Palmitic acid - coconut oil

[zkt]

Dayspring, I think it was, considers palmitic acid as atherogenic.
Not sure if this is a remmnant of conventional wisdom or what.
Then I ran into this study. Probably worth looking into.

JCI - Palmitic acid mediates hypothalamic insulin resistance by altering PKC-? subcellular localization in rodents

 

[cvictorg]

Dayspring, I think it was, considers palmitic acid as atherogenic.
Not sure if this is a remmnant of conventional wisdom or what.
Then I ran into this study. Probably worth looking into.

JCI - Palmitic acid mediates hypothalamic insulin resistance by altering PKC-? subcellular localization in rodents

Palmitic acid enhances lectin-like oxidized ... [Atherosclerosis. 2010] - PubMed - NCBI
Abstract

OBJECTIVE:
Elevated levels of nonesterified fatty acids (NEFA) in obesity and type 2 diabetes may contribute to the development of atherosclerosis. Therefore, we examined whether NEFA could regulate expression of scavenger receptors responsible for uptake of oxidized LDL (oxLDL) in macrophages, a critical step in atherogenesis.

METHODS AND RESULTS:
Expression level of scavenger receptors in NEFA-treated macrophage-like THP-1 and Raw264.7 cells were analyzed by real-time PCR. Palmitic acid showed the greatest enhancement of expression of lectin-like oxidized LDL receptor (LOX-1) among 7 NEFA examined (4 saturated and 3 unsaturated fatty acids). Upregulation of LOX-1 was selective as increases in expression level of other scavenger receptors (CD36, SR-AI, SR-BI, and CD68) were not observed. Western blotting analysis indicated that upregulation of LOX-1 also occurred at the protein level. Uptake of oxLDL by Raw264.7 cells was promoted by palmitic acid, and the enhanced uptake was abrogated when the cells were transfected with siRNA against LOX-1. Downregulation of Toll-like receptor (TLR) 2, TLR4, or IRAK4 with siRNA did not prevent LOX-1 upregulation, whereas inhibitors of p38 MAPK (p38) and reactive oxygen species (ROS) signal inhibited the upregulation of LOX-1 induced by palmitic acid.

CONCLUSIONS:
These results suggest that elevated level of palmitic acid may contribute to development of atherosclerosis through enhanced uptake of oxLDL via upregulation of LOX-1 in macrophages. The effects of palmitic acid may be mediated by ROS-p38 pathway rather than TLRs.

Loren Cordain – Caution: Saturated Fats – Disaster with Grains | Me and My Diabetes

http://paleohacks.com/questions/56875/sat-fat-ldl-receptor-oops#axzz1uyyyAaeU

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.

http://www.ajcn.org/content/73/2/198.full.pdf
Effect of 6 dietary fatty acids on the postprandial lipid profile, plasma fatty acids, lipoprotein lipase, and cholesterol ester transfer activities in healthy young men

http://apjcn.nhri.org.tw/server/apjcn/Volume11/vol11sup5/S433.pdf
Red palm oil in experimental atherosclerosis

The following findings provided a rationale for examining the effects of RPO in experimental atherosclerosis. Palm oil (PO) has been stigmatised as a hypercholesterolaemic fat because of its palmitic acid (16:0) content, despite human studies that show it does not raise serum cholesterol levels. 13,14 We have shown that the presence of palmitic acid at the SN2 position of a triglyceride renders that triglyceride more atherogenic.15–17 Cottonseed oil contains 24% palmitic acid but only 2% is at the SN2 position. Randomisation of cottonseed oil increases the amount of 16:0 at the SN2 position to 8.3% and trebles the severity of atherosclerosis.15 Lard and tallow both contain 20–24% palmitic acid. In lard, virtually all of the 16:0 is at the SN2 position and it is 113% more atherogenic than tallow. Randomisation of lard reduces the amount of 16:0 at the SN2 position by about 67% and reduces atherogenicity by 51%. Randomization of tallow increases the amount of 16:0 at the SN2 position by 124% and increases atherogenicity by 10%16 (Table 3). A study of synthetic triglycerides17 showed that 1,3-palmitoyl-2- oleoylglycerol was 53% less atherogenic than 1,2-palmitoyl- 3-oleoylglycerol.17

 

[zkt]

I dont know about you but I find this to be a bit problematic.

 

[cvictorg]

I dont know about you but I find this to be a bit problematic.

Maybe we should rethink the use of coconut oil for cooking and use grass fed butter instead

Your thoughts

 

[LW64]

Look at the rodent diet data in Table 2.

40 percent calories as fat with 46 percent calories as carbs is hardly a high-fat diet, AFAIC. And it certainly isnt low carb.

In humans, when carbs are restricted, two things hapen simultaneously: the body makes less saturated fat and also burns more of it. So, if you want to reduce the levels of fatty acids in your blood, you restrict carbs and increase your fat intake.

Comparison of low fat and low carbohydrate diets on c... [Lipids. 2008] - PubMed - NCBI

Limited effect of dietary saturated fat on plasma sat... [Lipids. 2010] - PubMed - NCBI

http://www.ajcn.org/content/83/2/227.full (Effect of a low-fat diet on fatty acid composition in red cells, plasma phospholipids, and cholesterol esters: investigation of a biomarker of total fat intake)

http://jn.nutrition.org/content/131/2/231 (Total Fat Intake Modifies Plasma Fatty Acid Composition in Humans)

 

[ergomaniac]

Maybe we should rethink the use of coconut oil for cooking and use grass fed butter instead

Your thoughts

[ame=http://en.wikipedia.org/wiki/Butterfat]Butterfat - Wikipedia, the free encyclopedia[/ame] this says 31% palmitic. 24% oleic.
i like olive oil for light cooking. and olives.

 

[zkt]

Maybe we should rethink the use of coconut oil for cooking and use grass fed butter instead

Your thoughts

Doubtless we need to reexamine the SFA effects in terms of chain length. Just went thru https://thinksteroids.com/community/threads/134304435

We were on the subject of chain length toward the end of the thread and it fizzled out. There appears to be substantial evidence for the atherogenecity of C16;N0 (palmatic acid) which constitutes 8% of coconut oil and some 20% of my beloved bacon and sausage.
Where is all the studies find ing coconut oil benefical from about a year ago.?
Bet LW has a lot to say on the subject. Just got the radiology report on my reenal anmd carotid arteries. Will post the findings as soon as I compare the latest to the past 6 years

 

[LW64]

Say hello to Delta 9 Desaturase:

[ame=http://en.wikipedia.org/wiki/Fatty_acid_desaturase]Fatty acid desaturase - Wikipedia, the free encyclopedia[/ame]

"...also known as Stearoyl-CoA desaturase-1, is used to synthesize oleic acid, a monounsaturated, ubiquitous component of all cells in the human body. ?9desaturase produces oleic acid by desaturating stearic acid, a saturated fatty acid either synthesized in the body from palmitic acid or ingested directly."

And...

Oleate prevents palmitate-induced... [Biochem Biophys Res Commun. 2005] - PubMed - NCBI

"... Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis."

Different effects of oleate vs... [Am J Physiol Endocrinol Metab. 2010] - PubMed - NCBI

"..."Oleate alone did not cause mtROS generation and mtDNA damage, and its addition to palmitate prevented palmitate-induced mtDNA damage, increased total ATP levels and cell viability, and prevented palmitate-induced apoptosis and inhibition of insulin-stimulated Akt (Ser(473)) phosphorylation."

Enough there to make you stop worrying?

 

[ergomaniac]

 

[stephen85]

Palmitic acid is probably the most typical soaked fatty acids present in animals and vegetation. Palmitic acid is a main portion of the essential oil from palm trees (hand oil and hand kernel oil). Butter, dairy products, whole milk and meat additionally contain palmitic acid.

 

[zkt]

Althought your studies are indicative of harmlessness they arent conclusive and mostly point to the well known fact that the body synthesises FA into longer chains. I need to reanalyze the datawith an open mind. This might be the point where the immune system first comes into play.

 

[LW64]

Althought your studies are indicative of harmlessness they arent conclusive and mostly point to the well known fact that the body synthesises FA into longer chains. I need to reanalyze the datawith an open mind. This might be the point where the immune system first comes into play.

You've been using it for a while. Is there anything about your present condition - good or bad - that you believe you can attribute to it's inclusion in your diet?


If I was eating a diet that was 40% fat and 46% carb (with a good chunk of it coming from sugar), I'd practically expect it to be atherogenic.

 

[ergomaniac]

Say hello to Delta 9 Desaturase:

Fatty acid desaturase - Wikipedia, the free encyclopedia

"...also known as Stearoyl-CoA desaturase-1, is used to synthesize oleic acid, a monounsaturated, ubiquitous component of all cells in the human body. ?9desaturase produces oleic acid by desaturating stearic acid, a saturated fatty acid either synthesized in the body from palmitic acid or ingested directly."

And...

Oleate prevents palmitate-induced... [Biochem Biophys Res Commun. 2005] - PubMed - NCBI

"... Low concentrations of oleate (0.1mM) completely inhibited palmitate-induced oxidative stress, SAPK activation, and apoptosis."

Different effects of oleate vs... [Am J Physiol Endocrinol Metab. 2010] - PubMed - NCBI

"..."Oleate alone did not cause mtROS generation and mtDNA damage, and its addition to palmitate prevented palmitate-induced mtDNA damage, increased total ATP levels and cell viability, and prevented palmitate-induced apoptosis and inhibition of insulin-stimulated Akt (Ser(473)) phosphorylation."

Enough there to make you stop worrying?

You've been using it for a while. Is there anything about your present condition - good or bad - that you believe you can attribute to it's inclusion in your diet?


If I was eating a diet that was 40% fat and 46% carb (with a good chunk of it coming from sugar), I'd practically expect it to be atherogenic.

im curious as to why try to add sfas if they are converted into mufas anyway. and why i cant cook with olive oil but i can cook with bacon drippings and butter. both of which contain mufas. along with the fact that most animal fats contain both sfas and mufas. coconut oil has less palmitic acid than butter or dairy fat. forget heavy cream. and whose effects are nullified by oleate according to the above. coconut oil also has a good amount of mcts for easy ketones as well as [ame="http://en.wikipedia.org/wiki/Lauric_acid"]lauric acid[/ame] which has potential medicinal properties it says. along with a positve effect on the immune system. you can google that.

 

[ergomaniac]

Palmitic acid is probably the most typical soaked fatty acids present in animals and vegetation. Palmitic acid is a main portion of the essential oil from palm trees (hand oil and hand kernel oil). Butter, dairy products, whole milk and meat additionally contain palmitic acid.

saturated not soaked. essential oils are not essential fatty acids. coconut oil contains little essential fatty acids.

 

[ergomaniac]

lauric acid which has potential medicinal properties it says. along with a positve effect on the immune system. you can google that.

about half of the fatty acid content in coconut oil this says.

 

[zkt]

You've been using it for a while. Is there anything about your present condition - good or bad - that you believe you can attribute to it's inclusion in your diet?
If I was eating a diet that was 40% fat and 46% carb (with a good chunk of it coming from sugar), I'd practically expect it to be atherogenic.

I mwntioned earlier that I had the yearly bilateral renal and carotid ultrasound. Havent yet compared the current data to the past several years BUT looks like there was substantial increase in stenosis. BUT last year was also when I started titrating the GC down. Its difficult, if not impossible, to attribute cause and effect, if there even is an observable effect, when changing mlore than one variable at a time, especially in an N=1 study.
But mostly I want to understand the effects of diet on the issue of atherosclerosis to the extent that my education and dedication will attain. I am far from that goal. When someone of the caliber of Dayspring says that palmitic acid is atherogenic I am compelled to investigate the issue with an open mind even if it means reversing field but have no dietary changes in mind at this time.
The only ones who eat sugar here are the hummingbirds.

 

[cvictorg]

On my last blood test I took (blood was drawn on 3/27/12) the Fatty Acid Profile C:12-C:22 test from Quest Labs - the blood sample was sent to Mayo Medical Labs in Rochester MN for analysis

Palmitic Acid C16;0 Reference Range is 1480-3730 nmol/mL

My test level was 1365 nmol/mL - so it's L

Now if I'm consuming butter, frying eggs in coconut oil, etc why is it not higher?

 

[zkt]

On my last blood test I took (blood was drawn on 3/27/12) the Fatty Acid Profile C:12-C:22 test from Quest Labs - the blood sample was sent to Mayo Medical Labs in Rochester MN for analysis

Palmitic Acid C16;0 Reference Range is 1480-3730 nmol/mL

My test level was 1365 nmol/mL - so it's L

Now if I'm consuming butter, frying eggs in coconut oil, etc why is it not higher?

Good question. Might guess that it is being converted to oleate at a rapid rate.
Certainly appreciate you data.

 

[LW64]

Now if I'm consuming butter, frying eggs in coconut oil, etc why is it not higher?

That is what I would expect if you have a low carb intake.

I am NOT disputing that palmitic acid is atherogenic. Under the right circumstances, it is. What I am claiming is that an optimal dietary approach to preventing over-accumulation of palmitic acid in the bloodstream (and SFAs in general) is to restrict carbs and increase fat intake.

Dietary carbohydrate - NOT dietary SFA - is the main driver of plasma levels of SFA. This is in the results of the papers I quoted in my first post. Those studies report LOWER plasma levels of SFA in response to diets that have many times the intake of SFA than plasma levels in persons who ate a low-fat diet. One other study showed a distinct LACK of association between dietary SFA and plasma levels of SFA - in other words, you are not what you eat.

Sure, it's counter-intuitive, but there's that human metabolism again - you are what your metabolism does with what you eat. If you're eating a large fraction of your calories as digestible carbs - and it doesnt have to be sugar because any digestible carb will end up as glucose in your bloodstream anyway - it raises your insulin level and that promotes fatty acid synthesis - palmitic acid! Net result? Higher plasma SFA levels.

Eat a high fat, low carb diet and your metabolism reduces it production of SFAs (I dont think it's ever zero) AND goes after SFAs as a source of energy, further reducing their number. Net result? Lower plasma SFAs.

Saturated Fat. On your Plate or in your Blood?

"The bottom line is that distribution of types of fatty acid in plasma is more dependent on the level of carbohydrate then the level or type of fat. Volek and Forsythe give you a good reason to focus on the carbohydrate content of your diet. What about the type of carbohydrate? In other words, is glycemic index important? Is fructose as bad as they say? We will look at that in a future post in which I will conclude that no change in the type of carbohydrate will ever have the same kind of effect as replacing carbohydrate across the board with fat. I’ll prove it."

 

[zkt]

1. 
   Date RRA LRA RICA LICA
   3-2012 <60% >60% 50-59% <50%
   3-11 NSS >60 ----- ----
   9-10 ----- ------ 50-69 <50
   10-9 >60 <60 ~50 <50
   1-9 ~60 >60 ----- ----
   1-8 NSS >60 ----- =------
   11-6 ----- ------ <50 <50
   10-6 NSS >60 ----- ------
   5-6 NSS >60 <50 <50
   2-5 >60 NSS ----- -------
   1,2-5 bilateral renal artery stent
   9-3 thalamic stroke
   9-3 ----- ------ NSS NSS
   /LIST]
   RRA: right renal artery
   RICA: right internal carotid artery
   NSS: no sig stenosis
   
   High SFA low carb diet shows no evidence of progression nor regression of arterial stenosis.
   However have continued crestor since 2006.