KATHMANDU — Drinking more water is generally advised — the common advice is to drink eight glasses per day –and has been associated with better kidney function and a reduced risk of kidney stones.
But drinking an extra four to six extra glasses of water per day won’t slow the decline of kidney functions for chronic kidney disease patients, according to a new study in Britain and Canada.
A study, published in JAMA (Journal of the American Medical Association) by researchers at LaLawson Health Research Institute in Ontario and Western University in London found that coaching patients with Chronic Kidney Disease (CKD) to drink more water does not slow down the decline of their kidney function.
“Despite widespread beliefs, little scientific data exists on the optimal amount of water to drink,” explains Dr. William Clark, Scientist at Lawson and Professor at Western’s Schulich School of Medicine & Dentistry.
“While many claims about the benefits of increased water intake remain untested, a growing body of evidence suggests that increased water intake improves kidney function through the suppression of the antidiuretic hormone.”
Researchers studied whether increased hydration made a difference in people with kidney disease. The clinical trial was published Tuesday in the Journal of the American Medical Association.
The randomized clinical trial included 631 patients at London Health Sciences Center and several other hospitals in Ontario with stage 3 kidney disease from April 2013 to June 2017. At stage 3, patients have lost up to 70 percent of their kidney function.
Half of the participants were coached to drink more water — 1 to 1.5 liters per day, depending on sex and weight. Those in the control group were asked to maintain usual intake or not decrease it by more than one-quarter to a half-liter per day. One liter of water is about 34 fluid ounces.
The researchers, after one year, found the increase of water consumption did not slow the loss of kidney function. They found, however, that the reduction significantly suppressed antidiuretic hormone release, particularly when the participant’s previous intake was low.
“This research indicates that for most patients with CKD, increasing fluid intake will not stop further loss of kidney function. It does allow us then to focus our efforts on other potential therapeutic options,” Clark said.
The researchers hope to conduct another study with a longer followup, according to them.
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Vitamin D can help tackle diabetes
Boosting vitamin D — often referred to as the sunshine vitamin because it is created in our skin in response to direct sunlight — can help tackle diabetes, according to a study from the Salk Institute.
The condition is caused by faulty beta cells in the pancreas. These cells manufacture and release insulin, the hormone essential for controlling glucose levels in the blood.
If beta cells produce too little insulin, or none at all, glucose can accumulate in the blood at levels that are toxic to cells and tissues.
Researchers from the Salk Institute have reported a potential new approach for treating diabetes by protecting beta cells.
Previous studies have found a connection between low vitamin D levels and a higher risk of diabetes, but the mechanisms involved have been challenging to unravel.
The researchers found that a particular compound — called iBRD9 — boosted the activity of vitamin D receptors when they were bound to vitamin D molecules. This had a protective effect on the beta cells.
They demonstrated that, in a mouse model of diabetes, iBRD9 brought glucose levels back down into the normal range.
When beta cells become dysfunctional, the body can’t make insulin to control blood sugar (glucose) and levels of glucose can rise to dangerous, even fatal, levels.
“We know that diabetes is a disease caused by inflammation,” explained senior author Ronald Evans adding, “In this study, we identified the vitamin D receptor as an important modulator of both inflammation and beta cell survival.”
The team accomplished this by conducting a screening test to look for compounds that improved the survival of beta cells in a dish. They then tested the combination in a mouse model of diabetes and showed that it could bring glucose back to normal levels in the animals.
“This study started out by looking at the role of vitamin D in beta cells,” said first author Zong Wei. “Epidemiological studies in patients have suggested a correlation between high vitamin D concentrations in the blood and a lower risk of diabetes, but the underlying mechanism was not well understood. It’s been hard to protect beta cells with the vitamin alone. We now have some ideas about how we might be able to take advantage of this connection.”
The underlying process has to do with transcription the way that genes are translated into proteins. Combining the new compound with vitamin D allowed certain protective genes to be expressed at much higher levels than they are in diseased cells.
The discovery’s implications can have far-reaching implications: It identifies a basic mechanism that can be translated into drugging many different targets in the clinic.
The findings appeared in the journal Cell.
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