This page is not to address the reported negative effects of Saturated Fatty Acids (SFA), rather to focus on its beneficial effects. Refer to this page regarding its supposed negative effects, and also this meta-analysis.
Fat, and particularly SFA has been vilified because it raises cholesterol. And purely on that basis, it has been deemed bad with the need to reduce our intake. More and more research is coming out that shows cholesterol has very little, if anything, to do with atherosclerosis. Yet SFA specifically still has a bad name. Below are some elements that show why this should not be the case or at least put a more nuanced view of its role in the body.
But first of all a truly negative point in general. Fats, and by that also SFAs, preferably should not be taken together with carbohydrates. Carbohydrates trigger a higher insulin release. This of course depends greatly on the amount. The type itself also plays a role in the speed of glucose inflow. Fat may actually help to reduce the absorption rate but insulin needs to push that excess glucose out of the blood stream. Insulin also lowers lipolysis and increases fat absorption so the dietary fat is directed to the fat cells at a higher degree. So if weight is of any concern then these are preferably not combined.
On an LDL particle, triglycerides, phospholipids and cholesterol are densely packed together. The phospholipids allow oxygen to come in and out of the LDL package. The fatty acids of the triglycerides being polyunsaturates are prone to oxidize. If the fatty acids are made up of saturated fats then we have a much stabler situation so that the fatty acid can maintain its function. When a PUFA oxidizes, it allows for a cascade of events which also affect the cholesterol ester in the LDL package.
If you believe in the theory that cholesterol causes atherosclerosis then you should be aware that the triglycerides/HDL ratio is currently the best risk indicator. The lower the ratio, thus the higher your HDL compared to the triglycerides, the better. A low carb diet reduces the triglycerides but SFA specifically increases HDL.
Dave Feldman - Cholesterol Code
Dave Feldman is known for his experiments regarding his lipid panel and has figured out how energy distribution is a major component of the lipid-proteins that carry around the fatty acids and other ‘cargo’ as he calls it.
To support the evidence that LDL is there to help distribute fat (and other raw material) to cells for energy, the research below shows how LDL levels increase during fasting.
CETP is interesting in that it helps with the transport of fatty acids from adipocytes on HDL towards VLDL and further on towards LDL. This happens depending on the level of expression of CETP and it increases in the case of starvation but also in case of dietary SFA intake. At the same time, the liver down-regulates LDL receptors. So it is protecting the energy from going out. The liver does recycle and excrete excess cholesterol by taking in LDL and HDL but it stops doing this under situations where more energy is needed/available.
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.335.2888&rep=rep1&type=pdf
Once you know how the system works, it is no wonder that carbs lower LDL. With an increase in insulin, fat release is lowered and this in turn also lowers LDL due to lower output from the adipocytes.
SFA yields the highest energy, followed by mono-unsaturated and trailed by poly-unsaturated.
Dr. Michael Eades explains it here as SFA driving the reverse electron transport (RET) which increases satiety, increased energy expenditure and spares glucose. Note that this is still a hypothesis.
This article shows the effect of replacing 5% carbs with SFA. We see the same fasting glucose levels yet a reduction in insulin.
Granted this is a study on mice but the mechanism is there. As the amount of SFA increases, the level of alcoholic liver disease goes down. However, there are 2 variables that changed here. One is the increase in SFA (SFA) and the other is a reduction in poly-unsaturated fat (PUFA). It is also likely that the reduction in PUFA caused a lower incidence rather than SFA having a protective effect or maybe both effects are at play. In any case, the least you can say is that SFA is neutral.
With the following research, there was no replacement of PUFA, rather SFA was added on top of the alcohol administered. This test provides evidence that SFA regulates the gene expression in the liver which causes the liver to produce less damaging PUFA when processing the alcohol. It is not clear what the end product of the ethanol is in this case but SFA actively regulating a reduction in PUFA is not neutral.
“Fatty acid profiling demonstrated that alcohol feeding dramatically increased hepatic unsaturated long chain fatty acyl species, particularly linoleic acid and oleic acid, which was attenuated by dietary MCT”
Saturated fats form the least toxic byproducts when used for cooking.
Acrolein formation, one of the lowest
What they are not mentioning… In this article they include coconut oil and olive oil but in the results these are left out. Is that because they contained undetectable levels? It is not mentioned by the authors so we can only speculate.
The next article discusses cooking with vegetable oils of which the results are obtained due to their instability. Saturated fat, being very stable, protects from or greatly reduces these effects.
Causes mitochondrial fusion Increases fatty acid beta-oxidation
Adiponectin is increased on both low and higher doses tested, compared to other fatty acids, stimulating energy metabolism. Resistin is also high in all doses helping to circulate the fatty acids for energy. This brings the results in line with the increase in energy from animal fats.