HR-Saturated fats good for the liver?

[gauf]

The following pubmed abstract mentions the role of fats in steatosis (primarily from alcohol).

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=15670659&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus

The part that caused me pause was....  "...1. Unsaturated fatty acids (corn oil, fish oil) exacerbate alcoholic liver injury by accentuating oxidative stress, whereas saturated fatty acids are protective."

I have NASH (and hep C), and I take omega 3 in the form of salmon oil. Am I exacerbating my cirhotic condition?
Thanks.

[St. George]

It should be Arachidonic not Archiodonic Acid.

[St. George]

Off treatment Omega 3's (flax, nuts,seeds) are good because they are anti-inflamatory by nature but on treatment a more pro-inflamtory effect is desired from the omega 6's (egg yolks, olive oil, dairy and red meat).  Look up Archiodonic Acid in Omega 6's and Interferon treatment.

[jmjm530]

Jamin,

I think there are two different issues here. One, what type of fats (and how much fat) might be good for your liver pre and post treatment. The other issue is that ribavirin absorbs better with fat during treatment. Therefore, eating "healthy" might be a priority before and after treatment, but during treatment -- at least for me - I ate what I would term "survival" -- meaning I ate whatever I could tolerate (which was little) with the intent of not losing too much more weight which might have kept me off treatment.
I also tried to include whatever fats I could tolerate (some foods made me nauceous) when I took my riba. Fortunately, my cholesterol went way down during tx (because of the interferon) so probably no real damage done.

Gauf,

Thanks for posting. Very interesting. You might find this site helpful when posting those very long URL's like in  this post. That way the width of the thread remains within the computer monitor :)    http://tinyurl.com/

[jamimapuddle]

I've been doing the fat thing with my riba pills.  I've been trying to use mostly 'healthy fats' like avocado, walnuts and olive oil. I also use the 'bad' stuff like milk, cheese, and eggs too. The only supplement I take is vit D.  Would it be better for me to stick with the 'bad' stuff or take those supplements you mentioned?
Is there anyway to get all that stuff through diet? I'm kind of NOT rich.

[gauf]

Thanks for that. My doc suspects I may have failed treatment due to steatosis (as geno 3, prone to this). And I am on diet and excercise regimen to improve this. My insulin has not been checked yet but he says he may prescribe something to offset this condition. I will have to take careful notes when next I see him. I take PPC.

[CockSparrow]

Thanks for the link and info. For some reason hadn’t paid much attention to AFLD.
There’s a Journal just on Alcohol and related diseases, bugger!
Alcohol (the Journal) has heaps of interesting articles in it. The issue with the article you posted has 4 or 5 related ones. Have to consider subscribing to it. Pity it costs $300, oh well.

What struck you about the article may have been the link between polyunsaturated fats and steatosis, but for me it was this.

Polyenylphosphatidylcholine may prevent liver injury by down-regulating cytochrome P450 2E1 activity, attenuating oxidative stress, reducing the number of activated hepatic stellate cells, and up-regulating collagenase activity.

Now where have I seen this mentioned B4??

Anyway thought you might be interested in this smallish study.

Insulin resistance and response to therapy in patients infected with chronic hepatitis C virus genotypes 2 and 3
Journal of Hepatology 48 (2008) 28–34

Results: The overall SVR was (77%). Patients with a SVR had lower mean serum insulin (10.7 ± 0.8 lU/ ml vs. 22.2 ± 4.9; P = 0.03), fibrosis stage (1.9 ± 0.1 vs. 2.7 ± 0.3; P = 0.007) and insulin resistance measured by the homeostasis model (HOMA-IR) (2.5 ± 0.2 vs. 6.1 ± 1.5; P = 0.03). Age, gender, ethnicity, alcohol consumption, treatment regimen, viral load, portal activity and steatosis did not influence the SVR.
By linear regression, body mass index (P < 0.001) and fibrosis stage (P < 0.001) were independently associated with HOMA-IR. After adjusting for fibrosis stage, patients with HOMA-IR of <2 were 6.5 times more likely to achieve SVR than those with HOMA-IRP 2.

Conclusions: Even in treatment-responsive genotypes 2 and 3, high HOMA-IR is associated with a reduced response.
Improving insulin sensitivity may be a useful adjunct to anti-viral therapy in these individuals

CS