Diabetes, the epidemic

By Mazie Aldrich
The Daily Sentinel

Published August 8, 2005

Look around you, of the five people closest to you, at least one is likely to become diabetic. Diabetes, it is not the “C” word that patients most dread hearing when they visit a physician, but it is every bit as deadly as cancer. Diabetes is the leading cause of adult blindness, kidney failure and non-traumatic amputations in the country and diabetes is the sixth leading cause of death in Alabama. Why? The cause of diabetes is unknown although several precipitating factors have been identified. Family history increases risk as well as racial or ethnic background and environmental factors such as viruses, nutrition and socioeconomic factors are all considered. Perhaps the answer lies within the sedentary lifestyle of Alabama residents, the lack of exercise, our craving for breads and other carbohydrates and our love of sweets. This is the first of four articles concerning diabetes, its cause and effects and how Jackson County physicians are attempting to educate the public about the severity of the problem in our county.

http://www.thedailysentinel.com

Diabetes Complications Can Be Prevented

Diabetes affects nearly 17 million Americans, according to government statistics. It's a condition that requires constant control and attention, or else sufferers may face complications.

Taking good care of diabetes can lower the chances of getting:

• Eye disease that can lead to a loss of vision or even blindness
• Kidney failure
• Heart disease
• Stroke
• Nerve damage that may cause a loss of feeling or pain in the hands, feet, legs, or other parts of the body

Stephen Furst is perhaps best known as Flounder in the movie "Animal House." What people don't know is that Furst almost lost part of his foot to amputation because he ignored the complications of diabetes.

November is Diabetes Awareness Month, and as Furst knows, awareness can mean the difference between life and death. Each year, 86,000 Americans undergo amputation due to nerve damage -- the medical term is neuropathy -- caused by diabetes, and experts say half of those amputations may have been prevented with proper awareness.

Very often, people with diabetes lose sensation in a leg and suffer a wound that may lead to amputation if left untreated. Furst developed severe wounds because he could not feel his injuries in the first place. That is why he now campaigns for awareness.

Experts at Wound Care Centers, which treat people with chronic wounds related to diabetes, offer the following tips to diabetics:

• Never walk around in your home without shoes.
• Make sure there are no foreign objects in your shoes.
• Make sure your shoes fit properly and are the right size.
• See a podiatrist regularly.

Tea can treat diabetes!

ISLAMABAD: A new study conducted by researchers at the University of Scranton suggests that tea might prevent diabetes and its ensuing complications, including cataracts.

Researchers led by Joe Vinson fed green and black tea to diabetic rats for three months and then monitored the chemical composition of the rats' blood and eye lenses.

At levels that would be equivalent to less than five cups of tea per day for a human, both teas significantly inhibited cataract formation in comparison to a control group which did not get tea.

The researchers found that both teas decreased glucose levels, which in turn affects other biochemical pathways that accelerate diabetic complications such as cataracts.

"Most people, scientists included, believe that green tea has more health benefits than black tea," Vinson added.

http://www.onlinenews.com.pk/details.php?id=85225

New Program Aimed at Helping Mexican-Americans with Diabetes, Rush University Medical Center

Diabetes is a growing problem in the United States today, and Hispanic Americans are especially hard hit by this illness. Hispanics are over 45% more likely to die from complications of diabetes than non-Hispanic whites. Researchers at Rush University Medical Center are offering a new program to study ways to help Mexican-Americans with diabetes.

(I-Newswire) - The program, called the MATCH Project, is currently enrolling Mexican-Americans diagnosed with type 2 diabetes mellitus who live in the Pilsen and Little Village neighborhoods. Participants in the study will receive information about diet, medications, physical activity, working with your doctor, and many other tips to help improve health. Participation in the program is free and completely voluntary.

"Diabetes is unique because it requires daily self-management in order to remain healthy," said Dr. Steven Rothschild, the principal investigator of the MATCH study at Rush. "The MATCH study hopes to identify new strategies that will close the health gap by helping Mexican-Americans become experts in their own diabetes care."

On average, Hispanics/Latinos are almost twice as likely to have diabetes as non-Hispanic whites of similar age. In fact, more than 10 percent of all Latino Americans ages 20 years or older have diabetes, and between the ages of 45 and 74, as many as 24 percent of Mexican Americans in the United States have diabetes. The group is also more likely to suffer from the complications of diabetes, such as kidney failure, heart disease, high blood pressure, and blindness, than non-Hispanic whites.

In addition to Rothschild, the study is led by an interdisciplinary team consisting of co-principal investigators Lynda Powell, PhD, a Rush epidemiologist, and Susan Swider, PhD, RN, from the Rush College of Nursing. Other Rush investigators include Molly Martin, MD, Susan Everson-Rose, PhD, and Kristin Flynn, PhD. The MATCH study is funded by a grant from the National Institutes of Health, and will run for approximately four years at Rush University Medical Center. For more information, contact Janet Footlik, PhD, at ( 312 ) 942-3139.

http://www.rush.edu


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Gestational diabetes on the rise

Doctors report they are diagnosing condition more often and in younger women.

By Anita Manning
USA Today


Among all the worries that plague pregnant women, one that had been relatively rare seems to be increasing along with the plumping of America.

Gestational diabetes -- a condition that occurs during pregnancy and usually disappears when the baby is born -- is being diagnosed more often and in younger women, doctors say.

"We're seeing teenagers with type 2 diabetes and teenagers with gestational diabetes," says Steven Gabbe, an obstetrician/gynecologist and dean of the Vanderbilt University Medical School. "It used to be that teenagers were very low-risk, but with increasing obesity, that's no longer the case."

About 135,000 pregnant women, roughly 2 percent to 8 percent of all pregnancies, are affected by gestational diabetes each year in the United States. But two Kaiser Permanente studies in the past year have found increasing rates in some regions and among younger women.

Treatment for pregnant women diagnosed with the condition usually starts with diet and exercise. But if that doesn't work, doctors may prescribe insulin or an oral medication.

The question of how aggressively to treat gestational diabetes is not resolved. A study in last month's New England Journal of Medicine found that when mothers have gestational diabetes, they and their babies do better if the diabetes is treated.

But many questions remain, and the National Institutes of Health is financing studies to determine at what point a mother's high blood sugar level begins to affect the developing fetus.

Treatment itself can have a downside, says Mark Landon of Ohio State University in Columbus, who leads the study of mild gestational diabetes.

"There are tremendous costs involved," not only for the tests and equipment to measure blood sugar levels several times a day but also because doctors tend to see gestational diabetes as a high-risk condition and are more likely to do Caesarean sections.

About 18 million Americans have diabetes, a condition in which the body does not produce enough insulin to keep blood sugars low enough to avoid causing long-term problems.

In pregnancy, the placenta makes hormones that counter the effect of insulin, says Martin Abrahamson, acting chief medical officer of the Joslin Diabetes Center in Boston.

If the mother's pancreas is not functioning well enough to make extra insulin, her blood sugar levels rise and cross into the unborn baby, causing the baby's pancreas to produce extra insulin.

"Insulin is a growth hormone as well as a hormone that reduces glucose," Abrahamson says. The flood of extra insulin the baby produces in response to the mother's high blood sugar causes the fetus to grow, resulting in overweight babies at birth.

Because the babies are so big, they might suffer injuries during birth, such as bone fractures, and might need to be delivered by C-section.

Because the baby's pancreas might not be able to switch off right away, it could continue producing too much insulin after birth, which can affect neurological development.

Those big babies also are more likely to grow up to be obese and to have diabetes themselves, Gabbe says.

http://www.indystar.com/apps/

Travel tips for people with diabetes

By Nanci Gonder/Missouri Office of Public Information

The nearly 300,000 adults in Missouri who have diabetes can enjoy relaxing, safe travel this summer-with some careful planning. The Missouri Department of Health and Senior Services Diabetes Prevention and Control Program offers travel tips for peple with diabetes developed by the National Diabetes Education Program.

"Missourians who have diabetes shouldn't be held back from traveling, but they need to take certain precautions before and during the trip," said Jo Anderson, coordinator for the Diabetes Prevention and Control Program.

For someone with diabetes, planning ahead is essential for safe travel. Immunizations, prescriptions, a letter explaining medication, identification tags in the local language and planning for time zone changes are a few details to consider before leaving the state.

"It is also important to have a check-up four to six weeks before your trip to make sure A1C, blood pressure and cholesterol (the ABC's of diabetes) are under control before you leave," said Anderson.

The A1C test, also known as glycated hemoglobin or HbA1c, shows the average amount of sugar in a person's blood over the last two to three months.

Prescription laws may be different in other countries, so travelers should prepare a list of International Diabetes Federation groups including IDF, 1 rue Defaeqz, B-1000 and Belgium, or visit www.idf.org. The American Consulate, American Express or local medical schools can provide a list of English-speaking doctors during an emergency.

Other general travel tips from the National Diabetes Education Program include:

- Have snacks, glucose gel or tablets nearby in case blood glucose levels drop.

- Make sure to keep medical insurance cards and medical insurance emergency numbers handy.

- Stay comfortable and reduce risk for blood clots by moving around every hour or two.

- Always tell at least one traveling companion that you have diabetes.

- Check blood glucose often. Changes in diet, activity and time zones can cause blood glucose levels to react in unexpected ways.


http://www.moberlymonitor.com/articles/2005/08/09/news/news12.txt

Cause of Diabetes-Related Erectile Dysfunction Is Clarified by Johns Hopkins Researchers

BALTIMORE, Aug. 9 (AScribe Newswire) -- A new study from the Brady Urological Institute at Johns Hopkins suggests an oversupply of a simple blood sugar could be a major cause of erectile dysfunction in diabetic men.

Researchers have found that one particular simple sugar, present in increased levels in diabetics, interferes with the chain of events needed to achieve and maintain erection and can lead to permanent penile impairment over time. The results, which have implications for new types of erectile dysfunction treatments targeting this mechanism of erection, are described in the August 16 issue of the Proceedings of the National Academy of Sciences.

Previous research had shown that diabetic erectile dysfunction was partially due to an interruption in an enzyme that starts the chain of vascular events leading to an erection. The Hopkins team suspected O-GlcNAc, a blood sugar present in hyperglycemic (high blood sugar) circumstances, to be that interrupting factor.

"We were interested to determine whether high glucose in diabetes mellitus modifies the endothelial nitric oxide synthase (eNOS) enzyme, which is responsible for the achievement and maintenance of erection," says Biljana Musicki, Ph.D., lead investigator of the study and a research associate in the Brady Urological Institute.

Erectile dysfunction is a common problem for more than half of men with diabetes. Musicki says that an estimated "50 percent to 75 percent of diabetic men have erectile dysfunction to some degree, [a rate] about threefold higher than in non-diabetic men." This is not the same type of erectile dysfunction seen in non-diabetics, and it is less effectively treated with conventional drugs like Viagra.

The study examined rats with type 1 diabetes mellitus as well as the overall mechanism of erection. "Erection begins when a sexual stimulus activates the enzyme neuronal nitric oxide synthase (nNOS) that causes short-term release of nitric oxide (NO) at the nerve endings in the penis," Musicki explains.

This initial release of NO causes rapid and short-term increases in penile blood flow and short-term relaxation of the penile smooth muscle, initiating an erection. The resulting expansion of penile blood vessels and smooth-muscle relaxation allows more blood to flow into the penis. This increased blood flow (shear stress) activates the eNOS in penile blood vessels causing sustained NO release, continued relaxation and full erection.

O-GlcNAc hinders this normal chain of events by inhibiting the activation of eNOS, and consequently reducing the release of NO and preventing the smooth muscle in the penis from relaxing. Without this relaxation, there is no shear stress to stoke the production of more NO and therefore, no normal, sustained erection.

The team also found that in comparison with the controls, the diabetic rats' erectile response was 30 percent lower, full erections were 40 percent smaller and these erections took 70 percent longer to achieve.

The study emphasizes the reduced blood vessel function present in patients with diabetes. "The mechanism we describe here stresses the critical importance of vascular function in the erectile response. It may suggest new ways of treating erectile dysfunction by targeting specifically this mechanism in penile erection," notes Musicki.

Additionally, speaking to more than just the sexual issues related to erectile dysfunction, the research addresses implications related to the overall understanding of penile health. According to Arthur Burnett, M.D., a professor of urology and head of the research team, "eNOS plays roles in both immediate erectile response and the overall health and function of the penile tissue."

Burnett, whose lab has studied penile erection since the early 1990s, continues, "the insight here is tremendous because it speaks to fundamental biological and vascular" mechanisms of diabetes. "This paper gets back to the physiological relevance of hyperglycemia and how it affects erection. We show here -- using erection as a model -- the vascular damage caused by diabetes and provide insights into vascular disease beyond this dysfunction," he adds.

The article, "Inactivation of phosphorylated endothelial nitric oxide synthase (Ser-1177) by O-GlcNAc in diabetes-associated erectile dysfunction," appears in the Aug. 16 issue of the Proceedings of the National Academy of Sciences and was published online Aug. 5. Melissa F. Kramer and Robyn E. Becker, also of the Brady Urological Institute, collaborated on this study.

This research was supported by the National Institute of Diabetes and Digestive and Kidney Diseases and the National Kidney Foundation of Maryland Professional Development Award.

http://newswire.ascribe.org/

Feeling Old? Time for a Mitochondrial Tune Up

Gene treatment targets mutations and defects in cellular powerhouses that contribute to aging and disease
By Liz Brown
Betterhumans Staff


Credit: NIH
Repair work: Prone to age-related damage, mitochondria could be fixed through DNA mending or replacement

Halting aging and the development of diseases such as Alzheimer's and Parkinson's may one day be as simple as seeing the doctor for a mitochondrial "tune up."

The tune up, currently in the early stages of development, would repair mutations that occur in mitochondria and are believed to contribute to many afflictions, from diabetes to heart disease.

From biology class, you may remember that mitochondria are the "powerhouses of the cell." These tiny organelles manufacture ATP, which is used as a source of energy. Besides manufacturing ATP, mitochondria are also involved in apoptosis, sending a "suicide" signal to cells.

Mitochondria are unique from other cell organelles because they contain their own DNA. This leaves them susceptible to genetic mutations in the form of DNA damage. Scientists believe that when a cell divides, mitochondria can lose important information, which can contribute to disease and aging.

Correcting defects

To combat this DNA damage, Shaharyar Khan and Rafal Smigrodzki of the University of Virginia are developing a therapy that could potentially prevent mitochondrial diseases and possibly many aspects of aging.

The therapy introduces engineered "correct" mitochondrial DNA to fix defects.

"In our current protocol, the DNA is mixed with a specially designed protein which coats it and enables it to pass through cell membranes to reach mitochondria," says Smigrodzki.

The method for delivery is called protofection. Already being tested in animals, protofection uses what are known as mitochondrial targeting sequences (MTS) to deliver treatment through the membrane of the mitochondria. These act like zip codes, making sure that treatment is delivered to the proper area of the organelle.

Delivering proteins

The approach is already showing promise for delivering therapeutic proteins to mitochondria in living animals.

Mark Payne of Wake Forest University School of Medicine in North Carolina, who is conducting similar research to the team in Virginia, says that researchers there have already delivered a test protein—green florescent protein—to most tissues in rats, including the brain, heart, liver, kidney and muscle.

Delivery of specific proteins could repair defects that cause specific diseases, much like repairing certain parts of a car. "We are currently working on two human diseases to determine if we can repair or stop the damage that occurs in the mitochondria," says Payne. One is a mitochondria defect that leads to sudden infant death syndrome (SIDS) and the other is involved in Friedreich's Ataxia, a rare genetic, neurodegenerative disease.

"Both of these diseases have transgenic animal models that we can test our hypothesis in," says Payne. "If we are successful in altering the disease course in the animal, we will perform additional testing and move towards human clinical trials," he says.

DNA replacement

While targeting individual proteins could help treat disease, Smigrodzki and Khan in Virginia have also begun tests on animals to see if they can successfully replace all mitochondrial DNA in a functioning animal. If all of the DNA can be replaced, it is possible that all mitochondrial diseases could be treated with a one-size-fits-all treatment rather than different treatments for different conditions.

"Currently, mitochondrial diseases are essentially untreatable," says Smigrodzki. "There is increasing evidence for significant mitochondrial involvement in Alzheimer's disease, Parkinson's disease and diabetes so mitochondrial replacement therapy could provide an effective causal (as opposed to current symptomatic) treatment."

However, Smigrodzki warns there is a long road of lab work ahead. "Once we prove the efficacy of protofection in animals, we need to show that it works in humans and then expand its use to other conditions, which should be enough to keep us busy for the next 15 to 20 years."

http://www.betterhumans.com/News/news.aspx?articleID=2005-02-23-3

Gene Discovery May Explain Recurring Infections

Newswise — A newly discovered gene mutation may account for many cases of immune deficiency, in particular two syndromes known as immunoglobulin A (IgA) deficiency and Common Variable Immunodeficiency (CVID), report researchers in the July issue of Nature Genetics. The discovery may lead to a new diagnostic test for these conditions, which make people highly susceptible to infections and often go unrecognized because of a lack of good tests.

IgA deficiency affects 1 in 600 people; CVID is less common but more severe. Children and adults with either condition suffer relentlessly recurring ear infections, sinus infections, bronchitis, pneumonias and gastrointestinal infections. IgA deficiency and CVID can occur in the same family, and also predispose people to autoimmunity, particularly affecting the thyroid gland and resulting in thyroid hormone insufficiency. Finally, people with CVID are susceptible to B-cell lymphomas.

The researchers, led by Raif Geha, MD, and Emanuela Castigli, PhD, in the Division of Immunology at Children’s Hospital Boston, found mutations in a gene known as TACI in 4 of 19 unrelated patients with CVID and in 1 of 16 unrelated patients with IgA deficiency. None of 50 healthy people tested had a TACI mutation. Four of the 5 patients with TACI mutations were studied further, and all 4 had relatives with the same mutations. Eleven of the 12 identified relatives with TACI or IgA deficiency reported a history of recurrent infections and were found to have low levels of immunoglobulin A (IgA), immunoglobulin G (IgG) or both.

TACI mutations interfere with two aspects of the immune response that involve maturation of B cells, the white blood cells that make immunoglobulins, which function as antibodies, to fight infections. Normally, TACI triggers B cells to switch from making immunoglobulin M (IgM), an antibody produced early in the body’s immune response, to making other immunoglobulins like IgA and IgG. More important, TACI signals B cells to produce antibodies with a high affinity for specific attackers. Because TACI mutations are dominant, people with even one copy of the mutation will be unable to mount a strong antibody response.

“A test for TACI would allow for diagnosis of more children and their relatives,” says Geha, senior author of the study and a professor of pediatrics at Harvard Medical School. “Many children who are sick are now missed, because they can have normal IgA and IgG levels, yet they still have poor antibody responses and get the same bacteria and viruses again and again.”

The gene discovery will immediately not change therapy, Geha adds. “For the time being, it’s prophylactic antibiotics or IV immunoglobulin infusions every three weeks,” he says.

Geha’s team previously demonstrated that TACI binds to two other proteins made by cells in the respiratory and gastrointestinal lining, known as APRIL and BAFF, to trigger the signal for B cells to mature. Geha believes that additional cases of immune deficiency result from mutations in the APRIL and BAFF genes, and plans to verify this in further studies.

Children’s Hospital Boston is home to the world’s largest research enterprise based at a pediatric medical center, where its discoveries have benefited both children and adults since 1869. More than 500 scientists, including eight members of the National Academy of Sciences, nine members of the Institute of Medicine and 10 members of the Howard Hughes Medical Institute comprise Children’s research community. Founded as a 20-bed hospital for children, Children’s Hospital Boston today is a 325-bed comprehensive center for pediatric and adolescent health care grounded in the values of excellence in patient care and sensitivity to the complex needs and diversity of children and families. Children’s also is the primary pediatric teaching affiliate of Harvard Medical School. For more information about the hospital and its research visit: http://www.childrenshospital.org/research/.

http://www.newswise.com/articles/view/512990/

BYETTA

SAN DIEGO, Calif. e INDIANAPOLIS, Ind., 29 de abril /PRNewswire-FirstCall/ -- Amylin Pharmaceuticals, Inc., y Eli Lilly and Companyanuncian que la Administración de Medicamentos y Alimentos (FDA) de EE.UU. ha aprobado la inyección de BYETTA(TM) (exenatide) como tratamiento coadyuvante para mejorar el control del nivel de azúcar en sangre en pacientes con diabetes tipo 2 que no han alcanzado el control adecuado con metformina y/o una sulfonilurea, dos medicamentos comunes para la diabetes administrados por vía oral. BYETTA, nombre comercial de exenatide, es el primero de una nueva clase de fármacos conocidos como miméticos de la incretina. BYETTA estará a la venta en farmacias el 1 de junio de 2005.

BYETTA mejora el control del nivel de azúcar en sangre mediante la reducción de los niveles de glucosa en ayunas y luego de las comidas, lo que conduce a un mejor control a largo plazo según medición de la hemoglobina A1C. BYETTA logra esto a través de varias acciones, como por ejemplo, la estimulación de la secreción de insulina sólo cuando el nivel de azúcar en sangre es elevado, y mediante el restablecimiento de la respuesta de insulina en la primera fase, capacidad de las células productoras de insulina del páncreas que se pierde en pacientes con diabetes tipo 2. La mayoría de los pacientes en los estudios clínicos a largo plazo de BYETTA también registraron una reducción de peso.

"La disponibilidad de un tratamiento que reduce el nivel de azúcar en sangre, y tiene el potencial de ayudar a restablecer la respuesta de las células productoras de insulina del cuerpo, constituye un interesante avance para los pacientes con diabetes tipo 2", afirmó el Dr. David Kendall, Director Médico del Centro Internacional de Diabetes en Minneapolis, Minnesota, e investigador para los estudios clínicos de BYETTA. "BYETTA es una herramienta verdaderamente única para manejar la diabetes tipo 2, y representa una alternativa adecuada a considerar cuando los pacientes no pueden controlar sus niveles de azúcar en sangre con uno o más medicamentos por vía oral".

"El manejo exitoso de la diabetes constituye una lucha diaria para millones de estadounidenses", indicó Ginger L. Graham, Presidente y Directora Ejecutiva de Amylin Pharmaceuticals, Inc. "Con frecuencia, los tratamientos actuales no permiten un control adecuado del nivel de azúcar en sangre, lo que genera frustración en pacientes y prestadores de atención médica. BYETTA, medicamento primero en su clase, es un nuevo tratamiento para quienes no logran controlar eficazmente el nivel de azúcar en sangre con los medicamentos actuales por vía oral".

"BYETTA ofrece una nueva opción interesante para las personas con diabetes tipo 2, y constituye un importante hito en la exitosa colaboración entre Amylin y Lilly", manifestó Sidney Taurel, Presidente del Directorio y Director Ejecutivo de Eli Lilly and Company. "Con los efectos demostrados de BYETTA en el nivel de azúcar en sangre, y su perfil de seguridad, los médicos y pacientes ahora cuentan con un nuevo abordaje para combatir la creciente epidemia de diabetes".

Además de aprobar BYETTA para el uso coadyuvante con medicamentos actuales administrados por vía oral, la FDA también estableció que BYETTA puede utilizarse como tratamiento independiente (monoterapia) en pacientes con diabetes tipo 2. Se prevé que cualquier dato adicional presentado para respaldar una indicación de monoterapia será analizado durante seis meses.

BYETTA está formulado para la autoadministración como una inyección subcutánea de dosis fija, aplicada antes de las comidas de la mañana y la noche. BYETTA estará disponible tanto en presentaciones de 5 microgramos por dosis y 10 microgramos por dosis en un dispositivo de inyección precargado.

Información de Seguridad y Tolerancia

En las tres pruebas controladas de 30 semanas, los efectos adversos asociados con BYETTA fueron, en general, de intensidad leve a moderada. El efecto adverso informado con mayor frecuencia fueron náuseas leves a moderadas según la dosis. En tratamientos prolongados en la mayoría de los pacientes que experimentaron náuseas en forma inicial, la frecuencia y gravedad se redujeron con el transcurso del tiempo.

Los pacientes que reciben BYETTA en combinación con una sulfonilurea presentan un mayor riesgo de hipoglucemia; para reducir este riesgo, se debe considerar disminuir la dosis de la sulfonilurea. En las pruebas clínicas controladas de 30 semanas, la hipoglucemia pareció depender de las dosis de BYETTA y una sulfonilurea. La mayoría de los episodios de hipoglucemia fueron de intensidad leve a moderada, y todos fueron resueltos mediante la administración oral de hidratos de carbono. En los estudios controlados de 30 semanas, no se observó un aumento en el riesgo de hipoglucemia cuando BYETTA fue utilizada en combinación con metformina en comparación con placebo.

Asimismo, debe informarse a los pacientes que el tratamiento con BYETTA puede generar reducción del apetito, de la ingesta de alimentos, y/o el peso corporal, y que no es necesario modificar la posología en razón de tales efectos.

BYETTA no debe administrarse a pacientes con diabetes tipo 1 ni debe utilizarse para el tratamiento de la cetoacidosis diabética, ni tampoco es un sustituto de la insulina en pacientes que la requieren. No se recomienda el uso de BYETTA en pacientes con enfermedad renal en etapa final o disfunción renal grave, ni en pacientes con enfermedad gastrointestinal grave. BYETTA debe administrarse con precaución en pacientes que reciben medicamentos por vía oral que requieren una rápida absorción gastrointestinal.

Si desea ver toda la Información sobre Prescripción, visitehttp://www.byetta.com/.

Acerca de BYETTA

BYETTA es el primero en una nueva clase de fármacos para el tratamiento de la diabetes tipo 2 llamados miméticos de la incretina, y exhibe muchos de los mismos efectos que la hormona incretina presente en humanos, denominada péptido similar al glucagón (GLP-1). GLP-1, secretada en respuesta a la ingesta de alimentos, tiene varios efectos en el estómago, hígado, páncreas y cerebro, que funcionan en concierto para regular el nivel de azúcar en sangre.(1) BYETTA fue aprobada por la FDA para el uso en personas con diabetes tipo 2 que no logran controlar sus niveles de azúcar en sangre a pesar de utilizar metformina, una sulfonilurea o ambos, los fármacos por vía oral más comúnmente recetados. Si desea ver toda la Información sobre Prescripción, visitehttp://www.byetta.com/.

Acerca de los Miméticos de la Incretina

Los miméticos de la incretina son una nueva clase de tratamientos utilizados para combatir la diabetes tipo 2. Un mimético de la incretina simula las acciones antidiabéticas o reductoras de la glucosa producidas por hormonas presentes naturalmente en el hombre, llamadas incretinas. Estas acciones incluyen estimular la capacidad del cuerpo para producir insulina en respuesta a niveles elevados de azúcar en sangre, inhibir la liberación de una hormona llamada glucagón luego de las comidas, demorar el ritmo al cual se absorben los nutrientes en el torrente sanguíneo, y reducir la ingesta de alimentos. BYETTA es el primer agente de esta nueva clase de medicamentos aprobado por la FDA.

Acerca de la Diabetes

La diabetes afecta a alrededor de 194 millones de adultos en todo el mundo(2) y más de 18 millones en Estados Unidos.(3) Cerca de 90 a 95% de los afectados sufren diabetes tipo 2, trastorno en el cual el cuerpo no produce suficiente insulina y/o las células del cuerpo no responden normalmente a la insulina.(3) La diabetes es la quinta causa principal de muerte por enfermedad en Estados Unidos(4) y representa un costo aproximado de US$132 mil millones por año en gastos médicos directos e indirectos. La diabetes tipo 2 en general se presenta en adultos mayores de 40 años, pero es cada vez más común en personas más jóvenes.(3)

Según el Estudio Nacional de Análisis de Salud y Nutrición de los Centros para Control y Prevención de Enfermedades, alrededor del 60% de los pacientes de diabetes no alcanzan los niveles objetivo de hemoglobina A1C (menos del 7% según pautas de la Asociación Americana de Diabetes(5)) con su actual régimen de tratamiento.(6)

Amylin Transmitirá por la Web Llamada en Conferencia con Inversores

Amylin Pharmaceuticals transmitirá por la web una llamada en conferencia para analizar la aprobación de BYETTA y los planes de comercialización el viernes 29 de abril de 2005 a las 12:00 p.m. ET (9:00 a.m. PT). Ginger L. Graham, Presidente y Directora Ejecutiva de Amylin Pharmaceuticals, conducirá la llamada.

La llamada se transmitirá en vivo por la web a través del sitio web corporativo de Amylin, y se podrá obtener una grabación de la misma después de su finalización. Para acceder a la transmisión web, conéctese ahttp://www.amylin.com/cerca de quince minutos antes de la llamada para registrarse, descargar e instalar el software de sonido necesario. Se podrá obtener una grabación por teléfono durante 24 horas, alrededor de una hora después de la finalización de la llamada. Se podrá acceder a dicha grabación en el 888-286-8010 (local) ó 617-801-6888 (internacional), número de identificación de la conferencia 65243380.

Acerca de Amylin y Lilly

Amylin Pharmaceuticals es una empresa biofarmacéutica comprometida con mejorar la vida a través del descubrimiento, el desarrollo y la comercialización de medicamentos innovadores. Se puede obtener más información sobre Amylin Pharmaceuticals, los productos que comercializa y sus desarrollos en metabolismo enhttp://www.amylin.com/.

A través de un compromiso de larga data con la atención de la diabetes, Lilly brinda a los pacientes tratamientos revolucionarios que les permiten vivir por más tiempo, más saludables y en forma más plena. Desde 1923, Lilly es líder en la industria en tratamientos innovadores para ayudar a los profesionales de la salud a mejorar la vida de personas que sufren diabetes, y continúa su investigación en medicamentos innovadores para responder a necesidades insatisfechas de los pacientes. Si desea más información sobre los productos actuales de Lilly para la diabetes, visitehttp://www.lillydiabetes.com/.

Lilly, empresa líder inspirada por la innovación, desarrolla una creciente cartera de productos farmacéuticos primeros y mejores en su clase mediante la aplicación de las últimas investigaciones de sus propios laboratorios en todo el mundo y de colaboraciones con importantes organizaciones científicas. Lilly, cuya sede central se encuentra en Indianapolis, Ind., brinda respuestas, a través de medicamentos e información, a algunas de las necesidades médicas más apremiantes del mundo. Se puede obtener más información sobre Lilly enhttp://www.lilly.com/.

Este comunicado de prensa contiene declaraciones a futuro acerca de Amylin y Lilly. Los resultados reales podrían diferir sustancialmente de los analizados o implícitos en este comunicado, debido a varios riesgos e incertidumbres, tales como el riesgo de que BYETTA no resulte ser una nueva opción terapéutica importante, no se reciban indicaciones adicionales para BYETTA, BYETTA no esté disponible comercialmente en el momento planeado y/o pueda verse afectado por nuevos datos o cuestiones técnicas imprevistas. El potencial de BYETTA también se podrá ver afectado por decisiones gubernamentales y comerciales sobre reintegro y fijación de precios, el ritmo de aceptación en el mercado y cualquier cuestión relacionada con la fabricación y el suministro. Ã%stos y otros riesgos e incertidumbres están descriptos en mayor detalle en los documentos de Amylin y Lilly presentados más recientemente ante la Comisión de Títulos Valores (SEC), tales como los respectivos Informes Anuales en el Formulario 10-K. Amylin y Lilly no asumen obligación alguna de actualizar estas declaraciones a futuro.

REFERENCIAS

(1) Kolterman, O, Buse J, Fineman M, Gaines E, Heintz S, Bicsak T, Taylor K, Kim D, Aisporna M, Wang Y, Baron A. Exendin-4 sintético (exenatide) reduce significativamente la glucosa postprandial y en ayunas en individuos con diabetes tipo 2. Journal of Clinical Endocrinology & Metabolism. 2003; 88(7):3082-3089.

(2) The International Diabetes Federation Diabetes Atlas. Disponible en:http://www.idf.org/home/index.cfm?unode=3B96906B-C026-2FD3-87B73F80BC22682A. Consultado el 12 de abril de 2005.

(3) Centros para Control y Prevención de Enfermedades, Ficha Técnica Nacional sobre Diabetes. Disponible en:http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2003.pdf.

(4) Kochanek KD, Murphy SL, Anderson RN, Scott C. Deaths: Datos finales para 2002. Informes nacionales sobre estadísticas vitales: vol 53 no 5. Hyattsville, Maryland: Centro Nacional de Estadísticas de Salud. 2004.

(5) Asociación Americana de Diabetes. Normas de atención médica en diabetes. Diabetes Care 2005;28:S4-36S.

(6) Harris MI, Eastman RC, Cowie CC, Flegal KM, Eberhardt MS. Diferencias raciales y étnicas en control de glucemia de adultos con diabetes tipo 2. Diabetes Care. 1999;22:403-408.

http://www.invertironline.com

SCIENTISTS UNCOVER NEW CLUES ABOUT BRAIN FUNCTION IN HUMAN BEHAVIOR

Researchers at the National Institute of Mental Health (NIMH), part of the National Institutes of Health, have discovered a genetically controlled brain mechanism responsible for social behavior in humans -- one of the most important but least understood aspects of human nature. The findings are reported in "Nature Neuroscience", published online on July 10, 2005.

The study compared the brains of healthy volunteers to those with a genetic abnormality, Williams Syndrome, a rare disorder that causes unique changes in social behavior. This comparison enabled the researchers to both define a brain circuit for social function in the healthy human brain, and identify the specific way in which it was affected by genetic changes in Williams Syndrome.

People with Williams Syndrome who are missing about 21 genes on chromosome seven are highly social and empathetic, even in situations that would elicit fear and anxiety in healthy people. They will eagerly, and often impulsively, engage in social interactions, even with strangers. However, they experience increased anxiety that is "non-social", such as fear of spiders or heights (phobias) and worry excessively.

For several years, scientists have suspected that abnormal processing in the amygdala, an almond-shaped structure deep in the brain, may be involved in this striking pattern of behavior. The amygdala's response and regulation are thought to be critical to people's social behavior through the monitoring of daily life events such as danger signals. Scientists know from animal studies that damage to the amygdala impairs social functioning.

"Social interactions are central to human experience and well-being, and are adversely affected in psychiatric illness. This may be the first study to identify functional disturbances in a brain pathway associated with abnormal social behavior caused by a genetic disorder," said NIMH Director Thomas R. Insel, M.D.

In this study, investigators used functional brain imaging (fMRI) to study the amygdala and structures linked to it in 13 participants with Williams Syndrome who were selected to have normal intelligence (Williams Syndrome is usually associated with some degree of mental retardation or learning impairment) and compared to healthy controls. Andreas Meyer-Lindenberg, M.D., Ph.D., and Karen Berman, M.D., from the NIMH Genes, Cognition, and Psychosis Program, and colleagues, then showed participants pictures of angry or fearful faces. Such faces are known to be highly socially relevant danger signals that strongly activate the amygdala. The fMRI showed considerably less activation of the amygdala in participants with Williams Syndrome than in the healthy volunteers. These findings suggest that reduced danger signaling by the amygdala in response to social stimuli might be responsible for their fearlessness in social interactions.

Next, researchers showed the study participants pictures of threatening scenes (a burning building or a plane crash), which did not have any people or faces in them and thus had no immediate social component. In remarkable contrast to the response to faces, the amygdala response to threatening scenes was abnormally increased in participants with Williams Syndrome, mirroring their severe non-social anxiety.

"The amygdala response perfectly reflected the unique profile of social and non-social anxiety in Williams Syndrome," said Meyer-Lindenberg. "Because our data showed that the amygdala did still function, although abnormally, in Williams Syndrome, we wondered whether it might be its regulation by other brain regions that was the cause of the amygdala abnormalities."

To investigate this, the scientists looked at the whole brain to identify other regions where reactivity was different between Williams's participants and healthy volunteers. They identified three areas of the prefrontal cortex, located in the front part of the brain, that have been implicated in decision-making, representation of social knowledge, and judgment. Those regions are the dorsolateral, the medial, and the orbitofrontal cortex. Specifically, the dorsolateral area is thought to establish and maintain social goals governing an interaction; the medial area has been associated with empathy and regulation of negative emotion; and orbitofrontal region is involved in assigning emotional values to a situation.

The researchers found a delicate network by which these three regions modulate amygdala activity. In Williams Syndrome, this fragile system was significantly abnormal, particularly the orbitofrontal cortex. This area did not activate for either task and was not functionally linked to the amygdala, as it was in healthy controls. Instead, the scientists observed increased activity and linkage in the medial region, which is consistent with the high level of empathy exhibited by people with Williams Syndrome.

"We had previously seen that the orbitofrontal cortex is structurally abnormal in Williams Syndrome, but we didn't know what role it played functionally in the disorder; it is now clear that this area can play a major role in producing social behavioral abnormalities," said Berman. "The over-activity of the medial-prefrontal cortex may be compensatory, but the result is still an abnormal fear response. The medial-prefrontal cortex still works and in fact it is working over-time because it may be the only thing that still regulates the amygdala in Williams Syndrome."

Other releases on this topic: http://www.nimh.nih.gov/press/prwilliams.cfm.

For more information visit the NINDS web site on Williams http://www.ninds.nih.gov/disorders/williams/williams.htm.

In addition to the NIMH Intramural Research Program, the research was also funded by a grant from the National Institute on Neurological Disorders and Stroke (NINDS) to co-author Dr. Carolyn Mervis, University of Louisville. Also participating in the research were Dr. Ahmad Hariri, Karen Munoz, Dr. Venkata Mattay, NIMH, and Dr. Colleen Morris, University of Nevada.

For a press release photo that depicts abnormal regulation of the amygdala
in participants with Williams Syndrome compared to controls please visit http://www.nih.gov/news/pr/jul2005/nimh-10.htm#brain.

New Warning on Antipsychotic Drugs Used to Treat Older People

The FDA has issued a public health advisory on the unapproved use of several antipsychotic drugs to treat behavioral disorders in older people.

The drugs, which include Abilify (aripiprazole), Zyprexa (olanzapine), Seroquel (quetiapine), Risperdal (risperidone), Clozaril (clozapine), and Geodon (ziprasidone), are approved only for the treatment of schizophrenia and mania. Clinical studies of these drugs to treat behavioral disorders in older patients with dementia have shown a higher death rate associated with their use, compared with patients receiving an inactive substance (placebo), according to the FDA.

The April 2005 advisory also applies to such antipsychotic drugs as Symbyax (olanzapine and fluoxetine HCl), which is approved for treatment of depressive episodes associated with bipolar disorder.

The FDA is requesting that the manufacturers of the drugs add a boxed warning to their drug labeling describing this risk, and noting that the drugs are not approved for the treatment of behavioral symptoms in older people with dementia. Older people receiving these drugs for this particular treatment should have their treatment reviewed by their health care providers.

The agency also is considering a warning for the labeling of older antipsychotic medications because limited data also suggest a similar increase in the risk of death for these drugs. The review of the data on the older antipsychotic drugs is ongoing.

Visit www.fda.gov/cder/drug/advisory/ antipsychotics.htm for additional information concerning the advisory.


http://www.rednova.com/

Antidepressants: 1st Choice for Nerve Pain

Antidepressants should be used as an initial treatment for the frequently disabling pain caused by nerve tissue damage, according to a new review of research on the issue.

Researchers reviewed 50 studies of 19 different antidepressants in the treatment of pain caused by nerve tissue damage, also known as neuropathic pain. They found that the older class of antidepressants called tricyclics can provide significant pain relief. These include medications such as amitriptyline, imipramine, clomipramine, desipramine, and nortriptyline.

Anticonvulsant drugs were also shown to alleviate neuropathic pain.

Nerve pain from diabetes, called diabetic neuropathy, occurs after chronically elevated blood sugars damage nerves throughout the body. A complication of shingles called postherpetic neuralgia causes nerve pain for weeks to years after the shingles rash has disappeared. And some cancer treatments -- radiation and some chemotherapy drugs -- can also result in nerve damage.

There is limited evidence that newer antidepressants, called selective serotonin reuptake inhibitors (SSRIs), may also provide neuropathic pain relief. Researchers say more studies are needed before they can be recommended for this use. SSRIs include Prozac, Celexa, Luvox, Zoloft, and Paxil.

Pain caused by nerve tissue damage often occurs as a burning, tingling, or stabbing sensation.

Researchers say antidepressants have been used for neuropathic pain for many years, and this review of research shows that it is still probably the best approach to take. Antidepressants are thought to ease pain caused by nerve damage by dampening pain signals sent to the brain.

Anticonvulsant drugs, such as Neurontin, Tegretol, and Dilatin, originally developed to treat epilepsy, are also often used to treat nerve pain, but researchers say they should be reserved as a second line of treatment. It remains unclear how these drugs work to dampen nerve pain.

Read WebMD's "Get the Facts about Diabetes-Related Nerve Problems"

Older Antidepressants Still Work for Nerve Pain

In the review, which appears in the current issue of the Cochrane Library, researchers evaluated studies on antidepressants and anticonvulsant drugs in the treatment of neuropathic pain involving more than 2,500 people.

The results showed that two-thirds of people with pain caused by nerve damage who took tricyclic antidepressants obtained at least moderate pain relief. But about one-fifth found the side effects of antidepressant treatment, such as drowsiness, dry mouth, and blurred vision, unacceptable and stopped taking the drugs.

The study showed that tricyclic antidepressants, particularly Amitril, were most effective in easing neuropathic pain caused by diabetes and shingles.

Although these results are promising, researchers say antidepressants do not cure or eliminate all pain.

"The amount of pain reduction is moderate at best. Typically the pain reduction averages around 40 percent in 50 percent of treated patients," says researcher Dennis C. Turk, PhD, of the University of Washington, in a news release. "This means that a significant proportion of patients do not obtain even moderate reductions in pain, and even those who do continue to experience significant pain."

Researchers say more studies are needed to evaluate the effects of newer antidepressants as well as alternative medicines, such as St. John's wort, before they can be recommended for treating neuropathic pain.

Read WebMD's "Learn More About Diabetes Complications"

Anticonvulsants May Also Help Nerve Pain

Researchers say the results of their review of anticonvulsants in treating neuropathic pain are both encouraging and conflicting.

Anticonvulsants were originally developed to treat epilepsy in the 1960s and have increasingly been used to treat pain. The drugs are thought to work by quieting abnormal firings of the nerves in the brain and central nervous system.

In their review, researchers analyzed 23 trials of anticonvulsant drugs involving more than 1,000 people.

They say the results of these studies are conflicting and suggest that each anticonvulsant drug needed to be evaluated independently to determine its effectiveness in treating neuropathic pain in comparison with other anticonvulsants and antidepressants.

For example, 15 studies of Neurontin showed that its effectiveness was comparable to another anticonvulsant, Tegretol, in relieving neuropathic pain. Neurontin has fewer side effects, but researchers say it is more expensive than other alternatives and cheaper treatments are also effective.

Therefore, researchers say anticonvulsants should be reserved as a second choice for treating pain caused by nerve tissue damage after first trying treatment with antidepressants.

By Jennifer Warner, reviewed by Brunilda Nazario, MD

SOURCES: Saarto, T. The Cochrane Database of Systemic Reviews, July 20, 2005. News release, Health Behavior News Service.

http://www.foxnews.com/story/0,2933,163015,00.html

Is ADHD a Real Disease?

It turns out that ADHD is a bogus disease. Yet, many public schools across the country now pressure parents to give Ritalin to their kids to "treat" this alleged disease.



[ClickPress, Thu Jul 21 2005] The vast majority of Ritalin and Adderall is given to school children to treat an alleged disease called ADHD. Children who suffer from ADHD are said to be inattentive, impulsive, and hyperactive. They often get bored easily in class, squirm in their seats, are always on the go, or don’t get along with other students or the teacher. In other words, many children diagnosed with ADHD may simply be bright, normal kids, full of energy and bored out of their minds sitting in public school classrooms.

In his testimony to the Pennsylvania House Democratic Policy Committee, Bruce Wiseman, National President of the Citizens Commission on Human Rights, stated that “thousands of children put on psychiatric drugs are simply ‘smart.’” He quoted the late Sydney Walker, a psychiatrist and neurologist, as saying, “They’re hyper not because their brains don’t work right, but because they spend most of the day waiting for slower students to catch up with them. These students are bored to tears, and people who are bored fidget, wiggle, scratch, stretch, and (especially if they are boys) start looking for ways to get into trouble."

Boredom is not the only reason children can exhibit symptoms of ADHD. Perfectly normal children who are over-active (have a lot of energy), rebellious, impulsive, day-dreamers, sensitive, undisciplined, bored easily (because they are bright), slow in learning, immature, troubled (for any number of reasons), learning disabled (dyslexia, for example), can also be inattentive, impulsive, or hyperactive.

Also, many factors outside the classroom can stress or emotionally affect children. Some of these factors are: not getting love, closeness, or attention from their parents; if a parent, friend, or sibling is sick or dies; if the parents are divorcing and there is anger, shouting, or conflict at home; domestic violence at home; sexual, physical, or emotional abuse by parents or siblings; inattention and neglect at home; personality clashes with parents or siblings; envy or cruelty directed at a child by classmates or by siblings at home, and many other factors.

Also, many other medical conditions can cause children to mimic some or all of ADHD’s symptoms. Some of these conditions are: Hypoglycemia (low blood sugar), allergies, learning disabilities, hyper or hypothyroidism, hearing and vision problems, mild to high lead levels, spinal problems, toxin exposures, carbon monoxide poisoning, metabolic disorders, genetic defects, sleeping disorders, post-traumatic subclinical seizure disorder, high mercury levels, iron deficiency, B-vitamin deficiencies (from poor diet), Tourette’s syndrome, Sensory Integration Dysfunction, early-onset diabetes, heart disease, cardiac conditions, early-onset bipolar disorder, worms, viral and bacterial infections, malnutrition or improper diet, head injuries, lack of exercise, and many others.

Because these medical conditions can cause some or all of ADHD’s symptoms, it becomes next to impossible for any teacher, principal, or family doctor to claim with any certainty that a child has ADHD. To be certain, a doctor would have to test the child for all these other possible medical conditions. Since parents or doctors rarely do this, every diagnosis of ADHD is suspect, to say the least.

Any of these medical conditions, normal personality variations, emotional problems, or outside-the-classroom stress-factors can disturb a child’s attention, natural enthusiasm, or desire to learn in class, and make the child exhibit symptoms of ADHD. Yet, as psychiatrist Peter R. Breggin, author of "Talking Back To Ritalin," and director of the International Center for the Study of Psychiatry and Psychology, notes, “These are the types of [normal] children who get diagnosed as suffering ADHD and who get subdued with stimulants and other medications.”

Many reputable authorities, such as Dr. Breggin, deny that ADHD, the disorder for which Ritalin is most commonly prescribed, even exists.

Parents, do not fall for the ADHD propaganda that public school authorities are now attempting to force on you and your children. ADHD turns out to be a bogus disease. Many public schools now use this bogus disease as a convenient excuse to pressure parents to give their normal, energetic, but bored children mind-altering drugs. I also urge you to read Dr. Breggin's book, "Talking Back To Ritalin."