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100019 tn?1335923317

Low cholesterol levels also predicted a lack of treatment success

"Low cholesterol levels also predicted a lack of treatment success."


Forgive me if this has already been posted and discussed.  I couldn't find a reference to it, but that doesn't always mean anything.

I thought the entire article was interesting, but especially that sentence in the last part of the article caught my attention.

I had a cholesterol test approx six months before Tx and again approx 6 months after TX, as part of a routine check up.  My cholesterol had dropped in half.  My doctor appeared to be rather bemused and had me re-take the test assuming it was incorrect, but it wasn't.  He said without taking medicine he thought it highly unusual to drop that much.  

Anyone else heard anything about low cholesterol ?
35 Responses
Avatar universal
I'll add to that list --- have you taken any dietary supplements in the interim such as Red Yeast Rice Extract? Red Yeast is basically a statin and can significantly reduce cholesterol in the same way pharm statins like Lipitor can.
Avatar universal
Did you lose a significant amount of weight, or change your diet, exercise, etc, between the two tests? I've heard of cholesterol dropping dramatically DURING treatment (mine did) but it returned to pre-tx levels (actually higher) within a month of being off the treatment drugs. Assuming your first test was correct, and diet/weight are about the same, if you haven't already, I would discuss the drop with a liver specialist (hepatologist) because as the article states, low cholesterol is sometimes associated with more severe liver disease. Have you had a recent biopsy? What is your platelet count and has it changed much? What is the size of your spleen under ultrasound? I'm not qualified to diagnose, but these are things your doctor might want to look into. Hopefully, it's just good news, but like your doc said -- cholesterol dropping by half is highly unusual unless something has changed.

All the best,

-- Jim
100019 tn?1335923317
I lost 50 lbs during tx, but gained all of it back within 6 months after tx.  No to the Red Yeast Rice Extract.

The only supplements I took (still do) is vitamin e, last month adding calcium, but that was after the tests.  

My next apt with the liver spec. is in Sept.  My first and last biopsy was August of '05, before tx.  The article caught my attention for all the reasons you just mentioned.  Until I see the dr. I have a hard time believing my liver could have gotten worse DURING tx.  Don't all the studies suggest liver improvement????  Don't know a thing about my spleen, but will certainly be bringing it to the attention of someone!

151263 tn?1243377877
I deliberately increased my cholesterol levels before and during my treatment. I was throwing back the ice cream, whole milk, pizza (especially pizza), french fries, milk chocolate, fudge brownies, whatever. I can't know if it helped during my treatment, especially considering I was taking VX950 along with IFN+riba, but I remained UND from week 2 onwards all the way through my 41 week treatment cycle (2 week post tx also UND) - but it mighta. The bummer part is, is that a high LDL level specifically was found to increase SVR rates. As you might know already, LDL is the "bad" cholesterol. So anyone with an existing problem with heart disease/arterial sclerosis would probably be ill advised to use this strategy. Although on the other hand the benefits of a temporary LDL elevation both just prior to treatment and during the first 3 months (or so) might outweigh the additional risk factor. Hard to say in the end, although the studies out there give a strong correlation between LDL and positive anti-viral response during SOC treatment.
Avatar universal
same thing here my cholesterol dropped 35 points halfway through treatment but rebounded back at the 3 month post test.....
96938 tn?1189803458
When I read about it months ago I viewed it as another signpost along the way and perhaps a missed opportunity. But I'm not sure.  Having had cirrhosis should have been enough for alarms to go off somewhere that modification of SOC might be a consideration.  I don't blame my tx doc  for relapse - heck, he's a great guy and willingly collaborates with a liverhead now on my behalf.  My issue is tx that is always squarely  inside the box for most people and maybe there is enough knowledge out there for docs to take note.  For about the last 20 years, maybe more, my LDL always tested in the 60's.  Can't tell you how many med professionals said 'wow,  or what do you eat or something like that'.  Sometimes dots don't get connected.
Avatar universal
I'm pretty sure you understand, but for others that might not have read carefully enough into this...

It's very unclear if raising your cholesterol by your own efforts pre-tx will have any effect at all on SVR. And, if in fact, the negative correlation between low cholesterol and SVR are due to more advanced fibrosis, then raising your cholesterol will obviously have no effect at all. This is not to say what you did has no merit, but it certainly has no proven merit.

-- Jim
86075 tn?1238118691
My good cholesterol has always been high (and considered good) and my bad cholesterol has always been low...guess I shouldn't celebrate that any longer...if anyone has any takes....
Avatar universal
I wouldn't read too much into that study beyond what the study actually says.  Many people have a lipid profile like yourself -- everything being equal an EXCELLENT profile -- and don't have any liver damage, or HCV for that matter. If you biopsy and/or Fibroscan says you don't have significant liver damage, that is what would count in my book. Of course, you could order up the original studies -- full-text -- and pour over them, like I probably would have had they been out before I started treating, but nothing that I've read in snippets suggests you have any problem.

-- Jim
100019 tn?1335923317
Forseegood : You're d**** if you do and you're d**** if you don't!

Jim, I second what you say.  I hope no one in any way thinks I'm suggesting they try raising their cholesterol.

This was just FYI - another piece of the puzzle.
Avatar universal
Just goes to show you.  Whats good for the goose isn't always good for the gander.   They can do a million studys and it will still come down to this virus is different for everyone.  Its in the Genes!!!!.

151263 tn?1243377877
Not sure I follow you completely, so I'll address a few of your comments point for point for clarity:

"It's very unclear if raising your cholesterol by your own efforts pre-tx will have any effect at all on SVR."

Well, I'm not sure how you would define "very unclear". But based on what I've read so far, there are a few studies that suggest this might very well be true. And the correlation between high pre-treatment LDL and subsequent UND/SVR rates was quite strong in the main study I've referenced here before and include again.  http://www.natap.org/2006/HCV/080806_02.htm  As with most studies it's not the end all be all nor the final word on the matter, but I think it's maybe a notch or two above "very unclear", which to me implies virtually useless information.  Plus there's a reasonably well understood mechanism concerning how the virus gains access to the hepatocytes that might be hindered via elevated LDL levels (which apparently serves to block viral access to the host cell). This is why the referenced study was conducted in the first place, to investigate this pre-existing theory behind the possible connection between viral replication rates and cholesterol levels. As you probably recall from a previous conversation quite some time ago, hepatitis researcher commented that the theory appeared to have merit and seemed logical (without blanketedly endorsing the idea or the study findings, of course).

"And, if in fact, the negative correlation between low cholesterol and SVR are due to more advanced fibrosis, then raising your cholesterol will obviously have no effect at all. This is not to say what you did has no merit, but it certainly has no proven merit."

I guess I'm just not following you here, or perhaps you've seen some research I'm not aware of (and feel free to enlighten me if you have). I'm aware that cirrhotics commonly have abnormally depressed cholesterol levels due to compromised liver functions (with cholesterol production being one of those functions). And I'm also aware that cirrhotics commonly experience lower overall SOC anti-viral performance in the form of time to UND and ultimate SVR rates. With those observations in mind, are you saying that I'm saying that those factors "prove" that low LDL predicts low SVR rates in cirrhotics or any other non-cirrhotic HCV+ patient for that matter??? If so, I'm not saying/suggesting that, all I'm saying/suggesting/referencing are studies like the one referenced above that use quite strong language and apparently reasonably well "reasoned" logic (again, as per HR) to explain this receptor blocking rationale (that appears borne out by these admittedly few studies). Here's just a few quotes from the study:

"Multivariate analysis of serum LDL level and SVR, after accounting for age and viral genotype, showed patients with higher LDL levels had significantly higher odds of achieving EVR, ETR, and SVR. Similarly, higher pretreatment serum cholesterol level was associated with higher odds of having EVR, ETR, and SVR."

"LDL and cholesterol levels prior to treatment were found to be higher in patients with positive EVR, ETR, and SVR. This difference remained significant independent of age. Multivariate analysis controlling for genotype and age showed that the higher the cholesterol and LDL levels prior to treatment, the greater the odds of responding to treatment...."

"For all patients LDL level was statistically significantly different between responders and nonresponders for EVR, ETR, and SVR (P = 0.0253, P = .0091, P = .0071, respectively; Fig. 1). Similarly, total cholesterol level differed significantly between responders and nonresponders for EVR, ETR, and SVR for all patients."

"The statistical significance of differences between responders and nonresponders in LDL and total cholesterol levels remained after controlling for these confounding variables (Table 4B). When we observed the effect of pretreatment LDL level, controlling for age and genotype, we found the odds of patients in the medium LDL group achieving EVR was 2.43 times that of patients in the low LDL group. Similarly, the odds of patients in the high LDL group achieving EVR was 2.43 times that of the patients in the medium LDL group. Likewise, looking at the effect of pretreatment cholesterol level while controlling for genotype and age showed the odds of patients in the medium cholesterol group achieving EVR was 1.93 times that of patients in the low cholesterol group, and similarly, the odds of patients in the high cholesterol group achieving EVR was 1.93 times greater than patients in the medium cholesterol group. The odds ratio of LDL predicting a treatment response was higher than that of total cholesterol."

As you can see, they use very strong and unambiguous language here, which as you know is rather rare for these types of studies. The researcher's confidence level appears quite high, and the reported data seems to be (sensibly) responsible for this confidence. Plus they have a sizeable test population, so the statistical significance isn't frivolous. Overall, not trying to make a mountain out of a mole hill. This high LDL level being beneficial for increased EVR/RVR and SVR rates theory remains at this point, just that: a theory. But in my opinion, I felt it was worth the added transient cardio risk to load up on the lard prior to and during my treatment. And because I did, in my judgment it exceeds the "very unclear" threshold you describe. Can't prove it in a court of law, but in this case I think the potential reward exceeds the risk. As always, YMMV.
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