First, a bit of background from the literature as to the
known causes or  contributing factors to colon cancer. 

the Colorectal Cancer Association of Canada (2008) lists
these risk factors: 1.) over age of  50 2.) previous
colorectal polyps 3.) history of inflammatory bowel
disease 4.) poor diet high in saturated fats (red meats
especially) and low in fiber,  fruits and vegetables 5.)
personal history of ovarian, breast, or endometrial ca.
6.) sedentary life style 7.) family history of
colorectal ca    -though the incidence of colorectal ca
is low in those under 20 there are  two recognized
hereditary syndromes that if known should prompt
screening  within the family they are      1.) familial
adenomatus polyposis (FAP) and it is related to a
mutation of  the tumor suppressor gene that leads those
who have it to developed may  pre-cancerous polyps
(hundreds and even thousands) in the colon that  should
be monitored (this is generally an autosomal dominant
transfer,  meaning that one parent, or both has the gene
as well, leading to a 50% to  100% chance of expressing
the gene in offspring!).            2.) hereditary
non-polyposis colorectal cancer (HNPCCP similar to FAP)
the  cancer my develop early and also presents with
polyps (presents with less  polyps than FAP). screening
for each can start as early as 12 years of age!

In addition to the Canadian Colorectal Cancer Society
the American Cancer  society (2008) adds 8.) smoking 9.)
people of African american and eastern European Jewish
descent have an  increased risk of developing the
disease 10.) alcohol use  11.) type 2 diabetes not so
strong links exist between 12.) Night shift workers have
a higher instance!!! though more data is needed  to
confirm and also testicular cancer survivors.

Prevention:   American Cancer Society (ACS, 2008) lists
early screening and removal of  polyps. Genetic testing
may be appropriate if there is a strong family history 
of polyps.

With regard to lifestyle there are several listed
recommendations from the  ACS and the Canadian
Colorectal Cancer Association of Canada.

1.) diet, healthy body weight, and exercise- a diet high
in insoluble and  soluble fibre, low in animal fats
particularly beef, lamb and pork. Exercise 
recommendation of 30min five times a weeks at minimum. 

2.) Vitamins: there is some literature that supports
Vitamin D, folate, and  magnesium rich diets or
supplements 

3.) ASA and cox 2 inhibitors may reduce the risk of
Colorectal ca (this is also  mentioned on pg 347 of the
Pathophysiololgy: the Basis of Biologic Diseases  in
Adults and Children (McCance & Heuther, 2006) the
section addresses the  inflammatory cascade as a factor
in the development of cancer. Though there  may be a
sound rationale, there could be dangerous side effects
to  prescribing or recommending an NSAID to a person
with compromised gastric  mucosa.

4.) Hormone replacement therapy in women may decrease
the incidence of  colorectal ca, but it is controversial
as it may contribute to its growth and   mortality in
some instances also.

How to answer the question:

In answer to this patients question as to how did he
'get' cancer, he has some  modfiable risks and some
non-modifiable risks:

His non-modifiable risk factors are: 1.) age- 90% of
people diagnosed with colorectal cancer are over 50
years old  (American Cancer Society, 1997 & 2008)

2.) Male gender- male are at a higher risk of colorectal
ca (McCance &  Huether, 2006 chapter 11).

3.) Race- African american or eastern European Jewish
descent (ACS, 2008)

4.) genetic and familiar predisposition 

5.) previous cancer of testes, (breast, endometrium, or
ovaries in women) or  inflammatory bowel disease. 

6.) (arguable) type 2 diabetes.

Modifiable:

1.) sedentary lifestyle, exercise, and diet 2.) ETOH 3.)
potentially poor management of type 2 diabetes 9 We say
that because he  describes what could be diabetic
neuropathies in his legs) 4.) (potentially) obesity

How he got cancer then can be explained that at some
point in his life he may  have accumulated one or more
of these risk factors and that along the  mucosal lining
of  his bowel a genetic mutation formed. It is difficult
to say  when or what happened but we do know that there
are several early  mechanisms that contribute to the
development of cancer. 

(from McCance and Huether 2006) a quick review of
cancers mechanisms:

cancer causing mutations in genes may occur due to  
-Clonal proliferation-as the cells reproduce over time
there is a higher  chance of error occurring and being
transcribed to the new generation the  error may lead to
a slight advantage of that cell over those around it.
for  example the cell may reproduce faster, or
demonstrate the immortality  feature of a cancer cell
where by it can duplicate with out the traditional 
cellular controls to limit reproductions. 

   -Alterations in Progrowth and Antigrowth mechanisms-
in progrowth the  cancer cell either develops a way of
stimulating its own growth by secreting  their own
growth factors (auto stimulation) or it develops
increased receptors  for existing growth stimulus
thereby becoming hypersensitive to them.

    -Angiogenis- speaks to the ability of a cancer cell
or group of cells to  secrete a factors that stimulate
the growth of new blood vessels a process  that is
usually reserved for wound healing and the female uterus
for  proliferation of the endometrial lining.

    -immortality- most cells with the exception of germ
& stem cells have  limited numbers of divisions before
they die. In germ cells and cancer cells  telomeres act
as protective caps to the chromosomes as they divide. as
a  protective mechanism, as the cell divides, if damage
occurs, the telomeres  get smaller until they can no
longer protect the chromosomes and they are  destroyed.
In cancer cells this process is disrupted and the
telomeres  regenerate allowing the cells to continue to
divide.          -Oncogenes and Tumor suppressor genes-
proto-oncogenes exist in the  body an are regulators of
growth factors, causing their secretion and there 
reception in other words they tell the cells to grow. In
a cancer cell there has  been a mutation (point
mutation, chromosomal translocation, etc.) this 
mutation has lead to the activation from proto-oncogene
to oncogene. The  oncogene allows and encourages
unchecked cell growth and reproduction.  the tumor
suppressor gene is the bodies natural way of regulating
abnormal  growth by telling the cell to stop growing.
One promotes growth the other  inhibits it    in a
cancerous cell one or both have stopped working, leading
to excessive  cell growth and proliferation of the
mutated cells.   

So to the patient we can explain that while there are
some factors which  predispose him to this cellular
cascade such as his diabetes, diet exercise,  weight,
alcohol use, age, genetics, and gender. As noted earlier
there are  preventative measure that could of and can
still be taken to manage the  disease and reduce the
risk of morbidity and death from this illness. 

Hope this is a good overview of a complex question,

Joanna, Andria, and Lorna

References:

American Cancer Society
(2008).http://www.cancer.org/docroot/CRI/
content/CRI_2_2_2X_What_causes_colorectal_cancer.asp?rnav=cri.
updated  last 03/05/08. 

Colorectal Cancer Association of Canada. (2008). Just
the facts: Prevention  Retrieved May 20, 2008, from
www.colorectal-cancer.ca/en/just-the-facts/ prevention. 


McCance, K.L., & Huether, S. E. (2006). Pathophysiology:
The biologic basis  for disease in adults and children.
Elsevier  Mosby: St. Louis.