Author Interviews, Blood Pressure - Hypertension, Kidney Disease, Salt-Sodium / 31.03.2016
Only a Few Neurons in Brain Responsible For Salt Hunger
MedicalResearch.com Interview with:
[caption id="attachment_23038" align="alignleft" width="150"]
Dr. Mathew Bailey[/caption]
Matthew Bailey PhD
Faculty Principal Investigator
British Heart Foundation Centre for Cardiovascular Science
The University of Edinburgh, Edinburgh, United Kingdom.
MedicalResearch.com: What is the background for this study?
Dr. Bailey: This study started with our interest in salt homeostasis and long term blood pressure, so it’s firmly rooted in the cardiovascular/renal disease risk factor arena. We were interested in salt-sensitivity- why does blood pressure go up in some people when they eat salt but not in others. I’m a renal physiologist, so we had a number of papers looking at renal salt excretion and blood pressure. We initially used a gene targeting approach to remove a gene (Hsd11b2) which acts as a suppressor of the mineralocorticoid pathway. It’s mainly expressed in the kidney and when we deleted the gene throughout the body we saw a number of renal abnormalities all associated with high mineralocorticoid activity. This was consistent with the “hypertension follows the kidney” theory of blood pressure control. There is a human disease called “Apparent Mineralocorticoid Excess”- there are people do not have the gene and are thought to have renal hypertension. Our study threw up some anomalies which we couldn’t easily interpret but suggested that the brain was involved. We moved to a more refined technology that allowed us to knockout a gene in one organ system but not another. We knew the gene was in the brain and localized to a very restricted subset of neurons linked to salt-appetite and blood pressure control. Previous studies had shown that these neurons were activated in salt-depleted rats (ie rats that needed to eat salt). We started there but didn’t anticipate that the effect on salt hunger and on blood pressure would be so large because renal function is -as far as we can tell- normal.
Dr. Mathew Bailey[/caption]
Matthew Bailey PhD
Faculty Principal Investigator
British Heart Foundation Centre for Cardiovascular Science
The University of Edinburgh, Edinburgh, United Kingdom.
MedicalResearch.com: What is the background for this study?
Dr. Bailey: This study started with our interest in salt homeostasis and long term blood pressure, so it’s firmly rooted in the cardiovascular/renal disease risk factor arena. We were interested in salt-sensitivity- why does blood pressure go up in some people when they eat salt but not in others. I’m a renal physiologist, so we had a number of papers looking at renal salt excretion and blood pressure. We initially used a gene targeting approach to remove a gene (Hsd11b2) which acts as a suppressor of the mineralocorticoid pathway. It’s mainly expressed in the kidney and when we deleted the gene throughout the body we saw a number of renal abnormalities all associated with high mineralocorticoid activity. This was consistent with the “hypertension follows the kidney” theory of blood pressure control. There is a human disease called “Apparent Mineralocorticoid Excess”- there are people do not have the gene and are thought to have renal hypertension. Our study threw up some anomalies which we couldn’t easily interpret but suggested that the brain was involved. We moved to a more refined technology that allowed us to knockout a gene in one organ system but not another. We knew the gene was in the brain and localized to a very restricted subset of neurons linked to salt-appetite and blood pressure control. Previous studies had shown that these neurons were activated in salt-depleted rats (ie rats that needed to eat salt). We started there but didn’t anticipate that the effect on salt hunger and on blood pressure would be so large because renal function is -as far as we can tell- normal.




















Dr. Refaat Hegazi[/caption]
MedicalResearch.com Interview with:
Dr. Refaat Hegazi, MD, PhD MS MPH
Abbott medical director and study author
MedicalResearch: What is the background for this study? What are the main findings?
Dr. Hegazi: The NOURISH study that was recently published in Clinical Nutrition showed that a specialized oral nutrition supplement (with high protein, HMB and Vitamin D) was associated with a 50 percent lower death rate in older, malnourished patients with a heart or lung disease, 90 days after leaving the hospital.
The study was conducted with the utmost scientific rigor and is one of the largest nutrition clinical studies of its kind. In the study, we evaluated the effects of this specialized nutrition supplement compared to a placebo supplement on the incidence of hospital readmission or death through 90-days after leaving the hospital. The population studied has never been evaluated before in this way.
Results showed no significant differences between the two groups for the primary composite (i.e. combined) endpoint of hospital readmissions or death. However, the study individual components and additional analyses showed:
Dr. Marie St-Onge[/caption]
Marie-Pierre St-Onge, Ph.D, FAHA
Assistant Professor, Department of Medicine
New York Obesity Nutrition Research Center
Institute of Human Nutrition
College of Physicians & Surgeons, Columbia University
New York, NY 10032
Medical Research: What is the background for this study? What are the main findings?
Dr. St-Onge: We have shown that sleep affects food intake: restricting sleep increases energy intake, particularly from fat (others also find increased sugar intake). We wanted to know if the reverse was also true: does diet affect sleep at night?
Medical Research: What should clinicians and patients take away from your report?
Dr. St-Onge: Diet quality can play an important role in sleep quality. Sleep can be affect after only a single day of poor dietary intakes (high saturated fat and low fiber intakes). It is possible that improving one’s diet can also improve their sleep.
Dr. Lindsey Taillie[/caption]