Heart Disease
How Arteries age
Figure A shows a normal artery with normal blood flow. Figure B shows an artery with plaque buildup.*
Plaque narrows the arteries and reduces blood flow to your heart muscle. It also makes it more likely that blood clots will form in your arteries. Blood clots can partially or completely block blood flow.*
* NHLBI (National Heart Lung and Blood Institute): Diseases and Conditions Index. Coronary Artery Disease: What Is Coronary Artery Disease? June 2008. (August 6, 2008).
Plaque accumulates
Plaque accumulation makes it harder for the heart to pump blood through the arteries. This is a root cause of heart cell death. Stroke risk increases. How The CR Way
can help
The CR way lowers major risk factors for plaque build up:
- Serum cholesterol
- Blood pressure
- LDL cholesterol
- Inflammation
Meanwhile, HDL cholesterol, which cleans cholesterol-forming plaque from the arteries, is raised.
The CR Way may even reverse artery blockage as some plaque is burned for energy needs.
How the heart ages
Cells Die
The heart repairs the age-related loss of cells by depositing collagen. But that forms fibrous tissue, which is less flexible. As a result, cardiac function becomes impaired while blood pressure increases and cardiac reserve decreases.
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How The CR Way
can help
The CR Way helps prevent cell loss – reducing collagen deposition, helping maintain heart function at more youthful levels.
Download PDF The left ventricle (the heart’s main pumping chamber) loses function.
As the number of cardiomyocytes (heart cells) declines, the remaining cells grow in size, causing the left ventricle to become enlarged. Risk of heart attack, heart failure, irregular heartbeats (arrhythmia) and sudden cardiac arrest is increased.
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How The CR Way
can help
The CR Way preserves left ventricle function.
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Mitochondria become impaired.
Mitochondria (vital energy producers that power cell function) become impaired, creating arrhythmias and dysfunction and eventual failure.
How The CR Way
can help
The CR Way protects against age-related decline of the energy production capabilities of the mitochondria, while decreasing oxidative-stress damage to mitochondrial proteins.