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Washington DC, Jun 29: Young children with narrow retinal artery diameters were more likely to develop higher blood pressure, and children with higher blood pressure levels were more likely to develop retinal microvascular impairment during early childhood, according to a new study.

The first study to show this connection in children was published today in Hypertension, an American Heart Association journal.

High blood pressure, the main risk factor for the development of cardiovascular disease (CVD), can manifest as early as childhood, and the prevalence of high blood pressure among children continues to rise. In previous studies, analysis of blood vessels in the retina has shown promise as a predictor of CVD risk among adults. In the study titled, "Retinal Vessel Diameters and Blood Pressure Progression in Children," researchers sought to predict the development of high blood pressure in children over four years based on retinal blood vessel measurements.

"Hypertension continues as the main risk factor for the development of cardiovascular diseases and mortality," says Henner Hanssen, M.D., the study's lead author and a professor in the department of sport, exercise and health at the University of Basel in Switzerland. 

"Primary prevention strategies are needed to focus on screening retinal microvascular health and blood pressure in young children in order to identify those at increased risk of developing hypertension. The earlier we can provide treatment and implement lifestyle changes to reduce hypertension, the greater the benefit for these children."

Researchers screened 262 children ages six to eight from 26 schools in Basel, Switzerland, in 2014, for baseline blood pressure and retinal arterial measurements. Both measures were taken again in 2018. Blood pressure measurements at both baseline and follow-up were performed in a sitting position after a minimum of five minutes of rest and were categorized based on the American Academy of Pediatrics' blood pressure guidelines. These guidelines utilize the same measurements as the American Heart Association/American College of Cardiology 2017 Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults.

Results from the analysis indicate: children with narrower retinal vessel diameters at baseline developed higher systolic blood pressure at follow-up; retinal vessel diameters could explain 29 -31 per cent of the changes in systolic blood pressure progression between 2014 and 2018; children with higher blood pressure levels at baseline developed significantly narrower arteriolar diameters at follow-up, depending on weight and cardiorespiratory fitness; and initial blood pressure measures explained 66-69 per cent of the change in retinal arteriolar diameter from baseline to follow-up.

"Early childhood assessments of retinal microvascular health and blood pressure monitoring can improve cardiovascular risk classification. Timely primary prevention strategies for children at risk of developing hypertension could potentially counteract its growing burden among both children and adults," said Hanssen.

Researchers noted limitations of their study include that they could not confirm blood pressure measurements over a single 24-hour period, so they would not account for "white coat" hypertension, a condition where patients have high blood pressure readings when measured in a medical setting.

Developmental stage including puberty status of each child was not accounted for in the study, as well as genetic factors or birth weight - variables that could impact blood pressure development and microvascular health.

In addition, reference values for appropriate retinal vessel diameters in children do not currently exist, so future studies are needed to determine age-related normal values during childhood.

London, Jul 2: The World Health Organisation says smoking is linked to a higher risk of severe illness and death from the coronavirus in hospitalised patients, although it was unable to specify exactly how much greater those risks might be.

In a scientific brief published this week, the U.N. health agency reviewed 34 published studies on the association between smoking and Covid-19, including the probability of infection, hospitalisation, severity of disease and death.

WHO noted that smokers represent up to 18% of hospitalised coronavirus patients and that there appeared to be a significant link between whether or not patients smoked and the severity of disease they suffered, the type of hospital interventions required and patients' risk of dying.

In April, French researchers released a small study suggesting smokers were at less risk of catching Covid-19 and planned to test nicotine patches on patients and health workers — but their findings were questioned by many scientists at the time who cited the lack of definitive data.

WHO says "the available evidence suggests that smoking is associated with increased severity of disease and death in hospitalized Covid-19 patients. It recommends that smokers quit.

New York, May 19: Cigarette smoke spurs the lungs to make more of the receptor protein which the novel coronavirus uses to enter human cells, according to a study which suggests that quitting smoking might reduce the risk of a severe coronavirus infection.

The findings, published in the journal Developmental Cell, may explain why smokers appear to be particularly vulnerable to severe COVID-19 disease.

"Our results provide a clue as to why smokers who develop COVID-19 tend to have poor clinical outcomes," said study senior author Jason Sheltzer, a cancer geneticist at Cold Spring Harbor Laboratory in the US.

"We found that smoking caused a significant increase in the expression of ACE2, the protein that SARS-CoV-2 uses to enter human cells," Sheltzer said.

According to the scientists, quitting smoking might reduce the risk of a severe coronavirus infection.

They said most individuals infected with the virus suffer only mild illness, if they experience any at all.

However, some require intensive care when the sometimes-fatal virus attacks, the researchers said.

In particular, they said three groups have been significantly more likely than others to develop severe illness -- men, the elderly, and smokers.

Turning to previously published data for possible explanations for these disparities, the scientists assessed if vulnerable groups share some key features related to the human proteins that the coronavirus relies on for infection.

First, they said, they focused on comparing gene activity in the lungs across different ages, between the sexes, and between smokers and nonsmokers.

The scientists said both mice that had been exposed to smoke in a laboratory, and humans who were current smokers had significant upregulation of ACE2.

According to Sheltzer, smokers produced 30-55 per cent more ACE2 than their non-smoking counterparts.

While the researchers found no evidence that age or sex impacts ACE2 levels in the lungs, they said the influence of smoke exposure was surprisingly strong.

However, they said, the change seemed to be temporary.

According to the data, the level of the receptors ACE2 in the lungs of people who had quit smoking was similar to that of non-smokers.

The study noted that the most prolific producers of ACE2 in the airways are mucus-producing cells called goblet cells.

Smoking is known to increase the prevalence of such cells, the scientists said.

"Goblet cells produce mucous to protect the respiratory tract from inhaled irritants. Thus, the increased expression of ACE2 in smokers' lungs could be a byproduct of smoking-induced secretory cell hyperplasia," Sheltzer explained.

However, Sheltzer said other studies on the effects of cigarette smoke have shown mixed results.

"Cigarette smoke contains hundreds of different chemicals. It's possible that certain ingredients like nicotine have a different effect than whole smoke does," he said.

The researchers cautioned that the actual ACE2 protein may be regulated in ways not addressed in the current study.

"One could imagine that having more cells that express ACE2 could make it easier for SARS-CoV-2 to spread in someone's lungs, but there is still a lot more we need to explore," Sheltzer said.