Connective tissue ruptures are important -and probably the first major event – in phenomena as diverse as both atherosclerosis and the formation of hemorrhoids.
Both phenomena are seriously misunderstood. Hemorrhoids are not swollen and distended veins; they are swollen and distended vascularized rectal tissue that has suffered an underlying connective tissue rupture, and excessive pushing during defecation does not cause this, but does contribute to the likelihood of externalizing hemorrhoids.
When structural abnormalities are already present in connective tissue anywhere in the body, less inflammation is necessary to stress the tissue beyond the breaking point, beyond the point of rupture. Ruptures are not easily repaired and not quickly reparable. Ruptures in coronary arteries are quickly plugged by a life-saving glue of which cholesterol is a major component (cholesterol acting as a life-saving substances, while being blamed for taking away life by seriously confused scientists), while those in the rectum are not.
When few or no structural abnormalities are present in the underlying connective tissue, more inflammation is required for rupture.
Driven by excesses of net inflammatory substances and deficiencies of net anti-inflammatory substances, local inflammation is only as strong as the body’s local defenses allow it to be. It is no omnipotent force as so many scientists envision.
Structural abnormalities have many sources, including both excesses of net harmful substances and deficiencies of net beneficial substances. One of the sources of structural abnormalities is a LOCAL deficiency of one or more nutrients, whether essential or not.
Whenever excesses and deficiencies that contribute to localized structural abnormalities are LOCAL, one does not expect that people who suffer from hemorrhoids are any more likely to suffer from atherosclerosis than people who enjoy their entire lives hemorrhoid-free.
When excesses and deficiencies are system-wide, the two types of rupture could in fact be correlated. For example, a genetic defect in a particular collagen or elastin gene whose protein is a key player in both types of connective tissue, or a chronic and serious vitamin C deficiency, which would perturb collagen structure body-wide.