The Paleo Diet - Loren Cordain [11]
Wild animal carcasses are lean, have little external fat, and exhibit virtually no fat between the muscles (marbling). In contrast, feedlot-produced cattle maintain a four- to six-inch layer of white fat covering the animal’s entire body. These artificial products of modern agriculture are overweight, obese, and sick. Their muscles are infiltrated with that fat that we call marbling, a trait that improves flavor but makes the cattle insulin resistant and in poor health, just like us. Wild animals rarely or never exhibit marbling.
Because feedlot-raised animals are exclusively fed grains (corn and sorghum) in the last half of their lives, their meat has high concentrations of omega 6 fatty acids at the expense of health-promoting omega 3 fatty acids. The meat of grain-fed livestock is vastly at odds with that of wild animals. Check out Appendix B in this book. A 100 gram (~ ¼4 lb.) serving of T-bone beefsteak gives you a walloping 9.1 grams of saturated fat, whereas a comparable piece of bison roast yields only 0.9 grams of saturated fat. You would have to eat ten times more bison meat to get a similar amount of saturated fat than the amount in a single serving of T-bone steak.
It would be difficult for our hunter-gatherer ancestors to eat anywhere near the amount of saturated fat that we get on a yearly basis in the typical Western diet. So, does dietary saturated fat promote heart disease? Should Paleo Dieters try to limit the fatty domesticated meats in their diet in order to reduce saturated fat? This question is not as clear-cut as it seemed twenty-five years ago, when Drs. Michael Brown and Joseph Goldstein of the University of Texas Southwest Medical Center were awarded the Nobel Prize in medicine for discovering that saturated fats down-regulated the LDL receptor. Their discovery and subsequent randomized, controlled human trials have unequivocally shown that certain saturated fats (lauric acid [12:0], myristic acid [14:0], and palmitic acid, [16:0]) but not all (stearic acid [18:0]), elevate blood cholesterol levels in humans, all other factors being equal. These facts are undeniable. Yet the next question is contentious and has divided the nutritional and medical community in recent years: do increased blood cholesterol levels necessarily predispose all people to an increased risk for cardiovascular disease?
As the scientific community has struggled with this question during the last few years, we should remember that the evolutionary template will almost always guide us to the correct answer. The clogging of arteries that eventually results in fatal heart attacks comes about through a process called atherosclerosis, in which plaque (cholesterol and calcium) builds up in the arteries that supply the heart itself with blood. It was originally thought that this buildup gradually narrowed and finally closed the arteries supplying the heart, thereby causing a heart attack. We now know that this model is inaccurate and too simple.
In the last ten to fifteen years, it has become apparent that inflammation is involved at every step of the way when arteries become clogged with plaque. In fact, the fatal event causing a heart attack is not the gradual narrowing of arteries supplying the heart but rather the rupturing of the fibrous cap that surrounds and walls off plaque that forms in the heart’s arteries. Chronic low-level inflammation triggers the fibrous cap to rupture, which in turn causes a clot to form in the arteries that supply the heart, resulting in a heart attack. Without chronic low-level inflammation, heart attacks probably would rarely or never occur.
So, do dietary saturated fats from fatty meats cause the artery-clogging process known as atherosclerosis? If we look at the evolutionary evidence, the answer is a resounding yes. Dr. Michael Zimmerman, a pathologist