VeriChip Corporation (”VeriChip”) (NASDAQ CHIP) and its development partner RECEPTORS LLC, a technology company whose AFFINITY by DESIGN™ chemistry platform can be applied to the development of selective binding products, announced that VeriChip plans to fund its existing development partnership with RECEPTORS to launch Phase II development of an in vivo glucosesensing RFID microchip. In Phase II of this program, which is expected to be completed in the second quarter of 2010, the critical binding environment and competitor agent components of the glucose sensor will be optimized for system stability, sensitivity and specificity.

VeriChip previously announced in November 2008 that RECEPTORS completed Phase I of the project and successfully prepared prototype examples for both the glucoseselective binding environment and the glucosecompetitive signaling component. These critical components were used to demonstrate the benchtop format application of the glucosesensing system to the detection of glucose levels. This demonstration is the proofofconcept foundation of the glucosesensing system.

Also in November 2008, VeriChips Chairman and CEO, Scott R. Silverman, purchased 5.4 million shares of VeriChip common stock from former controlling stockholder Digital Angel Corporation. Simultaneously, in a separate transaction, VeriChip purchased from Digital Angel all patents related to an embedded biosensor system for use in humans and the assignment of any rights of Digital Angel under a development agreement associated with the development of the implantable glucosesensing microchip. These two events positioned the Company to move forward with the development of the in vivo glucosesensing RFID microchip.

The goal of Phase II is to optimize the sensing system for its glucose response in the presence of blood and interstitial fluid matrix components and demonstrate the integration of the components into a stable and reproducible glucose sensor.

Robert E. Carlson, Ph.D., President and Chief Science Officer at RECEPTORS LLC, said, “The development of a viable in vivo glucosesensing device has been hampered by both the instability of the component reagents and the difficulty of integrating the diverse system requirements of longterm stability, simplicity, biocompatibility, etc. into a millimeter scale device. Phase II will build on the proofofconcept success of Phase I to produce the foundation upon which we will build the implantable glucose sensor.”

The partners published a white paper in December 2007 entitled, “Development of an Implantable Glucose Sensor,” which is available at verichipcorp.com.

About RECEPTORS LLC

RECEPTORS LLC develops SMART MATERIALS products for laboratory, clinical, industrial hygiene and healthcare use that selectively capture and measure chemical, biochemical and cellular targets from complex biological, environmental or industrial samples. The Companys patented AFFINITY by DESIGN™ platform has broad applicability, ranging from the isolation of disease pathway proteins for drug discovery and production of therapeutic antibodies, to the capture of bacteria and viruses for disinfection and diagnostic purposes. RECEPTORS LLC is a private company based in suburban Minneapolis, Minnesota. For further information please visit receptorsllc.com.

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Ipsen (ParisIPN), announced preliminary results from a Phase II openlabel clinical trial (MS316 study) that evaluates the coadministration of recombinant human growth hormone (rhGH) and recombinant human insulinlike growth factor1 (rhIGF1) in two separate daily injections as a potential treatment for children with otherwise unexplained short stature associated with low IGF1 levels. Ipsen also announced results from a longterm study of rhIGF1 (study 1419) in patients with severe primary insulinlike growth factor deficiency (sPIGFD) that demonstrated that longterm twicedaily therapy with rhIGF1 improved the adult and near adult heights of extremely short patients with sPIGFD. The data from these two studies were presented along with posters on rhIGF1 (Increlex®, mecasermin [rDNA origin] injection) at the 8th Joint Meeting of the Lawson Wilkins Pediatric Endocrine Society / European Society for Pediatric Endocrinology (LWPES/ESPE) in New York, NY.

These studies were performed under INDs (investigational new drug application protocols) and the coadministration of rhGH and rhIGF1 is not an approved administration regimen for Increlex®. At this point in time, Increlex® is marketed in the U.S. and other countries throughout the world for the treatment of growth failure in children with severe Primary IGFD using twicedaily injections.

“The structuring of its US platform in 2008 enabled Ipsen to build a fully fledged commercial presence in the US but also to gain access to a promising pipeline. The Group intends to capitalize on its unique growth disorders and endocrinology franchise. The interim data presented at the LWPES/ ESPE meeting validate ongoing investigations and we look forward to continuing our research progress with our partners on this effort,” said JeanLuc Bélingard, Chairman and Chief Executive Officer, Ipsen. “Ipsen Group remains fully committed to furthering its endocrinology research and product development in support to its fastest growing franchise in this highlyspecialized therapeutic area.”

The MS316 study is an ongoing Phase II, randomized, openlabel, activetreatment controlled trial evaluating the efficacy and safety of the coadministration of rhGH and rhIGF1 therapy versus rhGH alone in 106 children with short stature associated with low levels of IGF1. All participants received morning injections of either rhGH alone (45 μg/kg oncedaily) or coadministered with rhIGF1 (45 μg/kg rhGH and 50, 100 or 150 μg/kg rhIGF1 also once daily as two injections). Subjects had a baseline mean height standard deviation score (SDS) of 2.5. Thirtysix of the children enrolled in the study have completed one year of treatment. Firstyear height velocities were 9.2 cm for the patients receiving rhGH alone and 10.4, 10.7, and 12.1cm for the three rhGH/rhIGF1 groups. At the end of one year, changes in mean height SDS were 0.72 for the patients receiving rhGH alone and 0.88, 0.91, and 1.11 for the three rhGH/rhIGF1 groups. Among all patients, the most common adverse events (> 15%) were headache, upper respiratory infection, injection site reactions and fever. Other noteworthy but less frequent adverse events included vomiting, hypoglycemia and gynecomastia. In addition, 2 transient cases of papilledema (probable intracranial hypertension) occurred with coadministration. In both cases, treatment was discontinued and restarted without recurrence.

“The preliminary results for the MS316 study of a coadministration treatment of recombinant IGF1 and recombinant growth hormone in children with short stature associated with low IGF1 are encouraging,” said L. Kurt Midyett, MD, Medical Director, Childrens Mercy Hospital and Clinics, Kansas City, Missouri. “While there is a compelling scientific rationale for coadministration therapy, this remains a research endeavor at this point and I look forward to seeing the completed data compiled and analyzed for this potential coadministration treatment option.”

Ipsen also announced data on 16 patients with severe Primary IGFD treated with Increlex® until adult or nearadult height. These patients were part of the original registration trial for Increlex® (study 1419), which continues to collect longterm followup data on treatment until they reached adult height. The analysis was done with 9 male and 7 female patients. Patients received a mean dose of 112 μg/kg Increlex® twicedaily for a mean of 9.9 years. Five patients also received GnRHanalog. The mean estimated gain in height up to the time of nearadult height in patients taking Increlex® was 13.2 cm (range 0.4 to 23.4) and the mean estimated gain in adult height was conservatively estimated as 10.5 cm (range 2.9 to 22.3). While longterm Increlex® therapy improved adult height for extremely short patients with severe Primary IGFD, most patients did not experience enough catchup growth to bring their heights into the normal adult range. The most common side effects associated with Increlex® include dizziness, headache, nausea and vomiting.

“The data supporting the efficacy and safety of recombinant human IGFI (rhIGFI) (Increlex®) continue to grow, and these results demonstrate that children with severe Primary IGFI deficiency can improve their adult/near adult height with longterm IGFI therapy,” said Philippe F. Backeljauw, MD, Professor of Pediatrics, Cincinnati Childrens Hospital Medical Center. “These results provide increased confidence to treat patients with severe Primary IGFD with rhIGFI (Increlex®).”

Other Ipsen poster presentations included safety and efficacy data of Increlex® based on the IGFD Registry database, which now has over 700 patients enrolled since May 2006, and data on an 86week, openlabel trial of pharmacokinetic (PK)based oncedaily (QD) dosing of rhIGF1 in 45 treatmentnaïve prepubertal children with short stature associated with low IGF1 levels.

About Increlex® (mecasermin (rDNA origin) injection)

The active ingredient of Increlex® is recombinant human insulinlike growth factor1 (IGF1). IGF1 is the direct mediator of many of growth hormones (GH) effects on statural growth, and must be present for normal growth of bones and cartilage in children. Without adequate IGF1, children may not achieve normal height.

Increlex® has been marketed in the United States since early 2006 and in Europe since late 2007 for the treatment of growth failure in children with severe Primary IGFD. Severe Primary IGFD is defined by height at least three standard deviations below the mean and IGF1 levels at least three standard deviations below the mean for age and sex, and presence of normal or elevated GH level in the US, and IGF1 levels below the 2.5% percentile for age and sex, and GH sufficiency throughout Europe. In children with this disorder, low IGF1 levels may be due to growthhormone resistance or insensitivity associated with mutations in GH receptors, postGH receptor signaling pathways, or to defects in the IGF1 gene.

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In a onetwo punch, a familiar diabetes drug reduced tumors faster and prolonged remission in mice longer than chemotherapy alone, apparently by targeting cancer stem cells, report Harvard Medical School researchers in the Sept. 14 advance online Cancer Research.

“We have found a compound selective for cancer stem cells,” said senior author Kevin Struhl, the David Wesley Gaiser professor of biological chemistry and molecular pharmacology at HMS. “Whats different is that ours is a firstline diabetes drug.”

The findings add to a growing body of preliminary evidence in cells, mice, and people that metformin may improve breast cancer outcomes in people. In this study, the diabetes drug seemed to work independently of its ability to improve insulin sensitivity and lower blood sugar and insulin levels, all of which are also associated with better breast cancer outcomes.

The results fit within the cancer stem cell hypothesis, an intensely studied idea that a small subset of cancer cells has a special power to initiate tumors, fuel tumor growth, and promote recurrence of cancer. Cancer stem cells appear to resist conventional chemotherapies, which kill the bulk of the tumor.

“There is a big desire to find drugs specific to cancer stem cells,” Struhl says. “The cancer stem cell hypothesis says you cannot cure cancer unless you also get rid of the cancer stem cells. From a purely practical point of view, this could be tested in humans. Its already used as a firstline diabetes drug.”

The possible usefulness of a diabetes drug against cancer lends credence to an emerging idea that, in the vast and complex alphabet soup of molecular interactions within cells, relatively few biological pathways will turn out to be most important for many different diseases, Struhl suggested.

In experiments led by postdoctoral fellows Heather Hirsch and Dimitrios Iliopoulos, the combination of metformin and the cancer drug doxorubicin killed human cancer stem cells and nonstem cancer cells in culture. The researchers used four genetically distinct breast cancer cell lines.

In mice, pretreatment with the diabetes drug prevented the otherwise dramatic ability of human breast cancer stem cells to form tumors. In other mice where tumors were allowed to take hold for 10 days, the dual therapy also reduced tumor mass more quickly and prevented relapse for longer than doxorubicin alone. In the two months between the end of treatment and the end of the experiment, tumors regrew in mice treated with chemotherapy alone, but not in mice that had received both drugs. By itself, metformin was ineffective in treating tumors.

“This is an exciting study,” said Jennifer Ligibel, a medical oncologist at DanaFarber Cancer Institute and an HMS instructor in medicine, who was not involved in the study. Ligibel and colleagues at the National Cancer Institute of Canada Clinical Trials Group are developing a largescale phase II trial to study metformins impact on recurrence in women treated for early stage breast cancer.

“There is a lot of interest in studying metformin in breast cancer, but so far we do not have direct evidence that metformin will improve outcomes in patients,” Ligibel said. “Thats what this trial is for.”

So far, observational studies have suggested a lower risk of cancers, including breast cancer, and better response to chemotherapy in diabetics taking metformin, she said. Basic science studies also have suggested plausible biological mechanisms. The study from the Struhl lab suggests a potential new pathway through which metformin could have an effect on breast cancer cells, she said.

In their search for compounds that selectively destroy cancer stem cells, scientists hope to improve cancer outcomes. But the story is never as simple in human cancers, said Kornelia Polyak, a breast cancer researcher at DanaFarber Cancer Institute and HMS associate professor of medicine, who was not involved in the study

Cancer stem cells are a shifty target, Polyak said. For example, any cancer cell can acquire the properties of a cancer stem cell, and cancer stem cells can change into nonstem cancer cells, which can be just as deadly. Clinical trials in people are needed to test these ideas, Polyak said.

The Struhl paper is an offshoot of a larger project in his lab to systematically track how gene activity changes when cells transform into cancer. These changes were remarkably similar to gene dynamics in diabetes and other inflammatory conditions.

The researchers reasoned that if a common genetic pathway underlies different diseases, drugs that work against one disease might work against another. In a screen, the most effective drug inhibiting the transformation of cells into cancer was metformin, which led to the experiments in this paper.

The team was further encouraged by the low dose of metformin needed for the effect in the laboratory, compared to the amount needed for analogous molecular experiments in basic diabetes research. The relative dosage in people for treating or preventing cancer is unknown and untested.

HMS has applied for a patent for a combined therapy of metformin and a lower dose of chemotherapy, which is being tested in animals. The research was funded by the National Institutes of Health and the American Cancer Society.

Written by Carol Cruzan Morton

Full citation

Cancer Research, Sept. 14 advance online publication

“Metformin Selectively Targets Cancer Stem Cells, and Acts Together with Chemotherapy to Block Tumor Growth Q2 and Prolong Remission”

Heather A. Hirsch(1), Dimitrios Iliopoulos(1), Philip N. Tsichlis(2), and Kevin Struhl(1)

1Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School
2Molecular Oncology Research Institute, Tufts Medical Center, Boston, Massachusetts

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Carol Cruzan Morton

A breakthrough by an international team of researchers in Canada, France, the UK and Denmark has uncovered a new gene that could lead to better treatment of type 2 diabetes, as well as a better understanding of how this widespread disease develops.

Unlike most of the genes that have been shown to cause diabetes, the new gene, called Insulin Receptor Substrate 1 (IRS1), doesnt affect how insulin is created in the pancreas, but rather, how the body responds to insulin already in the bloodstream, say the researchers, whose work will be published in Nature Genetics Sept. 6.

“Most of the genes that weve identified as diabetes risk genes to date reduce the function of the pancreas, specifically of beta cells in the pancreas that make insulin,” explained Dr. Robert Sladek of McGill University and the Génome Québec Innovation Centre in Montreal, a corresponding author of the paper. “IRS1 has to do with the function of the other tissues in the body. Rather than reduce production of insulin, this gene reduces the effect of insulin in muscles, liver and fat, a process called insulin resistance.”

Insulin, a hormone produced in the pancreas, enables the bodys cells to absorb glucose from food and turn it into energy. Different types of diabetes are caused by the bodys inability to produce sufficient insulin, inability to use its own insulin properly, or a combination of both factors.

“IRS1 is the first inside the cell that gets activated by insulin,” Sladek continued. “It basically tells the rest of the cell, hey, insulin is here, start taking in glucose from the blood! If IRS1 doesnt work, the whole process is disrupted.”

The research was conducted by an international team including Sladek, Dr. Constantin Polychronakos of McGills Faculty of Medicine; Dr. Philippe Froguel of the CNRS and Lille 2 University in France and Imperial College London; Dr. Oluf Pedersen of the University of Copenhagen and Aarhus University in Denmark and their colleagues at many institutions across Europe and North America.

This study, which used genetic material drawn from more than 6,000 French participants divided into two separate groups, represents the final step in a series of collaborations between these researchers that has redrawn our understanding of diabetes genetics. In this instance, not only did the researchers pinpoint a new diabeteslinked gene, they found the genetic trigger, which leads to malfunction, in a totally unexpected place.

“Its a singlenucleotide polymorphism (SNP, pronounced snip), a single letter change in your DNA,” said Sladek. “Whats interesting about this particular SNP is that its not linked genetically to the IRS1 gene in any way; its about halfamillion basepairs away, in the middle of a genetic desert with no known genes nearby. In genetic terms, its halfway from Montreal to Halifax. And yet we can see that it causes a 40percent reduction in the IRS1 gene, and even more important, a 40percent reduction in its activity. Which means that even if insulin is present, it wont work.”

“We would like to congratulate Rob Sladek and his group for this breakthrough discovery. His work on the genetic basis of type 2 diabetes will certainly have an impact in the way clinicians diagnose and treat diabetes patients and is paving the way for translational research and personalized medicine,” said Catalina LopezCorrea, Vicepresident of Scientific Affairs at Génome Québec. She added, “This discovery once again confirms the scientific excellence and talent of Québecs scientists and the key role that genomics is playing in the study and treatment of complex diseases.”

Sladek hopes this discovery may lead to new therapeutic lines of attack in the future.

“Its possible that in diabetic patients, the signal to turn this gene on and off might be impaired. But we might be able to use one of the other pathways to turn it on,” he said.

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Type 2 diabetes, the most common form of diabetes, is increasing at an alarming state with more than 180 million people affected worldwide. With the rising incidence of obesity, a major risk factor for the onset of type 2 diabetes, this metabolic disorder represents a major health concern. A group from the Ecole Polytechnique Fédérale de Lausanne, now shows that there may exist new ways to fight these disorders.

The study, published in the current issue of the scientific journal Cell Metabolism (September 2, 2009), demonstrates that activation of the protein TGR5 can treat type 2 diabetes and reduce weight gain. In collaboration with Prof. Roberto Pellicciari and his team at the University of Perugia (Italy), and Intercept Pharmaceuticals (New York, USA; Perugia, Italy), the group at the EPFL, led by Dr Kristina Schoonjans and Prof. Johan Auwerx, have characterized the metabolic properties of a selective TGR5 activator (INT777), a drug with a promising future for the treatment of diabetes and obesity.

Earlier work from the same group showed that bile acids (endogenous molecules involved in digestion), via the activation of TGR5 in muscle and brown adipose tissue, are able to boost energy expenditure and to prevent or reverse dietinduced obesity in mice.

In the present study, the group of Dr Kristina Schoonjans and Prof. Johan Auwerx went further in studying the role of TGR5 in the gut where TGR5 is expressed in cells specialized in the production of gutderived hormones. The authors found that in these socalled enteroendocrine cells TGR5 controls the secretion of the hormone GlucagonLike Peptide 1 (GLP1), which plays a critical role in the control of pancreatic function and the regulation of blood sugar levels. In addition to this discovery and in collaboration with Prof. Roberto Pellicciari, who designed the novel potent and selective TGR5 activator, INT777, under a longstanding collaboration with Intercept Pharmaceuticals, the group at the EPFL has shown that under laboratory conditions this compound can effectively treat diabetes and reduce fat mass. The authors have furthermore demonstrated that these effects were related to the increase in both GLP1 secretion and energy expenditure.

This work is of great interest since it could herald a new approach in the treatment of type 2 diabetes and obesity. “Recently, two classes of drugs exploiting the properties of the hormone GLP1 have been marketed for the treatment of type 2 diabetes. The first strategy aims to increase the blood levels of GLP1 by limiting its degradation in the body. The second is to mimic the effects of GLP1 using drugs activating the GLP1 receptor (GLP1R) “, explains Charles Thomas, first author of the study. In this study, the authors propose a third therapeutic option based on increasing GLP1 secretion via administration of TGR5 agonist therapy. The results obtained by the authors are even more spectacular since in addition to stimulating the secretion of GLP1, INT777 activation of TGR5 in other tissues leads to an increase in energy expenditure responsible for a reduction in fat mass and obesity.

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Kristina Schoonjans
Ecole Polytechnique Fédérale de Lausanne

Researchers from North Carolina State University and Mayo Clinic have developed a computer model that medical doctors can use to determine the best time to begin using statin therapy in diabetes patients to help prevent heart disease and stroke.

“The research is significant because patients with diabetes are at high risk for cardiovascular disease and statins are the single most commonly used treatment for patients at risk of heart disease and/or stroke,” says Dr. Brian Denton, “and this model can help determine the best course of action for individual patients based on their risk of developing cardiovascular disease.” Denton is an assistant professor in NC States Edward P. Fitts Department of Industrial & Systems Engineering and lead author of the study.

Statins are a key component of current cardiovascular medical treatment guidelines, Denton says. They lower cholesterol levels and may significantly reduce the risk of heart attack and stroke, particularly in patients that are considered to be at high risk.

The researchers developed a new mathematical model that examines various possible treatment policies to see how they influence shortterm and longterm health outcomes for patients. The model shows how people are affected by diabetes, and how their health changes over time as patients age and the disease advances.

The new model incorporates patientspecific data. An established risk model calculates each patients probability of heart attack and stroke based on risk factors, such as their cholesterol, blood pressure, etc. This overall risk “score” is used to weigh the medical advantages of beginning statin therapy against the financial cost of the statins.

Overall, by accounting for the progression of diabetes, the patients specific risk score and the costbenefit analysis, the new model may help patients and doctors decide on the optimal time to begin statin therapy.

Denton says the new model has not yet been put into practice, but that the research team plans to develop a pilot to put the tool into the hands of medical professionals.

The research, “Optimizing the Start Time of Statin Therapy for Patients with Diabetes,” was funded in part by the Agency for Healthcare Research and Quality and the National Science Foundation, and was published earlier this month in the journal Medical Decision Making. The research was coauthored by Denton from NC State; Nilay D. Shah, Sandra C. Bryant and Steven A. Smith of the Mayo Clinic College of Medicine; and University of Pittsburgh graduate student Murat Kurt.

The Juvenile Diabetes Research Foundation has said that it has entered into a novel collaborative research agreement with the Genomics Institute of the Novartis Research Foundation (GNF) to create a diabetes drug discovery and development platform. The fouryear program is one of the largest and most comprehensive collaborations in the 40 year history of JDRF, a leader in setting the agenda for diabetes research worldwide and the largest charitable funder and advocate of type 1 research.

“This agreement with GNF opens exciting new avenues for JDRF to speed the translation of basic research into drugs and treatments for type 1 diabetes” said Alan J. Lewis, PhD, President and Chief Executive Officer of JDRF. “By creating this highly interactive collaboration with a world class organization with demonstrated expertise in discovering and developing innovative therapeutics for medical needs, we are looking to expand both the targets and the realm of possible treatments that can benefit people living with diabetes.”

Based in San Diego, GNF was founded in 1999. Funded by the Novartis Research Foundation, its mission is to develop and apply innovative technologies to the discovery of new biologic processes and new or improved therapeutics for people. With a team of 550 scientists and associates, it has an impressive track record of success in translational research, and has contributed significantly to Novartis pipeline of therapeutic candidates.

The partnership between JDRF and GNF aims to deliver a succession of drug candidates to the clinic over the next four years. The initial focus will be on pancreatic beta cell regeneration and survival, to restore beta cell function in diabetes. The program builds on current JDRF funding at GNF that has resulted in the discovery of beta cell regeneration drug targets and candidates, and allows for the inclusion of JDRFfunded projects and other discoveries into the program.

“Through this collaboration with JDRF, we are looking to create a unique program of translational research that fully exploits the strengths of each partner to produce a continuous source of novel insights, drug targets, and drug candidates,” said Peter Schultz, PhD, Lead GNF Investigator and Institute Director.

“This is an exciting evolution of JDRFs research strategy for discovering and developing diabetes therapeutics,” said Richard A. Insel, MD, Executive Vice President for Research at JDRF. “The partnership provides JDRF access to a highly talented group of scientists, stateoftheart drug discovery technology, and an organization with a proven track record of delivering drugs to the clinic to address a critical gap in research advancing basic research, often arising from academia, into drug discovery and development. The JDRFGNF partnership should jumpstart the creation of a multiproduct pipeline for beta cell regeneration, a therapeutic priority for JDRF.”

Projects within the collaboration will be chosen and managed by a combined review committee of JDRF and GNF representatives, with oversight from a Scientific Advisory Board and JDRF volunteers.

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Joana Casas

People with diabetes who live in less affluent neighborhoods are more likely to experience delays in treatment for hyperglycemia, according to a study published in the August issue of Diabetes Care. However, the researchers found, neighborhood income was only one factor in determining how quickly appropriate care was received.

People who were less adherent to medication, had A1C levels (a measure of how well blood glucose is controlled over time) lower than 9 percent, who had higher prescription drug copayments and who had not been to a doctor recently were also more likely to experience delays in receiving care for sustained hyperglycemia (high blood sugar levels), the study found.

“Findings highlight that no one person or thing is to blame when care quality falls short,” the researchers concluded. “Instead, receipt of quality care results from a complex system of factors. Although the decision to intensify diabetic medication is one usually associated with physicians, to be effective, interventions targeting improvements in pharmacological management should consider a broad array of factors. These include the financial barriers patients may face, the importance of access to routine visits, and possible psychological barriers to appropriate care.”

Hyperglycemia was measured using the A1C test, which looks at average blood glucose levels over a 23 month period. A person without diabetes would measure roughly 5 percent on the A1C test. The American Diabetes Association recommends that the goal for most people with diabetes be to keep A1C levels at or below 7 percent. The higher the A1C level, the higher the risk for diabetesrelated complications. Sustained hyperglycemia greatly increases the risk for diabetesrelated complications, such as nerve damage, amputations, blindness and stroke.

The study, led by researchers at the Henry Ford Health System, Center for Health Services Research in Detroit, found that 41 percent of people with sustained hyperglycemia failed to get appropriate care within six months; 25 percent failed to get care within a year; and 11 percent failed to get appropriate care for as much as two years. Once blood glucose levels exceeded 9 percent on the A1C test, however, patients were more likely to receive treatment, the study showed.

Diabetes Care, published by the American Diabetes Association, is the leading peerreviewed journal of clinical research into one of the nations leading causes of death by disease. Diabetes also is a leading cause of heart disease and stroke, as well as the leading cause of adult blindness, kidney failure, and nontraumatic amputations.

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Diabetica Research Solutions, Inc. (DRSI) drsirestoreenergy.com Diabetes is a disease of energy currently affecting 24 million people who have been diagnosed and approximately 55 million who are in a prediabetic condition. For so many of these people with diabetes, particularly those with type 2 diabetes, persistent fatigue is a constant complaint. According to a 2007 survey of 8,000 people with diabetes, approximately 85% of respondents reported that fatigue was their number one complaint. When asked how they dealt with their fatigue, 17% of respondents said they do nothing, 31% drink water, 23% drink coffee, 6% drink energy drinks and 23% drink sodas and diet sodas. Now, with the introduction of drsi™ Restore! Energy, theres a quick and effective way for diabetics and prediabetics to experience balanced, long lasting energy and stamina to help them through their daily routines.

drsi™ is a patent pending formula that consists of a proprietary blend of vitamins, minerals and added nutrients. We have added three times the number of electrolytes of the most popular sports drinks. With chromium picolinate and biotin, drsi™ may also assist in regulating blood sugar levels and has a low Glycemic Index. drsi™ provides balanced energy without the “spikes” and “crashes” often caused by traditional energy drinks and coffee which have been shown to be harmful to diabetics. Just as important as what drsi™ Restore! Energy has is what is doesnt have…No caffeine, no sugar, no stimulants and very few carbs.

All drsi™ ingredients have been well studied by the FDA and are recognized as dietary supplements considered “Generally Regarded as Safe,” (G.R.A.S. list) by the FDA. drsi™ is marketed under the Dietary Supplement Health and Education Act.

Kitty Castellini, President and CEO of Diabetes Living Today, a leading radio program that helps diabetics live better by providing information and insights to improve each day said, “The very first energy drink designed for diabetics! What a great concept to be able to finally have a new and wonderful product on the market thats not loaded with carbs.” She went on to say, “Being an active person and a daily energy drink person for several years myself, I was amazed by what I found in drsi™ Restore! Energy. The taste alone is pure pleasure and it has a wonderful aroma and color. I find that after drinking drsi™ Restore! Energy I have the energy to go all day. I should also mention the cooling sensation that my body feels from drinking it. I rate this product five stars out of five and a must for anyone living with diabetes.”

Many diabetics describe their persistent fatigue as living with a constant hangover. Excess sugar in their blood stream, often compounded by weight problems and dehydration, contribute to frequent fatigue. Left untreated, fatigue can lead to a continuing decline in the quality of life for many diabetics.

DRSI is a private corporation focused on developing and marketing nonprescription consumer health products to address quality of life issues in the rapidly growing diabetic community. drsi™ Restore! Energy is its flagship product and the only all natural, mega B vitamin complex with essential nutrients and the only energy formula designed to provide balanced, longlasting energy and stamina to energize diabetics.

At approximately $200 billion per annum, treating diabetes is one of the highest healthcare costs in the country and was recently targeted by the government for cost reductions, including through a variety of preventative programs. Diabetes is growing at one of the fastest rates of any disease and affects every ethnic and socioeconomic group.

Diabetics are unable to produce or utilize insulin efficiently to convert glucose into energy. As a result, the vast majority of diabetics suffer from various degrees of fatigue. Healthcare professionals universally recommend exercise as a primary means to help insulin work more efficiently and control blood sugar levels. Exercise is thus viewed as a critical preventative measure in helping to improve the physical wellbeing of diabetics and correspondingly a key component in reducing the cost of treating diabetes. With systemic fatigue, exercise can be a daunting undertaking for diabetics and a “Catch 22″ as they are too tired to exercise and without exercise they remain fatigued. drsi™ is the affordable, fastacting and effective way for diabetics to immediately counter persistent fatigue and gain the energy and stamina necessary to get through their daily routines.

drsi™ Restore! Energy is a powder formulation sold in easy to carry, tear away, airtight individual serving stick packs that are poured into a glass of 912 ounces of fresh water. It dissolves instantly into a quickly absorbed, refreshing, effervescent and great tasting drink that can be carried anywhere and enjoyed at anytime.

“In creating drsi™, we focused on the daily lifestyle needs of diabetics. We learned that the lack of energy and the persistent fatigue associated with diabetes is a primary obstacle keeping them from enjoying life and being as productive as they can be,” said Younis Zubchevich, CEO of DRSI. “While millions of Americans benefit from the energy spike provided by energy drinks, energy shots and coffee, diabetics had no specific, simple, cost effective way to improve their energy and stamina. We developed drsi™ to restore all of the natural vitamins and nutrients the body needs to create longlasting, balanced energy and hydration. We also made it great tasting. And, because the need for energy among diabetics is more constant than for others, we developed it in a powder formulation to remove the impulse out of the purchase process. At approximately less than half the perserving cost of energy drinks and coffee, drsi™ Restore! Energy allows diabetics to affordably and conveniently have it onhand with them whenever they need it and where ever they go rather than making frequent purchases of costly products like coffee and energy drinks that arent good for them.”

drsi™ Restore! Energy is initially available in a refreshing Lemon Lime flavor, comes in a box of 14 individual servings and sells for less than $1.00 per serving. drsi™ Restore Energy is available online at drsirestoreenergy.com and will soon be available at other web sites, through select diabetic supply providers and at leading retailers across the country.

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BRITAINS top diabetes specialists added their weight to calls for European drug regulatory bodies to launch an urgent investigation into the popular insulin treatment glargine (Lantus). The move by the Association of British Clinical Diabetologists (ABCD) follows this weeks publication of four studies, which raise possible concern about an increased risk of the development of cancer in people who use this longacting insulin therapy.

“For Britains growing number of people with insulintreated diabetes, many of whom use Lantus, there is a need for clarity, common sense and reassurance,” said ABCD Chairman, Dr Peter Winocour. “The European drug regulatory authorities are uniquely placed to provide this and we urge them to take action.

“We know from our work in hospitals across the NHS that there is a lot of concern in the diabetes community about these research findings, both among people with the condition as well as those who care for them.

“Although the latest research is inconclusive it neither confirms or excludes a link it has generated anxiety.”

While ABCD said it fully recognised patients concerns, it advised those who had found Lantus helpful on an individual basis against a change in treatment.

“At the present time, we do not recommend that people using Lantus change to another longacting insulin,” said Dr Winocour.

“Where people are concerned about the risk, and are keen to change Lantus insulin to an alternative, they should only do so after discussing the situation first with a diabetes specialist.

“On no account should people stop taking insulin to do so could cause them to become very ill.”

Lantus is a widely used insulin in the UK which has been available for almost 10 years. It has been of benefit to many patients, particularly those at risk of overnight hypoglycaemia.

Four studies involving the drug are published on the website of Diabetologia, a highlyrespected, peerreviewed scientific journal.

The largest study came from a German health insurance registry. It found there was no increased rate of the diagnosis of cancer associated with Lantus compared to other insulins. However, when the data were adjusted for dose, there was a modest association with overall incidence in the diagnosis of cancer, when Lantus was the only insulin prescribed.

A study performed in Sweden demonstrated no increase in overall incidence in the diagnosis of cancer, but there was there was an increased risk for breast cancer associated with Lantus insulin used alone.

Two further studies performed in the UK did not confirm these results.

The studies were based on reviews of case records recording diabetes treatment and the diagnosis of cancer.

Dr Winocour added “All the reports are observational epidemiological studies, which can only examine relationships and are unable to show cause and effect.

“They must be seen in this respect and considered inconclusive, not least having given differing results.”

An extensive and thoughtful editorial in Diabetologia reflected on the importance of the issue, as the suggested link between Lantus and the diagnosis of cancer was plausible.

A firm statement was made that there was no evidence from this research of any harm from glargine in type 1 diabetes, in men generally, or showing any association with premenopausal breast cancer.

Interpretation of these studies is complicated by confounding factors such as the type of older, more obese patients with type 2 diabetes who would be treated with glargine alone. Age and obesity are two factors which have been proven to increase the risk of cancer.

However, ABCD recommends that this suspicion of increased risk for the diagnosis of cancer with glargine insulin is investigated urgently by the European drug regulatory authorities, because of the concern that will be felt by people with diabetes and specialists caring for them.