The human body operates at about 95-100 degrees F. Notice that the saturated fats don't melt--i.e. become liquid--until you reach more than 110 degrees.
The unsaturated fats all remain liquid at temperatures well below human body temperature.
Fats travel in the body packed in triglycerides: three fatty acids bound to a glycerol backbone. The following depicts a triglyceride composed of three saturated fatty acids:
If you substitute a polyunsaturated fatty acid for one or more of those fats, the triglyceride will form weaker bonds to others. Also, if you use shorter chain saturated fats (e.g. coconut oil), there are fewer hydrogens available for binding, lowering the melting point of the fat.
Most dietary and endogenously produced triglycerides are like the second example, a mix of fatty acids, some saturated and some unsaturated. Nevertheless, the higher the number of saturated fatty acids in a mix of triglycerides, the higher its melting point. Thus, beef tallow, a mix primarily of long-chain saturated and monounsaturated fats, has a higher melting point than coconut fat, a mix of primarily medium and short chain fats, and both of these have a higher melting point than flax oil, in which the triglycerides consist primarily of polyunsaturated fats.
This is really obvious in our experience. Beef triglycerides are solid at room temp, and start to melt around 100 degrees. Coconut triglycerides melt at about 75 degrees, and fish and flax triglycerides stay fluid even at temperatures below freezing. This means beef triglycerides are more viscous/less fluid at body temperature than flax triglycerides.
Similarly, compare the texture of cold raw beef to cold raw salmon. The former is stiffer, in part because the fats in beef are more solid at refrigerator temperature than are the fats in salmon.
Nature also distributes the fats differently. Warm blooded animals and plants living in warm enviroments tend to have higher proportions of the saturated fats with higher melting points, e.g. beef and palm oils. Cold blooded animals and plants and animals originating in cold environments tend to have higher proportions of unsaturated fats with low melting points, e.g. reptiles, salmon, and flax. If salmon had a high proportion of saturated fats in their tissues, their bodies (muscles) would not be fluid enough to swim in Arctic oceans. If flax plants produced saturated fats, they would not be fluid enough to transport about the flax plant in the native environment.
The body uses different types of fatty acids specifically implementing their abilities to form more or less solid structures. For instance, the fat pads of the palms and feet have a high proportion of saturated fats, because this makes a more firm, noncompliant structure for padding. On the other hand, nerve membranes have a high proportion of highly unsaturated fats (specifically, arachidonic acid and DHA), presumably because these membranes must have a less firm structure in order to serve their purposes, which involve rapid fluctuations in sodium and potassium flow across the membranes.
These examples show that the melting points of fats (triglycerides) are very important in biological functions, and that nature naturally favors the use of unsaturated fats to keep things fluid and flexible, and the saturated fats to make things more stiff and noncompliant.
Taking a look at how nature uses these fats for differential effects, we might predict that these fats will have different effects on blood flow. increasing the amount of saturated fats in the triglycerides in mammalian blood stream will increase blood viscosity, which would impede flow of blood through the tiniest capillaries, impair delivery of oxygen and nutrients to and removal of wastes from the tissues (thus promoting ischemia and toxicity), and increase blood pressure. Since oils in general are viscous compared to water, it also predicts that reducing total fat, or replacing high-melting-point fats with low-melting-point fats, would have the opposite effects.
Tai et al fed rats diets supplying either 10% of energy as soyabean oil (control group) or 40 % energy from soyabean oil (USFA), palm oil (SFA) and vegetable shortening (TFA) for 8 weeks. They found: "rats fed high-fat diets exhibited significant increases in serum TAG levels (P < 0.01), plasma viscosity (P < 0.01), whole blood viscosity (P < 0.01) and internal viscosity (P < 0.01) compared to the controls."
Hall reviewed the available data and reported that although good-quality intervention data on dietary fatty acid composition and vascular function are scarce, so far what we have indicates the following:
1) A single high-fat meal can impair endothelial function compared to a low-fat meal, apparently due to increased circulating lipoproteins and nonesterified fatty acids which may induce pro-inflammatory pathways and increase oxidative stress.
2) Cross-sectional data suggest that saturated fat adversely affects vascular function whereas polyunsaturated fat (mainly linoleic acid (18 : 2n-6) and n-3 PUFA) are beneficial.
3) The superunsaturated, very low-melting-point fats EPA (20 : 5n-3) and DHA (22 : 6n-3) can reduce blood pressure, improve arterial compliance in type 2 diabetics and dyslipidaemics, and augment endothelium-dependent vasodilation.
Steer et al performed another human study. Saturated fatty acids impaired endothelial function, and alpha-linolenic acid (omega-3) improved endothelial function.
These findings alone might help explain why the Masai have atherosclerosis. The dairy-based Masai diet would increase blood viscosity, impair blood circulation, and induce vascular tissue ischemia, oxidative stress, and inflammation, compared to a lower fat diet.
As noted by Stephan, Mann et al tried to blame the atherosclerosis of the Masai on foods other than dairy fats, based on the fact that the disease appeared prevalent only in Masai after the age of 40 years, after the Muran period during which they lived almost exclusively on dairy products. Mann et al believed that some noxious agent introduced after the Muran period had to account for the atherosclerosis:
"We believe... that the Muran escapes some noxious dietary agent for a time. Obviously, this is neither animal fat nor cholesterol. The old and the young Masai do have access to such processed staples as flour, sugar, confections and shortenings through the Indian dukas scattered about Masailand. These foods could carry the hypothetical agent."
This line of reasoning has a major flaw: Simply, if flour, sugar, etc are the cause of the atherosclerosis, and both young and old Masai eat these things, then it should appear in both the young and the old Masai...both before and after the dairy period. But in fact, their own data, in the chart below, shows it substantially increasing in frequency only after their long period of a high fat dairy based diet.
If those non-dairy foods were the cause of Masai aortic fibrosis, and those foods were eaten by both young and old, but not those in the 20-40 age group, then the frequency of fibrosis should be high both before the Muran period (ages 10-20) and after (ages 40+). But in fact the frequency is substantially elevated only after the Muran period.
The data actually suggests four possibilities that occur to me: Either 1) aortic fibrosis is simply a fact of life for Masai after the age of 40, due to some aging factor, or 2) it is the 20 years of eating a high dairy fat diet that eventually causes the atherosclerosis to develop, or 3) the late life combination of dairy fats and flour etc. promotes atherosclerosis, or 4) there is some dietary factor other than the flour, etc. that promotes atherosclerosis in the aging Masai.
Given what we know about the effect of saturated fats on the viscosity of blood and endothelial function, I feel inclined to consider their high dairy fat diet a contributor to their atherosclerosis. The fact that the frequency of fibrosis in the young Masai (under 20 years of age) is practically the same as that of the Masai during the late Muran period (30-40 years of age) argues against non-dairy foods contributing to the process. I feel, at this time, more inclined to view their atherosclerosis as the result of 20 years of their vascular systems having to respond to high fat meals.
Song et al found that "rats on a diet rich in either saturated or unsaturated fat had higher blood pressure compared with chow-fed rats (approximately 130 vs 100 mmHg, respectively), along with hyperlipidaemia and insulin resistance." Repeat: High fat diets induced high blood pressure in rats, regardless of whether the diet was high saturated or high unsaturated fat.
Only a rat study?
Let's compare two human primitive populations, one with a long history of a high unsaturated fat diet--Eskimos--and one with a low fat, high carbohydrate diet--Yanomamo.
Andersen et al found elevated blood pressure but without modernized risk of ischemic heart disease in non-Westernized Inuit past the age of 40:
"Among the 812 Inuit aged 18 years or above blood pressure was unaltered until the age of 39 years (systolic, p=76; diastolic, p=0.36) and increased subsequently (both, p=0.001). Systolic blood pressure ≥140mmHg was more frequent when aged >40years (p=0.001) and diastolic blood pressure ≥90mmHg was more common in men (p=0.001) and in men and women aged ≥40years (p=0.001)."In contrast, Yanamamo natives of Brazil demonstrated no age-related increase in blood pressure. Yanomamo live largely on plantains, sweet potatoes, manioc, and various fruits, supplemented by insects, grubs, and hunted meat. The Inuit have a much higher intake of omega-3 fats, and a much higher total fat intake. These findings support the idea that chronic high fat intake promotes age-related elevations in blood pressure, even if a large portion of the fat consists of omega-3 fatty acids, even absent Western foods, and even if your ancestors have been eating an Inuit diet for more than ten thousand years.
"Blood pressure rose only after the age of 40 years in pre-western Inuit. Left ventricular hypertrophy peaked among 30-year olds and was independent of elevated blood pressure. It may be speculated that the common left ventricular hypertrophy was due to marked physical activity that contributed to the low occurrence of ischemic heart disease among pre-western Inuit."
As I have said before, we have no reason to believe that all primitive diets had the same health effects. The differences in blood pressure between Yanamamo and Inuit clearly provide evidence that different primitive diets have different health effects. By the way, the study of the Yanomamo was conducted in 1989 as part of the Intersalt project, while the study of the Inuit was conducted in 1962-1964. Both of these populations had exposure to Western civilization, the Yanomamos for 25 more years than the Inuit. The investigators of the Inuit blood pressure were satisfied that the Inuit they studied were not Westernized. Yanomamo in fact have the high carbohydrate diet that introduction of sugar, flour, etc would induce. I would find any attempt to blame the elevated blood pressure of Inuit on carbohydrates in the diet unconvincing.
Kjaergarrd et al also report that found electrocardiograms indicating coronary ischemia in 5.5% of non-westernized Inuit. It is a low rate compared to modern populations, but indicates that isolated Inuit were not totally immune to ischemic coronary disease.
By the way, Masai appear to have a special adaptation to dietary cholesterol not present in Caucasians. According to Taylor and Ho, controlled studies on the Masai show that they "have a much larger capacity for intestinal cholesterol absorption than whites and a greater ability to suppress endogenous cholesterol synthesis, averaging 50.5%, for compensation of their intestinal absorption of dietary cholesterol. This efficient feedback control is the only homeostatic mechanism that protects the Masai from developing hypercholesteremia." In other words, if you aren't of Masai descent, your high-dairy diet mileage may vary.