies, and this larger size was associated with increased cellular proliferation. Incretin-treated individuals showed an increase in pancreas dysplasia, an abnormal form of cell proliferation that is a risk factor for pancreatic cancer, as well as an expansion of alpha cells, endocrine cells that make the hormone glucagon.

This latter finding is likely a consequence of GLP-1–based therapies’ suppression of the release of glucagon by alpha cells, since decreasing the availability or action of the hormone glucagon has been shown in a variety of prior studies to induce a proliferation of pancreatic alpha cells. This alpha-cell expansion has been associated with the development of pancreatic neuroendocrine tumors. Three of the eight incretin-treated individuals had microadenomas and one has a neuroendocrine tumor composed of alpha cells.

Of the eight donors who were on incretin therapy, seven had been taking sitagliptin, sold in pill form as Januvia and marketed by Merck, and one had been on exenatide, sold as Byetta by Bristol-Myers Squibb. These and similar drugs are currently under investigation by the U.S. Food and Drug Administration for their possible links to pancreatitis and pancreatic cancer.

“These findings lend additional weight to concerns regarding the effects of long term GLP-1–related therapy, with respect to both unintended proliferative actions on the exocrine pancreas and now also a possible increased risk of neuroendocrine tumors,” the researchers write. “In addition to the surveillance previously recommended for the potential association of GLP-1– based therapy and pancreatic cancer risk, the current data imply that surveillance for a possible increased risk of pancreatic neuroendocrine tumors is warranted.”

Such surveillance approaches might include MRI imaging of the pancreas and screening for neuroendocrine tumors, Butler said.

“The present studies are only from a small number of individuals, and while the findings do raise concerns, it will be important that other approaches are now used in a larger group of living individuals to further investigate these findings,” he said.

A recent study led by Dr. Sonal Singh of Johns Hopkins University School of Medicine and Public Health and published in JAMA Internal Medicine suggested a doubling in the risk of hospitalization for acute pancreatitis with the GLP-1–based therapies and also recommended further research.

“Since most risk factors for acute pancreatitis are also linked to an increased risk of pancreatic cancer, these findings of changes in the human pancreas are very concerning,” said Singh, an assistant professor of medicine and international health. “Now that GLP-1–based therapies have been shown to increase the risk of pancreatic inflammation and abnormal cell proliferation, further studies are needed to urgently clarify whether these linkages lead to pancreatic cancer with long-term use.”

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Study co-authors, in addition to Butler and Atkinson, are Alexandra  E. Butler, Tatyana Gurlo and David W. Dawson, all of UCLA, and Martha Campbell-Thompson of the University of Florida.

Grants from National Institute of Diabetes and Digestive and Kidney Diseases (DK059579, DK061539 and DK077967), the Hillblom Foundation, and the Peter and Valerie Kompaniez Foundation funded this study. The Juvenile Diabetes Research Foundation funds the nPOD program.

For more news, visit the UCLA Newsroom and follow us on Twitter.

Carnitine supplements reverse glucose intolerance in animals

2009 study posted for filing

Contact: Mary Jane Gore
mary.gore@duke.edu
919-660-1309
Duke University Medical Center

DURHAM, N.C. – Supplementing obese rats with the nutrient carnitine helps the animals to clear the extra sugar in their blood, something they had trouble doing on their own, researchers at Duke University Medical Center report.

A team led by Deborah Muoio (Moo-ee-oo), Ph.D., of the Duke Sarah W. Stedman Nutrition and Metabolism Center, also performed tests on human muscle cells that showed supplementing with carnitine might help older people with prediabetes, diabetes, and other disorders that make glucose (sugar) metabolism difficult.

Carnitine is made in the liver and recycled by the kidney, but in some cases when this is insufficient, dietary carnitine from red meat and other animal foods can compensate for the shortfall.

After just eight weeks of supplementation with carnitine, the obese rats restored their cells’ fuel- burning capacity (which was shut down by a lack of natural carnitine) and improved their glucose tolerance, a health outcome that indicates a lower risk of diabetes.

These results offer hope for a new therapeutic option for people with glucose intolerance, older people, people with kidney disease, and those with type 2 diabetes (what used to be called adult-onset diabetes).

Muoio said that soon her team of researchers will begin a small clinical trial of carnitine supplementation in people who fit the profile of those who might benefit from additional carnitine – older people (60 to 80 years) with glucose intolerance.

The study is published in the Aug. 21 issue of the Journal of Biological Chemistry.

The Duke researchers began studying carnitine more closely when abnormalities in the nutrient emerged from blood chemistry profiles of obese and old animals. These chemical profiles report on hundreds of byproducts of cell metabolism called metabolites and give scientists an opportunity to identify markers of disease states.

Carnitine is a natural compound known for helping fatty acids enter the mitochondria, the powerhouses of cells, where fatty acids are “burned” to give cells energy for their various tasks. Carnitine also helps move excess fuel from cells into the circulating blood, which then redistributes this energy source to needier organs or to the kidneys for removal. These processes occur through the formation of acylcarnitine molecules, energy molecules that can cross membrane barriers that encase all cells.

Researchers at Duke had observed that skeletal muscle of obese rats produced high amounts of the acylcarnitines, which requires free carnitine. As these molecules started to accumulate, the availability of free, unprocessed carnitine decreased. This imbalance was linked to fuel-burning problems, that is, impairments in the cells’ combustion of both fat and glucose fuel.

“We suspected that persistent increases in acylcarnitines in the rats were causing problems, and we could also see that the availability of free carnitine was decreasing with weight gain and aging,” said Muoio. “It appeared that carnitine could no longer do its job when chronic metabolic disruptions were stressing the system. That’s when we designed an experiment to add extra carnitine to the rats’ diet.”

Muoio is also a professor in the departments of medicine, pharmacology and cancer biology.

 

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Other study authors included Robert C. Noland, Sarah E. Seiler, Helen Lum, Olga Ilkayeva, Robert Stevens, and Timothy R. Koves of the Sarah W. Stedman Nutrition and Metabolism Center. Koves is also with the Duke Department of Medicine. Robert M. Lust is with the Department of Physiology at East Carolina University in Greenville, N.C., and Fausto G. Hegardt is with the CIBER division Fisiopatología de la Obesidad y la Nutrición of the Instituto de Salud Carlos III in Spain.

The work was supported by grants from the National Institutes of Health, and the American Diabetes Association, and a John A. Hartford Duke Center for Excellence Award

Researchers find possible environmental causes for Alzheimer’s, diabetes : nitrates

2009 study posted for filing

Contact: Nancy Cawley Jean njean@lifespan.org Lifespan

Call for reducing nitrate levels in fertilizer and water, detoxifying food and water

Providence, RI – A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food with increased deaths from diseases, including Alzheimer’s, diabetes mellitus and Parkinson’s. The study was published in the Journal of Alzheimer’s Disease (Volume 17:3 July 2009).

Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer’s, Parkinson’s, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer’s, Parkinson’s, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases.

De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, “We have become a ‘nitrosamine generation.’ In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture.” She continues, “Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking.”

Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.

Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods.

Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer’s, Parkinson’s and Type 2 diabetes mellitus.

De la Monte comments, “All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies.”

The researchers recognize that an increase in death rates is anticipated in higher age groups. Yet when the researchers compared mortality from Parkinson’s and Alzheimer’s disease among 75 to 84 year olds from 1968 to 2005, the death rates increased much more dramatically than for cerebrovascular and cardiovascular disease, which are also aging-associated. For example, in Alzheimer’s patients, the death rate increased 150-fold, from 0 deaths to more than 150 deaths per 100,000. Parkinson’s disease death rates also increased across all age groups. However, mortality rates from cerebrovascular disease in the same age group declined, even though this is a disease associated with aging as well.

De la Monte notes, “Because of the similar trending in nearly all age groups within each disease category, this indicates that these overall trends are not due to an aging population. This relatively short time interval for such dramatic increases in death rates associated with these diseases is more consistent with exposure-related causes rather than genetic changes.” She also comments, “Moreover, the strikingly higher and climbing mortality rates in older age brackets suggest that aging and/or longer durations of exposure have greater impacts on progression and severity of these diseases.”

The researchers graphed and analyzed mortality rates, and compared them with increasing age for each disease. They then studied United States population growth, annual use and consumption of nitrite-containing fertilizers, annual sales at popular fast food chains, and sales for a major meat processing company, as well as consumption of grain and consumption of watermelon and cantaloupe (the melons were used as a control since they are not typically associated with nitrate or nitrite exposure).

The findings indicate that while nitrogen-containing fertilizer consumption increased by 230 percent between 1955 and 2005, its usage doubled between 1960 and 1980, which just precedes the insulin-resistant epidemics the researchers found. They also found that sales from the fast food chain and the meat processing company increased more than 8-fold from 1970 to 2005, and grain consumption increased 5-fold.

The authors state that the time course of the increased prevalence rates of Alzheimer’s, Parkinson’s and diabetes cannot be explained on the basis of gene mutations. They instead mirror the classical trends of exposure-related disease. Because nitrosamines produce biochemical changes within cells and tissues, it is conceivable that chronic exposure to low levels of nitrites and nitrosamines through processed foods, water and fertilizers is responsible for the current epidemics of these diseases and the increasing mortality rates associated with them.

De la Monte states, “If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption.”

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Other researchers involved in the study with de la Monte include Alexander Neusner, Jennifer Chu and Margot Lawton, from the departments of pathology, neurology and medicine at Rhode Island Hospital and The Warren Alpert Medical School of Brown University.

The study was funded through grants from the National Institutes of Health. Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH and diabetes.

De la Monte, Suzanne M., Alexander Neusner, Jennifer Chu and Margot Lawton. “Epidemilogical Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer’s Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis.” Journal of Alzheimer’s Disease, 17:3 (July 2009) pp 519-529.

The Journal of Alzheimer’s Disease (http://www.j-alz.com) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer’s disease. The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. Groundbreaking research that has appeared in the journal includes novel therapeutic targets, mechanisms of disease and clinical trial outcomes. The Journal of Alzheimer’s Disease has an Impact Factor of 5.101 according to Thomson Reuters’ 2008 Journal Citation Reports. The Journal is published by IOS Press (http://www.iospress.nl).

Founded in 1863, Rhode Island Hospital (www.rhodeislandhospital.org) in Providence, RI, is a private, not-for-profit hospital and is the largest teaching hospital of the Warren Alpert Medical School of Brown University. A major trauma center for southeastern New England, the hospital is dedicated to being on the cutting edge of medicine and research. Many of its physicians are recognized as leaders in their respective fields of cancer, cardiology, diabetes, emergency medicine and trauma, neuroscience, orthopedics, pediatrics, radiation oncology and surgery. Rhode Island Hospital receives nearly $50 million each year in external research funding. It is home to Hasbro Children’s Hospital, the state’s only facility dedicated to pediatric care, which is ranked among the top 30 children’s hospitals in the country by Parents magazine. Rhode Island Hospital is a founding member of the Lifespan health system.

Stopping diabetes damage with vitamin C

2009 study posted for filing

Contact: Diane Clay
diane-clay@ouhsc.edu
405-271-2323
University of Oklahoma

First test in humans gets dramatic results from blood sugar control and antioxidant

Researchers at the Harold Hamm Oklahoma Diabetes Center have found a way to stop the damage caused by Type 1 diabetes with the combination of insulin and a common vitamin found in most medicine cabinets.

While neither therapy produced desired results when used alone, the combination of insulin to control blood sugar together with the use of Vitamin C, stopped blood vessel damage caused by the disease in patients with poor glucose control. The findings appear this week in the Journal of Clinical Endocrinology and Metabolism.

“We had tested this theory on research models, but this is the first time anyone has shown the therapy’s effectiveness in people,” said Michael Ihnat, Ph.D., principal investigator and a pharmacologist at the OU College of Medicine Department of Cell Biology.

Ihnat said they are now studying the therapy in patients with Type 2 diabetes.

The goal of the work being done by Ihnat and British scientists from the University of Warwick led by Dr. Antonio Ceriello is to find a way to stop the damage to blood vessels that is caused by diabetes. The damage, known as endothelial dysfunction, is associated with most forms of cardiovascular disease such as hypertension, coronary artery disease, chronic heart failure, peripheral artery disease, diabetes and chronic renal failure.

By reducing or stopping the damage, patients with diabetes could avoid some of the painful and fatal consequences of the disease that include heart disease, reduced circulation and amputation, kidney disease and diabetic retinopathy, which can lead to blindness.

Insulin and many other drugs have long been used to control blood sugar, but Ihnat – in an earlier project with scientists in Italy and Hungary – found that cells have a “memory” that causes damage to continue even when blood sugar is controlled. By adding antioxidants like Vitamin C, Ihnat found that cell “memory” disappeared and cell function and oxidation stress were normalized.

“We have speculated that this happens with endothelial dysfunction, but we did not know until now if it was effective in humans. We finally were able to test it and proved it to be true,” Ihnat said. “For patients with diabetes, this means simply getting their glucose under control is not enough. An antioxidant-based therapy combined with glucose control will give patients more of an advantage and lessen the chance of complications with diabetes.”

While researchers do suggest diabetic patients eat foods and take multivitamins rich in antioxidants like Vitamin C, they warn that additional study is needed. The Vitamin C utilized in their study was given at very high doses and administered directly into the blood stream, so it is unlikely someone would get similar results with an over-the-counter vitamin supplement.

The team is now working to determine how antioxidants work at the molecular level to halt the destructive chain reaction set in motion by high blood sugar levels. In addition, they are evaluating several other antioxidants with an ultimate hope that their work will translate into simple, effective and inexpensive treatments for the control of diabetes.

 

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The Journal of Clinical Endocrinology & Metabolism is the world’s leading peer-reviewed journal for endocrine clinical research and cutting-edge clinical practice reviews.

Dr. Ihnat’s latest work, which is funded by the VA Medical Center, can be found online at http://jcem.endojournals.org/cgi/content/abstract/jc.2009-0762v1.

Daily vibration may combat prediabetes in youth : 20min daily was better than prescription drugs at reducing levels of hemoglobin A1

Contact: Toni Baker
tbaker@georgiahealth.edu
706-721-4421
Georgia Health Sciences University

AUGUSTA, Ga. – Daily sessions of whole-body vibration may combat prediabetes in adolescents, dramatically reducing inflammation, average blood glucose levels and symptoms such as frequent urination, researchers report.

In mice that mimic over-eating adolescents headed toward diabetes, 20 minutes of daily vibration for eight weeks restored a healthy balance of key pro- and anti-inflammatory mediators and was better than prescription drugs at reducing levels of hemoglobin A1c, the most accurate indicator of average blood glucose levels, said Dr. Jack C. Yu, Chief of the Section of Plastic and Reconstructive Surgery at the Medical College of Georgia at Georgia Health Sciences University.

In normal mice, just four days of vibration also dramatically improved the ability to manage a huge glucose surge similar to that following a high-calorie, high-fat meal. “It’s a very good sign,” said Yu. “If you eat a pound of sugar, your blood glucose will go up. If you are prediabetic, it will go up even more and take longer to come down.”

Interestingly, vibration did not produce similar changes in older, normal mice, Yu told researchers at the Third World Congress of Plastic Surgeons of Chinese Descent.

“This is our model: the average American teenager who eats too much,” said Yu, who regularly operates on obese and often prediabetic adolescent males who want their abnormally large breasts reduced. “The only way to burn fat is to exercise. We shake the bone for you rather than the body’s muscle shaking it. This is a highly efficient way to fool the bone into thinking we are exercising.”

It’s also one way to deal with the reality that many individuals simply will not exercise regularly, he said.

Yu, also a craniofacial surgeon who studies bone formation, said while it’s unclear exactly how vibration produces these desirable results, it seems linked to the impact of movement on bone health. Vibration mimics the motion bones experience during exercise when muscles are doing the work. The slight bending and unbending of bone triggers remodeling so it can stay strong. One result is production of osteocalcin, a protein essential to bone building, which also signals the pancreas to get ready for food. While this prehistoric relationship is tied to the hunt for food, it doesn’t work so well in 21st century living where folks are moving too little and eating too much, Yu said. The constant demand can produce resistance to the insulin required to use glucose as energy.

Additionally, the body tends to hold onto fat for energy and survival, which researchers think is key to the chronic inflammation found in obesity-related type 2 diabetes. The fat itself produces inflammatory factors; the immune system also can misidentify fat as an infection, resulting in even more inflammation but, unfortunately, not eliminating the fat.

The bottom line is an unbalanced immune response: too many aggressors like the immune system SWAT team member Th17 and too few calming regulating factors like FoxP3. Researchers looked in the mouse blood and found vibration produced a 125-fold increase in immune system homeostasis and similar results in the kidney. This included positive movement in other players as well, such as a five-fold reduction in what Yu calls the “nuclear fuel,” gammaH2AX, an indicator that something is attacking the body’s DNA.

The animal model researchers used has a defect in the receptor for leptin, the satiety hormone, so the mice uncharacteristically overeat. Vibration also significantly reduced the mouse’s diabetic symptoms of excessive thirst and diluted urine, resulting from excessive urination. The mice also seemed to like it, Yu said.

Next steps include learning more about how vibration produces such desirable results and large-scale clinical studies to see if they hold true in adolescents.

Prediabetics can avoid type 2 diabetes by making healthy diet changes and increasing physical activity, according to the American Diabetes Association.

Vibration technology was originally developed by the former Soviet Union to try to prevent muscle and bone wasting in cosmonauts. MCG researchers reported in the journal Bone in 2010 that daily whole body vibration may help minimize age-related bone density loss.

Yu and Biomedical Engineer Karl H. Wenger developed the whole-body vibrator used for the animal studies. Study coauthors include Wenger as well as GHSU’s Drs. Babak Baban, Sun Hsieh, Mahmood Mozaffari and Mohamad Masoumy.

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Plant-Based Diets Can Remedy Chronic Diseases

According to the World Health Organization (WHO), 63 percent of the deaths that occurred in 2008 were attributed to non-communicable chronic diseases such as cardiovascular disease, certain cancers, Type 2 diabetes and obesity—for which poor diets are contributing factors. Yet people that live in societies that eat healthy, plant-based diets rarely fall victim to these ailments. Research studies have long indicated that a high consumption of plant foods is associated with lower incidents of chronic disease. In the October issue of Food Technology magazine, Senior Writer/Editor Toni Tarver discusses recent discoveries in nutritional genomics that explain how plant-based diets are effective at warding off disease.

October 17, 2012

CHICAGO—According to the World Health Organization (WHO), 63 percent of the deaths that occurred in 2008 were attributed to non-communicable chronic diseases such as cardiovascular disease, certain cancers, Type 2 diabetes and obesity—for which poor diets are contributing factors. Yet people that live in societies that eat healthy, plant-based diets rarely fall victim to these ailments. Research studies have long indicated that a high consumption of plant foods is associated with lower incidents of chronic disease. In the October issue of Food Technology magazine, Senior Writer/Editor Toni Tarver discusses recent discoveries in nutritional genomics that explain how plant-based diets are effective at warding off disease.
The article indicates that bioactive compounds in plant foods play a role in controlling genetic and other biological factors that lead to chronic disease. For example, antioxidants in plant foods counter free radicals that can cause chronic inflammation and damage cells. And other plant compounds help control a gene linked to cardiovascular disease and plaque buildup in arteries and the genes and other cellular components responsible for forming and sustaining tumors.
William W. Li, M.D., President and Medical Director of the Angiogenesis Foundation in Cambridge, Mass., says that all consumers should look at their diets as if food is the medicine necessary to maintain healthy, disease-free lives. “Prevention is always better than a cure,” said Li. Foods that may help prevent cancer and other chronic diseases include artichokes, black pepper, cinnamon, garlic, lentils, olives, pumpkin, rosemary, thyme, watercress, and more.  For a more comprehensive list of medicinal foods, read “The Chronic Disease Food Remedy” in the October 2012 issue of Food Technology.

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About IFT For more than 70 years, IFT has existed to advance the science of food. Our nonprofit scientific society—more than 18,000 members from more than 100 countries—brings together food scientists, technologists and related professions from academia, government, and industry. For more information, please visit ift.org.

Popular diabetes treatment could trigger pancreatitis, pancreatic cancer

2009 study posted for filing

Contact: Enrique Rivero
erivero@mednet.ucla.edu
310-794-2273
University of California – Los Angeles

Drug’s adverse effects negated when combined with older diabetes drug

A drug widely used to treat Type 2 diabetes may have unintended effects on the pancreas that could lead to a form of low-grade pancreatitis in some patients and a greater risk of pancreatic cancer in long-term users, UCLA researchers have found.

In a study published in the online edition of the journal Diabetes, researchers from the Larry L. Hillblom Islet Research Center at UCLA found that sitagliptin, sold in pill form as Januvia, caused abnormalities in the pancreas that are recognized as risk factors for pancreatitis and, with time, pancreatic cancer in humans. Januvia is marketed by Merck & Co. Inc. Sitagliptin is a member of a new class of drugs that enhance the actions of the gut hormone known as glucagon-like peptide 1 (GLP-1), which has been shown to be effective in lowering blood sugar in people with Type 2 diabetes. The study is available at http://diabetes.diabetesjournals.org/cgi/content/abstract/db09-0058v1.

“Type 2 diabetes is a lifelong disease — people often take the same drugs for many years, so any adverse effect that could over time increase the risk for pancreatic cancer would be a concern,” said Dr. Peter Butler, director of the Hillblom Center and the study’s lead investigator. “A concern here is that the unwanted effects of this drug on the pancreas would likely not be detected in humans unless the pancreas was removed and examined.”

An observed connection between Byetta, a drug used to treat Type 2 diabetes that is related to Januvia in its intended actions, and pancreatitis has already been reported, prompting a Food and Drug Administration warning. Amylin Corp., which markets Byetta, has suggested that since there is no known mechanism linking the cases of pancreatitis with Byetta, the association might be chance. The UCLA study suggests that there may indeed be a link between drugs that enhance the actions of GLP-1 and pancreatitis — by increasing the rate of formation of cells that line the pancreatic ducts.

In the study, researchers used human IAPP transgenic (HIP) rats to test both sitagliptin and metformin; metformin, a member of an older, different class of diabetes drugs in use since the 1950s, has recently been found to have anti-tumor properties. The researchers sought to determine how the drugs, both singly and in combination, affected islet disease progression in the pancreas — particularly how they affected beta cells in the pancreas’s Islets of Langerhans. Beta cells are responsible for releasing insulin in people with normal metabolism, but they don’t produce insulin in sufficient amounts in diabetes patients. HIP rats approximate both the islets and metabolism of people with Type 2 diabetes. The drugs were tested in 40 rats for 12 weeks.

The researchers found that the two drugs in combination had a synergistic effect that helped preserve beta cells, improved their function and enhanced insulin sensitivity in the test rats. With the sitagliptin alone, however, the rats had abnormally high rates of cell production in their pancreatic ducts; a few developed an abnormality known as ductal metaplasia, and one developed pancreatitis.

But the metformin, trade name Glucophage, seems to counteract sitagliptin’s adverse effect.

“The apparent protection against the unwanted actions of sitagliptin in the exocrine pancreas are intriguing and may offer a potential way of using the GLP-1 class of drugs safely,” Butler said. “The protective effect may have been either by the actions of metformin to decrease blood glucose values or its recently appreciated properties as a tumor suppressive agent.”

Butler noted that the present study was undertaken in rats and that it is possible the adverse effects observed would not occur in humans.

“Given these findings, it is probably sensible to use the GLP-1 class of drugs only with metformin until other data is forthcoming,” he said.

 

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The National Institutes of Health, the Larry Hillblom Foundation and the Merck Research Foundation funded this study.

In addition to Butler, researchers included Aleksey V. Matveyenko, Heather I. Cox, Artemis Moshtaghian, Tatyana Gurlo, Ryan Galasso and Alexandra E. Butler, all of the Hillblom Center, and Sarah Dry of the department of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA.

The Larry L. Hillblom Islet Research Center at UCLA, established in 2004, is the first center dedicated to the study of the Islets of Langerhans, which include the insulin-producing cells in the pancreas. An understanding of the causes of islet cell destruction is key to finding a cure for diabetes. The center’s faculty members, recruited from around the world, provide leadership in the worldwide fight against the disease. The center is funded by a grant from the Larry Hillblom Foundation, which supports medical research in the state of California.

Low-carb diets prove better at controlling type 2 diabetes: Diabetes medications were reduced or eliminated in 95 percent of volunteers

2009 study posted for filing

Contact: Debbe Geiger
Debbe.Geiger@duke.edu
919-660-9461
Duke University Medical Center

DURHAM, NC — In a six-month comparison of low-carb diets, one that encourages eating carbohydrates with the lowest-possible rating on the glycemic index leads to greater improvement in blood sugar control, according to Duke University Medical Center researchers.

Patients who followed the no-glycemic diet experienced more frequent reductions, and in some cases elimination, of their need for medication to control type 2 diabetes, according to lead author Eric Westman, MD, director of Duke’s Lifestyle Medicine Program. The findings are published online in Nutrition and Metabolism.

“Low glycemic diets are good, but our work shows a no-glycemic diet is even better at improving blood sugar control,” he says. “We found you can get a three-fold improvement in type 2 diabetes as evidenced by a standard test of the amount of sugar in the blood. That’s an important distinction because as a physician who is faced with the choice of drugs or diet, I want a strong diet that’s shown to improve type 2 diabetes and minimize medication use.”

Eight-four volunteers with obesity and type 2 diabetes were randomized to either a low-carbohydrate ketogenic diet (less than 20 grams of carbs/day) or a low-glycemic, reduced calorie diet (500 calories/day). Both groups attended group meetings, had nutritional supplementation and an exercise regimen.

After 24 weeks, their glycemic control was determined by a blood test that measured hemoglobin A1C, a standard test used to determine blood sugar control in patients with diabetes. Of those who completed the study, the volunteers in the low-carbohydrate diet group had greater improvements in hemoglobin A1C. Diabetes medications were reduced or eliminated in 95 percent of the low-carbohydrate volunteers, compared to 62 percent in the low-glycemic group. The low-carbohydrate diet also resulted in a greater reduction in weight.

“It’s simple,” says Westman. “If you cut out the carbohydrates, your blood sugar goes down, and you lose weight which lowers your blood sugar even further. It’s a one-two punch.”

The diet is not easy for everybody. “This is a therapeutic diet for people who are sick,” says Westman. “These lifestyle approaches all have an intensive behavioral component. In our program, people come in every two weeks to get reinforcements and reminders. We’ve treated hundreds of patients this way now at Duke and what we see clinically and in our research shows that it works.”

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This research is funded by the Robert C. Atkins Foundation.

Vitamin B1 could reverse early-stage kidney disease in diabetes patients

2008 study posted for filing

Contact: Kelly Parkes-Harrison
k.e.parkes@warwick.ac.uk
44-078-245-40863
University of Warwick

Researchers at the University of Warwick have discovered high doses of thiamine – vitamin B1 – can reverse the onset of early diabetic kidney disease.

Kidney disease, or diabetic nephropathy, develops progressively in patients with type 2 diabetes. Early development of kidney disease is assessed by a high excretion rate of the protein albumin from the body in the urine, known as microalbuminuria.

The research is led by Dr Naila Rabbani and Professor Paul J Thornalley at Warwick Medical School, University of Warwick, in collaboration with researchers at the University of Punjab and Sheik Zaid Hospital, Lahore, Pakistan.

The team has discovered taking high oral doses of thiamine can dramatically decrease the excretion of albumin and reverse early stage kidney disease in type 2 diabetes patients.

In a paper published online in the journal Diabetologia, the team show 300 mg of thiamine taken orally each day for three months reduced the rate of albumin excretion in type 2 diabetes patients. The albumin excretion rate was decreased by 41% from the value at the start of the study. The results also showed 35% of patients with microalbuminuria saw a return to normal urinary albumin excretion after being treated with thiamine.

Forty patients with type 2 diabetes aged between 35 and 65 years old took part in the trial. They were randomly assigned a placebo or 3 x 100mg tablets of thiamine a day for three months.

The Warwick research group has already conclusively proven that type 2 diabetes patients have a thiamine deficiency. In an earlier study led by Professor Paul Thornalley at Warwick Medical School, the research team showed that thiamine deficiency could be key to a range of vascular problems for diabetes patients.

Dr Rabbani said: “This study once again highlights the importance of Vitamin B1 and we need to increase awareness. Professor Thornalley and I are planning a foundation at the University of Warwick to further education and research in thiamine deficiency.”

 

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Notes to editors

This study was funded by the Pakistan Higher Education Commission and Dr Rabbani holds a research fellowship with the British Heart Foundation, based at Warwick Medical School.

The paper appears in Diabetologia and is available online at http://www.springerlink.com/content/51l034044218455j/?p=814d61fe534b49ebbea262b559224387&pi=2

The previous study led by Professor Paul Thornalley appeared in Diabetologia in August 2007. It is available online at http://www.springerlink.com/content/r4723142882735l5/?p=de1637f799b94f9eaf1affc684404efb&pi=1

For more information or to speak to Professor Thornalley contact Kelly Parkes-Harrison, Communications Officer, University of Warwick, +44 (0)2476 150483, +44 (0)7824 540863, k.e.parkes@warwick.ac.uk

Garlic chemical tablet treats diabetes 1 and 2

2008 study posted for filing

Contact: Hiromu Sakurai
sakuraih@suzuka-u.ac.jp
Royal Society of Chemistry

Oral administration of vanadium-allixin compound lowers blood glucose levels in diabetic mice

A drug based on a chemical found in garlic can treat diabetes types I and II when taken as a tablet, a study in the new Royal Society of Chemistry journal Metallomics says.

When Hiromu Sakurai and colleagues from the Suzuka University of Medical Science, Japan, gave the drug orally to type I diabetic mice, they found it reduced blood glucose levels.

The drug is based on vanadium and allixin, a compound found in garlic, and its action described in an Advance Article from Metallomics available free online from today. The first issue of the new journal will be published in 2009.

In previous work they had discovered the vanadium-allixin compound treated both diabetes types when injected, but this new study shows the drug has promise as an oral treatment for the disease.

Type I diabetes (insulin dependent) is currently treated with daily injections of insulin, while type II (non-insulin dependent) is treated with drugs bearing undesirable side-effects – the authors note neither treatment is ideal.

The researchers aim to test the drug in humans in future work.

Study explains decrease in insulin-producing beta cells in diabetes: Current Theory is wrong

Contact: Karin Eskenazi
ket2116@columbia.edu
212-342-0508
Columbia University Medical Center

Findings suggest new approach to treatment

IMAGE:The life cycle of transcription factor FoxO1 closely mirrors the state of health of the pancreatic beta cell. In a healthy cell, FoxO1 (stained red) is inactive and co-localizes with…

Click here for more information. 

New York, NY (September 13, 2012) — Scientists generally think that reduced insulin production by the pancreas, a hallmark of type 2 diabetes, is due to the death of the organ’s beta cells. However, a new study by Columbia University Medical Center (CUMC) researchers shows that beta cells do not die but instead revert to a more fundamental, undifferentiated cell type. The findings suggest that strategies to prevent beta cells from de-differentiating, or to coax them to re-differentiate, might improve glucose balance in patients with type 2 diabetes. The study, conducted in mice was published today in the online edition of the journal Cell.

“The prevailing theory is that the death of beta cells is responsible for the decline in insulin production in type 2 diabetes,” said study leader Domenico Accili, MD, professor of Medicine and the Russell Berrie Foundation Professor at CUMC. “But when you look at a diabetic pancreas, you find very few, if any, dead beta cells. So, the organ dysfunction is out of proportion with the number of dead cells. Nobody has had a plausible explanation for this.”

Dr. Accili and co-author Chutima Talchai, PhD, suspected that some answers might lie in the activity of FoxO1 protein. FoxO1 — a transcription factor, or protein that controls when genes are switched on or off — serves as a kind of gauge of the body’s nutritional status. When a cell is well nourished, FoxO1 is inactive and stays in the cell body, or cytoplasm. In the face of a physiologic stress, such as high blood sugar, FoxO1 travels to the nucleus and ultimately disappears. “The starting point of our study was to ask, why does FoxO1 go to the nucleus in the early phases of diabetes, and is the decrease in FoxO1 a cause of diabetes or a consequence?” said Dr. Accili.

To address these questions, Dr. Talchai created a strain of mice whose beta cells lack FoxO1. Initially, the mice appeared normal, but after a physiologic stress, such as pregnancy or aging, the mice developed low levels of insulin and high levels of glucagon (a pancreatic hormone that counters the effects of insulin) — responses also seen in human diabetes.

The researchers then used a novel form of cell-lineage tracing to find out what happened to the beta cells. “To our surprise, we found that the beta cells had not disappeared but had changed into a different cell type. They had sort of walked back from fully committed insulin-making cells to an uncommitted progenitor-like, multipotent development stage,” said Dr. Accili. In addition, some of the beta cells became glucagon-producing cells, which would explain why people with diabetes have abnormally high glucagon levels. The same changes in beta cells were observed in other mouse models of diabetes.

“Our findings tell us that FoxO1 is necessary to maintain the identity of beta cells,” said Dr. Accili. “During metabolic stress, beta cells gradually lose FoxO1 and begin to de-differentiate, probably as a self-protective mechanism.”

The study has important implications for the treatment of type 2 diabetes. “Currently, we give patients medications that force beta cells to work even harder,” said Dr. Accili. “But it’s like flogging a dying horse. You can push beta cells only so far. Our findings would suggest that treatment should begin by giving beta cells a rest, by administering insulin. Then, we should give an agent that promotes the re-differentiation of beta cells. What that agent could be, we don’t know; but we do have some inkling from our work that certain signaling pathways, such as the wnt or notch pathways, could be targeted for this purpose.”

 

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The study is titled, “Pancreatic B-Cell Dedifferentiation As Mechanism Of Diabetic B-Cell Failure.” Contributors are Domenico Accili (CUMC), Chutima Talchai (CUMC and Chulalongkorn University, Bangkok, Thailand), Shouhong Xuan (CUMC), Hua V. Lin (Eli Lilly China Laboratories, Shanghai, People’s Republic of China), and Lori Sussel (CUMC). Dr. Talchai is a postdoctoral research scientist at CUMC and a New York Stem Cell Foundation-Druckenmiller Fellow.

The study was supported by grants from the Druckenmiller Fellowship of the New York Stem Cell Foundation, the National Institutes of Health (DK64819, DK58282, and DK63608), the Brehm Coalition, and the Russell Berrie Foundation.

The authors have filed a patent for an assay that can distinguish normal cells from de-differentiated cells. The authors declare no other financial or other conflicts of interest.

Columbia University Medical Center provides international leadership in basic, pre-clinical and clinical research, in medical and health sciences education, and in patient care. The medical center trains future leaders and includes the dedicated work of many physicians, scientists, public health professionals, dentists, and nurses at the College of Physicians and Surgeons, the Mailman School of Public Health, the College of Dental Medicine, the School of Nursing, the biomedical departments of the Graduate School of Arts and Sciences, and allied research centers and institutions. Established in 1767, Columbia’s College of Physicians and Surgeons was the first institution in the country to grant the M.D. degree and is among the most selective medical schools in the country. Columbia University Medical Center is home to the largest medical research enterprise in New York City and State and one of the largest in the United States.

Upon its official opening in October 1998, the Naomi Berrie Diabetes Center at Columbia University Medical Center established a new standard of care for the 1.6 million people with diabetes in the New York area—combining world-class diabetes research and education programs with unprecedented family-oriented patient care. Named for the mother of the late Russell Berrie, founder of RUSS™ Toys, the center is today recognized as the most comprehensive diabetes research and treatment center in the tri-state region and has been designated a national “Diabetes Center of Excellence.” Approximately one hundred faculty and students, affiliated with the Center, conduct basic and clinical research related to the pathogenesis and treatment of all forms of diabetes and its complications. For more information, visit www.nbdiabetes.org.

Increased dietary fructose (high fructose corn syrup) linked to elevated uric acid levels and lower liver energy stores

Contact: Dawn Peters sciencenewsroom@wiley.com 781-388-8408 Wiley

Obese patients with type 2 diabetes who consume higher amounts of fructose display reduced levels of liver adenosine triphosphate (ATP)—a compound involved in the energy transfer between cells. The findings, published in the September issue of Hepatology, a journal of the American Association for the Study of Liver Diseases, indicate that elevated uric acid levels (hyperuricemia) are associated with more severe hepatic ATP depletion in response to fructose intake.

This exploratory study, funded in part by grants from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), also suggests that uric acid levels may serve as a marker for increased fructose consumption and hepatic ATP depletion. Uric acid is produced by the breakdown of purines, natural substances commonly found in foods. According to the authors, increased dietary fructose can alter the body’s metabolism and energy balance. Energy depletion in the liver may be associated with liver injury in patients with non-alcoholic fatty liver disease (NAFLD) and in those at risk for developing this metabolic condition.

Fructose is a simple sugar that fuels the body, and is found in fruits and vegetables. High fructose corn syrup—a mixture of glucose and fructose—is used as a sweetener in consumer food products such as bread, cereal, and soda. Prior research reports that fructose consumption in the U.S. has more than doubled in the past 30 years. In fact, studies have shown that Americans’ fructose intake climbed from 15 grams per day in the early 1900s to 55 grams per day in 1994, which experts believe stems from an increase in soft drink consumption.

“There is an alarming trend of increased rates of obesity, type 2 diabetes and NAFLD in the U.S.,” said lead author Dr. Manal Abdelmalek from Duke University Medical Center. “Given the concurrent rise in fructose consumption and metabolic diseases, we need to fully understand the impact of a high-fructose diet on liver function and liver disease.”

For the present study, 244 obese and diabetic adults from the Look AHEAD Study were evaluated, with dietary fructose consumption estimated by the food frequency questionnaire. Liver ATP and uric acid levels were measured in 105 patients who participated in the Look AHEAD Fatty Liver Ancillary Study. Researchers assessed the change in liver ATP content using an IV fructose challenge in 25 subjects, comparing patients with low fructose consumption (less than 15 grams per day) to those with high fructose consumption (greater than 15 grams per day).

The team found that participants with a high intake of dietary fructose had lower liver ATP levels at baseline and a greater change in ATP content following the fructose challenge than those who consumed a lower amount of fructose. Patients with high uric acid levels (5.5 mg/dL or more) displayed lower ATP stores in response to fructose.

Dr. Abdelmalek concludes, “High fructose consumption and elevated levels of uric acid are associated with more severe depletion of liver ATP. Our findings suggest that increased dietary fructose intake may impair liver “energy balance.” Further research to define the clinical implications of these findings on metabolism and NAFLD is necessary.” The authors highlight the importance of public awareness of the risks associated with a diet high in fructose.

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This study is published in Hepatology. Media wishing to receive a PDF of this articles may contact sciencenewsroom@wiley.com.

Full Citation: “Higher Dietary Fructose Is Associated with Impaired Hepatic ATP Homeostasis in Obese Individuals with Type 2 Diabetes.” Manal F. Abdelmalek, Mariana Lazo, Alena Horska, Susanne Bonekamp, Edward W. Lipkin, Ashok Balasubramanyam, John P. Bantle, Richard J. Johnson, Anna Mae Diehl, Jeanne M. Clark, and the Fatty Liver Subgroup of the Look AHEAD Research Group. Hepatology; (DOI: 10.1002/hep.25741); Print Issue Date: September, 2012. URL: http://onlinelibrary.wiley.com/doi/10.1002/hep.25741/abstract

Author Contact:

To arrange an interview with Dr. Abdelmalek, please contact Rachel Bloch with Duke University at rachel.bloch@duke.edu or at +1 919-419-5069.

About the Journal:

Hepatology is the premier publication in the field of liver disease, publishing original, peer-reviewed articles concerning all aspects of liver structure, function and disease. Each month, the distinguished Editorial Board monitors and selects only the best articles on subjects such as immunology, chronic hepatitis, viral hepatitis, cirrhosis, genetic and metabolic liver diseases and their complications, liver cancer, and drug metabolism. Hepatology is published on is published by Wiley on behalf of the American Association for the Study of Liver Diseases (AASLD). For more information, please visit http://wileyonlinelibrary.com/journal/hep.

About Wiley

Founded in 1807, John Wiley & Sons, Inc. has been a valued source of information and understanding for more than 200 years, helping people around the world meet their needs and fulfill their aspirations. Wiley and its acquired companies have published the works of more than 450 Nobel laureates in all categories: Literature, Economics, Physiology or Medicine, Physics, Chemistry, and Peace.

Our core businesses publish scientific, technical, medical, and scholarly journals, encyclopedias, books, and online products and services; professional/trade books, subscription products, training materials, and online applications and Web sites; and educational materials for undergraduate and graduate students and lifelong learners. Wiley’s global headquarters are located in Hoboken, New Jersey, with operations in the U.S., Europe, Asia, Canada, and Australia. The Company’s Web site can be accessed at http://www.wiley.com. The Company is listed on the New York Stock Exchange under the symbols JWa and JWb

26th Health Research Report 19 MAR 2008 – Reconstruction

 

 

Editors Top Five:

 
1.      Mayo Clinic proceedings highlights research about cardiovascular benefits of omega-3 fatty acids
2.      Weight loss more effective than intensive insulin therapy for type 2 diabetics
3.      Extra vitamin D in early childhood cuts adult diabetes risk
4.      What effect does melatonin have in colitis?
5.      Only two per cent of paediatric drug trials reported using independent safety monitoring

 

 

In this Issue:

 

1.      Study finds bacteria may reduce risk for kidney stones
2.      Type 2 Diabetes May Be Caused by Intestinal Dysfunction
3.      When the chips are down — soak them!
4.      High levels of estrogen associated with breast cancer recurrence
5.      U of I scientists aim to overcome allergic reactions to soy
6.      UCLA study finds that broccoli may help boost the aging immune system
7.      One small step for man, one giant leap for advertising
8.      Curing addiction with cannabis medicines
9.      New bacteria contaminate hairspray
10.  Oregon study raises questions on synthetic progestins
11.  Magnesium associated with lower risk for some strokes in male smokers
12.  HPV vaccine reduces abnormal pap test results
13.  Mayo Clinic proceedings highlights research about cardiovascular benefits of omega-3 fatty acids
14.  Postoperative chemotherapy does not improve survival in gastric cancer patients
15.  Weight loss more effective than intensive insulin therapy for type 2 diabetics
16.  Study raises caution on new painkillers
17.  Is a cup of tea really the answer to everything — even anthrax?
18.  Killer fungus spells disaster for wheat
19.  Fertility in developing countries: words into action
20.  Extra vitamin D in early childhood cuts adult diabetes risk
21.  Rodent study finds artificial butter chemical harmful to lungs
22.  Study in Circulation Research details how diabetes drives atherosclerosis
23.  Legal exposure to asbestos-like material linked to lung damage 25 years later
24.  An anti-inflammatory response to the vegan diet
25.  Foodborne outbreaks from leafy greens on rise
26.  Solving the drug price crisis
27.  New study: Pycnogenol improves memory in elderly
28.  Pneumococcal disease rates down significantly post-vaccine
29.  What effect does melatonin have in colitis?
30.  Do bacterial combinations result in enhanced cytokine production? No!
31.  Grape skin compound fights the complications of diabetes
32.  Scientists successfully awaken sleeping stem cells
33.  Only two per cent of paediatric drug trials reported using independent safety monitoring
 
http://healthresearchreport.me/2008/03/19/26th-health-research-report-19-mar-2008-reconstruction/

Health Technology Research Synopsis

Health Research Report

26th Issue Date  19 MAR 2008

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/vitaminandherbstore

www.engineeringevil.com

High-fructose corn syrup sugar makes maturing human fat cells fatter, less insulin-sensitive

Contact: Aaron Lohr alohr@endo-society.org 240-482-1380 The Endocrine Society

Fructose, the sugar widely used as high-fructose corn syrup in soft drinks and processed foods, often gets some of the blame for the widespread rise in obesity. Now a laboratory study has found that when fructose is present as children’s fat cells mature, it makes more of these cells mature into fat cells in belly fat and less able to respond to insulin in both belly fat and fat located below the skin.

The results will be presented Sunday at The Endocrine Society’s 92nd Annual Meeting in San Diego by lead author Georgina Coade, a PhD student at the University of Bristol in the U.K.

“Our results suggest that high levels of fructose, which may result from eating a diet high in fructose, throughout childhood may lead to an increase in visceral [abdominal] obesity, which is associated with increased cardiometabolic risk,” Coade said.

Defined by a large waistline, abdominal obesity raises the risk of heart disease and Type 2 diabetes. The abdominal cavity contains one of two major types of fat in the body: visceral fat. The other type, subcutaneous fat, is found below the surface of the skin.

Although researchers have shown the negative effects of fructose on the fat distribution of rodents, the effects of this sugar on human adipocytes, or fat cells, are not clear, according to Coade. Therefore, she and her fellow researchers studied biopsy specimens of both subcutaneous and visceral fat from 32 healthy-weight children who had not yet gone through puberty.

From the biopsy samples, the investigators obtained preadipocytes—the precursors to fat cells that have the potential to differentiate, or mature, into fat-containing adipocytes. They then allowed the precursor cells to mature for 14 days in culture media containing normal glucose (the main sugar found in the bloodstream and the principal source of energy in the body), high glucose or high fructose. The researchers assessed cell differentiation by measuring activity of an enzyme (GPDH) and the abundance of the adipocyte fatty acid binding protein, which are both present only in mature fat cells.

Fructose, the research team found, had different effects to that of glucose and caused the fat cells to differentiate more—that is, to form more mature fat cells—but only in visceral fat.

For both types of fat cells, maturation in fructose decreased the cells’ insulin sensitivity, which is the ability to successfully take up glucose from the bloodstream into fat and muscles. Decreased insulin sensitivity is a characteristic of Type 2 diabetes.

Although prolonged exposure to fructose had a negative effect on insulin sensitivity, when Coade and her co-workers exposed mature fat cells, rather than preadipocytes, to fructose for 48 hours, the cells’ insulin sensitivity increased. The reason why is unknown. However, she said, “Fructose alters the behavior of human fat cells if it is present as the fat cells mature. We can maybe compare this [timing] to periods in children when they are making their fat.”

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The London-based organization Diabetes UK helped fund this study.

How a virus might make you diabetic later in life : Cytomegalovirus (CMV)

Contact: Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Cytomegalovirus (CMV) is one of the viruses that most infected people carry without ill effects. Once infected you are infected for life and, although it normally is dormant, it can become active again at any point in time. New research published in BioMed Central’s open access journal Immunity and Ageing shows that CMV infection is a significant risk factor for the type 2 diabetes in the elderly.

Obesity, inactivity and aging are known to be associated with insulin resistance, one of the first signs of incipient diabetes. However only a third of those with insulin resistance go on the develop type 2 diabetes. So what marks these people as different? Why do their pancreas’ fail? Genetic and environmental factors are thought to play a part but so also does inflammation. People with type 2 diabetes usually have raised levels of biological markers for inflammation such as elevated CRP and larger numbers of active white blood cells.

Chronic infections including CMV can ‘stress’ the immune system and when researchers from Leiden University Medical Centre and University of Tubingen Medical School compared glucose regulation with antibodies to CMV (or CMV seropositivity) in over 500 participants of the Leiden 85-plus Study they found that having CMV was associated with type 2 diabetes.

The researchers suggest that CMV could be either acting directly on pancreatic cells or  indirectly by causing the immune system attacking the pancreas. Dr Andrea Maier, who led the investigation explained, ” In our study we realised that although CMV seropositivity was associated with type 2 diabetes, higher levels of HnA1c and high non-fasting glucose the actual level of antibodies against CMV was not. ”

This study is looking at the effect of CMV on the very old. By their very nature these people have had longer to become infected with CMV and have low risks for other factors which are linked to diabetes or to cardiovascular disease. While it may not be possible to extrapolate these findings to the general population it seems likely that finding a way to overcome CMV infections may reduce diseases, such  as diabetes, later in life.

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Media contact

Dr Hilary Glover Scientific Press Officer, BioMed Central Tel:  +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com

Notes to Editors

1. Cytomegalovirus seropositivity is associated with glucose regulation in the oldest old. Results from the Leiden 85-plus Study Sijia Chen, Anton JM de Craen, Yotam Raz, Evelyna Derhovanessian, Ann CTM Vossen, Westendorp GJ Rudi, Graham Pawelec and Andrea B MaierImmunity & Ageing (in press)

Please name the journal in any story you write. If you are writing for the web, please link to the article. All articles are available free of charge, according to BioMed Central’s open access policy.

Article citation and URL available on request on the day of publication.

2. Immunity & Ageing is an open access, peer-reviewed, online journal that considers manuscripts on all aspects of ageing examined from an immunological point of view.

3. BioMed Central (http://www.biomedcentral.com/) is an STM (Science, Technology and Medicine) publisher which has pioneered the open access publishing model. All peer-reviewed research articles published by BioMed Central are made immediately and freely accessible online, and are licensed to allow redistribution and reuse. BioMed Central is part of Springer Science+Business Media, a leading global publisher in the STM sector. @BioMedCentral

Pumpkin: A fairytale end to insulin injections? Regenerates Pancreatic Cells

Compounds found in pumpkin could potentially replace or at least drastically reduce the daily insulin injections that so many diabetics currently have to endure. Recent research reveals that pumpkin extract promotes regeneration of damaged pancreatic cells in diabetic rats, boosting levels of insulin-producing beta cells and insulin in the blood, reports Lisa Richards in Chemistry & Industry, the magazine of the SCI.

A group, led by Tao Xia of the East China Normal University, found that diabetic rats fed the extract had only 5% less plasma insulin and 8% fewer insulin-positive (beta) cells compared to normal healthy rats (Journal of the Science of Food and Agriculture, 87(9) 1753-7 2007).

Xia says: ‘pumpkin extract is potentially a very good product for pre-diabetic persons, as well as those who have already developed diabetes.’ He adds that although insulin injections will probably always be necessary for these patients, pumpkin extract could drastically reduce the amount of insulin they need to take.

David Bender, sub-dean at the Royal Free and University College Medical School, London, says: ‘this research is very exciting… the main finding is that feeding pumpkin extract prevents the progressive destruction of pancreatic beta-cells… but it is impossible to say whether pumpkin extract would promote regeneration in humans.’  He added: ‘I think the exciting thing is that this may be a source of a medication that could be taken by mouth.’

The protective effect of pumpkin is thought to be due to both antioxidants and D-chiro-inositol, a molecule that mediates insulin activity. Boosting insulin levels has the effect of lowering blood sugar levels, which reduces levels of oxidative oxygen species that damage beta-cell membranes, preventing further damage and allowing for some regeneration. Beta cells levels in the diabetic rats are, however, unlikely ever to reach that of controls, because some of the cells will have been damaged beyond repair.

Diabetes affects more than 230m people, almost 6% of the world’s adult population, according to the World Diabetes Foundation. The rats used in this study represent type I diabetes, but the researchers believe the pumpkin extract may also play a role in type II diabetes.

*Requested Repost from my Newsletters 2007