If we follow the advice laid out in a previous post and increase fat while restricting PUFA, will the extra saturated fat be good or bad for our liver, HCV aside?
That depends, I suppose on whether you think alcohol and drugs and NAFLD are good models for virus-related liver damage. At present they are the only models we have. And we know that alcohol, acetaminophen, and fructose don't help people with Hep C. So I think they are very good models; all the mediators of liver damage from those causes are also present in the livers of people with Hep C (high ferritin, stellate cell activation, LPS sensitivity, lipid peroxidation, oxidative stress, and so on).
So personally I don't see it as any kind of leap to accept the relevance of papers like these. Besides, the proof of the suet pudding will appear in the eating thereof.
Hepatic Stellate Cells are the cells that make collagen in fibrosis. They are also called Ito cells, which explains why I missed all these Ito cell studies before (when I was collecting data on factors, including SFAs, that reduced hepatic stellate cell activity).
This is another line of evidence supporting the view that saturated fat in the diet is antifibrotic.
"When tallow was substituted for corn oil the Ito cells were not activated and the liver histology was normal".
Is it the PUFA restriction alone, or the addition of SFA?
My reading of these papers is that both play a role. Even 5% calories as PUFA causes some fibrosis on a low-fat diet, but none when corn oil is added to beef fat or coconut MCT to give a similar ratio.
These may only be animal tests, but I assure you, if a supplement performed half as well as saturated fat in animals, it would out-sell Silymarin.
Besides, we are talking about something everyone eats already.
This paper suggests that flaxseed oil may not be the best omega-3 supplement for alcoholics: linolenic acid is the vegetable form of omega-3.
In fact, this paper should be read in full and all the figures and tables studied, because there are 4 groups of control rats fed various fats without alcohol, and what happens to them is as interesting as the effects with alcohol.
![]()
That depends, I suppose on whether you think alcohol and drugs and NAFLD are good models for virus-related liver damage. At present they are the only models we have. And we know that alcohol, acetaminophen, and fructose don't help people with Hep C. So I think they are very good models; all the mediators of liver damage from those causes are also present in the livers of people with Hep C (high ferritin, stellate cell activation, LPS sensitivity, lipid peroxidation, oxidative stress, and so on).
So personally I don't see it as any kind of leap to accept the relevance of papers like these. Besides, the proof of the suet pudding will appear in the eating thereof.
Hepatic Stellate Cells are the cells that make collagen in fibrosis. They are also called Ito cells, which explains why I missed all these Ito cell studies before (when I was collecting data on factors, including SFAs, that reduced hepatic stellate cell activity).
This is another line of evidence supporting the view that saturated fat in the diet is antifibrotic.
"When tallow was substituted for corn oil the Ito cells were not activated and the liver histology was normal".
Is it the PUFA restriction alone, or the addition of SFA?
My reading of these papers is that both play a role. Even 5% calories as PUFA causes some fibrosis on a low-fat diet, but none when corn oil is added to beef fat or coconut MCT to give a similar ratio.
These may only be animal tests, but I assure you, if a supplement performed half as well as saturated fat in animals, it would out-sell Silymarin.
Besides, we are talking about something everyone eats already.
This paper suggests that flaxseed oil may not be the best omega-3 supplement for alcoholics: linolenic acid is the vegetable form of omega-3.
Besides, the benefits from PUFAs in Hep C (antiviral and metabolic) are only seen with DHA, arachadonic acid, and EPA (in descending order of potency), and these are only found in animal fats; oily fish, fatty red meat, organ meat, dairy fats, and egg yolks.
LOOK AT THIS TABLE: http://jn.nutrition.org/content/134/4/9 ... nsion.html
LOOK AT THIS TABLE: http://jn.nutrition.org/content/134/4/9 ... nsion.html
In fact, this paper should be read in full and all the figures and tables studied, because there are 4 groups of control rats fed various fats without alcohol, and what happens to them is as interesting as the effects with alcohol.
The control rats fed most saturated fats gained the least weight. Corn oil (high PUFA) was significantly more fattening than a mixture of beef fat and coconut MCTs, in a breed of rat designed to get fat on a "high fat" diet.
And here's one for the vegetarians: Olive oil is quite good at suppressing fibrosis, though perhaps not as brilliant as beef fat. (note that mutton, goat, venison, cocoa, and dairy fats ought to be similar to beef and coconut).
When I say "saturated fat" I really include monounsaturated fat, as it behaves chemically in pretty much the same way; it takes more than one unsaturated bond in close proximity (there are two such bonds near to one another in omega-6 lineolic acid) to promote lipid peroxidation.
Dietary olive oil prevents CCl(4)-induced tissue injury and fibrosis in the liver. Since oleic acid inhibited activation of HSCs, oleic acid may play a key role on this mechanism.
And here's one for the vegetarians: Olive oil is quite good at suppressing fibrosis, though perhaps not as brilliant as beef fat. (note that mutton, goat, venison, cocoa, and dairy fats ought to be similar to beef and coconut).
When I say "saturated fat" I really include monounsaturated fat, as it behaves chemically in pretty much the same way; it takes more than one unsaturated bond in close proximity (there are two such bonds near to one another in omega-6 lineolic acid) to promote lipid peroxidation.
Dietary olive oil prevents CCl(4)-induced tissue injury and fibrosis in the liver. Since oleic acid inhibited activation of HSCs, oleic acid may play a key role on this mechanism.
