Studies? Where Is Evidence PUFAs Are Preferentially Stored Not Burned?

[ecstatichamster]

As I understand Dr. Peat, PUFAs are stored in cells rather than burned as fuel. So they can get dumped into the bloodstream as free fatty acids and create prostaglandins and participate in all sorts of inflammatory reactions.

But where is evidence of this? I have seen other evidence that satfat is stored and PUFAs burned first...

Any studies that back up Peat?

Thank you!

 

[tca300]

He might make that assumption based on the observation that older people have more PUFA stored ( accumulation, higher ratio of PUFA to SAT ) in thier bodies than younger people. Saturated FFA's that arent bound to albumin can cause a "soap like action" blocking bloodflow ( via aggregation) and is harmful. Neither are desirable imo.

"Despite the instability of polyunsaturated fatty acids, which tend to break down into toxic fragments, and despite their tendency to be preferentially liberated from fat cells during stress, the proportion of them in many tissues increases with age (Laganiere and Yu, 1993, 1987; Lee, et al., 1999; Smidova, et al., 1990;Tamburini, et al., 2004; Nourooz-Zadeh J and Pereira, 1999 ). This progressive increase with age can be seen already in early childhood (Guerra, et al., 2007). The reason for this increase seems to be that the saturated fatty acids are preferentially oxidized by many types of cell, (fat cells can slowly oxidize fat for their own energy maintenance). Albumin preferentially delivers saturated fatty acids into actively metabolizing cells such at the heart (Paris, 1978) for use as fuel. This preferential oxidation would explain Hans Selye's results, in which canola oil in the diet caused the death of heart cells, but when the animals received stearic acid in addition to the canola oil, their hearts showed no sign of damage." Fats, functions and malfunctions.

 

[ecstatichamster]

still looking for studies on this...thanks!

 

[Stramonium]

Have you check the references in his articles?

 

[Milena]

Differential effects of saturated versus unsaturated dietary fatty acids on weight gain and myocellular lipid profiles in mice - doesn't seem to be the case, here.
Uptake of individual fatty acids into adipose tissue in relation to their presence in the diet - interesting but almost incomprehensible to me. Other studies have also concluded that O3 oil are not preferentially taken up, showing the opposite of lipogenesis.
Every study, I found was saying the same thing, but one did note the correlation was strong for animal studies but not definitive in the human studies done.
Perhaps Ella may enlighten you as lipids are her field.

 

[marteagal]

I'm not sure if this will be helpful at all; sorry if not. The following is from the Introduction of a random "Peat-independent" article I came across a few weeks ago:

"It has been shown on fluid analysis of necrosectomy samples, which were from obese patients, that the predominant long chain fatty acids (up to 73%) were unsaturated fatty acids (UFA), comprising primarily of oleic acid and linoleic acid. This is similar to what other investigators have noted where UFA's accumulate in the pancreas adipocytes and can be 6 - 11 fold higher in necrosed pancreas samples as compared to a normal pancreas [33,43]. Similarly, in obese patients with NAFLD the quantities of UFA's were noted to be significantly increased in abdominal fat [44]. Hence, there is sufficient evidence that the predominant fatty acids that accumulate in abdominal and visceral fat in obesity are UFA's, which ties in well with our current dietary trends and recommended daily allowance according to which the saturated fat should be <30% with correspondingly more unsaturated fat (http:// www.health.gov/dietaryguidelines/dga2000/document/choose. htm)." (Acharya et al. (2014) Role of pancreatic fat in the outcomes of pancreatitis)

References cited:

[33] Pinnick KE, Collins SC, Londos C, Gauguier D, Clark A, Fielding BA. Pancreatic ectopic fat is characterized by adipocyte infiltration and altered lipid composition. Obes (Silver Spring) 2008;16:522e30.

[43] Panek J, Sztefko K, Drozdz W. Composition of free fatty acid and triglyceride fractions in human necrotic pancreatic tissue. Med Sci Monit 2001;7:894e8.

[44] Araya J, Rodrigo R, Videla LA, Thielemann L, Orellana M, Pettinelli P, et al.
Increase in long-chain polyunsaturated fatty acid n e 6/n e 3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease. Clin Sci (Lond) 2004;106:635e43.

 

[Milena]

I'm not sure if this will be helpful at all; sorry if not. The following is from the Introduction of a random "Peat-independent" article I came across a few weeks ago:

"It has been shown on fluid analysis of necrosectomy samples, which were from obese patients, that the predominant long chain fatty acids (up to 73%) were unsaturated fatty acids (UFA), comprising primarily of oleic acid and linoleic acid. This is similar to what other investigators have noted where UFA's accumulate in the pancreas adipocytes and can be 6 - 11 fold higher in necrosed pancreas samples as compared to a normal pancreas [33,43]. Similarly, in obese patients with NAFLD the quantities of UFA's were noted to be significantly increased in abdominal fat [44]. Hence, there is sufficient evidence that the predominant fatty acids that accumulate in abdominal and visceral fat in obesity are UFA's, which ties in well with our current dietary trends and recommended daily allowance according to which the saturated fat should be <30% with correspondingly more unsaturated fat (http:// www.health.gov/dietaryguidelines/dga2000/document/choose. htm)." (Acharya et al. (2014) Role of pancreatic fat in the outcomes of pancreatitis)

References cited:

[33] Pinnick KE, Collins SC, Londos C, Gauguier D, Clark A, Fielding BA. Pancreatic ectopic fat is characterized by adipocyte infiltration and altered lipid composition. Obes (Silver Spring) 2008;16:522e30.

[43] Panek J, Sztefko K, Drozdz W. Composition of free fatty acid and triglyceride fractions in human necrotic pancreatic tissue. Med Sci Monit 2001;7:894e8.

[44] Araya J, Rodrigo R, Videla LA, Thielemann L, Orellana M, Pettinelli P, et al.
Increase in long-chain polyunsaturated fatty acid n e 6/n e 3 ratio in relation to hepatic steatosis in patients with non-alcoholic fatty liver disease. Clin Sci (Lond) 2004;106:635e43.

Wow! Good job:)

 

[Drareg]

As I understand Dr. Peat, PUFAs are stored in cells rather than burned as fuel. So they can get dumped into the bloodstream as free fatty acids and create prostaglandins and participate in all sorts of inflammatory reactions.

But where is evidence of this? I have seen other evidence that satfat is stored and PUFAs burned first...

Any studies that back up Peat?

Thank you!

Are you thinking the body gets PUFA in the diet but uses them,burns them off?
They get stored when you over eat?

 

[ecstatichamster]

Are you thinking the body gets PUFA in the diet but uses them,burns them off?
They get stored when you over eat?

Dr. Peat says they get stored and satfat is burned FIRST.

I am looking for proof of this.

 

[shepherdgirl]

Wouldn't it depend upon whether one lives in a cold or hot climate? Has this been taken into account in any of the studies?

 

[JohnA]

Really thought-provoking discussion, guys. I'm starting to reconsider my faith in McDougall's "the fat you eat is the fat you wear" principle.

Does anyone know whether the fat created via lipogenesis tends to be saturated or unsaturated? My hunch is that a properly functioning metabolism will convert more of the fat to saturated.

 

[Drareg]

Dr. Peat says they get stored and satfat is burned FIRST.

I am looking for proof of this.

I see, your question made me ask the question if we eat a meal with sat fat ,PUFA,sugar protein but it's just what I need to replenish energy levels do PUFA still get stored?
In other words does fat still get stored if you undereat so to speak,keeping in mind you are not overweight to begin with for the sake of questioning relative to ideals?

If so is there direct evidence of this?

 

[HDD]

I see, your question made me ask the question if we eat a meal with sat fat ,PUFA,sugar protein but it's just what I need to replenish energy levels do PUFA still get stored?
In other words does fat still get stored if you undereat so to speak,keeping in mind you are not overweight to begin with for the sake of questioning relative to ideals?

If so is there direct evidence of this?

I thought it was about the ratio of saturated/ unsaturated. Hence, the frying out the fat in bacon or chicharrones and refrying in coconut oil, cooking eggs in coconut oil, or adding coconut oil to peanut butter. I don't recall if this ratio was something I read directly from Peat or a discussion on this forum.

 

[schultz]

Wouldn't it depend upon whether one lives in a cold or hot climate? Has this been taken into account in any of the studies?

Good point.

@ecstatichamster why not just ask Ray? It seems like a hard topic to research. I don't even know what to search in pubmed. I did find a few animals studies suggesting that PUFA is preferentially burned. What was funny is that the paper suggests that PUFA has better digestibility since the animals could eat less of the PUFA diet and still gain the same weight as the Sat diet. From a Peat perspective, the PUFA is just lowering the metabolic rate.

 

[ecstatichamster]

Good point.

@ecstatichamster why not just ask Ray? It seems like a hard topic to research. I don't even know what to search in pubmed. I did find a few animals studies suggesting that PUFA is preferentially burned. What was funny is that the paper suggests that PUFA has better digestibility since the animals could eat less of the PUFA diet and still gain the same weight as the Sat diet. From a Peat perspective, the PUFA is just lowering the metabolic rate.

Peat has explained PUFAs were first used to fatten food farm animals more efficiently.

I will email him.

 

[Kyle M]

I don't have a reference handy but the idea is based on his other idea that PUFA inhibit enzymes and SFA do not. This includes respiratory enzymes and transport enzymes, so SFA will be more amenable to getting moved around the cell and plugged into metabolic reaction than PUFA. Also something about the greater water solubility of PUFA, which might be how the enzyme inhibition works in the first place, but this supposedly also preferentially releases PUFA from storage under the influence of hormone sensitive lipase, since the greater hydrophilicity of PUFA will tend to pull them into the circulation.

 

[ecstatichamster]

Ray wrote back:

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.

 

[Drareg]

I thought it was about the ratio of saturated/ unsaturated. Hence, the frying out the fat in bacon or chicharrones and refrying in coconut oil, cooking eggs in coconut oil, or adding coconut oil to peanut butter. I don't recall if this ratio was something I read directly from Peat or a discussion on this forum.

It's interesting to think about cooking techniques like that for cooking out a lot of the PUFA if it's possible like traditional confit for example.

Either way would saturated fat and PUFA in any ratio get stored if calories are spot on rather than over feeding is an interesting question,is there evidence for this,probably difficult to tell with current technology.

 

[artlange]

Dr. Peat says they get stored and satfat is burned FIRST.

I am looking for proof of this.

this was quoted in ray's article Fats, functions and malfunctions. as Paris 1978
Eur J Biochem. 1978 Feb 1;83(1):235-43. The role of serum albumin in the uptake of fatty acids by cultured cardiac cells from chick embryo. Paris S, Samuel D, Jacques Y, Gache C, Franchi A, Ailhaud G.


pubmed
The role of serum albumin in the uptake of fatty acids by cultured cardiac cells from chick embryo. - PubMed - NCBI
Eur J Biochem. 1978 Feb 1;83(1):235-43.
The role of serum albumin in the uptake of fatty acids by cultured cardiac cells from chick embryo.
Paris S, Samuel D, Jacques Y, Gache C, Franchi A, Ailhaud G.
Abstract
Fatty acids enter the cultured cardiac cells from chicken embryo through two mechanisms, one involving a saturable process, the other resembling passive diffusion. Studies of the saturable component, at fixed concentrations of palmitate or of oleate and at increasing concentrations of albumin, show that this protein increases the rate of palmitate uptake with a maximum at palmitate/albumin molar ratios between 7 and 10 while it decreases the rate of oleate uptake under all conditions. Albumin cannot be replaced by other serum proteins; its effect is specific to saturated fatty acids, can be mimicked by the detergent Tween 40 and involves the binding of the fatty acid to the protein, prior to its delivery to the cell. Both with labelled saturated and unsaturated fatty acids the presence of albumin lowers the proportion of unesterified fatty acids and enhances the proportion of esterified fatty acids recovered in the cardiac cell after uptake. A similar effect of albumin was also found with hepatocytes and permanent cell lines. A specific role for serum albumin is presented, which assumes a 'dispersing' effect of this protein towards dimers (or higher aggregates) of saturated fatty acids and the entry of fatty acids into the cell as monomers.

PMID:
564268
[Indexed for MEDLINE]
Free full text

 

[Luann]

I was wrestling with this question too. Trying to figure out if fasting would burn off PUFA's or if it would only steal the saturated fats.

I just googled the changes to adipose composition after fasting. From some studies it looks like the PUFA is quick to get liberated but then it concentrates in the fat cells. So it is not burned. In fact the fat tissue after fasting has a higher linoleic acid to SFA ratio which means that less saturated species of fat are getting lost through fat burning.