Now the difference from lowest to highest is not really that great, right? This is true and, furthermore, the amount of saturated fat in butter and coconut oil greatly exceeds that of safflower oil, so, if saturated fat were a big driver of cholesterol, you would expect a much greater difference. This is the point of the authors I mentioned above: saturated fat should not be demonized, because it simply does not change cholesterol that much even in very large quantities. Now I respectfully disagree with that – remember I’m all about maximizing erectile strength – and I’ll discuss why below. But, for now, I concede the point that saturated fat does not make a massive difference in most of the typical, high cholesterol Americans out there.
Before we leave this study, let’s look at the numbers that really count: LDL. LDL is the “bad cholesterol” and both small and large particles can lead to arteriosclerosis. So let’s look at what happened in the above study to LDL levels:
- Butter: 4.5 mmol/l = 174 mg/dl
- Coconut Oil: 4.2 mmol/l = 162 mg/dl
- Safflower Oil: 3.9 mmol/l = 150 mg/dl
In this case, the type of oil used makes a bit more of a difference – 16% from lowest to highest. And please keep reading: I make an important point regarding LDL below.
NOTE: Yes, I know that coconut oil has some great properties. For example, did you know that, while coconut oil will raise LDL some, it bumps by HDL more proportionately according to some research?  The reason is that it is a rich source of lauric acid. In fact, some very heart healthy cultures based their diet off of coconut oil and fish. See my page on The Diet of the Tokeluau and Pukapuka. There is also an older study that shows that beef fat does not have nearly the negative impact on lipids as one might think.  All I can say, though, is please keep reading.
2. Normal Cholesterol. There was a theory that a certain genotype (E4 or APOE4) responded much more strongly to saturated fat than the general population. One study looked at all the different genetic variations in those with normal cholesterol levels and came to this conclusion: 
“Relative to the average American diet, both the Step 1 and Low-Sat diets significantly reduced total cholesterol, LDL cholesterol, and HDL cholesterol in all three apoE genotype groups. No evidence of a significant diet by genotype interaction, however, could be identified for any of the measured lipid and lipoprotein end points.”
Basically, this study showed that that everyone (with normal cholesterol) responds to saturated fat.
3. Mildly High Cholesterol. Another study a year later again looked at these same genotypes, but this time in those with “mildly high cholesterol.” What they found was somewhat similar: all genotypes were responsive but the most responsive was the Apo E4 group.  What they did was create a diet with about half of the saturated fat of the original diet and it dropped total cholesterol and LDL levels about 15% and 9%, respectively in the E4 group. Again, other groups dropped but not as much.
So the bottom line is that there is lots of evidence that reducing saturated fat will reduce your cholesterol levels, but the magnitude of the reduction may be determined by your genotype. The above experts are right in the sense that much of the population does not experience a huge drop.
However, their emphasis of this point I think is a huge mistake. First of all, those with the E4 genotype are probably put at risk. But the other point is this: those of us on Low Fat Diets realize that lowering BOTH saturated and total fat will usually dramatically lower total cholesterol and LDL. The Tarahumara Indians – arguably the healthiest culture on planet earth – have cholesterol levels below 130. My last reading was also below 130. And the solid majority of people that go on a Low Fat Diet can get their cholesterol below 150.
NOTE: Some studies show that dropping total fat does just as much to lower cholesterol as lowering saturated fat. 
So, in my opinion, these health writers are implying that you can’t really significantly lower your total cholesterol. Well, this just simply is not the case and, again, it is common knowledge in the Low Fat community that cholesterol can be lowered easily and quickly. And, by the way, it’s not just by reducing fat in the diet that cholesterol can be lowered: many foods do the same as does losing weight. (You’ll lose about a point in cholesterol for every pound you lose.) You don’t have to blame bad genetics on your high cholesterol: it’s almost always possible to get it down into a safe zone with just lifestyle changes.
Now on this page I am not going to get into the cholesterol controversy. I’ve written about that on other pages. And, to be honest, I don’t think total cholesterol matters that much anyway. The number that really counts is LDL, or the “bad” cholesterol. If you care about keeping your arteries clean and clear, then you should care about LDL. All the researchers and clinicians that I know of that regress plaque and reverse heart disease pay attention to LDL. See my page on LDL Thresholds to Arrest or Reverse Heart Disease.
Wonder why the American Diet kills your arteries very slowly over decades and not months? Well, the studies above show that high saturated fat tweaks up your LDL just enough to help contribute to arterial plaque buildup but very slowly. Pretty insidious, eh? Almost diabolical some would say. Instead of killing you overnight, saturated fat may be a factor (along with inflammation) that kills you very gently and slowly – molecule by molecule. The typical pattern is that the penile arteries fill up with plaque first, because they are smaller, and the cardiac and neck arteries follow about five years later, leading to a major event like heart attack, stroke or angina. See my page on the The Dangers of Erectile Dysfunction for the research in this regard.
REBUTTAL? Yes, there are a couple of large epidemiological studies that show that saturated fat really doesn’t matter. And this is more or less what one would expect based on the above cholesterol/LDL numbers. Of course, there are many factors that contribute to arteriosclerosis and arterial hardening of the arteries, but the biggest is LDL and saturated fat has a pretty small impact in that area. However, I don’t drink decaffeinated coffee either. Decaff coffee actually increases LDL a little – very similar to saturated fat – for reasons that are poorly understood. I play it safe and avoid decaff coffee, though, as I don’t need that extra boost to my LDL.
And, if you don’t think total cholesterol matters, I’d ask you to consider the APOE4 genetic group that I mentioned above. Their skewed lipid profiles put them at risk for “atherosclerosis, Alzheimer’s disease, impaired cognitive function, reduced hippocampal volume, HIV, faster disease progression in multiple sclerosis, unfavorable outcome after traumatic brain injury, ischemic cerebrovascular disease, sleep apnea, accelerated telomere shortening and reduced neurite outgrowth.”  The lesson to be learned is that it does not pay to ignore your LDL numbers.
And there are other reason to be cautious about satured fat as well:
- Saturated fat lowers nitric oxide and I’m all about nitric oxide.
- Almost all wild game does not have much saturated fat
- Modern indistrial meats are only loaded with saturated fat because of unnatural, artificial livestock practices.
- A little saturated fat can help with Vitamin E digestion. But the truth is that humans need only small amounts of saturated fat. (Some experts believe we do not need any saturated fat.)
- Only body manufactures all the cholesterol that we need. We need do not need high saturated fat industrial meats to “help” us out.
NOTE: To be clear, if you’ve read my page on Low Fat Meats, then you know that I have no issue with a range fed, humanely treated animals sources of protein.
1) J of Lipid Res, Aug 1995, 36:1787-1795, “Effects of coconut oil, butter, and safflower oil on lipids and lipoproteins in persons with moderately elevated cholesterol levels”
3) Am J Clin Nutr, 2003 May, 77(5):1146-55, “Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials”
4) Am J Clin Nutr, Aug 1985, 42(2):190-197, “Plasma lipid and lipoprotein response of humans to beef fat, coconut oil and safflower oil”
5) Arterioscler Thromb Vasc Biol, 1997 Nov, 17(11):2914-23, “ApoE genotype does not predict lipid response to changes in dietary saturated fatty acids in a heterogeneous normolipidemic population. The DELTA Research Group. Dietary Effects on Lipoproteins and Thrombogenic Activity”
6) Am J Clin Nutr, 1998, 68:1215 22, “Effect of apolipoprotein E polymorphism on serum lipid response to the separate modification of dietary fat and dietary cholesterol”
8) Br Med J. Mar 2, 1963, 1(5330):571 576, “Diet and Plasma Cholesterol in 99 Bank Men”