Health Highlights: Nov. 30, 2015

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Here are some of the latest health and medical news developments, compiled by the editors of HealthDay:

Salt Warning Symbol on Menus To Take Effect in NYC

As of Tuesday, chain restaurants in New York City will be required to put a salt-shaker emblem next to menu items with more than the recommended daily limit of 2,300 milligrams of sodium, or about a teaspoon of salt.

The first-of-a-kind rule is the latest in a series of measures by city officials to promote healthier eating, The New York Times reported.

"With the high sodium warning label, New Yorkers will have easily accessible information that can affect their health," Health Commissioner Dr. Mary Bassett said when the new warning was approved by the Board of Health in September.

Most Americans' intake of salt is too high, putting them at increased risk for high blood pressure and heart problems, experts warn.

The average American consumes about 3,400 mg of salt per day and New York City's new rule is welcomed by public health advocates, The Times reported.

It will apply to about 10 percent of menu items in New York City outlets of chain restaurants with at least 15 locations nationwide, according to the health department.

While the rule takes effect Tuesday, fines for violating it won't be levied until March 1, The Times reported.

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Study Discovers How Alzheimer's Destroys Brain Cell Connections

Scientists who discovered how connections between brain cells are destroyed in the early stages of Alzheimer's disease say their findings could lead to new treatments for the condition in its early stages.

"One of the first signs of Alzheimer's disease is the loss of synapses -- the structures that connect neurons in the brain," team leader Vladimir Sytnyk, School of Biotechnology and Biomolecular Sciences, University of New South Wales, Australia, said in a university news release.

"Synapses are required for all brain functions, and particularly for learning and forming memories. In Alzheimer's disease, this loss of synapses occurs very early on, when people still only have mild cognitive impairment, and long before the nerve cells themselves die," he explained.

"We have identified a new molecular mechanism which directly contributes to this synapse loss -- a discovery we hope could eventually lead to earlier diagnosis of the disease and new treatments," Sytnyk said.

The researchers focused on a protein called neural cell adhesion molecule 2 (NCAM2), which plays a major role in connections between synapses. Analysis of brain tissue from dead people revealed that Alzheimer's patients have low levels of this protein in the brain's hippocampus.

Mice and laboratory studies showed that NCAM2 is broken down by beta-amyloid, a protein that is the main component of Alzheimer's-related brain plaques.

"Our research shows the loss of synapses is linked to the loss of NCAM2 as a result of the toxic effects of beta-amyloid," Sytnyk said.

"It opens up a new avenue for research on possible treatments that can prevent the destruction of NCAM2 in the brain," he added.

The study was published in the journal Nature Communications.

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