The Web of Hunger 
More Is Not Necessarily Better 
Researchers are learning that an excess of a required nutrient 
may present as much of a cancer risk as a deficiency 
by T. Colin Campbell 
The current spate of publicity con- 
cerning the possible role of diet and 
nutrition in certain kinds of human 
cancer has led to much public mis- 
understanding and confusion. At var- 
ious times, animal fat and an excess 
of protein, calories, and sugar have 
been implicated as possible carcino- 
gens, whereas inadequate amounts of 
vitamin C, vitamin E, vitamin A, zinc, 
and selenium (a soil mineral that is 
found in most vegetables and cereal 
grains) have been thought to enhance 
the risk of cancer. 
There are about forty substances 
required by the human body to main- 
tain health and sustain growth. Con- 
sidered individually, each of these nu- 
trients can influence the risk of cancer 
in only one of three possible ways: 
have no effect; inhibit the develop- 
ment of cancer; enhance the risk. Nu- 
trients, however, are not consumed sin- 
gly but in groups in which their be- 
havior may be altered. Therefore, if 
there is ever to be more clarity, we 
must seek to understand the effects 
of multiple nutrient intakes and ana- 
lyze dietary patterns in terms of the 
ways in which the simultaneous ac- 
tions of nutrients can modify the risk 
of cancer. 
In order to better appreciate these 
nutrient effects, a brief description of 
the carcinogenic process is helpful. 
The simplest model divides the process 
into three phases: initiation; cell modi- 
fication; and metastasis, or invasion 
of other tissues. 
In the initiation phase, a normal 
cell is converted into a neoplastic one 
— that is, a cell that grows without 
restriction — through the process of 
mutation. The mutation occurs when 
a chemical reacts with and changes 
the cell’s genetic material, or deoxy- 
ribonucleic acid (DNA), so that sub- 
sequent generations of daughter cells 
derived from the parent cell are per- 
manently altered. A wide variety of 
natural chemicals, such as aflatoxin 
(a mold product found primarily on 
improperly stored peanuts and corn) 
and a chemical found in black pepper, 
as well as some synthetic chemicals 
are capable of acting as initiators dur- 
ing this phase. After ingestion, most 
of these initiators are metabolized by 
an enzyme system to reactive products 
that bind tightly to certain sites on 
the DNA molecule. If not removed 
or neutralized, these initiators ulti- 
mately transform normal cells into 
neoplastic cells, which can be either 
benign or malignant. When that hap- 
pens, the initiation phase is completed. 
Some of these initiated cells then 
progress over a period of years through 
the second, or modification, phase to 
the ultimate cancer cell that charac- 
terizes malignant tumor tissue. This 
long period is considered a latent one, 
in large measure because cells pro- 
gressing through the series of stages 
involved cannot be readily detected. 
Some compounds may positively pro- 
mote the growth of these latent cells, 
whereas others may inhibit that 
growth. The human body may, in some 
cases, recognize these “new” cells as 
foreign bodies — as it does with foreign 
bacteria — and destroy them by means 
of its immunological defense system. 
If this happens, the carcinogenic proc- 
ess is intercepted and fully developed 
tumor cells never appear. If, on the 
other hand, these latent cells escape 
the body defenses and receive nour- 
ishment for growth, they eventually 
give rise to dangerous malignant cells. 
Whereas many factors may promote 
the development of these latent cells, 
others may repress that development. 
We are now beginning to understand 
that a wide variety of biochemical and 
physiological mechanisms may ac- 
count for these modifier effects. 
In the third phase of cell transfor- 
mation — which does not always take 
place — the fully developed cancerous 
cells begin to take on properties that 
permit transport to, and invasion of, 
other tissues, a process known as me- 
tastasis. This phase has often been 
described in terms of histological, or 
tissue, characteristics, although much 
new information is rapidly becoming 
available on biochemical and/or bio- 
physical characteristics. Our present 
knowledge of the effects of nutrients 
on this third phase is incomplete. Nu- 
trients may or may not affect me- 
tastasis. 
This three-phase concept is quite 
useful if we consider how dietary man- 
agement might be used to repress or 
prevent the exceedingly complex dis- 
ease of cancer. In theory, prevention 
ought to be achievable in either of 
two ways. The elimination of all di- 
etary initiators is one hypothetical pos- 
sibility. But since their total elimi- 
nation is not practical, manipulation 
of the agents producing cell modifi- 
cation offers a second possibility. 
When consumed at inappropriate lev- 
els of intake, most nutrients tested 
may act as cell modifiers. In addition 
to the presence of essential nutrients 
in foods, there may also be a wide 
variety of other nonnutrient chemicals 
such as aflatoxin. Some of these non- 
nutrient compounds may act as 
initiators, some may be virtually in- 
nocuous, and still others may act as 
modifiers. 
With respect to nutrients, what is 
an inappropriate level of intake? All 
nutrients, of course, are required in 
the human diet at some minimum level 
in order to satisfy a wide variety of 
bodily functions. But we are now be- 
ginning to recognize that an excessive 
intake of nutrients may be harmful. 
When evaluating the effects of nu- 
trients on the risk of cancer, we should 
attempt to identify the optimum in- 
12 
