Short or poor sleep can worsen kidney function: Study

November 21, 2016

New York, Nov 21: According to a new study, short and poor quality of sleep may adversely affect kidney function in patients with chronic kidney disease (CKD). “Short sleep and fragmented sleep are significant yet unappreciated risk factors for CKD progression,” said one of the researchers, Ana Ricardo, from the University of Illinois at Chicago in the US.

sleep“Our research adds to the accumulating knowledge regarding the importance of sleep on kidney function, and underscores the need to design and test clinical interventions to improve sleep habits in individuals with CKD,” she added.

Although there is increasing evidence that sleep disorders are common in individuals with CKD, its link with CKD progression is unknown.

To investigate, Ricardo and her colleagues examined the sleep patterns of 432 adults with chronic kidney disease. Participants wore a wrist monitor for five to seven days to measure sleep duration and quality, and their health was followed for a median of five years.

Participants slept an average of 6.5 hours/night, and during follow-up, 70 individuals developed kidney failure and 48 individuals died.

The researchers calculated that each additional hour of nighttime sleep was linked with a 19 per cent lower risk of developing kidney failure.

There was also a significant association between sleep quality and kidney failure risk -- each one per cent increase in sleep fragmentation was linked with a four per cent increase in the risk of developing kidney failure.

Also, patients who experienced daytime sleepiness were 10 per cent more likely to die during follow-up than those who were not sleepy during the day, said the study presented at American Society of Nephrology (ASN) Kidney Week 2016 at McCormick Place in Chicago, Illinois.

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Agencies
May 20,2020

Washington D.C., May 20: While a dairy-rich diet is helpful in meeting the body's calcium requirement, outcomes of a large international study links eating at least two daily servings of dairy with lower risks of diabetes and high blood pressure.

The dairy-rich diet also proved to lower the cluster of factors that heighten cardiovascular disease risk (metabolic syndrome). The study was published online in journal BMJ Open Diabetes Research & Care.

The observed associations were strongest for full-fat dairy products, the findings indicated.

Previously published research has suggested that higher dairy intake is associated with a lower risk of diabetes, high blood pressure, and metabolic syndrome. But these studies have tended to focus on North America and Europe to the exclusion of other regions of the world.

To see whether these associations might also be found in a broader range of countries, the researchers drew on people taking part in the Prospective Urban Rural Epidemiology (PURE) study.

Participants were all aged between 35 and 70 and came from 21 countries: Argentina; Bangladesh; Brazil; Canada; Chile; China; Colombia; India; Iran; Malaysia; Palestine; Pakistan; Philippines, Poland; South Africa; Saudi Arabia; Sweden; Tanzania; Turkey; United Arab Emirates; and Zimbabwe.

Usual dietary intake over the previous 12 months was assessed by means of Food Frequency Questionnaires. Dairy products included milk, yogurt, yogurt drinks, cheese and dishes prepared with dairy products, and were classified as full or low fat (1-2 percent).

Butter and cream were assessed separately as these are not commonly eaten in some of the countries studied.

Information on personal medical history, use of prescription medicines, educational attainment, smoking and measurements of weight, height, waist circumference, blood pressure and fasting blood glucose were also collected.

Data on all five components of the metabolic syndrome were available for nearly 113,000 people: blood pressure above 130/85 mm Hg; waist circumference above 80 cm; low levels of (beneficial) high-density cholesterol (less than 1-1.3 mmol/l); blood fats (triglycerides) of more than 1.7 mmol/dl; and fasting blood glucose of 5.5 mmol/l or more.

Average daily total dairy consumption was 179 g, with full-fat accounting for around double the amount of low fat: 124.5+ vs 65 g.

Some 46, 667 people had metabolic syndrome--defined as having at least 3 of the 5 components.

Total dairy and full-fat dairy, but not low-fat dairy, was associated with a lower prevalence of most components of metabolic syndrome, with the size of the association greatest in those countries with normally low dairy intakes.

At least 2 servings a day of total dairy were associated with a 24 percent lower risk of metabolic syndrome, rising to 28 percent for full-fat dairy alone, compared with no daily dairy intake.

The health of nearly 190,000 participants was tracked for an average of nine years, during which time 13,640 people developed high blood pressure and 5351 developed diabetes.

At least 2 servings a day of total dairy was associated with a 11-12 percent lower risk of both conditions, rising to a 13-14 percent lower risk for 3 daily servings. The associations were stronger for full fat than they were for low-fat dairy.

This is an observational study, and as such can't establish the cause. Food frequency questionnaires are also subject to recall, and changes in metabolic syndrome weren't measured over time, all of which may have influenced the findings.

Nevertheless, the researchers suggest: "If our findings are confirmed in sufficiently large and long term trials, then increasing dairy consumption may represent a feasible and low-cost approach to reducing [metabolic syndrome], hypertension, diabetes, and ultimately cardiovascular disease events worldwide."

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News Network
February 21,2020

Washington, Feb 21: The fat around arteries may play an important role in keeping the blood vessels healthy, according to a study in rats that may affect how researchers test for treatments related to plaque buildup, as seen in conditions leading to heart attack.

The study, published in the journal Scientific Reports, noted that the fat, known as perivascular adipose tissue, or PVAT, helps arteries let go of muscular tension while under constant strain.

According to the researchers, including Stephanie W. Watts from the Michigan State University in the US, this feature is similar to how the bladder expands to accommodate more liquid, while at the same time keeping it from spilling out.

"In our study, PVAT reduced the tension that blood vessels experience when stretched," Watts said.

"And that's a good thing, because the vessel then expends less energy. It's not under as much stress," she added.

According to Watts and her team, PVAT has largely been ignored by researchers believing its main job was to store lipids and do little more.

Until now, she said, scientists only divided blood vessels into three parts, the innermost layer called the tunica intima, the middle layer called the tunica media, and the outermost layer called the tunica adventitia.

Watts believes PVAT is the fourth layer, which others have called tunica adiposa.

Tunica, she said, meant a membranous sheath enveloping or lining an organ, and adiposa is a synonym for fat.

"For years, we ignored this layer -- in the lab it was thrown out. In the clinic it wasn't imaged. But now we're discovering it may be integral to our blood vessels," Watts said.

"Our finding redefines what the functional blood vessels are, and is part of what can be dysfunctional in diseases that afflict us, including hypertension. We need to pay attention to this layer of a blood vessel because it does far more than we originally thought," she added.

Earlier studies, Watts said, had shown that PVAT plays a role in the functioning of blood vessels, finding that it secretes substances that can cause blood vessels to relax as well as substances that can cause it to contract.

In the current study, the researchers decided to test whether PVAT provides a structural benefit to arteries by assisting the function of stress relaxation.

They tested the thoracic aorta in rats, and found those with intact PVAT had more stress relaxation than those without.

The study revealed that the pieces of artery with surrounding fat had measurably relaxed more than those without.

Watts and her colleagues then tested other arteries, and were able to duplicate the same response.

"It's not something you see only in this particular vessel or this particular species or this particular strain. But that maybe it's a general phenomenon," she said.

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Agencies
May 19,2020

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.

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