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

[ecstatichamster]

That study is surely bunk. Saturated fats have been used successfully to treat liver disorders.

But it was an over feeding study.

 

[Spokey]

Yeah, but an overfeeding study with poor controls leading to the conclusion SFA is worse for the Liver that PUFA is bunk if there's already direct evidence to the diametric contrary. It's a bad study with an engineered conclusion. It says nothing about SFA, but maybe something about mixed diets, study design and drawing premature conclusions from them. Maybe.

 

[Mito]

From the study....“The SAT but not the other diets also increased markers of endotoxemia and upregulated genes related to gram-negative bacterial infection in adipose tissue. These changes could have contributed to SAT-induced lipolysis and de novo ceramide synthesis, because in mice, endotoxin induces both adipose tissue inflamation (11) and ceramide-dependent IR (10).”

This matches a post by @tyw:
“(2) The more double bonds in a fat, the LESS endotoxin gets into the serum. A PUFA like DHA will cause less endotoxin to be transferred into the bloodstream, as compared to a Saturated Fat like Coconut Oil. [paper (a)]”
Endotoxin And Fat Consumption

 

[Spokey]

From the study....“The SAT but not the other diets also increased markers of endotoxemia and upregulated genes related to gram-negative bacterial infection in adipose tissue. These changes could have contributed to SAT-induced lipolysis and de novo ceramide synthesis, because in mice, endotoxin induces both adipose tissue inflamation (11) and ceramide-dependent IR (10).”

This matches a post by @tyw:
“(2) The more double bonds in a fat, the LESS endotoxin gets into the serum. A PUFA like DHA will cause less endotoxin to be transferred into the bloodstream, as compared to a Saturated Fat like Coconut Oil. [paper (a)]”
Endotoxin And Fat Consumption

Yep, but that says endotoxin is the causal agent of the liver damage, not SFA as implied by the title. SFA can kill bacteria, antibiotics do the same and can paradoxically produce toxic shock by the liberation of LPS from dead bacteria. This is an endotoxin management problem, not an SFA problem.

 

[Mito]

but that says endotoxin is the causal agent of the liver damage,

That might be true but it doesn’t change the result of the study with regard to saturated fat increasing liver triglycerides significantly more than unsaturated fat or carbohydrates (in the context of an energy excess i.e. overweight/overfed subjects).

 

[Mito]

Great -- now saturated fat is bad, and because I haven't hesitated to consume it over the past year, my fat-laden liver is now probably worse than ever? Or maybe this is just being posted to spur more contentious debate.

Remember this was an overfeeding study of overweight subjects with BMI’s around 32.

 

[Spokey]

Show me a study that produces liver damage with pure SFA in the absence of endotoxin.

 

[x-ray peat]

This seems to explain whats going on. Too much anything isnt good.

Lipotoxicity - Wikipedia
Cause
Adipocytes, the cells that normally function as lipid store of the body, are well equipped to handle the excess lipids. Yet, too great of an excess will overburden these cells and cause a spillover into non-adipose cells, which do not have the necessary storage space. When the storage capacity of non-adipose cells is exceeded, cellular dysfunction and/or death result. The mechanism by which lipotoxicity causes death and dysfunction is not well understood. The cause of apoptosis and extent of cellular dysfunction is related to the type of cell affected, as well as the type and quantity of excess lipids.[3]

Liver
An excess of free fatty acids in liver cells plays a role in Nonalcoholic Fatty Liver Disease (NAFLD). In the liver, it is the type of fatty acid, not the quantity, that determines the extent of the lipotoxic effects. In hepatocytes, the ratio of monounsaturated fatty acids and saturated fatty acids leads to apoptosis and liver damage. There are several potential mechanisms of by which the excess fatty acids can cause cell death and damage. They may activate death receptors, stimulate apoptotic pathways, or initiate cellular stress response in the endoplasmic reticulum. These lipotoxic effects have been shown to be prevented by the presence of excess triglycerides within the hepatocytes. [6]

here is the liver study referenced above
Lipotoxicity in Nonalcoholic Fatty Liver Disease: Not All Lipids Are Created Equal

 

[managing]

SFA - coconut oil, butter, and blue cheese

PUFA - olive oil, pesto, pecans, butter

Carbs - OJ, sugar sweetened beverage, candy

I think all this proves is:

a) butter is an SFA, not a PUFA
b) Olive oil is not nearly so bad as seed oils
c) pecans aren't nearly so bad as seed oils
d) pesto is made with . . . olive oil

And the whole moldy cheese thing already addressed.

 

[Mito]

I think all this proves is:

a) butter is an SFA, not a PUFA
b) Olive oil is not nearly so bad as seed oils
c) pecans aren't nearly so bad as seed oils
d) pesto is made with . . . olive oil

And the whole moldy cheese thing already addressed.

SAT - coconut oil, butter, and blue cheese (76% SFA/21% MUFA/3% PUFA)

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

 

[Spokey]

Wikipedia. Hmm. That's not a study. It's an article contrived of suspect observations and even more suspect conclusions. And again we have direct evidence to the contrary, SFA protects from liver damage.

For example:

Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. - PubMed - NCBI
Virgin coconut oil reverses hepatic steatosis by restoring redox homeostasis and lipid metabolism in male Wistar rats. - PubMed - NCBI

 

[managing]

SAT - coconut oil, butter, and blue cheese (76% SFA/21% MUFA/3% PUFA)

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

What I am getting at is, butter is included in both.

And Olive Oil is MUFA, not PUFA. If they wanted a well defined study would be CO and the PUFA group would be Canola. Throw in a MUFA group while you are at it that is just EVOO. And make the "sugar" group real sugar, ie fruit, not "candy". Its a real garbage design. You have to wonder whether they are incompetent, or deceitful.

 

[x-ray peat]

Wikipedia. Hmm. That's not a study. It's an article contrived of suspect observations and even more suspect conclusions. And again we have direct evidence to the contrary, SFA protects from liver damage.

For example:

Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. - PubMed - NCBI
Virgin coconut oil reverses hepatic steatosis by restoring redox homeostasis and lipid metabolism in male Wistar rats. - PubMed - NCBI

haha yes I felt guilty using it but I think it summarized the key issue which is too much fat for the body to store at one time. I think you are right that SFAs are protective when eaten in normal amounts but are unhealthy and even dangerous when eaten in excess.
I did post a link to the referenced study on effects of excess fat on the liver.
Lipotoxicity in Nonalcoholic Fatty Liver Disease: Not All Lipids Are Created Equal
A surplus of FFA in non-adipose cells may enter deleterious pathways leading to cell dysfunction (lipotoxicity) and apoptotic cell death (lipoapoptosis) [10,12]. FFA can induce these effects through several mechanisms that may differ across different cell types. We have recently uncovered some key aspects linking hepatocyte FFA overloading, to hepatocellular apoptosis and liver injury[13]. The results demonstrated that the ratio of monounsaturated fatty acids (MUFA) to saturated fatty acids (SFA) determines whether liver cells are damaged by the flux of exogenous FFA, and thus the nature rather than the quantity of FFA determines hepatic stress.

 

[Spokey]

"may enter deleterious pathways leading to cell dysfunction" Hmm.

Olive oil contains Omega-9 which Ray has already written about with regard to anti-inflammatory mead acid. Again, I've yet to see the study showing damage in a human from SFA in absence of LPS; they don't exist.

 

[x-ray peat]

"may enter deleterious pathways leading to cell dysfunction" Hmm.

Olive oil contains Omega-9 which Ray has already written about with regard to anti-inflammatory mead acid. Again, I've yet to see the study showing damage in a human from SFA in absence of LPS; they don't exist.

That study I linked to has a number of studies in it that demonstrate exactly that. The only way you can isolate any effects of endotoxins is to run the experiment in vitro. Otherwise you could always say that the SFAs are allowing in endotoxins. I would also add that you are just assuming that it is the endotoxins causing all the damage in vivo. The endotoxin theory just doesnt hold up when liver cells are damaged exactly the same way whether in vivo or in vitro due to excess fatty acids.

"We demonstrated that incubation of human and murine hepatocytes with FFA results in a dose- and saturation-dependent mitochondrial dysfunction [22]. The saturated FFA palmitate at concentrations that mimic the levels of this FFA present in the circulation of humans with metabolic syndrome induced significant mitochondrial membrane permeabilization and increased ROS production. Another group showed that saturated FFA induce JNK-dependent hepatocyte lipoapoptosis by activating the pro-apoptotic proteins Bim and Bax which trigger the mitochondrial apoptotic pathway [23]."

 

[Spokey]

"The only way you can isolate any effects of endotoxins is to run the experiment in vitro."

You can do experiments in animals with no bacteria. This has been done numerous times.

I don't buy the in vitro extrapolation to in vivo conclusions (especially given the dubious quality of the work).
If they were sound, I venture the animal experiment would have been done already, whereas the evidence that LPS and PUFA can directly damage the liver in animals and humans does exist already.

 

[x-ray peat]

"The only way you can isolate any effects of endotoxins is to run the experiment in vitro."

You can do experiments in animals with no bacteria. This has been done numerous times.

You asked for human studies; the no bacteria study you propose would be unethical.
Both in vitro human cell studies and in vivo human studies show the same damage. No endotoxins needed to explain it.

Again I dont think its saying that SFAs are bad but only when they are in excess and the adipose cells cant store it all. Lipotoxicity seems to be fairly well established even if some of the details arent fully fleshed out.

 

[Spokey]

The in-vivo studies are uncontrolled, and there are studies that show the opposite, saturated fat consumption inversely correlated with liver health.

If it can be shown in bacteria-free animals, which would be the next logical step, I don't really need the human study. But those studies do not exist either.

 

[michael94]

speaking of sfa anyone else like white choc m&ms
no iron, available in bulk at smart n final
Keep in freezer then soak in water to get the candy layer/dye off and discard the murky water

me gusta

 

[michael94]

o yea reeses pieces are the same although they have some iron
made with defatted peanuts and hydrogenated fat