Saturated Fat TERRIBLE For Liver Health & Diabetes. Compared To PUFA

[Nuancé]

You've gone beyond "Nuance" here, and you are just full on trolling at this point. If Saturated Fat can repair and restore the function of seriously damaged livers of alcoholics, why wouldn't it be beneficial for "common people" as well? Especially since NAFLD is fairly "common" in and of itself.

Besides that, there are now several animal studies, and at least two human studies (one of those studies lasting several years), posted to this thread refuting the title of this thread, and answering your initial question. I guess you can keep on shifting the goal post to "yes, okay, but what about Eskimos living in Peru that only consume 4 glasses of gin each week, where are the studies on them?" if you really want to.

Nothing is black and white, again... don't be absolutist. PUFA can have interest also in some cases, just like SFA. They are not fundamentally good or bad.
If SFA can help alcoholic why not, but if it put you at risk for diabetes, endotoxins etc... there is a benefit/risk ratio in EVERYTHING !

NAFLD and NASH are sometimes linked to... ORANGE haha. Does that mean that we should definitively avoid oranges ? Absolutely not, I even have eaten an orange this morning.

Raw orange intake is associated with higher prevalence of non-alcoholic fatty liver disease in an adult population - PubMed

"
Abstract
Objectives: Non-alcoholic fatty liver disease (NAFLD) is one of the most common public health issues worldwide. Oranges are the most popular fruit consumed in the world. Admittedly, flavonoids in oranges act as antioxidants and improve liver steatosis. However, oranges also are rich in fructose, which is a risk factor in the progress of NAFLD. Therefore, we hypothesize that orange intake may be a double-edged sword in the development of NAFLD."

"
Methods: We randomly recruited 27,214 adults into the Tianjin Chronic Low-Grade Systemic Inflammation and Health Cohort Study. NAFLD was diagnosed by liver ultrasonography. Raw orange intake was assessed by a validated self-administered food frequency questionnaire. Multiple logistic regression analysis was used to evaluate the association between orange intake and the prevalence of NAFLD.

Results: There was a 27.18% prevalence of NAFLD among the participants. Consumption of orange was positively associated with the prevalence of NAFLD after adjustment for all potential confounding factors (Ptrend = 0.04). The odds ratios (95% confidence interval) of the categories of orange intake in the NAFLD were 1.00 (reference) for less than once per week, 1.02 (0.95-1.11) for 1 to 6 times per week, and 1.17 (1.03-1.33) for ≥7 times per week, respectively.

Conclusions: The present study demonstrated that orange intake is positively associated with the prevalence of NAFLD."

Anyway, can we talk about nuts reducing MDA and oxidized LDL in intervention studies on humans or not ??!

 

[Nuancé]

Nothing is black and white, again... don't be absolutist. PUFA can have interest also in some cases, just like SFA. They are not fundamentally good or bad.
If SFA can help alcoholic why not, but if it put you at risk for diabetes, endotoxins etc... there is a benefit/risk ratio in EVERYTHING !

NAFLD and NASH are sometimes linked to... ORANGE haha. Does that mean that we should definitively avoid oranges ? Absolutely not, I even have eaten an orange this morning.

Raw orange intake is associated with higher prevalence of non-alcoholic fatty liver disease in an adult population - PubMed

"
Abstract
Objectives: Non-alcoholic fatty liver disease (NAFLD) is one of the most common public health issues worldwide. Oranges are the most popular fruit consumed in the world. Admittedly, flavonoids in oranges act as antioxidants and improve liver steatosis. However, oranges also are rich in fructose, which is a risk factor in the progress of NAFLD. Therefore, we hypothesize that orange intake may be a double-edged sword in the development of NAFLD."

"
Methods: We randomly recruited 27,214 adults into the Tianjin Chronic Low-Grade Systemic Inflammation and Health Cohort Study. NAFLD was diagnosed by liver ultrasonography. Raw orange intake was assessed by a validated self-administered food frequency questionnaire. Multiple logistic regression analysis was used to evaluate the association between orange intake and the prevalence of NAFLD.

Results: There was a 27.18% prevalence of NAFLD among the participants. Consumption of orange was positively associated with the prevalence of NAFLD after adjustment for all potential confounding factors (Ptrend = 0.04). The odds ratios (95% confidence interval) of the categories of orange intake in the NAFLD were 1.00 (reference) for less than once per week, 1.02 (0.95-1.11) for 1 to 6 times per week, and 1.17 (1.03-1.33) for ≥7 times per week, respectively.

Conclusions: The present study demonstrated that orange intake is positively associated with the prevalence of NAFLD."

Anyway, can we talk about nuts reducing MDA and oxidized LDL in intervention studies on humans or not ??!

 

[Nuancé]

I wonder if it is the vegetable ghee rather than actual ghee? I wonder how many immigrants buy the vegetable ghee versus actual ghee?

Good question, but here they talk about oxidized cholesterol. Vegetables fats doesn't have cholesterol, so they can't contain that. Their PUFA content can become rancid, depending on oxygen exposure, light, heat, storage, presence of iron etc despite that of course.

But oxysterols are like rancid PUFA, linked to nearly every kind of civilization diseases, heart disease, stroke, alzheimer, cancer, etc. Fats are fragile and don't like agressive cooking or prolonged storage definitively, especially when they are processed like oil, fish oil...
Only vegetable rich saturated fat foods seems strong enough against oxidation, coconut being the reference, cocoa butter, shea butter, palm oil, and also the monounsaturated fat rich foods like avocados, macadamias or olives.

 

[schultz]

Good question, but here they talk about oxidized cholesterol. Vegetables fats doesn't have cholesterol, so they can't contain that. Their PUFA content can become rancid, depending on oxygen exposure, light, heat, storage, presence of iron etc despite that of course.

But oxysterols are like rancid PUFA, linked to nearly every kind of civilization diseases, heart disease, stroke, alzheimer, cancer, etc. Fats are fragile and don't like agressive cooking or prolonged storage definitively, especially when they are processed like oil, fish oil...
Only vegetable rich saturated fat foods seems strong enough against oxidation, coconut being the reference, cocoa butter, shea butter, palm oil, and also the monounsaturated fat rich foods like avocados, macadamias or olives.

I didn't read the little study you had posted, but it seemed like, from the abstract, that they recognized two groups of immigrants who both develop atherosclerosis. Both of these groups are known to consume "ghee" so the researchers decided to test ghee because of a hypothesis they had on oxidized cholesterol. But did they actually find out whether the majority of these immigrants are actually consuming real ghee? Immigrants tend to have limited funds and I would imagine most of them would buy vegetable ghee.

I'll go through the paper I guess and just check myself.

 

[schultz]

Interesting, I keep that in mind... but nobody here is alcoholic I hope haha, I was talking more about "common people". :)

And ghee is really controversial, ghee can be extremely rich in oxidized cholesterol compared to butter, which is terrible for cardiovascular health :

Cholesterol oxides in Indian ghee: possible cause of unexplained high risk of atherosclerosis in Indian immigrant populations - PubMed

"
Abstract
Two populations of immigrants to London and to the West Indies from the Indian subcontinent have higher than expected morbidity and mortality from atherosclerosis but do not show the commonly accepted major risk factors. This study investigated the hypothesis that ghee, a clarified butter product prized in Indian cooking, contains cholesterol oxides and could therefore be an important source of dietary exposure to cholesterol oxides and an explanation for the high atherosclerosis risk. Substantial amounts of cholesterol oxides were found in ghee (12.3% of sterols), but not in fresh butter, by thin-layer and high-performance-liquid chromatography. Dietary exposure to cholesterol oxides from ghee may offer a logical explanation for the high frequency of atherosclerotic complications in these Indian populations.

"

Okay I went over the paper and it has a few gems in it...

The introduction actually says that these groups with increased atherosclerosis actually consume low amounts of saturated fat.


"In these populations the rate of myocardial infarction is 1.5 - 2 times that in the indigenous populations, yet these people do not have high intakes of saturated fat or cholesterol, high rates of cigarette smoking, higher than normal mean serum cholesterol or low-density-lipoprotein cholesterol, or hypertension."


This researcher did not actually check if they were using vegetable ghee. He got his data from another researcher "McKeigue". I didn't look at the McKeigue paper yet.


"McKeigue et all reported that Asians living in London use ghee as cooking oil."


He then cites the McKeigue paper in the discussion section and it is pretty awesome...


"In the study of McKeigue and colleagues the Londoners of Asian origin had a theoretically lower atherosclerosis risk in terms of each known risk factor studied than the British controls, yet their observed relative risk for myocardial infarction was 1.8 and their mortality was 1.2 times higher than that of the controls. Dietary fat intake as a percentage of kilocalories, and intake of saturated fatty acids and cholesterol were significantly lower among the Asians than the controls. Percentage of calories from polyunsaturated fatty acids was more than twice higher in the Asians than in the controls. Serum cholesterol was lower and high-density-lipoprotein cholesterol was higher in the Asians than in the controls, and the fatty-acid composition of their serum cholesterol esters was enriched in linoleic acid. All of the above features predict a lower risk of myocardial infarction in the Asian than in the British-born group. As McKeigue et al stated, the observed high relative risk was unexplained by their data."


I especially like that last part about their serum cholesterol being enriched in linoleic acid.

 

[Wilfrid]

Raw moulded cheeses, like blue cheese, are actually very effective against endotoxins.
Those cheeses contain milk bioactive peptides and biomolecules (like fungi) which enhance alkaline phosphatase activity.
This enzyme dephosphorylates and thus detoxifies pro-inflammatory microbial components like lipopolysaccharide, making them unable to trigger inflammatory responses and generate chronic low-grade inflammation (including insulin resistance, glucose intolerance, type-2 diabetes, metabolic syndrome and obesity to name a few.....).
So, if anything, I think that consumption of raw blue cheese is protective rather than harmful. Jean Paul Lalles has made some very good research on it.

 

[Vinny]

Raw moulded cheeses, like blue cheese, are actually very effective against endotoxins.
Those cheeses contain milk bioactive peptides and biomolecules (like fungi) which enhance alkaline phosphatase activity.
This enzyme dephosphorylates and thus detoxifies pro-inflammatory microbial components like lipopolysaccharide, making them unable to trigger inflammatory responses and generate chronic low-grade inflammation (including insulin resistance, glucose intolerance, type-2 diabetes, metabolic syndrome and obesity to name a few.....).
So, if anything, I think that consumption of raw blue cheese is protective rather than harmful. Jean Paul Lalles has made some very good research on it.

Thanks for this information

 

[PaRa]

Raw moulded cheeses, like blue cheese, are actually very effective against endotoxins.
Those cheeses contain milk bioactive peptides and biomolecules (like fungi) which enhance alkaline phosphatase activity.
This enzyme dephosphorylates and thus detoxifies pro-inflammatory microbial components like lipopolysaccharide, making them unable to trigger inflammatory responses and generate chronic low-grade inflammation (including insulin resistance, glucose intolerance, type-2 diabetes, metabolic syndrome and obesity to name a few.....).
So, if anything, I think that consumption of raw blue cheese is protective rather than harmful. Jean Paul Lalles has made some very good research on it.

Will try French Real Roquefort again

 

[opson123]

If anyone dislikes the taste of blue cheese, as I do, I recommend trying it with gingerbread cookies. The combo tastes really good. Great for Christmas.

 

[Lollipop2]

Okay I went over the paper and it has a few gems in it...

The introduction actually says that these groups with increased atherosclerosis actually consume low amounts of saturated fat.


"In these populations the rate of myocardial infarction is 1.5 - 2 times that in the indigenous populations, yet these people do not have high intakes of saturated fat or cholesterol, high rates of cigarette smoking, higher than normal mean serum cholesterol or low-density-lipoprotein cholesterol, or hypertension."


This researcher did not actually check if they were using vegetable ghee. He got his data from another researcher "McKeigue". I didn't look at the McKeigue paper yet.


"McKeigue et all reported that Asians living in London use ghee as cooking oil."


He then cites the McKeigue paper in the discussion section and it is pretty awesome...


"In the study of McKeigue and colleagues the Londoners of Asian origin had a theoretically lower atherosclerosis risk in terms of each known risk factor studied than the British controls, yet their observed relative risk for myocardial infarction was 1.8 and their mortality was 1.2 times higher than that of the controls. Dietary fat intake as a percentage of kilocalories, and intake of saturated fatty acids and cholesterol were significantly lower among the Asians than the controls. Percentage of calories from polyunsaturated fatty acids was more than twice higher in the Asians than in the controls. Serum cholesterol was lower and high-density-lipoprotein cholesterol was higher in the Asians than in the controls, and the fatty-acid composition of their serum cholesterol esters was enriched in linoleic acid. All of the above features predict a lower risk of myocardial infarction in the Asian than in the British-born group. As McKeigue et al stated, the observed high relative risk was unexplained by their data."


I especially like that last part about their serum cholesterol being enriched in linoleic acid.

Great sleuthing job! Confirmed your suspicions. I loved loved the part about low consumption of sat fats - lol.

 

[Peater Piper]

I think consuming a large amount of long chain saturated fats is generally a bad idea unless you're fairly active or consuming quite a bit of coffee. Otherwise, it tends to accumulate in the liver. Yes, it can be protective if you happen to poison yourself, so try to avoid the latter. It can also increase iron absorption and lower absorption of other minerals.

 

[B___Danny]

@Nuancé All you have to know is that your body creates its own saturated fat. Your body only creates its own molecules of something it needs a lot of (saturated fat, cholesterol, glucose, hormones). If polyunsaturated fats were better the body would make those in large amounts rather than saturated.

 

[tankasnowgod]

Nothing is black and white, again... don't be absolutist. PUFA can have interest also in some cases, just like SFA. They are not fundamentally good or bad.
If SFA can help alcoholic why not, but if it put you at risk for diabetes, endotoxins etc... there is a benefit/risk ratio in EVERYTHING !

Eating Saturated Fat does not put you at risk for diabetes or "endotoxins." SFAs have an antimicrobial effect, so they lower endotoxin exposure over time. There can be a transient increase when first increasing SFAs in the diet, but longer term studies show lower exposure. The only real interest in PUFA I have at this point is minimizing my exposure, as much as possible. Feel free to drink corn oil and eat 500 calories worth of walnuts for dinner if you want, I'm not interested.

Anyway, can we talk about nuts reducing MDA and oxidized LDL in intervention studies on humans or not ??!

I'm not interested in this issue, so no. Again, this had nothing to do with this original topic of the thread.

At this point, I'm hitting the "ignore" button on your posts, as you are bringing no real value here, and just want to argue. I suggest others do the same if they wish.

 

[jb116]

Eating Saturated Fat does not put you at risk for diabetes or "endotoxins." SFAs have an antimicrobial effect, so they lower endotoxin exposure over time. There can be a transient increase when first increasing SFAs in the diet, but longer term studies show lower exposure. The only real interest in PUFA I have at this point is minimizing my exposure, as much as possible. Feel free to drink corn oil and eat 500 calories worth of walnuts for dinner if you want, I'm not interested.



I'm not interested in this issue, so no. Again, this had nothing to do with this original topic of the thread.

At this point, I'm hitting the "ignore" button on your posts, as you are bringing no real value here, and just want to argue. I suggest others do the same if they wish.

Thanks for that, I wanted to bring that up too that SFA may increase only transience but they actually inhibit the TL4R. PUFAs activate them.

 

[haidut]

it put you at risk for diabetes, endotoxins etc

Actually, there is evidence from human studies that it is PUFA, and not SFA (and precisely PUFA from nuts btw) that puts you at risk for diabetes, increased endotoxin, etc. There is so much evidence on the forum about this, a simple search for something like "PUFA diabetes" would have brought up tens of threads. Some of it below.
Nut (PUFA) Consumption May Cause Diabetes Even Without Obesity
PUFA May Drive Obesity, Insulin Resistance, Liver Issues In Diabetes II Patients
PUFA Makes Girls Fat / Lazy / Diabetic And Exercise Futile
PUFAs Cause Obesity And Diabetes. Coconut Oil & Fructose Are Protective
PUFA Deficiency Highly Protective Against Endoxotin
Coconut Oil "completely Abolished Responses To Endotoxin"

If consumption of something like say nuts is found to lower MDA then in all likelihood it is due to its vitamin E content or some other antioxidant present together with the PUFA to protect the plant itself from the PUFA. But even then, it does not mean that the lower MDA will end up protecting from diseases (e.g. diabetes) the PUFA causes in the long run (see above threads). It is not a coincidence high-PUFA oils like wheat germ oil have high contents of vitamin E as the plant needs an antioxidant to prevent the PUFA from going rancid and killing the plant. Animals like cold-water fish that have high-PUFA stores (omega-3) do not need vitamin E as they live in very cold water, but when that omega-3 is eaten by people without vitamin E their MDA levels skyrocket. In fact, nothing raises MDA more than EPA/DHA. So, when the isolated PUFA is tested in studies it invariably demonstrates negative results, to the point that PUFA peroxidation products are reliable biomarkers for degenerative diseases like Alzheimer.
Increased Pufa Oxidation May Be Biomarker For Alzheimers
Blocking PUFA Metabolism May Reverse Alzheimer Disease (AD)
Another Study Links PUFA To Alzheimer Disease (AD)

@tankasnowgod

 

[Kozak]

Funny how you talk about "Well Done Studies," and then cite the following three that you did. The first and last are free living studies, so hardly "well done" in that sense, as they aren't able to control for diet at all. The second is ridiculous, as it uses 100 grams of Blue Cheese a day. Insane. Massive confounder, as using a moldy cheese is almost certainly filled with excess endotoxin, and other problematic substances.

As for the Well Conducted studies you ask for, Haidut has posted several times about the Nanji studies where researchers induced fatty liver (and I believe even NASH and cirrhosis) with diets of Poly Unsaturated Fat and Alcohol, and reversed these conditions simply by switching to Saturated Fat, even when the animals were still being fed alcohol.

A suggestion, as a newbie (if you aren't a troll), you should spend more time searching the forum first, rather than writing a post about studies that have already been discussed previously.

I second that

 

[Nuancé]

Actually, there is evidence from human studies that it is PUFA, and not SFA (and precisely PUFA from nuts btw) that puts you at risk for diabetes, increased endotoxin, etc. There is so much evidence on the forum about this, a simple search for something like "PUFA diabetes" would have brought up tens of threads. Some of it below.
Nut (PUFA) Consumption May Cause Diabetes Even Without Obesity
PUFA May Drive Obesity, Insulin Resistance, Liver Issues In Diabetes II Patients
PUFA Makes Girls Fat / Lazy / Diabetic And Exercise Futile
PUFAs Cause Obesity And Diabetes. Coconut Oil & Fructose Are Protective
PUFA Deficiency Highly Protective Against Endoxotin
Coconut Oil "completely Abolished Responses To Endotoxin"

If consumption of something like say nuts is found to lower MDA then in all likelihood it is due to its vitamin E content or some other antioxidant present together with the PUFA to protect the plant itself from the PUFA. But even then, it does not mean that the lower MDA will end up protecting from diseases (e.g. diabetes) the PUFA causes in the long run (see above threads). It is not a coincidence high-PUFA oils like wheat germ oil have high contents of vitamin E as the plant needs an antioxidant to prevent the PUFA from going rancid and killing the plant. Animals like cold-water fish that have high-PUFA stores (omega-3) do not need vitamin E as they live in very cold water, but when that omega-3 is eaten by people without vitamin E their MDA levels skyrocket. In fact, nothing raises MDA more than EPA/DHA. So, when the isolated PUFA is tested in studies it invariably demonstrates negative results, to the point that PUFA peroxidation products are reliable biomarkers for degenerative diseases like Alzheimer.
Increased Pufa Oxidation May Be Biomarker For Alzheimers
Blocking PUFA Metabolism May Reverse Alzheimer Disease (AD)
Another Study Links PUFA To Alzheimer Disease (AD)

@tankasnowgod

Some studies are interesting, really, although I'm not a fan of rodents studies. Sadly, there is also studies linking SFA with diabetes, fatty liver, heart disease etc... I'm not saying that one side is perfect, I'm saying that it's the biggest controversy that probably exists in nutrition. :)

I've never seen intervention studies showing alarming data concerning raw nuts about these subjects (only for aflatoxins and lipid peroxidation products in roasted/grilled/store bought butter nuts to be totally honest).
Fish and fish liver it's something else, I've seen worrying informations on frozen, smoked, high temperature cooked or processed fish, not really fresh fish.
My home is near the second largest fishing port in France, so I'm lucky enough to have fresh fish, lean or fatty, crustaceans, shellfish etc... some people only have access to canned products or frozen products, even though it's not always a problem.

Effects of sardine-enriched diet on metabolic control, inflammation and gut microbiota in drug-naïve patients with type 2 diabetes: a pilot randomized trial

"
The aims of this pilot study were to investigate the effects of a sardine-enriched diet on metabolic control, adiponectin, inflammatory markers, erythrocyte membrane fatty acid (EMFA) composition, and gut microbiota in drug-naïve patients with type 2 diabetes.
Methods

35 drug-naïve patients with type 2 diabetes were randomized to follow either a type 2 diabetes standard diet (control group: CG), or a standard diet enriched with 100 g of sardines 5 days a week (sardine group: SG) for 6 months. Anthropometric, dietary information, fasting glycated hemoglobin, glucose, insulin, adiponectin, inflammatory markers, EMFA and specific bacterial strains were determined before and after intervention.
"

"
Results
There were no significant differences in glycemic control between groups at the end of the study. Both groups decreased plasma insulin (SG: −35.3 %, P = 0.01, CG: −22.6 %, P = 0.02) and homeostasis model of assessment - insulin resistance (HOMA-IR) (SG: −39.2 %, P = 0.007, CG: −21.8 %, P = 0.04) at 6-months from baseline. However only SG increased adiponectin in plasma compared to baseline level (+40.7 %, P = 0.04). The omega-3 index increased 2.6 % in the SG compared to 0.6 % in the CG (P = 0.001). Both dietary interventions decreased phylum Firmicutes (SG and CG: P = 0.04) and increased E. coli concentrations (SG: P = 0.01, CG: P = 0.03) at the end of the study from baseline, whereas SG decreased Firmicutes/Bacteroidetes ratio (P = 0.04) and increased Bacteroides-Prevotella (P = 0.004) compared to baseline.
"

Sardines being a bit better here for plasma insulin and HOMA-IR than control, and significantly better for adiponectin concentration, a six months intervention study with 100gr (near 4 oz) of sardines five days a week.

I've found a study once on canned cod liver, showing that she wasn't dangerous toward health.

https://onlinelibrary.wiley.com/doi/abs/10.1002/1521-3803(20020101)46:1<40::AID-FOOD40>3.0.CO;2-H

"Lipid resistance to oxidation was found to decrease after thermal treatment of livers. However, the lipid oxidation level in canned liver stored for 3–8 months was not high and averaged, for the entire can content, 0.47 ± 0.4 Meq O, the oil being more susceptible to oxidation that the solids. It is concluded that canned cod liver is a very good source of n‐3 PUFA, particularly with respect to DHA. Heavy metal, DDT, and PCB contamination and the presence of lipid oxidation products in the canned products tested remain at a level producing no perceivable health hazard and could in no way interfere with consumption of recommended amounts of n‐3 PUFAs."

I would probably avoid canned fish liver personally, but this little study is interesting.

 

[Atman]

@Nuancé
Since you are not a big fan of animal studies, I strongly encourage you to do a simple human experiment yourself:

For 2-4 weeks cook all your food with sunflower oil and log your general well being, skin condition etc.
Then for another 2-4 weeks do the exact same thing but with coconut oil and/or butter.

I bet you will come to a fairly distinct conclusion and your desire to lose yourself in the analysis of myriads of questionable studies will perish.
Eventually it will makes sense to you, that the introduction of vast amounts of PUFAs to the human diet in the 20th century was not a good idea.

 

[Vinny]

@Nuancé


For 2-4 weeks cook all your food with sunflower oil and log your general well being, skin condition etc.

I think he mentioned several times at least something like, that he would discuss the influence of WHOLE foods, and he agrees that ISOLATED oils are detrimental.

 

[Atman]

I think he mentioned several times at least something like, that he would discuss the influence of WHOLE foods, and he agrees that ISOLATED oils are detrimental.

Butter and coconut oil are also "!!ISOLATED!!" oils, yet they have been used successfully in human diets for millennia. This whole isolated vs whole dichotomy is almost as useless as the natural/organic vs artificial distinction.
This self experiment I mentioned can also be done with "!!WHOLE!!" foods like sunflower seeds and coconut flesh/milk.