Colorectal cancer is the second
leading cause of cancer death in the United States and the third most
common cause of cancer death in the world. Your lifetime risk of
developing colorectal cancer is a bit less than 1 in 20.
But there is a light on the
horizon. Since 2000, the diagnosis rate for those 50 and older has
dropped by a third with recent work on screening and prevention
showing how we can improve the numbers even further.
Colon cancer starts in the
lining cells of the large intestine in a “two hit”
process.
The first step, theorized to be
an exposure to an environmental toxin or infectious agent in a
genetically predisposed individual, initiates the rapid growth of a
single cell which then, over time, grows into a benign polyp.
A second change then occurs in
one of these rapidly growing polyp cells results in the first cell of
a colon cancer. If this polyp is removed at this early stage, the
small cancer is cured.
Left in place, however, the
cancer slowly increases in size until at some point it grows through
the wall of the colon. It has been estimated that the time from
benign polyp to colon wall cancer is in the neighborhood of 10 years.
This physiology is the basis
for screening colonoscopy. Identify and remove polyps and you will
prevent, and in some cases, cure colon cancer.
The effectiveness of
colonoscopy screening is the likely explanation of the drop in the
rate of colon cancer diagnosis over the last 20 years. It has been
estimated that over 60% of people over 50 years old have been
screened.
The first of the new
developments is an easier but equally effective screening test.
Advances in immunologic testing allows low risk individuals to
collect a small stool sample for testing. Individuals with low risk
have no personal or family history of colon cancer or polyps. The
stool is then tested for remnants of abnormal proteins shed by
polyps. The colonoscopy is reserved to evaluate for and remove polyps
only in those who are stool test positive.
This annual fecal
immunochemical test (FIT) gives physicians an additional tool to take
advantage of that 10 year screening window. More screening equals
earlier removal (and cure) of more small colon cancers. The FIT is
inexpensive, seemingly as effective as colonoscopy screenings, and
more readily available to patients.
The next advance suggests we
may be getting closer to the idea of preventing colon cancer rather
than just finding it in its early, curable stages. It looks like
colon cancer might be an infectious disease.
Thirty years ago, we found that
stomach ulcers are often the result of a bacterial infection (H.
Pylori) of the digestive tract, rather than the result of acid
irritation alone. We now have suggestive evidence that a certain
bacteria may be associated with those cell changes that lead to colon
polyps and colon cancer.
High concentrations of a family
of bacteria (Fusobacterium) were found in colon cancer tissue removed
from more than 1000 people at surgery. Even more interesting was
finding the same bacteria in an occasional colon metastases (cancer
that had spread), implying an even stronger linkage. The benefits of
targeting and eliminating this specific colon bacteria (with
antibiotics or diet) is being investigated.
And finally, while studying the
role of colon bacteria as a cause of colon cancer, there were clues
as to how our diet may play a role in the initiation or inhibition of
cancerous cell growth. That means making changes in our diet might
decrease our personal risk of developing colon cancer.
It’s old news that
vegetarians have less colon cancer, 20 - 30 percent less than
non-vegetarians. But why?
One possibility could be the
elimination of a cancer cell stimulant. Studies of groups on high
versus low meat diets revealed a three fold variation in the
concentration of nitrosamines, a potentially cancer causing compound,
in their stool.
Another might be the addition
of an actual inhibitor of cancer growth. The microbiome produces
short-chain fatty acids as it metabolizes dietary fiber. Laboratory
experiments exposing colon cancer cells to one of them, butyrate,
slows and can even stop cancer cell growth. Take away the butyrate
and the cells resume growing.
More fruits and vegetables,
less red meat, and it appears you can impact your colon cancer risk.
Even after colon cancer’s
development, diet changes impact a patient’s future course. In a
study of 1,000 people already diagnosed with colon cancer spread
beyond the colon, those who modified their lifestyle to a healthier
diet with added exercise decreased their risk of dying over the next
seven years. The risk was decreased by 42 percent compared to those
who did not change their diet.
Better screening, prevention
with simple diet changes, and the chance that we might eliminate one
reason for that first cancer cell are three reasons I’m optimistic
that the trend line for colon cancer diagnosis (and deaths) will
continue on a downward trend.
References:
https://medicalxpress.com/news/2018-09-vegetarian-colon-cancer.html
https://www.medscape.com/viewarticle/916283
------ references added post publication ---------
https://nutritionfacts.org/video/flashback-friday-whats-your-gut-microbiome-enterotype/
https://www.medscape.com/viewarticle/916283
------ references added post publication ---------
https://nutritionfacts.org/video/flashback-friday-whats-your-gut-microbiome-enterotype/
A risk factor may be a virus in meat (and dairy too). https://nutritionfacts.org/2020/09/24/the-role-of-meat-and-dairy-viruses-in-cancer/
Aspirin may decrease CRC by its effect on the microbiome. https://www.medscape.com/viewarticle/937141
Egg and colon cancer risk via TMAO
Less meat/alcohol and more dairy = less colon cancer
https://www.medscape.com/viewarticle/958688
