Saturated Fats (SFA) Increase Glucose Oxidation While PUFA Decrease It

[Cirion]

This makes sense. I have read at least half a dozen success stories and the story is almost always the same (with slight variants)

-> Focus on increase temps/pulses.
-> Work on lowering dietary fat intake and replace with carbs. Go as low in PUFA in particular as possible to accelerate PUFA elimination
-> Once a lean body is achieved, and the person feels good (presumably PUFA depleted), SFA"s can be increased to a reasonable amount and not cause issues, and in fact improve metabolism further

So basically even if one mostly intakes SFA's, total fat intake should still be low, at least until PUFA is depleted. Makes sense

 

[cyclops]

I think the key difference is that this is a study for fat metabolism under stress. I mentioned this in my original post but maybe the message got lost or was unclear. When you eat fat in a meal and are not under stress then SFA gets oxidized (especially the SCFA and MCT portions of it) while PUFA gets stored. However, under stress and thus increased lipolysis it is PUFA that gets released since storage contains mostly PUFA and this is what causes the damage. So, until tissue stores are mostly SFA lipolysis should be kept as low as possible.
@Mauritio @rei @Cirion

And how do we lose body fat again? Specifically PUFA stores if we dont want them to get released?

 

[cyclops]

So basically even if one mostly intakes SFA's, total fat intake should still be low, at least until PUFA is depleted. Makes sense

Similar to my question above, what is the mechanism by which PUFA is safely depleted if not lipolysis?

 

[Hugh Johnson]

Also, what about the infamous randle cycle?

Does even PURE saturated fats activate the randle cycle? like hydrogenated coconut oil, MCT oil....

Randle cycle just means the cells move their fuel mix to less sugar and more fat. It's not a bad thing, in moderation, and as long as the cells are not forced to burn PUFA.

 

[Cirion]

Cyclops... good question... in for answers

my strategy for now is not to go ZERO fat but to eat almost 100% SFA's (MCT oil, coconut oil) for the fats I do intake, switching to hydrogenated coconut oil shortly and of course high sugar.

I think it's not realistic to go zero fat for most people. But I think it does make sense to go zero (or almost zero) PUFA. It's just that going zero PUFA is easy if all fat intake is also zero.

 

[TeaRex14]

Also, what about the infamous randle cycle?

Does even PURE saturated fats activate the randle cycle? like hydrogenated coconut oil, MCT oil....

I think it's to a "lesser" degree. I'm not sure where to find it, but Kyle Mamounis had a excellent paper on that. He did a talk at the ancestral health about CO2, fatty acid/glucose metabolism, and the randle cycle. Anecdotally, I also don't notice any weight gain on a high carb diet while eating fairly modest amounts of coconut oil. Butter will make me fat though.

 

[Wagner83]

Tyw repeatedly stated that pufas were preferentially burned compared to sfas which are stored, I seem to remember he was ridiculed for such claims. At the time his ideas were to be in slight calorific deficit and move a bit more to burn the pufas if he ate any.

 

[Hugh Johnson]

And how do we lose body fat again? Specifically PUFA stores if we dont want them to get released?

They get released all the time. You want them released slowly so that the liver can take them out safely. Fast release during stress is the problem.

 

[cyclops]

Fast release during stress is the problem.

And to be clear the main "stress" we are usually talking about here is just not eating right? Not having sugar to burn, so the body liberates fat stores?

 

[Cirion]

I think it's to a "lesser" degree. I'm not sure where to find it, but Kyle Mamounis had a excellent paper on that. He did a talk at the ancestral health about CO2, fatty acid/glucose metabolism, and the randle cycle. Anecdotally, I also don't notice any weight gain on a high carb diet while eating fairly modest amounts of coconut oil. Butter will make me fat though.

That's seemingly my experience as well. I went heavy on the fats from goat dairy, butter, cheese starting off but it made me, well, fat. I think part of the problem is that those other fats tend to add up in PUFA's. Even coconut oil has PUFAs though so that's why I wanna use hydrogenated coconut oil.

 

[Kartoffel]

I think the key difference is that this is a study for fat metabolism under stress. I mentioned this in my original post but maybe the message got lost or was unclear. When you eat fat in a meal and are not under stress then SFA gets oxidized (especially the SCFA and MCT portions of it) while PUFA gets stored. However, under stress and thus increased lipolysis it is PUFA that gets released since storage contains mostly PUFA and this is what causes the damage. So, until tissue stores are mostly SFA lipolysis should be kept as low as possible.
@Mauritio @rei @Cirion

But that seems not to be the case. Most fats in our adipose tissue are oleic acid, followed by variou saturated fatty acids, while PUFA are something between 10-25% depending on dietary intake. And there are animal studies suggesting that the body prefers to quickly oxidize linoleic acid (18:2) in particular while barely storing any. When you feed rats cocoa fat or olive oil for 8 weeks, they quickly store a lot of it as triglycerol in the muscle. On the other hand, safflower oil doesn't increase it, at all. Hence, at least muscle cells seem to prefer storing SFA while burning PUFA when activated/stressed.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302136/

 

[ecstatichamster]

I asked Dr. Peat about this a couple years ago.

Dr. Peat, you have said that PUFAs are stored in adipose tissue in the body, and that sat fat is preferentially burned. So burning off PUFAs to deplete excessive PUFAs takes a long time.

I can’t find any cites on this. Many cites say PUFAs are burned first.

Can you direct me? I will share your email with the raypeatforum so they can get the benefit too.
----

And Dr. Peat wrote:

There are more references in my newsletters, including some on fat composition changes with aging, but I don’t have them with me.

Are dietary saturated, monounsaturated, and polyunsaturated fatty acids deposited to the same extent in adipose tissue of rabbits?
Lin DS, Connor WE, Spenler CW
Am J Clin Nutr. 1993 Aug ; 58(2): 174-9
The objective of this study was to determine the effect that different dietary fatty acids would have on the fatty acid composition of adipose tissue. Thirty adult rabbits were starved 3-4 wk to deplete adipose tissue stores. They were then refed five different fats (linseed, rapeseed, cocoa butter, palm, and safflower oils) to regain initial body weights. The fatty acids of the adipose tissue, in general, reflected the diet. Positive correlations between the amount of the five commonly consumed fatty acids (palmitic, stearic, oleic, linoleic, and linolenic acids) in the diet and their deposition into the adipose tissue were observed. All polyunsaturated and monounsaturated fatty acids were well incorporated into the adipose tissue, even linolenic acid. The deposition of dietary saturated fatty acids (ie stearic acid) was limited. Our data showed that the fatty acids of dietary fats may greatly affect adipose fatty acid composition. Thus, adipose stores of essential fatty acids can be greatly augmented by diet.

FullText

Br J Nutr. 2001 Sep;86(3):371-7.
Polyunsaturated fatty acid-rich diets: effect on adipose tissue metabolism in
rats.
Gaíva MH, Couto RC, Oyama LM, Couto GE, Silveira VL, Riberio EB, Nascimento CM.
Department of Nutrition and Dietetics, Mato Grosso Federal University (UFMT),
Mato Grosso, Brazil.
The aim of the present study was to evaluate the effect of diets rich in n-6 and
n-3 fatty acids on adipose tissue metabolism. Starting at weaning, male Wistar
rats were fed ad libitum, for 8 weeks with one of the following diets: C, rat
chow; S, rat chow containing 15 % (w/w) soyabean oil; F, rat chow containing 15 %
(w/w) fish oil; SF, rat chow containing 15 % (w/w) soyabean and fish oil (5:1,
w/w). Casein was added to the fat diets to achieve the same 20 % (w/w) protein
content as in the control chow. Food intake and body weight were measured weekly.
The rats were killed by decapitation and the retroperitoneal (RET) and epididymal
(EPI) white adipose tissues were removed and weighed. Tissue lipid and protein
content, in vivo lipogenesis rate, uptake of diet-derived lipids, in vitro
lipolytic rate, adipocyte area, lipoprotein lipase, ATP citrate lyase, and malic
enzyme activities were evaluated. Carcass lipid and protein contents were also
measured. Energy intake was reduced while carcass lipid content was increased in
the three fat-fed groups. However, carcass protein and body weight gains were
elevated only with diets F and SF. Lipolysis rate was diminished by diets F and
SF, while the uptake of diet-derived lipids was elevated by the diet S in both
RET and EPI tissues. These metabolic alterations may have contributed to the
increase in in vivo lipogenesis rate in the presence of decreased ATP citrate
lyase and malic enzyme activities induced by the three lipid diets. These results
indicate that enrichment of the diet with polyunsaturated fatty acids causes
changes in adipose tissue metabolism that favour fat deposition. Different
metabolic pathways were preferentially affected by each type of fatty acid used.

J Hepatol. 2004 Nov;41(5):721-9.
Polyunsaturated fatty acid deficiency reverses effects of alcohol on
mitochondrial energy metabolism.
Piquet MA, Roulet M, Nogueira V, Filippi C, Sibille B, Hourmand-Ollivier I,
Pilet M, Rouleau V, Leverve XM.
Departement d'Hepatologie et Nutrition, CHU, F-14033 Caen cedex, France.
[email protected]
BACKGROUND/AIMS: Polyunsaturated fatty acids (PUFA) deficiency is common in
patients with alcoholic liver disease. The suitability of reversing such
deficiency remains controversial. The aim was to investigate the role played by
PUFA deficiency in the occurrence of alcohol-related mitochondrial dysfunction.
METHODS: Wistar rats were fed either a control diet with or without alcohol
(control and ethanol groups) or a PUFA deficient diet with or without alcohol
(PUFA deficient and PUFA deficient+ethanol groups). After 6 weeks, liver
mitochondria were isolated for energetic studies and fatty acid analysis.
RESULTS: Mitochondria from ethanol fed rats showed a dramatic decrease in oxygen
consumption rates and in cytochrome oxidase activity. PUFA deficiency showed an
opposite picture. PUFA deficient+ethanol group roughly reach control values,
regarding cytochrome oxidase activity and respiratory rates. The relationship
between ATP synthesis and respiratory rate was shifted to the left in ethanol
group and to the right in PUFA-deficient group. The plots of control and PUFA
deficient+ethanol groups were overlapping. Phospholipid arachidonic over
linoleic ratio closely correlated to cytochrome oxidase and oxygen uptake.
CONCLUSIONS: PUFA deficiency reverses alcohol-related mitochondrial dysfunction
via an increase in phospholipid arachidonic over linoleic ratio, which raises
cytochrome oxidase activity. Such deficiency may be an adaptive mechanism.

J Nutr. 1991 Nov;121(11):1811-9.
Dietary fat saturation affects glucose metabolism without affecting insulin
receptor number and affinity in adipocytes from BHE rats.
Pan JS(1), Berdanier CD.
(1)Department of Foods and Nutrition, University of Georgia, Athens 30602.
The effects of dietary fat source on epididymal fat cell insulin receptor binding
and affinity and on glucose transport and use by genetically diabetic rats were
studied. Male BHE rats were fed 6% fat/64% sucrose diets. The fat consisted of 1%
corn oil plus 5% beef tallow, menhaden oil or corn oil. Glucose tolerance was
assessed at 100, 300 and 600 d of age. At 100 d of age the fat pads were excised,
isolated adipocytes prepared and insulin receptor number, receptor affinity,
3-O-methyl glucose uptake and glucose use determined. Insulin receptor number and
binding affinity were not affected by dietary fat type. The transport and
subsequent use of glucose were greater in fat cells from rats fed beef tallow
compared with those from rats fed corn oil or menhaden oil. All three groups
exhibited a deterioration in glucose tolerance with age. Although we observed
greater glucose transport, oxidation and conversion to fatty acids in beef
tallow-fed rats, we saw no differences in these measurements between cells from
corn or menhaden oil-fed rats. Thus, we conclude that the effects of these
dietary lipids are attributable to effects of saturated fatty acids on
intracellular events rather than on the insulin receptor per se, and that the
type of unsaturated fatty acid [(n-3) vs. (n-6)] is of little importance to the
regulation of glucose metabolism by isolated adipocytes.

 

[ecstatichamster]

I believe that the reason there is difficulty finding answers here (and I've tried for many many hours) is that this is a highly politicized topic. That means that scientists getting grant money are towing the line.

Dr. Peat I am sure is completely right. But there is so much of this blather about the satfat demon for decades, that it is hard to find backup.

I think that the makeup of fat cells does change as we age, and that PUFA accumulation is the reason our metabolism falls so much as we age. And I think that this is hard to fix.

There is a basal metabolic level where fat is always being burned. The key is to minimize FFAs and minimize PUFAs and probably all fats. Then the fat will be burned "in place" rather than PUFA fats being spilled into the blood that much.

 

[TeaRex14]

That's seemingly my experience as well. I went heavy on the fats from goat dairy, butter, cheese starting off but it made me, well, fat. I think part of the problem is that those other fats tend to add up in PUFA's. Even coconut oil has PUFAs though so that's why I wanna use hydrogenated coconut oil.

I think the higher PUFA concentration plays a factor. But also butter and dairy tend to have longer chain saturated fats, which take longer to metabolize. Coconut oil is mostly medium and short chain SFAs.

 

[Cirion]

This thread has inspired me to stop drinking even 1% milk. I think milk without fat is not great though, so now I put MCT oil in my skim milk :P

On the road to <1 g a day PUFA... or at least <2g

 

[cyclops]

Then the fat will be burned "in place"

It sounds like you are describing a process wherein fat can be burned other then releasing FFA, but what does "burned in place" mean? Are you saying the fat is burned for energy right in the cell?

 

[ecstatichamster]

It sounds like you are describing a process wherein fat can be burned other then releasing FFA, but what does "burned in place" mean? Are you saying the fat is burned for energy right in the cell?

the basal metabolic rate burns fat all the time. So keep fat in diet very low, keep plenty of sugar, and fat will simply burn away in the cells without spilling into the bloodstream (except during sleep)

 

[cyclops]

the basal metabolic rate burns fat all the time. So keep fat in diet very low, keep plenty of sugar, and fat will simply burn away in the cells without spilling into the bloodstream (except during sleep)

Thanks hamster...this was exactly the info I was looking for. I didn't know fat could be burned in the cell. For some reason I thought lipolysis was the only way fat could be burned. I was always confused about this.

 

[ecstatichamster]

Thanks hamster...this was exactly the info I was looking for. I didn't know fat could be burned in the cell. For some reason I thought lipolysis was the only way fat could be burned. I was always confused about this.

at rest the body burns 1800 kCal a day on average, and it is mostly fat. The fat cells themselves have a basal metabolism. The body is constantly burning fat.

 

[cyclops]

at rest the body burns 1800 kCal a day on average, and it is mostly fat. The fat cells themselves have a basal metabolism. The body is constantly burning fat.

You just keep the good news coming!