Thanks, Joseph.

For instance, regarding diet sodas:

“In the typical western diet refined sugars comprise 16-18% of the total daily energy. Clearly, there are numerous health problems associated with this enormous intake of empty calories. However, for many people it is difficult to make sudden behavioral changes, particularly when it comes to comfort foods, such as highly sugared processed foods (ice cream, cake, cookies, candy etc). Although fruits would be a much better choice for taming the sweet tooth, diet sodas can help people to make this transition. We never have suggested that diet sodas were part of pre-agricultural diets…”

I believe this means that to put an american (I’m from Europe, and our diet is not as uggly as the american diet, which is the worst diet on the planet) on a clean 100% paleo may be hard, just like it is hard to get a drug addict to quit cold turkey. So, sodas are a transition, nothing else.

Regarding low fat meats, you have to understand that domesticated meats have nothing to do with wild meats

http://www.thepaleodiet.com/articles/Final%20Fatty%20Acid%20PDF.pdf

http://www.thepaleodiet.com/articles/Meat%20Paradox%20Final.pdf

And here are Cordain’s statements:
What would you say to people who disagree with your assertion that saturated fats cause heart disease?

First off, let’s get the record straight. I have never said that saturated fats are the sole dietary cause of “heart disease.” Coronary heart disease (CHD) consists of myocardial infarctions (heart attacks) and angina pectoris and accounts for 54% of the deaths from a larger category of heart and blood vessel illnesses called cardiovascular disease (CVD) which accounts for 40.6% of all deaths in the U.S. CVD not only includes CHD, but also stroke, congestive heart failure, hypertension, rheumatic heart disease, congenital cardiovascular defects, artery diseases and others. The physiological mechanism underlying CHD is atherosclerosis, a complex process involving interactions among environmental factors (both nutritional and non-nutritional) and the genome. Environmental factors such as exercise, smoking, and inflammation clearly influence the development and progression of atherosclerosis. Numerous nutritional factors can serve to either (1) promote or (2) inhibit atherosclerosis via modulation of one or more of the steps involved in the atherosclerotic process.

Dietary saturated fats are nutritional elements that may promote atherosclerosis. As consumption of certain saturated fatty acids (12:0, 14:0, 16:0, but not 18:0) increases, the number of hepatic (liver) and peripheral low-density lipoprotein (LDL) receptors decreases which in turn causes serum concentrations of LDL cholesterol to rise (a process called down regulation). Down regulation occurs because internalization of 12:0, 14:0 and 16:0 within cells reduces the expression of genes which code for the LDL receptor protein. At low blood LDL cholesterol concentrations (20-50 mg/dl), LDL cholesterol molecules move freely in and out of the arterial intima (the portion of the artery where atherosclerosis arises). When blood levels of LDL cholesterol molecules rise, LDL molecules tend to become “stuck” in the intima where they undergo oxidation and glycation to become “modified LDL.” Modified LDL stimulates arterial endothelial cells to display adhesion molecules which latch onto circulating monocytes and T cells. The endothelial cells then secrete chemokines which bring the monocytes and T cells into the intima where they mature into macrophages. T cells release cytokines causing inflammation and cell division within the artery. The macrophages are different from all other cells in the body in that they display a scavenger receptor which is not down regulated by LDL cholesterol molecules. The macrophages “feast” upon modified LDL cholesterol in the intima and become filled with these fatty droplets and become foam cells. Cytokines cause smooth muscle cells to grow over the lipid core of multiple foam cells forming a tough fibrous cap which becomes the characteristic plaque which defines atherosclerosis. Finally, inflammatory cytokines secreted by foam cells weaken the fibrous cap by digesting the collagen matrix. If the weakened cap ruptures, a substance secreted by the foam cells called “tissue factor” interacts with clot promoting elements in the blood causing a thrombus (clot) to form. If the clot is large enough to halt blood flow, it causes a myocardial infarction (heart attack).

Dietary saturated fats do not always elevate blood LDL concentrations. When consumed under hypocaloric (reduced energy) conditions they may improve most blood lipid parameters including total and LDL cholesterol, HDL cholesterol, and total triacylglycerol (TG). This phenomenon typically explains why Atkins-like diets (such as recently reported this spring in the New England Journal of Medicine) may be as or more effective than hypocaloric, low-fat, high-carbohydrate diets. However, under isocaloric (normal energy) conditions, studies of healthy normal subjects show increased consumption of saturated fats significantly raises blood LDL concentrations.

A further confounding factor in this scenario is the presence of a specific type of LDL cholesterol molecule in the blood called “small dense LDL.” The rate of influx of LDL into the intima is not only related to the blood concentration of LDL cholesterol, but also to the size of the LDL molecule. Small dense LDL have a greater flux into the intima than normal LDL and they are more likely to get “stuck” in the intima because of increase binding to proteoglycans. The primary metabolic source of small dense LDL is very low density lipoprotein molecules (VLDL) whose blood concentration is greatly influenced by dietary carbohydrate, particularly high-glycemic-load carbohydrates. Hence foods with high glycemic loads such as those made with refined sugars and grains may also operate synergistically with high dietary saturated fats to promote atherosclerosis. Additionally, high-glycemic-load carbohydrates are positively correlated with plasma concentrations of C reactive protein, an important marker for systemic inflammation, a key element of the atherosclerotic process, as I previously noted.

The gold standard procedure for demonstrating cause and effect between diet and disease is called a dietary intervention. Subjects are either fed or not fed a certain food or nutrient and then either presence or absence of a disease or disease symptom is monitored over time. With CHD, the results of dietary interventions in which saturated fats have been lowered, frequently have been unable to demonstrate a reduced mortality from CHD. The problem with the majority of these studies is that they were conducted prior to the knowledge that high-glycemic-load carbohydrates were an important promoting factor in CHD etiology. Further, most of these studies did not control for inhibitory dietary factors such as omega-3 fatty acids, fiber, phytochemicals, antioxidants etc. Hence, the interpretation of whether or not dietary saturated fats cause CHD in these interventions is confounded by a number of crucial variables. In animal studies, including primates, these confounding dietary factors can be completely controlled and atherosclerosis is routinely induced by solely feeding high amounts of saturated fats.

To what extent do you think the level of small-dense LDL cholesterol explains the “badness” of LDL? This is relevant to The Paleo Diet because small-dense LDL is strongly correlated with triglycerides. On some conceptions of The Paleo Diet, a more Atkins-like approach is taken: liberal saturated fat, very low carb. The result is often somewhat elevated LDL, but very low triglycerides. The low triglycerides probably indicate low levels of small-dense particles in the LDL fraction. This is why the Eades are not concerned about increases in LDL on their plan (for example). What is your take on this?

Excellent point. We need more information to determine if very-low-carbohydrate, high-fat diets reduce small-dense LDL in all people or only in certain genetically predisposed people ala the multiple studies done by Dreon et al. Further it will be necessary to determine whether or not the total increase in LDL (even with a concomitant decrease in small-dense LDL) still accelerates the atherosclerotic process. It seems most likely that small-dense LDL is derived from triacylglycerols carried in the VLDL fraction, hence the possibility looms that a major determinant of atherosclerosis is the ratio of total LDL/small-dense LDL. To my mind, the evidence points to the notion that atherosclerosis results from many environmental factors including those dietary elements that simultaneously raise LDL (high-saturated-fat diets) and triacylglycerols (high-glycemic-load diets). Both of these dietary characteristics could not have been part of any Paleolithic diet.

“There is absolutely no doubt that hunter-gatherers favored the fattiest part of the animals they hunted and killed. As far back as 2.5 million years there is incredible fossil evidence from Africa showing this scenario to be true. Stone tool cut marks on the inner jawbone of antelope reveal that our ancient ancestors removed the tongue and almost certainly ate it. Other fossils show that Stone Age hunter-gatherers smashed open long bones and skulls of their prey and ate the contents. Not surprisingly, these organs are all relatively high in fat, but more importantly analyses from our laboratories showed the types of fats in tongue, brain, and marrow are healthful, unlike the high concentrations of saturated fats found in fatty domestic meats. Brain is extremely high in polyunsaturated fats including the health-promoting omega-3 fatty acids, whereas the dominant fat in tongue and marrow are the cholesterol lowering monounsaturated fats.

Since most of us would not savor the thought of eating brains, marrow, tongue, liver, or any other organ meat on a regular basis, a few 21st century modifications of the original Paleolithic diet are necessary to get the fatty acid balance “right.”

THis is why he recommends, for instance, olive oil, which, evidently, wasn’t part of the diet of our H/G ancestors, but, In Spain, where I live, is highly used.

Butter was not part of the diet of our Paleo ancestors, but many people who follow the “saturated fat is good and very healthy” approach also include it, so the arguments that he includes foods that are not Paleo doesn’t cut it.

As for eggs, if you eat the typical ones, your Omega 6/Omega 3 ratio will go through the roof.
If you choose eggs from wild chickens (who don’t feed on grains), the n6/n3 ratio will be around 2/1.
Also, it should be reminded that eggs may be involved in auto-immunity, so not everyone can eat them.

As so, the only dietary difference I can find is about saturated fat.

See the following interview, which is very interesting:

http://hoe.kgnu.net/hoeradioshow.php?show_id=331

Of course, Mark does a great job pointing out that stress management, proper exercise and sleep are very important.

Don’t get me wrong, I think Mark’s perspective is a great one and he is a living proof that he’s right, but after reading Cordain’s papers on grains and auto-immunnity, I decided to follow his guidelines and my RA is in remission, and I intend to pursue my studies in Immunology to study dietary antigens in RA, so I have read everything the guy has published (not his laypersons articles, but his scientific ones) and I encourage everyone to read his great scientific papers, who, by the way, are available for free at his website (who else does that???), and then make up their mind.

Merry Chritsmas to all of you and please do not think I’m atacking you, since I’m just defending someone who is being attacked on a very unfare way.

Joseph