Saturated Fat Is More Metabolically Harmful For The Human Liver Than Unsaturated Fat Or Simple Sugar

[michael94]

speaking of hydrogenation

did you know if you hydrogenate glucose and fructose you get sorbitol and mannitol? ...
I wonder if hydrogenation of sugars is any way related to hydrogenation of fats. Or if its simply irrelevant. Any ideas? One issue I see is they use nickel catalyst to do the hydrogenation.

Industrial synthesisEdit
Mannitol is commonly produced via the hydrogenation of fructose, which is formed from either starch or sucrose (common table sugar). Although starch is a cheaper source than sucrose, the transformation of starch is much more complicated. Eventually, it yields a syrup containing about 42% fructose, 52% glucose, and 6% maltose. Sucrose is simply hydrolyzed into an invert sugarsyrup, which contains about 50% fructose. In both cases, the syrups are chromatographically purified to contain 90–95% fructose. The fructose is then hydrogenated over a nickel catalyst into a mixture of isomers sorbitol and mannitol. Yield is typically 50%:50%, although slightly alkaline reaction conditions can slightly increase mannitol yields.[16]

ok this is very important and no one talks about it outside of these research cliques
apparently sorbitol made with nickel or iron catalysts leak metals into the mixture
very big problem
probably why sugar alcohols made in this why can be a problem, possibly toxic
Carbon supported Ru catalysts as promising alternative for Raney-type Ni in the selective hydrogenation of d-glucose - ScienceDirect

this is huge, how can i contact ray about this or would someone be willing to send an email on my behalf I will compose the question. thx

 

[ecstatichamster]

Perhaps this study is true for three weeks. Over time of months or years, the overfeeding of pufa fat would be more dangerous to the organism than satfat.

 

[ddjd]

Saturated Fat Is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars

OBJECTIVE
Nonalcoholic fatty liver disease (i.e., increased intrahepatic triglyceride [IHTG] content), predisposes to type 2 diabetes and cardiovascular disease. Adipose tissue lipolysis and hepatic de novo lipogenesis (DNL) are the main pathways contributing to IHTG. We hypothesized that dietary macronutrient composition influences the pathways, mediators, and magnitude of weight gain-induced changes in IHTG.

RESEARCH DESIGN AND METHODS
We overfed 38 overweight subjects (age 48 6 2, BMI 31 6 1 kg/m2, liver fat 4.7 6 0.9%) 1,000 extra kcal/day of saturated (SAT) or unsaturated (UNSAT) fat or simple sugars (CARB) for 3 weeks. We measured IHTG (1H-MRS), pathways contributing to IHTG (lipolysis ([2H5]glycerol) and DNL (2H2O) basally and during euglycemic hyperinsulinemia,insulin resistance,endotoxemia,plasmaceramides,andadipose tissue gene expression at 0 and 3 weeks.

RESULTS
Overfeeding SAT increased IHTG more (+55%) than UNSAT (+15%, P < 0.05). CARB increased IHTG (+33%) by stimulating DNL (+98%). SAT significantly increased while UNSAT decreased lipolysis. SAT induced insulin resistance and endotoxemia and significantly increased multiple plasma ceramides. The diets had distinct effects on adipose tissue gene expression.

CONCLUSIONS
Macronutrient composition of excess energy influences pathways of IHTG: CARB increases DNL, while SAT increases and UNSAT decreases lipolysis. SAT induced greatest increase in IHTG, insulin resistance, and harmful ceramides. Decreased intakes of SAT could be beneficial in reducing IHTG and the associated risk of diabetes.

i would totally agree because from personal experience the short chain saturated fatty acids particularly present in dairy completely clog up my liver, increase estrogenic symptomns, increased bloatedness etc.

this study posted by @tca300 explains that the longer chain fatty acids present in MUFA and SFA are better for the liver and gallbladder. so 12 and greater. Lauric C12, Myristic C14, Palmitic C16, Stearic C18, Oleic C18:1, Linoleic C18:2, are the most common longer chain fatty acids.

10 grams of 12+ carbon length fat seems to maximally empty the gallbladder.
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI

Its a fact that fatty chains under 12 carbons dont stimulate bile flow, or at least much much less. i believe this is what causes the NAFLD.

for example, cacao fat makes my liver feel fantastic as opposed to butter fat which causes terrible bloating. the longer chain fats are better for bile production, because cocoa fat has a higher percentage of longer chains than dairy.

 

[tca300]

I worry about where certain "reaserchers" get their study grants from, as well as a biased dogmatic perception of saturated vs unsaturated fats. After all, mammals including humans when carbohydrate consumption is high enough to induce de novo lipogenesis palmitic acid is the primary fat made first and foremost. Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet.

I believe that mechanism wouldn't exist if they were indeed as terrible as the corrupt system suggests.

Alcoholic Liver Disease: Update on the Role of Dietary Fat

Nanji, A.A. and S.W. French, Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res, 1986. 10(3): p. 271-3.

Nanji, A.A., C.L. Mendenhall, and S.W. French, Beef fat prevents alcoholic liver disease in the rat. Alcohol Clin Exp Res, 1989. 13(1): p. 15-9.

Ronis, M.J., S. Korourian, M. Zipperman, R. Hakkak, and T.M. Badger, Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr, 2004. 134(4): p. 904-12.

Kirpich, I.A., W. Feng, Y. Wang, Y. Liu, D.F. Barker, S.S. Barve, and C.J. McClain, The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res, 2012. 36(5): p. 835-46.

Nanji, A.A., K. Jokelainen, G.L. Tipoe, A. Rahemtulla, and A.J. Dannenberg, Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. J Pharmacol Exp Ther, 2001. 299(2): p. 638-44.

Hwang, J., Y.H. Chang, J.H. Park, S.Y. Kim, H. Chung, E. Shim, and H.J. Hwang, Dietary saturated and monounsaturated fats protect against acute acetaminophen hepatotoxicity by altering fatty acid composition of liver microsomal membrane in rats. Lipids Health Dis, 2011. 10: p. 184.

 

[lvysaur]

UNSAT - olive oil, pesto, pecans, butter (57% MUFA/22% PUFA/21% SFA)

The point everyone seems to be overlooking: rven their UNSAT diet is mostly MUFA. If people eat out and use vegetable oil to cook, their fat intake is not going to be only 22% PUFA hahaha

 

[Antonello]

i would totally agree because from personal experience the short chain saturated fatty acids particularly present in dairy completely clog up my liver, increase estrogenic symptomns, increased bloatedness etc.

this study posted by @tca300 explains that the longer chain fatty acids present in MUFA and SFA are better for the liver and gallbladder. so 12 and greater. Lauric C12, Myristic C14, Palmitic C16, Stearic C18, Oleic C18:1, Linoleic C18:2, are the most common longer chain fatty acids.

10 grams of 12+ carbon length fat seems to maximally empty the gallbladder.
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI
The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. - PubMed - NCBI

Its a fact that fatty chains under 12 carbons dont stimulate bile flow, or at least much much less. i believe this is what causes the NAFLD.

for example, cacao fat makes my liver feel fantastic as opposed to butter fat which causes terrible bloating. the longer chain fats are better for bile production, because cocoa fat has a higher percentage of longer chains than dairy.

Are you able to digest dairy fat after your cleansing with cacao fat?

 

[Hugh Johnson]

The liver is a metabolically active organ, it's not good to store PUFA there. Better store it elsewhere. Besides overfeeding fat means you have to store the calories somewhere and non-alcoholic fatty liver in absence of PUFA seems mostly harmless.

 

[_lppaiva]

Now, I'm no expert, and this is my first post (Hey guys), but I would like to see if my line of reasoning would be correct.

Studying RP's work for a while, and seeing haidut's post, I've learned to not take these studies at face value and actually try to apply my knowledge to it.

So they got a bunch of overweight individuals, loaded with PUFA, and increased their Saturated fat intake, that most likely started to displace the PUFA, liberating then into the bloodstream, which they themselves state is the major contributer to intrahepatic triglycerides. "Fatty acids in intrahepatic triglycerides can originate from adipose tissue lipolysis, hepatic de novo lipogenesis, and dietary fat (4). Lipolysis provides most of the FAs used for synthesis of intrahepatic triglycerides.". And stated that the major cause of it was saturated fats.

The fact that unsaturated fat increase DIDN'T induce intrahepatic triglycerides due to the downregulating the metabolism, not allowing for the release of more PUFA while continuing to store it. "Saturated fats significantly increased while unsaturated fats decreased lipolysis", this can be further proved by the point that the amount of weight gain in both groups is the same, but one induces intrahepatic triglycerides. "Saturated but not polyunsaturated fat has been reported to increase intrahepatic triglycerides (IHTGs) in young nonobese adults, despite similar weight gain (2). "

There are still, however, some flaws to my theory, as Sugar also increased intrahepatic triglycerides even though de novo lipogenesis only provides SFA (perhaps the SFA provided by sugar can also displace PUFA?). And the ceramides part that I don't know much about:
"Ceramides are synthesized de novo from SFAs, such as palmitate, and interfere with glucose metabolism by inhibiting insulin signaling". Are ceramides made from SFA really? In this case SFA would induce Insulin resistance right?

Anyway,
What do you guys think? Anything to add? Any hasty conclusions I made? Otherwise this study really is a bummer

 

[bdawg]

i think its a valid line of reasoning when haidut posted recently in another thread that FASN discourages the glucose pathway, and FASN only synthesizes saturated fat

Its main function is to catalyze the synthesis of palmitate (C16:0, a long-chain saturated fatty acid) from acetyl-CoA and malonyl-CoA, in the presence of NADPH.[8]

were all aware of PUFAs effects, but it would be good to get further clarity on saturated fats too

PUFAs reduce FASN (though increases lipolysis as well but also reduces tryglycerides) so damn im confused rn

Dietary n-6 and n-3 PUFAs (polyunsaturated fatty acid), but not mono-unsaturated or saturated fatty acids, co-ordinately suppress the transcription of several hepatic genes encoding glycolytic and lipogenic enzymes [e.g. FASN (fatty acid synthase); acetyl-CoA carboxylase, SCD1 (stearoyl-CoA desaturase 1) and pyruvate kinase] [1–6]. This suppressive effect of PUFA is associated with a significant reduction in the rate of hepatic malonyl-CoA production and fatty acid biosynthesis

The decrease in malonyl-CoA facilitates fatty acid oxidation by releasing carnitine palmitoyltransferase from inhibition by malonyl-CoA [7]. In addition, PUFAs activate peroxisome proliferator-activated receptor α and thereby increase the expression of genes encoding enzymes of fatty acid oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA oxidase) [5,8,9]. The net result is a diversion of fatty acids away from triacylglycerol (triglyceride) synthesis and secretion, and towards fatty acid oxidation and ketogenesis.

Polyunsaturated fatty acid suppression of fatty acid synthase (FASN): evidence for dietary modulation of NF-Y binding to the Fasn promoter by SREBP-1c

 

[hmac]

From my perspective, the floor in this study is more simple than many of the floors that have been suggested. 1000 calories of pecan nuts and pesto (oil + pine nuts) is considerably less digestible than 1000 calories of butter and coconut oil. Anyone who's ever eaten a lot of nuts and checked what comes out the other end will realise this.

In reality, those overfeeding on the saturated fat may have been absorbing close to the stated 1000 extra calories, whereas those eating the pecans may have only been getting 600 calories. Therefore, the results potentially suggest only that those who over consume more calories get more fatty livers.

It's important not to be totally wedded to any theory though. Reality is mysterious, we never know as much as we think we do.

 

[GelatinGoblin]

Rise thread, Rise!

 

[GorillaHead]

So guys I am recently trying a new diet Mainly consisting of saturated fats. Any concerns for insulin resistance ?

 

[Motorneuron]

Bump

 

[Ras]

So guys I am recently trying a new diet Mainly consisting of saturated fats. Any concerns for insulin resistance ?

Just keep the choline high enough, and you should be fine.