I know saturated is great and I have no doubts about its greatness but I would love to know how it is metabolized by our bodies. Conventional Wisdom says it stays saturated and therefore "clogs our arteries", but when people use that as an argument against me I don't know how to respond. Would love to have some obvious "ammo" to rub into there face.
asked byrob_4 (1146)
Get FREE instant access to our Paleo For Beginners Guide & 15 FREE Recipes!
on March 03, 2011
at 06:07 PM
I think your question is about how saturated fats are metabolized into their building blocks, fatty acids. The best answer is that dietary levels of anything aren't as correlated with serum levels as you might think. So eating a lot of fat, after an adaptation period, doesn't mean high lipid levels. The same goes for eating a lot of sugar. The debate then hinges on what the adverse effects of the adaptation to that diet is.
What follows is a precis of the Wikipedia article. I'm running an experiment, but once it finishes, I'll supplement it with some of my biochemistry texts at home and edit for clarity. Meanwhile, I wanted to give a preliminary answer.
Saturated fat is broken down by digestion into fatty acids that are transported through the bloodstream and into cells. Once in cells, the fatty acid may be chewed up 2 carbon lengths at a time to provide acetyl-CoA, one of two required reactants for the Krebs cycle. The other, pyruvate, can come from either glycolysis or the combination of two molecules of acetyl-CoA. This is all inside the cell.
[From my recollection]
Outside the cell it was thought that saturated fat precipitated onto blood vessel walls because it was hydrophobic. Normally transport vehicles (lipoproteins) would handle it but if someone ate too much saturated fat, it would start to float around un-chauffered and glom onto things. No one believes this because saturated fat never floats around in the blood stream, only fatty acids which are polar enough not to precipitate under normal physiologic conditions. Now the idea is that saturated fat dysregulates (i.e. messes up) macrophages. Normally they help, among their other roles, repair daily blood vessel wall injuries that happen just due to movement. The problem is a high amount of saturated fat was thought to make the macrophages stay to long at the cite of a blood vessel wall tear thus exacerbating rather than stopping the normal inflammatory reaction. These macrophages, laden with fatty acids, came to be called foam cells. Indeed foam cells from plaques have a lot of saturated fat.
on March 05, 2011
at 01:51 AM
And this is specifically for mac389. You can search my posts on eicosanoids for more details since your seem to be that kinda guy. Here is a copy of one of the paragraphs there that specifically mentions where cardiac CRP comes into the equation from the eicosanoid pro inflammatory side of their receptor function.
The synthesis of arachidonate, much of the DGLA derived from ingested linoleic acid or GLA is diverted into membrane phospholipids due to the inefficiency of the Δ5-desaturase catalyzing the conversion of DGLA to arachidonic acid. Incorporation of DGLA into membrane phospholipids competes with the incorporation of arachidonate so that diets enriched in GLA result in an alteration in the ratio of membrane arachidonate to DGLA. Release of membrane DGLA occurs through the action of PLA2 just as for release of arachidonate. Once DGLA is released it will compete with arachidonate for COXs and LOXs. The products of COX action on DGLA are series-1 prostaglandins (PGE1) and thromboxanes (TXA1). These eicosanoids are structurally similar to the series-2 eicosanoids except, of course, they have a single double bond. Although structurally similar, the series-1 eicosanoids have distinctly different biological actions. And this is why there is a ton of confusion of what this class of fats does.......PGE1 and TXA1 are anti-inflammatory, they induce vasodilation, and they inhibit platelet aggregation. When DGLA is a substrate for 15-LOX the product is 15-hydroxyeicosatrienoic acid (15-HETrE). 15-HETrE is a potent inhibitor of 5-LOX which is the enzyme responsible for the conversion of arachidonic acid to LTB4. LTB4 is a potent inflammatory molecule through its action on neutrophils, thus, DGLA serves to inhibit inflammation via the linear eicosanoid pathway as well. The more omega 6 oils you eat with lineolic acid the more this favors this breakdown to the inflammatory eicosainoid production and hence a rise in your cardiac CRP in inflammation measurement.
on March 03, 2011
at 05:16 PM
Depends if there is pre existing inflammation......that is why getting a cardiac CRP when you start and vit D status is vital because without this info you really dont know if sat fat will hurt or help you. You also should in my view as a doc get your omega 6/3 ratios checked too because many of us believe that the omega 6 levels are critical and often more critical in the inflammatory cascade. If your Cardiac crp is below one I see no issues with saturated fats at all..........if they are not......yu need to focus on reducing your inflamamtion before you go pedal to the metal paleo......that is how I handle myself and my patients. Cardiac CRP is a direct measure of how leaky our mitochondria are.......the more leaky we are the sicker and more cancer we get and the more apoptosis our organs see due to aging and AGE's and ALE's.........The story is not as cut and dry as many in our paleo community seem to think. Once your healthy sat fat poses no issues. Infact stearic acid, which is saturated fat, actually lowers your cholesterol.