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100019 tn?1335919717

Low cholesterol levels also predicted a lack of treatment success

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

http://www.medicinenet.com/script/main/art.asp?articlekey=82349

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 ?
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Avatar universal
This is strange.  My high LDL is how I found out I had hep-c.  They suggested lipator or something like that and I said wait a minute, isn't that stuff hard on your liver?  They said yes and ordered a liver panel and back came hep-c.  From what I have read here my LDL should have been lower since I have had this virus for so long. Since I never got a biopsy I guess at least for me I don't know if my liver had anything to do with the LDL.  Now before anyone jumps on me I did get an Ultrasound and it was the best thing I could have done as they discovered a real silent killer. One that kills more people then hep-c.  That is an aorta aneurysm which I had repaired last year. If the ultrasound did not find this 5 years ago It would have killed me sooner than the hep-c.  Go figure  Sometimes its better to be lucky than good.
                                                                                                                                       Ron
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96938 tn?1189799858
Mine did too.  After years of LDL in the 60's it broke through to 105 during tx#1.  After relapse, and before tx#2, it was back in the 60's.  Haven't had it tested during tx#2. In my interest to minimize things to focus on, I don't care about much more than pcr's and cbc's now.
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Avatar universal
I didn't realize you were currently treating, I hope you're making good progress and things are going as well as can be expected. I'll try and address your response as best I can below:

I guess we're simply going to have to agree to disagree that cholesterol and LDL levels can be significantly adjusted via dietary intake in most people. I know there are exceptions to this rule, but the rule it remains for most people. I've always thought that it's essentially common knowledge that diet plays a significant role in blood serum cholesterol levels in most people, but this thread has me re-thinking the "common knowledge" part. I guess the current trend in thinking amongst many ordinary people is that diet has little or no influence on cholesterol levels. Not sure why that might be, but I think what upbeat alluded to hints to why this might be. The drug companies have been working hard in recent years (via commercials, advertisements and even studies) to change our perceptions on that count for the purposes of selling us more drugs (as opposed to advocating/promoting drug-free naturalistic remedies like improving one's diet, losing weight and exercising). But whatever the reason, the fact remains that diet DOES significantly influence cholesterol levels in most people and we are what we eat in that regard (and myself and many many others are living proof of that). You also state:

"Speaking of effect of high levels of LDLs pre-treatment on SVR levels, I ditto all people of this board who suggested that it is very unlikely that this number affect either way…I analyzed quiet excessively a few months ago when I first time read this article.  If somebody is interested in my ideas on this subject, I will cover it next time."

Well sure, if you have a concise theory/explanation as to why you feel that elevated LDL levels do not influence (i.e. benefit) SOC antiviral response rates (i.e. you think the referenced studies are baloney), then by all means lets hear it.

"I’m an engineer, like you (I believe), but just different kind of engineering.  I was trained to design and develop different medical equipment/ instrumentation …"

That's really interesting! What kind of equipment do you design? I've spent more than a few hours running HPLC's (chromatography) and flame atomic absorption (AA) spectrophotometers and some other fancy stuff. I used to talk to the guy who came by to service our units (Perkin Elmer rep) and learned quite a bit about our machines from him. I still sprinkle a little salt on the stove burner once in a while just to see that brassy yellow sodium flame - loved that stuff.

Anyway, in closing I just want to quickly summarize why I think deliberately increasing LDL just prior to and during a few weeks/months during treatment is a good idea:

First, lets assume this theory of increased LDL levels actually does work and it significantly increases your odds of achieving an RVR/EVR and subsequent SVR. Obviously, that would be a fantastic benefit/advantage you might glean should you choose to employ this strategy (by bulking up on the bacon and eggs for a while). Or, if you already have an elevated level of cholesterol/LDL, you simply do nothing to lower it during the earlier timeframe of treatment (under your dr's supervision of course). You'd be significantly more likely to get rid of the virus once and for all (with all the benefits that entails), while also minimizing the likelihood of repeated exposures to the treatment drugs and both their short and long term side effects (some of which can be permanent and life altering in a very bad way). I mean, what's not to like???

Ok, what's not to like is that you've temporarily raised your cholesterol level into an unhealthy range that is known to cause or exacerbate arterial plaque/sclerosis. Alright, so everyone knows arterial plaque/sclerosis is bad, my goodness no one wants clogged arteries. That can cause high blood pressure, stroke and angina!! Ok, fair enough, but there's just one problem with this concern/fear, and that problem is that clogged arteries don't happen overnight. And they certainly don't happen over the course of a few weeks or months. It happens slowly over years and years and years and years - DECADES. It normally takes decades of bad health habits and persistently elevated cholesterol levels to clog up your arteries, and sometimes even that won't do it (ever known a crusty old fart who ate sausage every day, drank highballs and smoked pall malls his whole life and yet still lived to 95?? I have!). Arterial sclerosis happens, but it isn't going to happen within a few weeks or a few months. And also remember that while eating bad food for a while is bad for you, taking interferon and ribavirin (and perhaps a PI) are bad for you too...very bad for you in fact. Yet we're willing to take these poison pills and temporarily harm our minds and bodies to achieve a greater good. Why should eating hamburgers and ice cream for a shorter period time be viewed any differently?? (especially considering the harm they do is certainly more benign than what IFN+riba does)

Lastly, lets assume this high LDL = increased SVR rate theory turns out to be a bunch of hooey. And lets say you employed this strategy prior to learning this - what price have you paid by deliberately raising your LDL level for a few weeks/months during your treatment? Well, you probably deposited some more plaque inside of your arteries, and man that's not good. But how much did you deposit??? Well, that's hard to say exactly, I'm sure it would vary from person to person depending on just how much they elevated their cholesterol and how long they elevated it. But what's not hard to say is that based on the fact that it takes decades to clog up a person's arteries (unless you're a very special case), the amount of plaque you deposited could be described as essentially and effectively NIL. i.e.---> negligible. But wait! Even if you didn't consider the 'additional' damage done to your circulatory system during that brief "window of fat" negligible and wanted to do something to reverse it - you could! If you're willing to go the distance via strict dietary controls and/or through the use of statins to improve your lipid profile, you can actually adjust your total cholesterol and HDL/LDL ratio in a manner that will actually cleanse plaque from your arteries. That's right, plaque deposits can actually be (slowly) reversed if you get your numbers lined up right (as I have before through olive oil and omega 3's via salmon and flaxseed oil). So even if you  were terribly uptight about your 230 cholesterol level during the first 3 months of treatment, then simply become a healthy nazi for awhile and reverse whatever tiny effect if might have had on during that 3 months (or thereabouts).

So with all of that in mind, I think this study has heft to it (and the others piling up supporting it). So much so I think it's virtually a no-brainer for anyone considering going into SOC treatment anytime soon. (with the usual disclaimers concerning special exceptions/exclusions for those who fall into riskier categories and/or where their doctor specifically forbids the strategy for some other medically legitimate reason).
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135456 tn?1301437624
My doctor told me that interferon is known to cause blood levels of cholesterol to rise, mine did.
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Avatar universal
Cholesterol is an important substance for human life and growth.  However, it is not essential in the biological terms (meaning, that it does not have to be supplied through food, because required for life amount is produced by liver).

If a person consumes any amount of the substance naturally produced by body, the healthy human body will react in two possible ways:
a) the body will excrete the excess as a waste product
b) The body may adjust and start producing less amount of the substance, so the sum is constant (usual effect observed with supplemental hormonal intake with active glands present.  Example: supplemental intake of estrogen by pre-menopausal females for enhancement of female features will not help females without removal of ovaries.  But for the gentlemen, considering sex change, estrogen consumption will produce feminine features.
However, there is some sort of threshold – if you consume too much of the substance naturally produced by body - body may not be able to adjust by simply shutting down its own glands or excreting as a waste product (or metabolizing it).  Example: male body builders.  It is common knowledge that extreme consumption of male enhancing products may shut down/ damage/ destroy multiple organs (while a wonderful human organism trying to figure out the path ways of the excess elimination).  You have to remember that we are the latest evolution product with highly developed “survival system”, so it takes us a while until our bodies give up the battle of adjustment.

Speaking of cholesterol, so called “bad” (LDL) is crucial for survival … I did not have a refreshment course in biochemistry, so I’m trying to recollect my 15 years old knowledge (and forgive me, if I’m not presenting it correctly – there is always a good excuse – interferon induced brain fog), Low Density Lipids transport fats from a digestive system through the blood stream to the liver for fat metabolism with help of bile – sorry, may be I oversimplified.  However, some people genetically designed with, for example, larger LDL particles, allowing to transport probably more fat, but the same time asking for trouble of fat with cholesterol particles deposition inside of the blood vessels.  In other words, larger particles of fat and LDL mixture have less chance to get to the liver due to early precipitation in the vessels.  After that point scientists may exercise their brains endlessly...

This was just one easy explainable example of genetic variance effect on the metabolic pathway.  There are many more reasons for different rates of removal excess cholesterol by human body.  But in many cases science is still trying to learn and explain differences in peoples’ “survival skills”.  The easiest solution is to recommend fat restricted diet – this is something that all people can do and definitely, even if it does not have any benefit on cholesterol level, it will give many other benefits, resulting in prolonging human life.  For example, I’m considered, underweight and have been all life.  And underweight people (even though appearing normal and slim) are not considered the best for the healthy and long life.  When my mother (also very slim) was recovering after surgery (in another country), she overheard medial personal discussing her case as saying “if she had a little bigger body mass, she definitely would survive, otherwise, it is not likely” (they did not know that she already was becoming alert).

Speaking of effect of high levels of LDLs pre-treatment on SVR levels, I ditto all people of this board who suggested that it is very unlikely that this number affect either way… I analyzed quiet excessively a few months ago when I first time read this article.  If somebody is interested in my ideas on this subject, I will cover it next time.
The reason I was interested in this subject that genetically (or due to other undiscovered problems), my cholesterol was high from age 23 (and being deadly skinny like models), may be earlier, but I did not check it before… it definitely did not concerned me a bit... I just enjoyed the fact that I could come up with different jokes for my parents/ grandparents friends.  At 26 (in 1995) I was diagnosed with hep. C during routing physical exam - who knows how long I had it, but a Dr. noticed somewhat elevated ALTs and decided to check further.  When a nurse recommended over the phone a visit to a hepatologist due to suspected hep. C, my first question was “How is my cholesterol”?   I new that Hep. C is some sort of viral disease of liver, but I did not think that there are any treatments… and I did not have any insurance… so why worry? if I can do nothing about it.  Well, of course I had high cholesterol, as always (FYI, I never really liked or eat greasy food, with the exception of occasional pizza).   Long story short, my first interferon + riba for 48 weeks clinical trial was unsuccessful, I did not have 2 log drop at the end of 48 weeks and was declared unresponder.

Not so long ago, I completed 98+ weeks of high dose daily Infergen with riba… my cholesterol was quiet low prior and during treatment, probably due to liver function decrease/cholesterol production.. will be interesting to see the results.

Mremeet: To answer your question, I’m not a Dr.  I’m an engineer, like you (I believe), but just different kind of engineering.  I was trained to design and develop different medical equipment/ instrumentation … so I had an extensive chemistry training (my second background) and we used bio chemistry text books designed for medical students, of course, many chapters were not included in the study course, but I studied anyway because I was extremely fascinated with all this stuff, even eventually I was included in the research team with my professor – this how I ended up having one more degree… which, unfortunately, I don’t utilize in my daily work, but found it is quiet useful for my personal research.

Cheers and all the best to everybody!!
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Avatar universal
I bet it does help you  to svr when your body is harboring a little more fat than it should it just makes since wish we could poll the svrs and get thier pre tx lipid labs......
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Avatar universal
Maybe its just the drug companys pushing their drugs.  Lipitor says only 20% of cholesterol comes from food and 80% is made by your body.  

                                                                                                                                       Ron
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Avatar universal
upbeat - While it's true that some (relatively rare) people can basically eat anything they want and it will not appreciably affect their cholesterol levels, for the vast majority of us diet absolutely impacts cholesterol and LDL - and it impacts it significantly. Take a look at what the CDC says:

http://www.cdc.gov/cholesterol/prevention.htm

"People can have an excess of cholesterol because of DIET [emphasis added] and because of the rate at which cholesterol is processed in the body. Most of the excess cholesterol comes from DIET." [emphasis added]

"If it is found that your cholesterol is high, your doctor may prescribe various treatments depending on your risk for developing heart disease. These include lifestyle changes such as DIET [emphasis added], weight control, and physical activity. Certain drugs can also be prescribed to manage your cholesterol."

"A number of things can affect the cholesterol levels in your blood. These include the following:

DIET [emphasis added] - Certain foods have types of fat that raise your cholesterol level. These types of fats include saturated fat, trans fatty acids or trans fats, and dietary cholesterol. Saturated fats come largely from animal fat in the diet, but also some vegetable oils such as palm oil. Trans fats are made when vegetable oil is hydrogenated to harden it. Research suggests that trans fatty acids can raise cholesterol levels. Dietary cholesterol is found in foods that come from animal sources such as egg yolks, meat, and dairy products.

Weight - Being overweight tends to increase LDL levels, lowers HDL levels, and increases total cholesterol level.

Physical Inactivity - Lack of regular physical activity can lead to weight gain, which could raise your LDL cholesterol level.

Heredity - High blood cholesterol can run in families. An inherited genetic condition results in very high LDL cholesterol levels. This condition is called familial hypercholesterolemia.

Age and Sex - As people get older, their LDL cholesterol levels tend to rise. Men tend to have lower HDL levels than women. Younger women tend to have lower LDL levels than men, but higher levels at older ages (after age 55 years)."

motheroffour - You ask about riba binding to fat: I don't know on a molecular level if it binds to fat, but I do know that we were advised to always take our riba (and VX950) with a fat rich snack prior to every dose (and this is also mentioned in the package insert). The fat helps the riba be more fully absorbed into our bodies, thereby increasing its blood serum concentration (and subsequent effectiveness). You also raise the issue concerning decreased overall SVR rates amongst obese patients (with high BMI) and how this apparently contradicts the theory of high LDL corresponding to higher SVR rates (because obese patients tend to have higher LDL levels). Firstly, it's not true that all obese people have unhealthy cholesterol levels (including elevated LDL), although generally they are more likely to. But it is true that people with high BMI's do tend to SVR less often (when treated with SOC) when compared to thinner people. And although I don't think it's fully understood exactly why obese people tend to experience lower antiviral performance, I think there's a a pretty obvious reason that probably plays a major role that's unrelated to LDL. First is that much of the SOC SVR statistical data that was compiled in the fairly recent past was based on fixed riba dose regimens. It was common in the earlier days of SOC treatment for patients to receive a fixed dose of 800mg of ribavirin. The dose was not adjusted to accommodate for variances in weight, and was NOT optimum for heavier patients (with "heavier" being defined as basically anyone over 150 lbs or so). As you can imagine, a woman weighing 130lbs taking 800mg of riba a day will have a much higher riba blood serum concentration than Lumpy Lewinski weighing in at 400 lbs and also taking 800mg/daily. Even when weight based ribavirin dosing became more commonly accepted, the max dose usually given is 1200mg, as per the product insert (although some doctors will prescribe more "off-label" if you're game for it). But even 1200mg isn't going to get the aforementioned Lumpy's riba serum concentration up to a level comparable to someone 1/3rd his weight. I'm less knowledgeable about weight based interferon dosing and its impact on SVR rates in regards to high BMI patients, but again there's a fixed "ceiling dose" approved by the drug companies that many doctors will not go above regardless of how heavy their patients might be. I believe offlabel higher-than-standard dosing of interferon may be helpful for those with high BMI's, but again I'm not very knowledgeable about that aspect of treatment for high BMI's. Lastly, there's other factors that may negatively impact SVR performance in high BMI patients - like a suspected link between decreased SVR rates in those with insulin resistance or outright diabetes, for instance. Obviously diabetes and insulin resistance are very commonly associated with obesity and high BMI's.

So as you can see the picture is much more complicated when assessing cause and effect when predicting SVR performance for high BMI patients, especially in regards to cholesterol levels addressed in this thread.
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Avatar universal
Strange.  I was always under the impression that food had very little to do with LDL and everything to do with your Genes. From what I understand you can only lower your LDL slightly with diet,

                                                                                                                                         Ron

                                                                                                                                          
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Avatar universal
Did someone at one time say that Riba binds to fat?  Perhaps those with high cholesteral...in general...(dismissing people with genetic high cholesteral who are of normal weight)....have more "fat" that the Riba binds to ergo "sticking" in the person longer and doing a better job of mopping up the viral remnants.  It's possible that it's something that simple, although it flies in the face of the theory that obese/heavy patients have a more difficult time clearning HCV which I think I also read,  so I  couldn't really buy into the "cholesteral bulking" as a potential avenue to easier clearning I guess.
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Avatar universal
"I already said (see my last post) that I wasn't intentionally being dismissive, and in fact your theory may have merit. How many times do I have to clarify my statements? I stick to what I said in my last post regarding your theory ,and for the last time will say I'm sorry if you found the statements "dismissive" because that was not my intent."

You don't have to clarify your statements at all. But it's disingenuous on the one hand to claim you're not being dismissive (on whatever level to you wish to concede, if any) whilst simultaneously persisting in providing lengthy rebuttal-like dissertations about why you think what I did specifically in regards to deliberately raising my LDL level was not corresponding with the referenced study nor the concepts detailed therein (with the subsequent impliance they had little or no merit). In short, it’s classic passive aggressive posturing. I never claimed, suggested nor insinuated in my original statement that it was a "proven" fact that deliberately elevating LDL would translate into elevated odds of getting an SVR. No one came down from the mountain in a toga with a flowing gray beard bearing chiseled stone tablets declaring in a reverbed out Heston-like voice: ALL YE WHO SEEK SVR SHALL EAT MANY MANY CHEEEBOOGAH!! IT HAS BEEN WRITTEN, SO SAYETH MREMEET!! I perfectly qualified my initial statement and it was valid as it stood (if you have doubts, re-read it). And yet you initially responded with a 'corrective' counter statement that was somewhat dismissive (yes, that's right dismissive) and gave off the impression that me raising my LDL prior to treatment was all but foolhardy. You said: "It's very unclear if raising your cholesterol by your own efforts pre-tx will have any effect at all on SVR [you then later reiterate this sentiment because you've apparently decided that dietary LDL's don't have quite the same oomph as liver produced LDL's, and yet offer no plausible explanation as to why you feel that's true]. And then go on to say: "This is not to say what you did has no merit, but it certainly has no proven merit." Um, yeah, who said it had "proven merit?" All I said was all I said, and all I said was that there was some good evidence (which has been thoroughly cited) that *strongly* suggested it MAY have merit (with an emphasis on strongly). So with that in mind, why the overly dismissive counter statement? And yes, it was both overly dismissive and countering, you can claim it wasn't (and perhaps honestly believe it), but it was. And as I asked in my previous post (that you did not respond to), why do you feel so strongly that dietary LDL’s would function differently within the context of possibly inhibiting viral-hepatocyte invasion when compared to liver produced LDL’s? (which again, was at the core of your “dismissiveness”)

As to alcohol, as I already stated I included that as an example of yet another nebulously defined HCV related treatment theory. And also because you’ve been dismissive of it in the past too, and not that I’m interested in rehashing it (as I’d suspect you aren’t either). As to the concept that not everyone’s LDL can be raised via the consumption of lard sandwiches, yes I know that’s true and is why I mentioned it in my previous posts. But suffice to say, for the vast majority of folks, diet DOES play a role in cholesterol and LDL levels (and yes age does too).

Thanks for the congrats on the hopefully impending SVR, appreciate the sentiment. The end.
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Avatar universal
Against better sense, let  me try to bridge the gap a little.

Mre, my cholesterol profile seems similar to yours in the respect that I have a total cholesterol around 180 if I eat very well and it goes up to 220-250 range if I let's say pig out. That said, not everyone has this reaction. I have friends on a very high fat diet -- McDonald's and all -- who have very low cholesterol and then, of course, there are those that eat well and have very high cholesterol. So yes, eating a high fat diet in many of us raises LDL, but in those who are able to metabolize cholesterol in a different way, it may not to any signficant way.

-- Jim

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Avatar universal
Are you a doctor? When you say "If you were able to increase the LDLs levels simply by increasing consumption of fat, that fact signifies underlying metabolic problems...we usually associate it with age."   If you don;t mind me asking, who's "we"? To my knowledge, it's well understood and acknowledged in western science that LDL levels are either directly or indirectly influenced by the consumption of fats, especially saturated fats. Speaking for myself, I have a pretty lengthy labwork dossier indicating what my cholesterol profile has been for over ten years. It's almost always quite healthy, with a total cholesterol around 180 and an excellent ratio of LDL to HDL. The only time it get's a little out of line, is if my diet persistently goes astray. As soon as I started deliberately hitting the high fat food (just prior to my tx), it jumped right up into the 250-ish range, and my HDL/LDL ratio skewed right out of wack. My LDL's were much higher as a consequence of my dietary change. I'm not a doctor, but as far as I know this is pretty typical of what happens to most people once they hit the fatty foods.

Thanks again for the kind words...
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Avatar universal
Mre: As already stated, I agree it's not "proven" according  to the exacting standards associated with mathematical proofs. It's just that my impression of your initial response to my initial statement concerning high LDL vs increased EVR/RVR/SVR rates was one of being overly dismissive.
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I already said (see my last post) that I wasn't intentionally being dismissive, and in fact your theory may have merit. How many times do I have to clarify my statements? I stick to what I said in my last post regarding your theory ,and for the last time will say I'm sorry if you found the statements "dismissive" because that was not my intent.

Re: Alchohol
-----------------
Not sure why that thread was addressed to me, as I have made no statements  about alchohol here, nor do I intend to today, other than to say that my hepatologist urged me to have a few drinks a week (post treatment)  for cardio issues -- which right now, trump any liver problems I still may or may not have. And that's a statement, not an opening for discussion, at least on my end.

Again, congratulations on your SVR, and hopefully we will leave this discussion with the same respect as before it started.

All the best,

-- Jim
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Avatar universal
I don't want to start a lengthy discussion, but my statement was based on the backbone of the biochemistry, aka The citric acid cycle (also known as the tricarboxylic acid cycle, the TCA cycle, the Krebs cycle).  If you were able to increase the LDLs levels simply by increasing consumption of fat, that fact signifies underlying metabolic problems ... we usually associate it with age.  

Cheer up, life is good with or without imbalanced cholesterol!

All the best
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Avatar universal
Tallahass quote: "...in the normally functioning body, where all organs live and interact in peace and harmony :-), no amount of pizza and fat will increase cholesterol levels... unless you consume pizza in huge amounts for years without sufficient physical activity"

Huhhh? What in the world are you talking about? Cholesterol levels (including LDL) most certainly ARE influenced/affected by diet. Eating an abundance of greasy and fatty foods high in saturated fat WILL increase cholesterol/LDL levels in the vast majority of people who do so (although there are relatively rare exceptions). Not sure where you got the notion to the contrary, but take my word for it (and the medical community's in general) that it's not true.

" ... followed by weight gain ...f followed by reduced muscle mass... followed by reduced metabolism... and at this point the peace and balance in the body will be replaced with hormonal chaos and a bunch of other problems, including inability of the body to maintain the proper amount of cholesterol."

Well, I'm not sure what you fully mean by "peace and harmony" amongst the organs, but I think you're misinterpreting the scope of what I mean when I say deliberately increasing LDL levels may be beneficial prior to and during a portion of SOC treatment. No one is suggesting eating a garbage diet ad infinitum, only for a very limited timeframe for the very specific reason of permanently ousting another *very* serious and persistent threat to the "peace and harmony" amongst the organs. After the ousting has been successful, then of course return to a happy, healthy diet high in fiber, rich in omega 3's and all that.

And thanks you for the kind words of congrats for my 6 week UND - keeping my fingers crossed in the meantime.
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Avatar universal
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Controvertible Theory/Concept #2 - Alcohol increases viral replication rate and therefore increases viral load. Therefore, abstaining from alcohol can lower viral replication rates, and therefore lower viral loads, and therefore increase odds of being successfully treated with SOC.

Is this theory actionable or within my realm of influence? - Yes, I can abstain from drinking.

Vagaries - Mixed evidence (via studies) is available that suggests both that alcohol does and does not have a significant effect on viral loads. Especially in regards to light and moderate drinking (with additional vagaries associated with how "light" and "moderate" are defined). Anecdotally I've known people that have drank copiously for decades and have little or no significant liver fibrosis. I also know of some who appear to be near tea totallers which significant fibrosis. Observed viral loads in drinkers genrally don't "seem" that different from non-drinkers.

Upsides of accepting/adhering to this theory - Abstaining from alcohol may actually reduce viral loads, the theory might be true to one extent or another. This would impart an advantage by lowering viral load prior to commencement of treating. Lower starting viral loads are associated with higher rates of RVR and subsequent SVR. Abstaining from heavy to moderate drinking will probably reduce the progression of fibrosis. Abstaining from heavy to moderate (or even light) drinking may also alleviate other health issues, including things like improved blood sugar regulation, lessening of sleep apnea (in those vulnerable to it), reducing urination at night (all of which improves sleep patterns and therefore overall wellness), facilitate weight loss (i.e. beer belly), improve mental function, emotional status and ability to engage and adhere to a regular exercise program (or SOC treatment for that matter). And so on, and so on...

Downsides of accepting/adhering to this theory - Moderate to light drinking may turn out to have little or no real effect on viral loads, and therefore impart no significant benefit prior to or during SOC treatment. Moderate to light alcohol consumption can be very enjoyable and has always been an important part of my adult life. I like drinking a fine microbrew and damned if I want to give it up for some semi-supported study that may turn out to be proven largely untrue a few years from now. Light alcohol consumption may have other tangential health benefits like reducing stress and possibly lowering cholesterol levels.

Actionable Conclusion - Just to be on the safe side, I decided to stop all alcohol consumption ~90 days prior to commencement of drug trial in hopes of lowering starting VL. I also abstained from any alcohol consumption during the entire course of treatment for the reasons mentioned in "upsides". I like drinking (moderately), but imposing a temporary abstinence is a very manageable action considering the potential upside (in consideration of how badly I want an SVR) with virtually no downsides (physiologically speaking). Even if it doesn't impart a huge likely benefit, considering the dicey odds of treatment success for geno 1's, it's worth paying the price in abstinence during the pre-treatment and treatment interval.
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Avatar universal
jimquote: "Regardless, my main point was that just because a study shows that low LDL is associated with lower SVR rates does not mean that intervening (such as with fatty foods) to raise cholesterol will have a positive effect on SVR. And I doubt that HR would make that statement as well, other than to say as I did (he probably says it nicer :) ) that it *may* have merit but is not proven."

As already stated, I agree it's not "proven" according  to the exacting standards associated with mathematical proofs. It's just that my impression of your initial response to my initial statement concerning high LDL vs increased EVR/RVR/SVR rates was one of being overly dismissive. It sounded to me (and perhaps others) as if you were degrading the quality of the referenced study to the level of "Oh come on, there's also a study that 'proves' cheeseburgers prevent cancer - fahhgettaboutit!!" I think the LDL-->SVR connection has more (probable) merit than that and it warrants serious consideration. In fact, I believe the seriousness of it rises to the level of "actionable intelligence" from an HCV patient's perspective considering or preparing for SOC treatment (which I'll explain in more detail about below). Also, above you seem to intimate that an LDL level that's been elevated via diet may somehow not impart the same "antiviral goodness" that someone with high LDL levels even in the absence of a crappy diet has (i.e. someone who has high LDL levels as a result of their own liver producing the bulk of their LDL's). The study does not suggest that, and I can't think of why that might be true - Low Density Lipoproteins are Low Density Lipoproteins. If the anti-viral mechanism of LDL's inhibiting permeation of the virus into the host cell is accurately described within the referenced study (and others), then why would LDL's derived from diet be any less effective than LDL's produced by the liver itself? (which almost certainly derives them from the diet anyway) Furthermore, what otherwise healthy (non-starving) human being doesn't have an admixture of LDL's sourced from both the liver and diet? Especially in regards to this particular study, which was conducted in the US. Considering we're the fattest b@stards in the world, how many of the referenced study participants were "typical Americans" in this sense? (i.e. with the usual diet induced high cholesterol levels associated with poor health habits and/or obesity) And yet these same study participants are the very ones producing the data repeatedly demonstrating a strong correlation between LDL levels and RVR/EVR/SVR. Considering all of these factors, I see no reason whatsoever to be doubtful that high LDL levels largely associated with a high fat diet will possess the same viral inhibiting qualities that another comparable person might have with a healthy (low fat) diet but their liver simply produces too much LDL.

In summary, the way I view this study and what I described earlier as its "actionable intelligence", is how I view many concepts and theories concerning the treatment of HCV. As with with nearly all concepts, theories and ideas about hepatitis C and its treatment, there's almost without exception vagaries, statistical uncertainties and a general lack of conclusive proof of one thing or another to wrestle with (which can be very frustrating!). Instead we're left with a mish-mashed menagerie of probabilities, likelihoods, indicative trends, all the way down to anecdotal "this worked for me!"-isms along with other hints and allegations. From a patient's perspective, sorting through all this and deciding what's actionable and what's not can be a real challenge. So what I've done is come up with a sort of truth table to ascertain if concept x or theory y (that's within my realm of influence) is worth pursuing when dealing with my virus. Here are two examples of what I mean (and obviously each indivual will have their own personal interpretation of these issues):
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Controvertible Theory/Concept #1 - High pre-treatment cholesterol levels (and specifically LDL levels) appears to impart a significantly increased likelihood of RVR, EVR and ultimately SVR.

Is this theory actionable or within my realm of influence? - Yes, consuming high fat foods can and will elevate LDL levels.

Vagaries - This theory is relatively new and hasn't really been exhaustively tested by a wide array of researchers. There isn't a very large body of research specifically tailored to vetting (or refuting) this theory just yet. However, recent research supporting the theory does appear to be piling up as demonstrated here, for instance: http://www.hivandhepatitis.com/hep_c/news/2007/022707_b.html

Upsides of accepting/adhering to this theory - Deliberately increasing LDL levels prior to commencement of treatment (and during treatment) may very well significantly increase antiviral performance and improve odds of achieving RVR, EVR and SVR. A calorie rich diet high in fat will also help stave off excess weight loss during treatment, which is a common side effect during a course of SOC. SOC treatment also appears to have a cholesterol lowering effect in some patients. Boosting HDL/LDL levels with dietary supplementation may actually improve overall lipid profile in some.

Downsides of accepting/adhering to this theory - The high LDL levels that are found to be associated with improved HCV antiviral performance are unhealthy from a cardio/aterial sclerosis perspective. This could be especially problematic for a person with a pre-existing condition associated with heart disease, stroke etc and may not be suitable for those that fall within that category. (doctor consult required for those with pre-existing conditions)

Actionable Conclusion - I don't have a pre-existing problem with heart disease or stroke (yet anyway). The evidence compiled so far seems compelling enough to risk deliberately increasing LDL levels temporarily both before and during treatment in an attempt to glean the possible benefit of improved antiviral performance (which could be substantial according to the existing studies). Also, the LDL levels do not necessarily have to be elevated during the entire treatment cycle. High LDL levels may only be necessary/useful just prior to treatment and during the early phase of viral clearance. A possible plan of action would be to increase LDL just prior to treatment and maintain high LDL only until a few weeks after an UND status is achieved. This may result in a very "risk manageable" and relatively short duration of high LDL, lasting perhaps anywhere from a few weeks to a few months. Especially so considering how many hamburgers, pizza and french fries I've eaten in my life already! (part deux below)
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Avatar universal
Jim, ditto, ditto, ditto!

HR did not address the issue of intervention with fatty foods for potential increase of SVR, because in the normally functioning body, where all organs live and interact in peace and harmony :-), no amount of pizza and fat will increase cholesterol levels... unless you consume pizza in huge amounts for years without sufficient physical activity ... followed by weight gain ...f followed by reduced muscle mass... followed by reduced metabolism... and at this point the peace and balance in the body will be replaced with hormonal chaos and a bunch of other problems, including inability of the body to maintain the proper amount of cholesterol.

On the other hand, if cholesterol consumption from the diet is low, the normally functioning body should produce just right amount necessary for life.  Definitely, the diet should be balanced and have sufficient amount of the "construction material" to "build" more cholesterol necessary for survival.

FLGuy, I think your "bad" cholesterol in the 60-s and without observed drastic decrease in the levels just means that you have one of the best genetic configurations! The same can be said about Forseegood, enjoy it!

So many theories, so many ideas!

Mremeet, congratulations with UND results!! Great job ... may be YOUR pizza made the difference! :-)  All the best to everybody!
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Avatar universal
My H's total cholesteral was not high 25 years ago and neither was mine.  Both of us were about 180 on average.  However, my h's cholesteral has been steadily decreasing albeit slowly over 25 years to about 150 and mine has stayed steady at about 180.  My H was diagnosed wtih probable stage 4 and a fibrosis score of 3 prior to the onset of treatment so I have to believe that yes, liver damage lowers cholesteral.  H was also a steady but slow responder.   to me, it would be more meaningful of the correlation studies of cholesteral to SVR were broken down by stage of liver disease.
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Avatar universal
Just re-read your post, and I now see that you weren't suggesting HR was endorsing your idea -- just the study findings -- therefore my statments above re HR's take on your theory should have been omitted.

BTW I did find the thread in the MH abyss, and "HR" does think the study has merit but he doesn't address the issue of intervention with fatty foods one way or another.
http://www.medhelp.org/forums/hepatitis/messages/44113.html

-- Jim
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Avatar universal
First of all, "very unclear" to me does not mean useless information, and in fact the last sentence of my post states that indeed what you say might have merit, i.e. it might be true.

Next, I have absolutely no quibble with the study conclusions that low LDL is negatively associated with SVR.

As to the issue of fibrosis and low LDL, I think we're in agreement, but I wasn't trying to make it part of your argument.  I was simply stating that cirrhotics often have low LDL as well as lower SVR rates, and I was therefore suggesting that perhaps this could have accounted for the lower SVR rates in the low LDL group. The study author's also give some credence to that notion here:

"he presence of severe fibrosis was shown to be an independent predictor of SVR in IFN-based therapy for patients with chronic hepatitis C.[19] There is a decrease in serum cholesterol and LDL levels as the severity of liver disease increases.[20] Thus, the inability of patients with low LDL levels to achieve SVR could be secondary to advanced liver fibrosis. However, this effect is unlikely to completely explain the observed association because the effect on cholesterol is generally seen only in very advanced disease. Patients with HCV genotype 2 or 3, most of whom achieve SVR and are thus treated empirically, accounted for about half our study population. Thus, unlike patients with genotype 1, liver biopsy is often not performed in patients infected with non-genotype 1 HCV. A chi-square test with available data for stage of fibrosis and SVR, however, did not show any significant correlation. Therefore, fibrosis stage was not included as a covariate in the multivariate analysis. Among those patients with genotype 2, LDL level remained a significant prognostic indicator for SVR."


Regardless, my main point was that just because a study shows that low LDL is associated with lower SVR rates does not mean that intervening (such as with fatty foods) to raise cholesterol will have a positive effect on SVR. And I doubt that HR would make that statement as well, other than to say as I did (he probably says it nicer :) ) that it *may* have merit but is not proven. Please don't go looking for HR's post in the MH backfile abyss, but if you have the thread handy, why dont you post it. '

Lastly, the study authors deal with the ramifications of the study but never suggest what you did -- not to say you said they did. What they did say was this:

"A better understanding of the mechanisms underlying HCV infection and efficacy of interferon treatment will suggest advances to improve the outcome of therapy. The potential involvement of the LDL receptor in HCV infection provides a new approach to therapy in the future. Such advances may include the use of LDL receptor-blocking analogues that may slow viral replication and progression of the disease, prevent reinfection of a transplanted liver, or improve the rate of sustained viral response. "

Again, as I stated -- obviously not very well the first time -- I think your approach has merit and indeed may one day become a recommended tx strategy. I just don't think that it has proven merit.

Hope this clarifies and once again congratulations on your SVR!

All the best,

-- Jim

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Avatar universal
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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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!!!!.

                                                                                                                                           Ron
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