By Nicholas Regush (ABCNEWS.com)
Let me lay it on the line for you: I have never once thought - or written - that hepatitis C is a psychological problem. I have no doubt whatsoever that people have developed liver scarring and that many have developed liver disease and died from it.
But after 30 years of reporting on science, I can sometimes smell a skunk. This time, the skunk is a so-called virus called hepatitis C virus (HCV), which is blamed for much of the severe liver disease people suffer.
I certainly feel compassion for people who become ill with liver disease. But I have less than nice feelings for scientific enterprise that is shallow and takes red-flag shortcuts, which is exactly what I have concluded has occurred with the science underlying the claim that a hepatitis C virus has been properly identified.
When you get beyond all the biotech smoke and mirrors and you need to take time to travel through this fantasyland to appreciate the nuances - there are disturbing issues about HCV that must be raised, particularly when it is said to have infected some 4 million Americans, the vast majority of whom have no symptoms and have been frightened out of their wits that they'll eventually develop fatal liver disease.
HCV is said to spread through direct contact with contaminated blood; that means through such routes as sex, sharing needles for drug use and, of course, blood transfusions, particularly from the 1960s through the '80s when the blood supply wasn't adequately tested for HCV. The stakes here are obviously very high for people diagnosed with HCV and for society in general. We'd better have good fundamental science serving as the foundation for very expensive testing programs, treatment regimens and public health promotion about a "hidden epidemic" on the rampage.
Keep in mind that it takes only a handful of researchers and some good marketing to set others on a course that, even if misdirected, becomes difficult to reverse. This is particularly true in today's world of molecular biology, in which basic discoveries, in the form of molecular products or tests, are often accepted without challenge as baselines for further research, and, of course, the scramble for research dollars.
Most doctors who see patients must accept this basic science on blind faith, due to their own lack of scientific expertise or the time to read the research papers. They then pass on their accepting views to patients, who typically assume they've been told "the truth."
In 1987, a scientific research team went on the hunt for a virus to explain liver disease linked to what was then called non-A non-B hepatitis. The team, including scientists from the CDC, Chiron Corp. and others, claimed to have detected HCV.
But to this day, no one has ever been able to isolate such a virus in an intact form, nor has anyone been able to grow it in a culture. And no one has been able to fish out such a virus, purify it (meaning separate it from a cell), inject it into an animal and cause hepatitis.
No one has ever been able to document, according to basic long-held standards of virology, that such a proposed virus is infectious. No one.
From the beginning, the researchers presumed too much in making their claim. They began by injecting blood from hepatitis patients into chimps. In half of the animals, they noted signs of infection in the form of a biological marker of hepatitis called alanine aminotransferase. The injected blood, however, did not cause hepatitis.
That should have been a big red flag.
The marker they detected may have had nothing to do with a virus. In any case, the scientists began fishing in liver tissue to find one. What they found, with the use of high-tech amplification tools, was essentially a small piece of genetic information (encoded in ribonucleic acid, or RNA).
On the basis of tests to reconstruct pieces of what they believed was a virus; they presumed that this bit of RNA was foreign and viral - even though they had no basic evidence that their "catch" behaved like a virus.
But never mind. Just clone the pieces of genetic information; work out the genetic sequences; using indirect methods, generate proteins presumably coming from a virus's genetic code; create an antibody test against this genetic information; test many patients who turn out to be positive against this genetic information - and lo and behold, you have an epidemic.
Then, of course, all of the followers of the leaders must then publish thousands of scientific papers (which they did) studying the bits and pieces of genetic information presumed to be a virus. And they must do so to keep their labs going, particularly at a time when everyone is clawing for research support to keep their academic enterprise alive.
This is not science. When you generate the basis of an epidemic and nowhere have you properly isolated the virus and shown it to be infective and disease-causing, you are making a mockery of the scientific method. Now what about this "genetic information" that is presumed to be a virus?
Some scientists have already suggested, on the basis of highly-detailed research (published in 1997) on cells from healthy human subjects who aren't antibody positive to HCV, that some of that so-called viral genetic information may be similar to what is found normally in human cells - specifically, cell-escaping sequences of DNA via its RNA messenger.
In other words, some of the genetic information thought to be a virus may actually have a human origin. How very intriguing.
Rule Out Before Ruling In
But to a thoughtful molecular biologist, such a proposition makes a lot of sense. One of the people I consulted was Richard Strohman, professor emeritus of molecular and cell biology at the University of California. Strohman points out what any reasonable molecular biologist should know: toxic hits, say, for example, smoking and alcohol consumption, can traumatize the liver and cause some genetic instability in its cells.
In other words, the human cell itself can certainly be the source of the kind of genetic information caught in a molecular fishing expedition and presumed to be viral. Before jumping on a viral bandwagon, every effort should be made to thoroughly rule this out.
It bothers Strohman that in the case of HCV, it has not. It also bothers him that the supposed detection of the HCV has been credited for lowering the post-transfusion rate of non-A non-B hepatitis. Better screening equals much less infection, or so goes the logic. But this is another example of pole-vaulting. There may be other reasons for the decline, including the elimination of many donors at risk for AIDS.
In last week's column, I raised the challenge to the scientific community to send me some evidence that a virus exists.
The fact is, a virus might indeed exist and contribute to non-A non-B hepatitis, but the evidence so far is only indirect and circumstantial and, I believe, highly misleading, given the extreme to which it has been pushed.
I have some time I can set aside later this summer to debate anyone from the molecular biology establishment who has been at the forefront of the discovery of HCV. No pretenders to the throne or angry followers of the leaders need apply.
In the meantime, given the huge amount of tax dollars being appropriated and the numerous biotech industry programs that have emerged to fight HCV, I plan this week to contact a congressional committee known for its investigation of scientific issues and ask that they seriously consider launching a probe of the science behind this vapor-like virus. Next week, I'll focus on some on the important issues hepatitis patients are raising about their disease and the science and doctoring behind it.
Hepatitis C is said to be a silent blood borne epidemic that affects many millions who are unaware that they are ill. But do these people really have this virus?
Consider this a challenge in progress. This scientific adventure raises the question of whether the hepatitis C virus, blamed for a major silent epidemic of liver disease and even cancer, actually exists. That's right. You read this correctly: I am raising a question that may disturb scientists and hepatitis C patients alike.
But I'm raising it anyway because it is vital to do so in the interests of public health. I'm issuing a challenge to the scientific community to present me with the published, peer-reviewed scientific evidence that such a virus actually exists- namely that it has been properly isolated, according to accepted, fundamental principles of virology.
The C Files
Thus far, I should tell you, the evidence for the existence of such a virus underwhelms me. Before tackling this issue bluntly, I've decided to offer those who believe the science supporting the virus is adequate the opportunity to educate me on the subject. (We'll even run your letters.) You can do this by providing me with key references for proof that hepatitis C virus is real and not some meaningless biotech concoction posing as a real virus.
I plan to ignore any speculative theories, pole-vaults in reaching conclusions and the usual harangues from the medical and scientific community about the stupidity and irresponsibility of journalists.
I have little patience for emotional approaches to this important scientific issue.
Many months ago, I wrote a column about hepatitis C, arguing that government officials botched proper testing of the blood supply for the virus. (A number of lawsuits are in progress, claiming the government was negligent.) In other words, I had automatically accepted the conventional wisdom that such a virus exists.
I'm not blaming myself here; there is only so much research that one can do at any time, and we are often condemned, as I'm sure you will agree, to rely heavily on the views of others, particularly when there appears to be strong scientific consensus.
Inquiring Readers Want to Know
In response to that column, I have received a regular flurry of e-mail from readers who ask me to write more about hepatitis C, particularly about how this epidemic has been neglected by the government and medical community. So, in response to these letters, and out of genuine curiosity, I have slowly, but systematically, exploring the scientific literature.
What I discovered surprised me.
But first, let's look at the conventional wisdom on hepatitis C: Official estimates are that about 4 million Americans have been infected by the virus, that many don't know they're infected, and that some of these people (it's not clear how many) who now have no symptoms, will go on, perhaps in 20 or 30 years, to develop a scarring of their liver known as cirrhosis, which, in some cases, will lead to liver cancer.
The conventional wisdom says that this is a virus spread through direct contact with contaminated blood; that means through such routes as sex, sharing needles for drug use and, of course, blood transfusions, particularly in the '60s, '70s and '80s, before the blood supply was appropriately monitored. For many of the people, perhaps as many as half who have positive hepatitis-C antibody tests, the manner in which they may have contracted the virus remains a mystery.
Antiviral drugs, often in combination, are the main fighting force against hepatitis C, though, again according to the conventional wisdom, they appear to be only modestly effective in about half of patients and have serious side effects. When scanning the literature, most of this type of information pops up again and again.
And media reports on the science do not question the conventional wisdom, at least not the numerous ones I've perused. Yet, the more I read the science, the more troubling it appears.
Challenge of the Week
As regular readers of this column know, I have taken it upon myself to call some of the conventional wisdom in medicine into question if adequate science has been bypassed in favor of speculation, hype and/or commercial gain. What has especially energized me, of late, is the debate I still hope to have with Dr. Rodrigo Munoz, president of the American Psychiatric Association, over the science underlying the prescription of antidepressant drugs.
Unfortunately, it looks as though Munoz is shying away from a public encounter with me, even after suggesting to me in an e-mail that he might be willing to take a crack at it. Oh, well, maybe a prominent hepatitis C expert, perhaps even someone involved in the discovery of hepatitis C, will want to have a free-ranging public debate on what it means to isolate a virus.
Old Research Raises Still-Valid Questions Regush has been flooded with letters in response to his first two columns on hepatitis C, most lambasting him for questioning the mainstream view on the disease.
First, some reassuring and potentially empowering information about a disease named hepatitis C. Of all the studies I've examined in the past several weeks, one older one looms large as the first to offer patients a measure of hope and food for thought.
It's a large-scale, long-term study published back in 1992 in the New England Journal of Medicine (Volume 327, No.27, pages 1906-1911), and while it should not be seen as definitive, it is most instructive as a way of thinking about the disease.
The study, which followed transfusion-related non-A non-B hepatitis patients for 18 years and matched them with control subjects who received transfusions but didn't have the disease, informs us that it appears to be uncommon for the disease to result in dire problems. The study concluded that those believed to have been infected with the hepatitis C virus (associated with most cases of non-A non-B) live as long overall as those with no infection.
There was, however, a small increase over time in the number of deaths specifically associated with liver disease in patients with non-A non-B, suggesting that it takes a very long time indeed for the disease to take its final toll. What can we make of such data?
The optimist might conclude that the virus won't reduce overall survival rates over time, and that increased numbers of liver-disease-related deaths that the study documented in infected patients might actually be due to intervening factors, including alcohol consumption.
But as an editorial in the same issue of the Journal cautioned, a much longer-term follow-up of patients may well show a tide of death related to the virus. And the editorial also called for more research on the effects of the disease, and not just on how long people live.
What this study immediately tells me is that evidence for a viral cause of non-A non-B is open to question. It raises a big red flag because of the time it appears to take this virus to do its dirty work. Other data suggest that it doesn't even cause symptoms beyond a conventional flu-like illness in many people, even for decades. When science lines up behind a virus whose damage potential extends into many decades, I get suspicious.
Is Evidence Lacking?
So I did some checking. There is no good evidence that such a virus exists. I concluded that the scientists who made the initial discovery made fanciful leaps; consequently these leaps became the basis for further studies and entrenched beliefs.
My view is that the cause of non-A non-B hepatitis remains unknown. Some 4 million Americans are said to be already infected with the hepatitis C virus. If I knew that I were among them, I would make it a major commitment to uncover everything I possibly could about this virus and the claims underlying its identification.
I would stop at nothing to get a good fix on the virus because that knowledge would certainly affect how I live my life, how I would assess my chances of becoming ill and which treatments I might deem appropriate.
Strength in Numbers
I would try to associate with others affected by the disease who also had a burning desire to raise questions about the virus. I would make an effort to acquaint myself with the fundamental science and I would be particularly interested in following up any challenges to that science. I would consider it foolhardy to automatically accept the conventional wisdom.
What is considered mainstream today in science might well be built on the basis of medical politics and corrupted research. I would take special care not to associate with organizations or support groups that would insist on following the CW and which would be immediately antagonistic to non-conventional thinking about the disease.
And I would be particularly cautious about joining up with any patient group that was supported by pharmaceutical funds or led by lay people and doctors alike who appeared to be toeing some official line, or, for that matter, using the vehicle of a support group or voluntary association to enlarge their egos. I would much rather seek the support of independent spirits who gave me the empowered feeling that I was free to pursue any and all information about the disease.
I am writing this because of the nature of many of the letters that I have been flooded with in response to my first two columns on this issue. Most have come from patients or patient support groups that lambasted me for questioning the mainstream view on non-A non-B hepatitis.
Rather than raise questions or indicate that they were interested in knowing more about my views, they settled for name-calling and, in some cases, threats to my well-being. Well, I don't care much if people call me names and I can either live with threats or refer them to police authorities if they get out of hand. What I find very disturbing is the fact that so many people would be unwilling to further explore the nature of their disease.
Rather than pummel me, these patients and support groups should delve into the questions being raised about non-A non-B, not only by me but by others, including some prominent scientists. One would think that taking this route might become an empowering experience. In any case, to those patients and support group members who did write that they would look into the issues that I raised, I can only applaud your willingness to have an open mind.
This is what it will take to get to the bottom of what this disease is all about. And please stay tuned. In the weeks and months ahead, I'll occasionally update you on my own burning desire to make scientists working on non-A non-B accountable for their claims. I'll also let you know if anyone involved in the discovery of the so-called hepatitis C virus has the guts to take up my challenge to publicly debate me on the scientific issues.
Eur J Clin Chem Clin Biochem 1997 Dec;35(12):899-905
Dr. Mercola's Comment:
Nicholas Regush at ABC appears to be the most progressive journalists I have ever seen. I will be contacting him to see if he is willing to set up a Dateline or 20/20 follow up for the information I will be presenting at the autism lecture this week.
Last week I mentioned that the current chemical assault being used by traditional medicine is CLEARLY not the answer. Many were interested in what my treatment for hepatitis C involves as. This is especially evident after reviewing the articles on hepatitis C posted in this week’s newsletter.
My approach for hepatitis C involves first and foremost making sure there is rigid compliance to the dietary recommendations listed in Read This First.
Once that is implemented one need to minimize other toxic influences to the immune system. Amalgam fillings are typically present and need to be removed along with a comprehensive mercury detoxification program by a competent clinician. Elimination of toxic deposits in the body, especially pesticides through sauna detoxification is another helpful approach.
However, I believe the critical element involves normalizing the autonomic nervous system by uncoupling the emotional traumas and conflict that typically seem to impair its optimal functioning. Applied Psycho Neurobiology is the current strategy I am using.
The following article also supports the hepatitis theory described above:
Hepatitis C virus (HCV) specific sequences are demonstrable in the DNA fraction of peripheral blood mononuclear cells from healthy, anti-HCV antibody-negative individuals and cell lines of human origin. By Dennin RH, Chen Z
No convincing support has been provided so far for the existence of extrahepatic hepatitis C virus particles that should correspond to the sometimes extremely high concentration of 'HCV-RNA' in serum or plasma. If a naturally occurring HCV-specific DNA were to be found, a concept for at least some phenomena in terms of the pathophysiology of HCV should become conceivable.
DNA was extracted from peripheral blood mononuclear cells of eleven healthy, anti-HCV-negative individuals, including five long term blood donors, and cells from different cell lines. DNA was subjected to nested polymerase chain reaction omitting a reverse transcriptase step with primers of the 5'NC as well as part of the core region of HCV.
Direct polymerase chain reaction, i.e. without a reverse transcriptase step, revealed HCV-specific sequences in the DNA fraction of peripheral blood mononuclear cells of different origin: healthy anti-HCV negative individuals, furthermore in HeLa and MT2 cells.
The fragments found were of expected length as well as of shorter and of longer than expected length with respect to the sequence of the HCV genome framed by the primers applied.
The results derived from additional hybridization, restriction endonuclase analysis, and sequencing demonstrated HCV-specific sequences in the expected fragments with both a high degree of homology and deletions, respectively, substitutions, as compared to a prototype strain.
However, the longer than expected fragments also contained sequences not specific for HCV.