Below is a correspondence between Dr. Cordain and Luke Milano regarding Innuit mummies and cardiovascular disease:
Luke Milano:
Hi Professor Cordain,
I listened to your interview with Jimmy Moore where you discussed the results of two Innuit mummies examined by the researcher from Pennsylvania. If I'm understanding you correctly, you acknowledge that high fat intake may have contributed to the arterial plaque but there was no evidence of heart attack. You stated that inflammation is necessary for rupture of the fibrous cap that precipitates the heart attack.
The whole subject of plaque, rupture, inflammation and saturated fat and their relationship to each other is a hot topic of discussion but no one that I know of has truly presented a thorough analysis. Perhaps this would present an opportunity for you to be the one to pull the proverbial sword out of the stone.
First point of clarification; damage to the endothelial lining is the start of the process. It is my understanding that inflammation is either necessary or is a key factor in this regard. Your interview was not specific as to what role inflammation played in initial damage to the endothelial lining. Secondly, those who oppose saturated fat consumption argue that it is the "flat" molecular structure of saturated fats that contribute to plaque formation, as these flat molecules lay down more easily to cover the damaged areas of the endothelial lining. (As opposed to unsaturated fats which have a "bent" or "kinky" molecular structure )
Then there is the issue of foam cells. It has been argued that macrophages consume the LDL along the endothelial lining. However macrophages do not have a built in governor to prevent them from overconsumption of LDL and once they are "maxed out" they become foam cells, and it is these foam cells that consitute the arterial plaque. Built into this process is calcium incorporated in the plaque representing 20% of the volume which brings about the "hardening" of the arteries. However it has been argued that the calcium content is functional and purposeful as it provides "structure" to the plaque and hence diminishs the chance of rupture.
But it has been argued that it is cholesterol that is the "spackle" so to speak that is used to repair damage to the endothelial lining. Cholesterol is delivered by the VLDL in the bloodstream ( more correctly cholesterol esters )
So these are the questions that need clarification. Is inflamation necessary for damage to the endothelial lining? WIll saturated fat ( flat molecule ), LDL or cholesterol cause damage to the endothelial lining merely by its presence in greater volume? What is the role of saturated fat ( flat molecule ) in relation to creation of cholesterol or LDL? It would seem that the "flat molecule" theory is a moot point as cholesterol and LDL have their own molecular makeup. Do foam cell cadavers, so to speak, create the spackle to repair the breaks in the endothelial lining and come to consitute the bulk of arterial plaque?
One example would be high blood pressure. The higher pressure creates friction along the sides of the blood vesseel ( endothelial lining ) and results in small breaks, fissures, etc. How are these breaks sealed? By flat moleculed saturated fat in the bloodstream? By LDL? By macrophage? Can repair be made without the macrophage forming foam cells? What is the role of calcium in this process? This is a topic worthy of discussion because proponents of chelation therapy argue that chelation can reduce the calcium content of plaque. Even if this is physiologically possible, reduction may have short term benefits to patients because it reduces plaque volume but is hazardous long term because greater chance of rupture is created from the calcium loss.
Granted, this email is convoluted. Almost by necessity, important initial questions in unexplored areas tend to be convoluted. But my questions address issues that have not been clearly and fully addressed by the scientific community. I have long admired your work and believe that you perhaps better than anyone else can bring clarity to these questions.