The hepatitis B vaccine is widely promoted, even mandated, based on the proposition that the hepatitis B virus is both serious and widespread. Unfortunately, the statistics and "science" used to promote this idea are of questionable validity.

The Centers for Disease Control and Prevention (CDC) have made highly discrepant claims about the incidence of new infections each year.  In their "....Comprehensive Strategy for Eliminating Transmission..." (of hepatitis B in the United States), they claim that between 1980 and 1991 there were an estimated 200,000 to 300,000 new cases of hepatitis B each year.  In a 1998 article the CDC estimates 323,462 were infected annually between 1976 and 1980, while 334,863 were infected annually from 1988-1994.  However, in their Hepatitis B Fact Sheet, the estimate rises to "an average of 450,000" new cases in the 1980's.

Which is it, CDC?

They allegedly arrive at these numbers using "catalytic modeling" based on serum sampling of hepatitis B markers employed to derive the proportion of unreported and asymptomatic cases.  Were they not to do so, the reported cases  would be strikingly low, ranging from 18,003 (in 1991) to 26,611 (in 1985), hardly enough to get very excited about.

While the notion that one might want to determine missing cases is certainly valid, in this case errant methodology appears to have been used, since the particular markers upon which we are told the estimates are based do not necessarily measure the things they are purported to measure.

 Using serum sampling of 14,488 people, the CDC found that "The prevalence of serologic markers for HBV infection (HBsAg, anti-HBs, or anti-HBc) in this population was 4.8%." In the CDC study upon which their estimates are based, it was stated, "In NHANES II, serologic evidence of present or past HBV infection was defined as a positive test for anti-HBs or HBsAg, while in NHANES III, a positive test for anti-HBc was used to define infection". (Journal of Infectious Diseases)

These methods of measurement, however, do not necessarily denote either current or chronic infection.  In fact, quite to the contrary, anti-HBs represents immunity and is present in those cases where there has been recovery from hepatitis B. Anti-HBc may indicate "resolved infection".  In addition, "Anti-HBc appears shortly after HBsAg among people with acute disease and generally persists for life. It is therefore not a good marker for people with acute disease."  (Vaccines)

Even the significance of HBsAg, a marker for acute or chronic HBV infection, is not clear-cut:  "In 95 percent of patients with acute hepatitis B, HBsAg disappears from the serum within one year." (American Family Physician) The mere finding via sampling of subclinical cases also says nothing about the significance of such a finding.  "Most of these patients (with chronic persistent hepatitis) do not progress to chronic active hepatitis or cirrhosis: however, those with HBeAg in the serum are more likely to do so".  (American Family Physician)

By lumping together acute, chronic and recovered hepatitis B cases, an approach, which includes using contrary and ambiguous indicators, and markers which haven't even been approved by the FDA, the results become inflated and meaningless, particularly given that most cases recover.  In addition, by taking a slice in time and treating it as if it is a constant, they are also disregarding the overwhelming proportion of cases which eventually resolve. It is usually only chronic, active infection that poses a long-term threat, not recovery. 

To bolster the appearance that the risk of getting hepatitis B was rising, the CDC stated that "reported incidence of acute hepatitis B increased by 37% from 1979 to 1989".

The truth is, however, that reported cases actually DECLINED 12% between 1985 and 1989. By the time the hepatitis B recombinant vaccine was recommended in 1991 for all infants and children, the reported incidence of hepatitis B was down to 18,003 (all ages), another 23% drop in two years. (Put another way in Vaccines:  "In the United States, reports of acute hepatitis B increased by 37% from 1979 to 1985, but since 1986 declined to 1979 levels.")

Topping it all off, the CDC is now reporting that hepatitis B incidence dropped to around 80,000 in 1999, the implication being that vaccination has had a huge impact.  This, in spite of the fact that according to the American Journal of Public Health, as recently as 1994 there was no significant decrease in prevalence, "despite the availability of hepatitis B vaccine". 

The CDC also has stated that "The estimated 1 million-1.25 million persons with chronic HBV infection in the United States are potentially infectious to others."  "Potentially infectious" - now what's that supposed to mean?  Particularly given that hepatitis B is largely a "lifestyle" disease, with transmission dependent on either engaging in risky behaviors or living in close contact with someone with infectious hepatitis B virus (HBV) (the important exception, of course, being an infant born to a hepatitis B positive mother, in which case the mother can be screened).

The truth is, the United States, except for certain ethnic groups in Alaska, is actually considered a low prevalence area for chronic hepatitis.

And what about long-term risk from chronic hepatitis B? According to Murray, "It is not unusual for hepatitis B virus antigenemia to resolve after 20 to 30 years".  Even the chronic carrier state will eventually resolve, at least for some.

As for the alleged risk of acquiring liver damage or hepatocellular carcinoma from hepatitis B, and implied to be quite large by the CDC,  according to American Family Physician, "In the United States, alcoholic cirrhosis more commonly leads to primary hepatic cancer than does chronic hepatitis B infection".  According to the journal Cancer, "Hepatocellular carcinoma (HCC) occurs more frequently in patients with hepatitis C virus (HCV)-related chronic liver disease than those with hepatitis B virus-related disease."  And in the American Journal of Epidemiology it was reported that "rather than chronic hepatitis B virus infection, hepatitis C virus infection and alcoholism were the two dominant risk factors that signaled the risk of liver damage among these Taiwanese aborigines". 

What is the true incidence of the chronic hepatitis B carrier state in the U.S. and its significance? 

How many chronic hepatitis B carriers in the U.S. go on to develop chronic, active hepatitis?

How many of those with chronic, active hepatitis in the U.S. go on to develop serious, long-term consequences?

What percent of hepatitis B cases in the U.S. end up eventually resolving and how is this taken into account when estimating long-term risk?

How much hepatocellular carcinoma in the U.S. is directly attributable to hepatitis B?

Is Public Health over-stating the risk of cancer resulting from hepatitis B?

What justification is there to recommend, not only universal infant hepatitis B vaccine, but vaccine for those adolescents and adults not participating in risky behaviors?

Even if there is what many would consider an arguably small risk from hepatitis B vaccine, where is the justification for taking any risk?

Are the CDC estimates of hepatitis B incidence, prevalence and risk based on sound science?

How much coming out of the CDC can we believe?