Bad calories have variations too, with some being more harmful than others 

Tedros Adhanom Ghebreyesus, the World Health Organisation's (WHO) Director-General, said that a clinical trial of hydroxychloroquine (HCQ) on COVID-19 patients has come to "a temporary pause", while the safety data of the the anti-malaria drug was being reviewed.

According to the WHO chief, The Lancet medical journal on May 22 had published an observational study on HCQ and chloroquine and its effects on COVID-19 patients that have been hospitalized, reports Xinhua news agency.

The authors of the study reported that among patients receiving the drug, when used alone or with a macrolide, they estimated a higher mortality rate.

"The Executive Group of the Solidarity Trial, representing 10 of the participating countries, met on Saturday (May 23) and has agreed to review a comprehensive analysis and critical appraisal of all evidence available globally," Tedros said in a virtual press conference on Monday.

The review will consider data collected so far in the Solidarity Trial and in particular robust randomized available data, to adequately evaluate the potential benefits and harms from this drug, he said.

"The Executive Group has implemented a temporary pause of the HCQ arm within the Solidarity Trial while the safety data is reviewed by the Data Safety Monitoring Board. The other arms of the trial are continuing," Tedros added.

WHO initiated the Solidarity Trial, a plan to evaluate the safety and efficacy of four drugs and drug combinations against COVID-19 more than two months ago, which include HCQ.

According to the WHO, over 400 hospitals in 35 countries are actively recruiting patients and nearly 3,500 patients have been enrolled from 17 countries under the Solidarity Trial.

Tedros added that the safety concern over the drug related only to the use of HCQ and chloroquine in COVID-19, and "these drugs are accepted as generally safe for use in patients with autoimmune diseases or malaria".

"WHO will provide further updates as we know more," he added.

Taking multiple courses of antibiotics within a short span of time may do people more harm than good, suggests new research which discovered an association between the number of prescriptions for antibiotics and a higher risk of hospital admissions.

Patients who have had 9 or more antibiotic prescriptions for common infections in the previous three years are 2.26 times more likely to go to hospital with another infection in three or more months, said the researchers.

Patients who had two antibiotic prescriptions were 1.23 times more likely, patients who had three to four prescriptions 1.33 times more likely and patients who had five to eight 1.77 times more likely to go to hospital with another infection.

"We don't know why this is, but overuse of antibiotics might kill the good bacteria in the gut (microbiota) and make us more susceptible to infections, for example," said Professor Tjeerd van Staa from the University of Manchester in Britain.

The study, published in the journal BMC Medicine, is based on the data of two million patients in England and Wales.

The patient records, from 2000 to 2016, covered common infections such as upper respiratory tract, urinary tract, ear and chest infections and excluded long term conditions such as cystic fibrosis and chronic lung disease.

The risks of going to hospital with another infection were related to the number of the antibiotic prescriptions in the previous three years.

A course is defined by the team as being given over a period of one or two weeks.

"GPs (general physicians) care about their patients, and over recent years have worked hard to reduce the prescribing of antibiotics,""Staa said.

"But it is clear GPs do not have the tools to prescribe antibiotics effectively for common infections, especially when patients already have previously used antibiotics.

"They may prescribe numerous courses of antibiotics over several years, which according to our study increases the risk of a more serious infection. That in turn, we show, is linked to hospital admissions," Staa added.

It not clear why hospital admissions are linked to higher prescriptions and research is needed to show what or if any biological factors exist, said the research team.

"Our hope is that, however, a tool we are working for GPs, based on patient history, will be able to calculate the risks associated with taking multiple courses of antibiotics," said Francine Jury from the University of Manchester.

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.