Wednesday, November 27, 2019
The Herman Trend Alert
November 27, 2019
New Treatments for Heart Disease
Atherosclerosis is a type of heart disease in which the cholesterol in our bodies aggregates into the walls of the blood vessels causing what we call "plaque." This build-up eventually becomes so thick that it causes the narrowing of the blood conduits and if unchecked, can kill us. In fact, it is the leading cause of death worldwide. Recently, a team of researchers in the United Kingdom from the University of Sheffield identified a protein that plays a vital role in the development of atherosclerosis---the first step to finding effective treatments.
The Benefit of Tribbles 1
For the first time, researchers have demonstrated that the protein known as Tribbles 1 (TRIB1) is expressed by the very cells that are linked to the formation of the artery-clogging plaques. Called "Macrophages," they are responsible for removing cellular garbage and other waste from our bodies to keep us healthy---including the insides of our blood vessels. These garbage collectors patrol our bloodstream; when they detect fatty deposits lodged in the walls of our blood vessels, they move absorb the cholesterol and transport it away.
The Trouble with Tribbles 1
Sadly, when they try to absorb too much, some forms of cholesterol overwhelm these macrophages. Macrophages that absorb large quantities of these fatty deposits become swollen, cholesterol-laden cells known as foam cells. These foam cells become lodged in the walls of the arteries. There, they do nothing but create inflammation and attract more macrophages to those areas. After trying to absorb the fatty deposits, the newly attracted macrophages also become trapped, become overwhelmed, and die. The site eventually becomes a macrophage graveyard, and the dead and dying foam cells form the basis of the familiar arterial plaques that accompany atherosclerosis.
Using Tribbles 1 to Reduce Disease Progression
Interestingly, the researchers showed that by decreasing the presence of TRIB1, disease progression was reversed. If these researchers can find a way to block or reduce the activity of TRIB1, they could create a therapy to prevent the formation of the bloated foam cells and atherosclerotic plaques; this action would allow the macrophages to eliminate the waste without themselves becoming trapped---thus cleaning out clogged blood vessels--- a solution to atherosclerosis.
Other Treatments Hold Promise as Well
This TRIB 1 approach is only one of the therapies currently being developed to address the cause of atherosclerosis. Repair Biotechnologies is also researching a therapy that could improve how macrophages break down cholesterol, making them more robust and able to carry it away more effectively. SENS Research Foundation has developed an approach that works by removing an especially lethal form of oxidized lipid directly from the macrophages. Expect good news from SENS soon.
Just the Start of the Good News to Come
Given that atherosclerosis and its resulting heart attacks and strokes kills so many people worldwide, we expect that even more resources will be aimed at this serious disease. For those of us with high cholesterol, these solutions cannot come soon enough!
Special thanks to the Lifeboat Foundation and Life Extension Advocacy Foundation for highlighting this important breakthrough.
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Read this Herman Trend Alert on the web: http://www.hermangroup.com/alert/archive 11-27-2019.html.
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