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Preventing the development of Hypertension, Obesity and Diabetes in Mid-life is Necessary to Lower Heart Failure Risk

People without diabetes lived on average between 8.6 and 10.6 years longer without heart failure

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New York, November 29, 2016: Preventing the development of hypertension, obesity and diabetes in mid-life — between the age of 45 and 55 years — can result in an 86 per cent lower risk of heart failure throughout the remainder of life, says a research.

Millions of people worldwide currently suffer from heart failure as well as face a significantly reduced quality of life and higher mortality rate.

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The study found that hypertension, obesity and diabetes — major risk factors as well as highly prevalent in individuals — are preventable risk factors for heart failure, the researchers said.

Further, people with diabetes were found to have a particularly strong association with shorter heart failure-free survival, as those without diabetes lived on average between 8.6 and 10.6 years longer without heart failure.

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Men at age 45 years without any of the three risk factors lived an average of 10.6 years longer free of heart failure, while women at age 45 without any of the three risk factors lived an average of 14.9 years longer without heart failure.

“The study adds to the understanding of how individual and aggregate risk factor levels, specifically in middle age, affect incident heart failure risk over the remaining lifespan,” said John T. Wilkins from the Northwestern University at Evanston, in Illinois, in the US.

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Prevention of hypertension, obesity and diabetes by ages 45 and 55 years may substantially prolong heart failure-free survival, decrease heart failure-related morbidity and reduce the public health impact of heart failure, the researchers noted.

The study was published in the journal JACC: Heart Failure. (IANS)

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New Drug Offers Treatment For Diabetes-Related Blindness

The researchers now plan to conduct a full-scale clinical trial, Gamble said

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New drug offers hope for diabetes-related blindness.

In a major breakthrough, Australian scientists have developed a new drug that offers treatment for people suffering from diabetic retinopathy — the main cause of blindness from diabetes.

The debilitating disease occurs when tiny blood vessels in the retina, responsible for detecting light, leak fluid or haemorrhage.

While treatment options include laser surgery or eye injections of anti-vascular endothelial growth factor (VEGF), they are not always effective or can result in side effects, highlighting the need for alternative therapeutic approaches.

The team from the Centenary Institute in Sydney developed a novel drug CD5-2, which in mouse models was found to mend the damaged blood retinal barrier and reduce vascular leakage.

“We believe CD5-2 could potentially be used as a stand-alone therapy to treat those patients who fail to respond to the anti-VEGF treatment. It may also work in conjunction with existing anti-VEGF treatments to extend the effectiveness of the treatment,” said lead author Ka Ka Ting from the Institute.

“With limited treatment options currently available, it is critical we develop alternative strategies for the treatment of this outcome of diabetes,” Ting added.

Diabetes
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The key process involved in diabetic retinopathy pathology is the breakdown of the blood-retinal barrier (BRB), which is normally impermeable. Its integrity relies on how well capillary endothelial cells are bound together by tight junctions. If the junctions are loose or damaged, the blood vessels can leak.

In the study, reported in the journal Diabetologia, CD5-2 was found to have therapeutic potential for individuals with vascular-leak-associated retinal diseases based on its ease of delivery and its ability to reverse vascular dysfunction as well as inflammatory aspects in animal models of retinopathy.

Previous studies have shown that CD5-2 can have positive effects on the growth of blood vessels.

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“This drug has shown great promise for the treatment of several major health problems, in the eye and in the brain,” said Professor Jenny Gamble, head of Centenary’s Vascular Biology Programme.

The researchers now plan to conduct a full-scale clinical trial, Gamble said. (IANS)