Teen BMI can predict the risk of cardiovascular death in adulthood, according to a recent study.

In light of the worldwide increase in childhood obesity, Hebrew University's Jeremy Kark, together with Dr. Gilad Twig of the Sheba Medical Center, Dr. Hagai Levine of the Braun School and other colleagues in Israel, set out to determine the association between body-mass index (BMI) in late adolescence and death from cardiovascular causes in adulthood.

Their study was based on a national database of 2.3 million Israeli 17 year olds in whom height and weight were measured between 1967 and 2010. The researchers assessed the association between BMI in late adolescence and death from coronary heart disease, stroke, and sudden death in adulthood by mid-2011.

The results showed an increase in the risk of cardiovascular death in the group that was considered within the "accepted normal" range of BMI, in the 50th to 74th percentiles, and of death from coronary heart disease at BMI values above 20.

The researchers concluded that even BMI considered "normal" during adolescence was associated with a graded increase in cardiovascular and all-cause mortality during the 40 years of follow-up. This included increased rates of death from coronary heart disease, stroke, and total cardiovascular causes among participants.

As BMI scores increased into the 75th to 84th percentiles, adolescent obesity was associated with elevated risk of death from coronary heart disease, stroke, sudden death from unknown causes, and death from total cardiovascular causes, as well as death from non-cardiovascular causes and death from all causes. Participants also had an increased risk of sudden death.

Kark said that the findings appear to provide a link between the trends in adolescent overweight during the past decades and coronary mortality in midlife. The continuing increase in adolescent BMI, and the rising prevalence of overweight and obesity among adolescents, may account for a substantial and growing future burden of cardiovascular disease, particularly coronary heart disease.

The study appears in New England Journal of Medicine.

Researchers have for the first time found it possible to generate simultaneous immune response against diseases such as Hepatitis C virus and HIV, raising the possibility of a combined vaccination.

An estimated 2.3 million people globally are co-infected with HIV and HCV. HCV is the leading cause of non-AIDS deaths in co-infected individuals.

"While we have drugs to treat both HIV and HCV, these are out of reach for many and do not prevent reinfection," said lead researcher Lucy Dorrell, professor at University of Oxford in London.

"Knowing that it may be possible to vaccinate a single individual against both diseases opens up huge possibilities for rolling back epidemics of disease and co-infection," added one of the researchers Ellie Barnes, professor.

The findings showed that vaccine priming against HCV and HIV induced immune response in the body, measured by the number of HIV and HCV specific T-cells found in a sample of blood.

These immune responses were further increased following the boost vaccination.

In addition, co-administration of HCV and HIV components of the boost did not impair the magnitude or breadth of either HCV or HIV specific T-cell responses compared to each alone.

All vaccines were given as an intramuscular injection and both were well tolerated.

The study showed that the 'prime boost' approach is compatible with co-administration of vectors encoding for HIV and HCV antigens -- molecules capable of inducing an immune response to the immune system.

Following this, booster vaccinations are given with the same combination of HCV and HIV fragments.

The Phase 1 study enrolled 32 healthy volunteers in three groups. Group one received only HCV investigational vaccines at weeks 0 and 8.

The second group received only HIV investigational vaccines following the same dosing schedule.

The final group received both HCV and HIV investigational vaccines that were co-administered.

The study was presented at The International Liver Congress 2016 in Barcelona, Spain.

A team of researchers, including an Indian-origin scientist, has identified key inflammatory mechanisms underlying Type 1 diabetes and obesity-related kidney dysfunction.

Diabetic kidney disease is the leading cause of end-stage kidney disease and is a major risk factor for cardiovascular disease.

The findings showed that an increase in amounts of Sphingomyelin -- a type of fatty acid commonly found in cell membranes and nervous tissue -- has the potential to trigger the inflammatory mechanisms that can damage functioning of kidneys.

Sphingomyelin has been known to drive an increase in the ratio of adenosine triphosphate (ATP) and adenosine monophosphate (AMP) -- molecules involved in intracellular energy transfer in kidneys -- in glomerular cells of the kidney in mice with diabetes, obesity or both.

Diabetes and obesity leads to an increase in the ATP levels and decreases the AMP levels, disrupting the balance leading to the dysfunctioning of the kidneys.

"We believe that sphingomyelin fuels increases in ATP and decreases in AMP that result in inflammation which leads to cell dysfunction, fibrosis and endothelial damage underlying diabetic kidney disease," said Sharma, professor at the University of California San Diego in the US.

The team analysed the kidneys of experimental mice with Type 1 diabetes and mice fed on a high-fat diet.

The results also showed that deficiency in the production of insulin in the body or the resistance to externally induced insulin leads to an increase in amounts of sphingomyelin.

"We found that insulin deficiency and insulin resistance, two hallmarks of diabetes, seem to be associated with increased sphingomyelin in the kidney, which trigger damaging inflammatory mechanisms," Sharma noted in the paper published online in the journal EbioMedicine.

The insights could have major impact on developing new biomarkers and novel therapeutics for diabetic and obesity-related kidney diseases.

"It may be possible to create new treatments by blocking ATP and the inflammatory pathways consequent to that or by developing ways to reduce the amount or activity of sphingomyelin in the kidney," Sharma concluded.

According to a new study, eating of oily fish like salmon during pregnancy may reduces the risk of developing respiratory diseases like asthma in babies.

At six months of age, there is no difference in allergy rate between the children whose mothers ate oil fish and those who did not during pregnancy, as shown in the early result of the study

The early results of the study showed that at six months of age there was no difference in allergy rate between the children whose mothers ate salmon and those who did not.

However, at age of two and half years, children whose mothers ate oily fish during pregnancy are less likely to have asthma.

"Our findings indicate that early nutrition interventions, even during pregnancy, can have long lasting effects on health," said Philip Calder, professor at University of Southampton in Britain.

The study proved that fatty acids -- or a lack of them -- are involved in a broad spectrum of common diseases ranging from diverse allergies through to atherosclerosis and inflammatory conditions such as Crohn's disease.

The research was a randomised controlled trial in which a group of women ate salmon twice a week from week 19 of pregnancy.

Allergy tests were then performed on the children at six months and then at two to three years of age.

Results were compared to a control group whose mothers did not eat salmon during pregnancy.

The findings were presented at the recent Experimental Biology Congress in San Diego, US.

Obesity not only increases the risk of heart failure, but increased belly fat, combined with an ageing population, can also lead to a significant increase in the risk of heart failure, a study says.

The study showed a clear correlation between higher Body Mass Index (BMI), waist circumference and the risk of heart failure.

The researchers saw that with every 10 cm increase in waist circumference was linked to a 29 percent higher risk of heart failure from the analyses of 360,000 participants.

"Overweight individuals had a 35 percent increased risk of heart failure as compared with normal weight individuals and our findings indicate that overweight should be considered a clear risk factor for heart failure," said first author Dagfinn Aune from Norwegian University of Science and Technology in Norway.

Research showed that a BMI between 25 and 30 kg/m2, which is considered overweight, is also associated with increased risk.

A higher waist-to-hip ratio was also correlated with a progressively greater risk of developing heart failure.

The studies looked at the link between body mass index and the risk of death from heart failure and suggested a 26 percent higher risk for an increase of five BMI units.

"Overweight and obesity increase the risk for heart muscle disease, which is an established risk factor for heart failure," said Aune.

The findings hold great significance for clinical guidelines on preventing heart failure and they are also important from a public health perspective.

"Physical activity and a more plant-based diet with lots of fruits and vegetables and whole grains are important to prevent overweight and obesity," Aune said.