The China Study by Thomas Campbell

62 THE CHINA STUDY

diet halfway through their lifetime started growing tumors again. These

findings on full-blown tumors confirmed our earlier findings using foci.

Namely, nutritional manipulation can turn cancer "on" and "off."

We also measured early foci in these "lifetime" studies to see if their

response to dietary protein was similar to that for tumor response. The

correspondence between foci growth and tumor growth could not have

been greater (Chart 3. 9a). 36,43

How much more did we need to find out? I would never have dreamed

that our results up to this point would be so incredibly consistent, bio-

logically plausible and statistically significant. We had fully confirmed the

original work from India and had done it in exceptional depth.

Let there be no doubt: cow's milk protein is an exceptionally potent

cancer promoter in rats dosed with aflatoxin. The fact that this promotion

effect occurs at dietary protein levels 00-20%) commonly used both in

rodents and humans makes it especially tantalizing-and provocative.

OTHER CANCERS, OTHER CARCINOGENS
Okay, so here's the central question: how does this research apply to hu-
man health and human liver cancer in particular? One way to investigate
this question is to research other species, other carcinogens and other
organs. If casein's effect on cancer is consistent across these categories,
it becomes more likely that humans better take note. So our research be-
came broader in scope, to see whether our discoveries would hold up.
While our rat studies were underway, studies were published^44 ,45
claiming that chronic infection with hepatitis B virus (HBV) was the
major risk factor for human liver cancer. It was thought that people who
remained chronically infected with HBV had twenty to forty times the
risk of getting liver cancer.
Over the years, considerable research had been done on how this
virus causes liver cancer.^46 In effect, a piece of the virus gene inserts
itself into the genetic material of the mouse liver where it initiates liver
cancer. When this is done experimentally the animals are considered
transgenic.
Virtually all of the research done in other laboratories on HBV trans-
genic mice-and there was a lot of it-was done primarily to understand
the molecular mechanism by which HBV worked. No attention was
given to nutrition and its effect on tumor development. I watched with
some amusement for several years how one community of researchers
argued for aflatoxin as the key cause of human liver cancer and another