Add nuts to your diet for sake of health, longevity

COVID-19 mostly kills through an overreaction of the immune system, whose function is precisely to fight infections, say scientists who have decoded the mechanisms, symptoms, and diagnosis of the disease caused by the SARS-Cov-2 coronavirus.

In a study published in the journal Frontiers in Public Health, the researchers explained step-by-step how the virus infects the airways, multiplies inside cells, and in severe cases causes the immune defences to overshoot with a "cytokine storm".

This storm is an over-activation of white blood cells, which release too-great amounts of cytokines -- inflammation-stimulating molecules --into the blood, they said.

"Similar to what happens after infection with SARS and MERS, data show that patients with severe COVID-19 may have a cytokine storm syndrome," said study author Daishun Liu, Professor at Zunyi Medical University in China.

"The rapidly increased cytokines attract an excess of immune cells such as lymphocytes and neutrophils, resulting in an infiltration of these cells into lung tissue and thus cause lung injury," Liu said.

The researchers explained that the cytokine storm ultimately causes high fever, excessive leakiness of blood vessels, and blood clotting inside the body.

It also causes extremely low blood pressure, lack of oxygen and excess acidity of the blood, and build-up of fluids in the lungs, they said.

The researchers noted that white blood cells are misdirected to attack and inflame even healthy tissue, leading to failure of the lungs, heart, liver, intestines, kidneys, and genitals.

This multiple organ dysfunction syndrome (MODS) may worsen and shutdown the lungs, a condition called acute respiratory distress syndrome, (ARDS), they said.

This, the researchers explained, happens due to the formation of a so-called hyaline membrane -- composed of debris of proteins and dead cells -- lining the lungs, which makes absorption of oxygen difficult.

Most deaths due to COVID-19 are therefore due to respiratory failure, they said.

The researchers explained that in the absence of a specific antiviral cure for COVID-19, the goal of treatment must be to the fight the symptoms, and lowering the mortality rate through intensive maintenance of organ function.

For example, an artificial liver blood purification system or renal replacement therapy can be used to filter the blood through mechanical means, they said.

The team noted that especially important are methods to supplement or replace lung function, for example with non-invasive mechanical ventilation through a mask, ventilation through a tube into the windpipe, the administration of heated and humidified oxygen via a tube in the nose, or a heart-lung bypass.

The researchers stressed the importance of preventing secondary infections.

They noted that SARS-Cov-2 also invades the intestines, where it causes inflammation and leakiness of the gut lining, allowing the opportunistic entry of other disease-causing microorganisms.

The researchers advocate that this should be prevented with nutritional support, for example with probiotics -- beneficial bacteria that protect against the establishment of harmful ones -- and nutrients and amino acids to improve the immune defences and function of the intestine.

"Because treatment for now relies on aggressive treatment of symptoms, preventative protection against secondary infections, such as bacteria and fungi, is particularly important to support organ function, especially in the heart, kidneys, and liver, to try and avoid further deterioration of their condition," Liu added.

The health and future of every child and adolescent worldwide is under immediate threat from ecological degradation, climate change and exploitative marketing practices that push fast food, sugary drinks, alcohol and tobacco at children, said a new report on Wednesday.

No single country is adequately protecting children's health, their environment and their futures, according to the report by a commission of over 40 child and adolescent health experts from around the world.

The commission, convened by the World Health Organization (WHO), the United Nations children's agency, Unicef, and medical journal the Lancet, found that while the poorest countries need to do more to support their children's ability to live healthy lives, excessive carbon emissions --disproportionately from wealthier countries -- threaten the future of all children.

"Despite improvements in child and adolescent health over the past 20 years, progress has stalled, and is set to reverse," said former Prime Minister of New Zealand and Co-Chair of the Commission, Helen Clark.

"It has been estimated that around 250 million children under five years old in low- and middle-income countries are at risk of not reaching their developmental potential, based on proxy measures of stunting and poverty. But of even greater concern, every child worldwide now faces existential threats from climate change and commercial pressures," Clark said.

The report, titled "A Future for the World's Children?", includes a new global index of 180 countries, comparing performance on child flourishing and sustainability, with a proxy for greenhouse gas emissions, and equity, or income gaps.

India ranked 131 among the 180 countries in the index.

The index shows that children in Norway, the Republic of Korea, and the Netherlands have the best chance at survival and well-being, while children in the Central African Republic, Chad, Somalia, Niger and Mali face the worst odds.

However, when the authors took per capita CO2 emissions into account, the top countries trail behind: Norway ranked 156, the Republic of Korea 166, and the Netherlands 160.

Each of the three emits 210 per cent more CO2 per capita than their 2030 target.

The US, Australia, and Saudi Arabia are among the ten worst emitters.

If global warming exceeds 4 degree Celsius by the year 2100 in line with current projections, this would lead to devastating health consequences for children, due to rising ocean levels, heatwaves, proliferation of diseases like malaria and dengue, and malnutrition, said the report.

The only countries on track to beat CO2 emission per capita targets by 2030, while also performing fairly (within the top 70) on child flourishing measures are: Albania, Armenia, Grenada, Jordan, Moldova, Sri Lanka, Tunisia, Uruguay and Vietnam.

The report also revealed the distinct threat posed to children from harmful marketing. Evidence suggests that children in some countries see as many as 30,000 advertisements on television alone in a single year, while youth exposure to vaping (e-cigarettes) advertisements increased by more than 250 per cent in the US over two years, reaching more than 24 million young people.

Children's exposure to commercial marketing of junk food and sugary beverages is associated with purchase of unhealthy foods and overweight and obesity, linking predatory marketing to the alarming rise in childhood obesity, said the report.

The number of obese children and adolescents increased from 11 million in 1975 to 124 million in 2016 - an 11-fold increase, with dire individual and societal costs.

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.