Excess Sodium Intake Remains Common in the United States

Nearly all Americans – regardless of age, race, gender or whether they have high blood pressure (hypertension) – consume more sodium than is recommended for a healthy diet. That is the conclusion of a new report published by the Centers for Disease Control and Prevention (CDC) in today’sMorbidity and Mortality Weekly Report (MMWR).

According to the latest findings, more than 90 percent of children and 89 percent of adults aged 19 and older eat too much sodium, that is, more than the recommended limits in the 2015-2020 Dietary Guidelines for Americans, not including salt added at the table. The newly released guidelines – which are developed around current scientific evidence and released every five years – recommend limiting sodium to less than 2,300 mg per day for people over the age of 14 and less for those younger. Evidence links excess sodium intake to high blood pressure and other health problems.

“The finding that nine of ten adults and children still consume too much salt is alarming,” said CDC Director Tom Frieden, MD, MPH. “The evidence is clear: too much sodium in our foods leads to high blood pressure, a major risk factor for heart disease and stroke. Reducing sodium in manufactured and restaurant foods will give consumers more choice and save lives.”

CDC researchers analyzed dietary data from the 2009-2012 National Health and Nutrition Examination Surveys (NHANES) to calculate how much sodium Americans are eating. Nearly 15,000 people were included in this study.

Sodium consumption high among those at risk of heart disease

Excess sodium intake is a problem across gender, race, and health status. Some differences were seen:

• Among adults, a larger proportion of men (98 percent) than women (80 percent) consume too much sodium.
• About 90 percent of adult whites consume excess sodium compared with 85 percent of blacks.
• Estimated sodium and calorie consumption peaks between the ages of 19 and 50.
• Among people at greater risk of developing heart disease or stroke – such as people age 51 and older, African Americans and individuals with high blood pressure or pre-hypertension (blood pressure higher than normal but not in the “high” range) – more than three out of four exceed 2,300 mg per day.
• Adults with hypertension consume slightly less sodium than other adults, and may be trying to follow physicians’ advice to reduce sodium. However, 86 percent of adults with hypertension still consume too much.

These new findings show that little has changed in sodium consumption over the past decade. More than three quarters of sodium in the American diet is estimated to come from processed and restaurant food, which gives consumers little choice when it comes to lowering daily intake. A key strategy for lowering population-wide sodium intake is gradually reducing sodium in the food supply. Some food companies have begun to voluntarily reduce sodium in their products and others are being encouraged to take similar steps.

The report also highlights the important role healthcare professionals can play in advising patients on how to limit salt in the diet. About one in three U.S. adults – or about 70 million people – already have high blood pressure and only half have it under control. Heart disease, stroke, and other cardiovascular diseases kill more than 800,000 Americans each year and cost nearly $320 billion a year in health care and lost productivity.

“Sodium reduction is a key part of preventing heart disease and stroke,” said Sandra Jackson, an author of the report and an epidemiologist in CDC’s Division for Heart Disease and Stroke Prevention. “Reducing sodium is an achievable and effective strategy to improve heart health for everyone, but it’s going to take all of us working together to make it possible.”

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Neurons that have been exposed to GDF10 grow more connections as a result.UCLA

Stroke occurs when blood flow to the brain is disrupted. Without oxygen- and nutrient-rich blood, brain cells start to die. Recovery after stroke depends on a process called axonal sprouting, in which healthy neurons send out new projections, or extensions. These “sprouts” generate new connections between brain cells or reestablish some of the connections that were lost or damaged during stroke, resulting in partial recovery.

Previous studies suggested that a protein called growth and differentiation factor 10 (GDF10) was involved in the early stages of axonal sprouting. Dr. S. Thomas Carmichael and his colleagues at the University of California, Los Angeles, took a closer look at GDF10 to identify how it contributes to the process. Their work was supported in part by NIH’s National Institute of Neurological Disorders and Stroke (NINDS). The findings were published online on October 26, 2015, inNature Neuroscience.

By examining animal models of stroke as well as brain tissue from human autopsies, the team found that GDF10 was activated very early after stroke. Using rodent neurons and human neurons derived from stem cells, the researchers showed that GDF10 stimulated axonal growth and increased the length of the axons.

To see whether GDF10 is important for functional recovery after stroke, the researchers treated mouse models of stroke with GDF10 in a biopolymer hydrogel, which releases the protein to the site of injury over a 2- to 3-week period. Treated animals performed various motor tasks significantly faster and with fewer errors after stroke than control animals. In contrast, when the researchers blocked GDF10 production, the animals didn’t perform as well on the motor tasks, suggesting that repair mechanisms were impaired without GDF10.

To understand the pathways by which GDF10 might be working, the researchers isolated cortical neurons after stroke and examined their gene expression profiles. To see if the mechanisms of repair are similar to axonal sprouting during normal development when mice are forming new connections, they also examined cortical neurons from young mice. The analysis revealed that GDF10 affected a set of genes after stroke that was distinct from those involved in development.

“We found that regeneration is a unique program in the brain that occurs after injury. It is not simply Development 2.0, using the same mechanisms that take place when the nervous system is forming,” Carmichael says.

“These findings help to elucidate the mechanisms of repair following stroke,” says Dr. Francesca Bosetti, stroke program director at NINDS. “Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery.”

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NIH-funded research pinpoints protein that sprouts into action, activating stroke repair

Looking at brain tissue from mice, monkeys and humans, scientists have found that a molecule known as growth and differentiation factor 10 (GDF10) is a key player in repair mechanisms following stroke. The findings suggest that GDF10 may be a potential therapy for recovery after stroke. The study, published in Nature Neuroscience, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health.

Sprouting connections in the brain: Adding GDF10 to neurons in a dish results in the formation of new connections between brain cells. This process may lead to recovery after stroke. Image courtesy of S. Thomas Carmichael, M.D., Ph.D., David Geffen School of Medicine at the University of California Los Angeles.

“These findings help to elucidate the mechanisms of repair following stroke. Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery,” said Francesca Bosetti, Ph.D., stroke program director at NINDS.

Stroke can occur when a brain blood vessel becomes blocked, preventing nearby tissue from getting essential nutrients. When brain tissue is deprived of oxygen and nutrients, it begins to die. Once this occurs, repair mechanisms, such as axonal sprouting, are activated as the brain attempts to overcome the damage. During axonal sprouting, healthy neurons send out new projections (“sprouts”) that re-establish some of the connections lost or damaged during the stroke and form new ones, resulting in partial recovery. Before this study, it was unknown what triggered axonal sprouting.

Previous studies suggested that GDF10 was involved in the early stages of axonal sprouting, but its exact role in the process was unclear. S. Thomas Carmichael, M.D., Ph.D., and his colleagues at the David Geffen School of Medicine at the University of California Los Angeles took a closer look at GDF10 to identify how it may contribute to axonal sprouting.

Examining animal models of stroke as well as human autopsy tissue, Dr. Carmichael’s team found that GDF10 was activated very early after stroke. Then, using rodent and human neurons in a dish, the researchers tested the effect of GDF10 on the length of axons, the neuronal projections that carry messages between brain cells. They discovered that GDF10 stimulated axonal growth and increased the length of the axons.

“We found that GDF10 caused many different neurons in a dish to grow, including human neurons that were derived from stem cells,” said Dr. Carmichael.

His group also found that GDF10 may be important for functional recovery after stroke. They treated mouse models of stroke with GDF10 and had the animals perform various motor tasks to test recovery. The results suggested that increasing levels of GDF10 were associated with significantly faster recovery after stroke. When the researchers blocked GDF10, the animals did not perform as well on the motor tasks, suggesting the repair mechanisms were impaired — and that the natural levels of GDF10 in the brain represent a signal for recovery.

“We were surprised by how consistently GDF10 caused new connections to form across all of the levels of analysis. We looked at rodent cortical neurons and human neurons in dish as well as in live animals. It’s a demanding gauntlet to run, but the effects of GDF10 held up in all of the levels that we tested,” said Dr. Carmichael.

It has been widely believed that mechanisms of brain repair are similar to those that occur during development. Dr. Carmichael’s team conducted comprehensive analyses to compare the effects of GDF10 on genes related to stroke repair with genes involved in development and learning and memory, processes that result in connections forming between neurons.

Surprisingly, there was little similarity. The findings revealed that GDF10 affected entirely different genes following stroke than those involved in development or learning and memory.

“We found that regeneration is a unique program in the brain that occurs after injury. It is not simply Development 2.0, using the same mechanisms that take place when the nervous system is forming,” said Dr. Carmichael.

More research is necessary to determine whether GDF10 can be a potential treatment for stroke recovery.

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