In today’s Wall Street Journal*, Jonathan Rockoff reports on new cancer treatments that are “personalized” depending on whether one is carrying a certain mutated gene. When individuals with specific types of cancer carry the mutated gene, and are treated with these new medications, the results are impressive. Almost 50% of cancer patients taking these medications had shrinkage of tumors compared with 5.5% of those on conventional chemotherapy.
Some patients taking the medications report side effects such as fatigue and joint pain which led their physicians to lower their dose. Fatigue and joint pain are signs of immune dysfunction, typically excessive levels of inflammatory responses by the immune system. The key is to help the body return to immune homeostasis (immune balance).
Immune inflammation has two main functions: a) defending the body from infection, and b) healing the body when an infection has occurred, or if the body injured.
People are becoming increasingly aware that inflammation is also associated with other conditions such as atherosclerosis (1), autoimmune conditions, and even the development of cancer [2, 3].
The relationship between immune inflammation and cancer is not well understood, but it appears that inflammatory responses feed cancer cells and cancer cells trigger inflammatory responses.
The relationship between cancer and inflammation is not simple (4). But studies suggest that if approximately 15 percent of cancer , is associated with microbial infection one would expect that if infections were reduced world-wide, so would cancer.
There are certain “hallmarks of cancer” :
Are often “immortal”. In a test tube, whereas “normal” cells will divide a number of times before they die off, cancer cells keep dividing and multiplying for a long time—they seem to disregard the natural “death” cycle.
Appear to stimulate blood vessels to grow to them bringing them “good blood circulation” and nutrients.
Are independent—they can grow without input or control from other cells.
Lack “contact-inhibition”. [Normal cells will stop growing when they touch one another, cancer cells will “overgrow” each other.]
Are able to invade other tissues and spread throughout the body (metastasize).
Some scientists consider pre-malignant tumors as being “wound-like” . The body recognizes the presence of the tumor and starts to combat it using inflammation as its weapons system.
The inflammatory response produces immune factors that recruit other inflammatory immune cells into the area to “heal” the “lesion”. Unfortunately however, due to the nature of cancer cells, some of these molecules may only stimulate the growth of more cancer cells resulting in more tissue invasion and metastasis . This is why immune homeostasis is essential to our health.
Taking the following steps may help decrease the chances of getting cancer:
a) Stop the use of tobacco.
b) Drink alcohol in moderation (if you consume alcohol).
c) Have moderate sun exposure (10 minutes/day) and plenty of fresh air.
d) Eat plant-based foods, especially those high in phytonutrients: berries, dark, green, leafy vegetables, cauliflower, broccoli, nuts (in moderation), are great choices.
e) Increase your physical activity. (Physical activity is associated with a reduced risk of cancers of the colon and breast, improved quality of life among cancer patients, and cancer survival (8)).
f) Maintain a healthy weight (obese people have higher rates of cancer)
g) Avoid risky sexual and chemical-abuse behaviors that may expose you to certain infections that may lead to cancer (for example: HIV/AIDS, hepatitis, etc.)
h) Screen regularly for cancer
Also, to help the body achieve inflammatory immune homeostasis, along with eating a healthful diet and controlling your portion sizes, consumption of on a daily basis of hyperimmune egg is prudent.
1. Crandall MA, Corson MA. Curr Treat Options Cardiovasc Med. 2008 10:304.
2. Balkwill F, Mantovani A. Lancet. 2002 357:539.
3. Coussens LM, Werb Z. Nature. 2002 420:860.
4 Hanahan D, Weinberg RA. Cell. 2000 100:57.
5. Kuper H, et al. J Intern Med. 2000 248:171.
6. Coussens LM, et al. Genes Dev. 1999 13:1382.
7. Rakoff-Nahoum S. Yale J Biol Med. 2006 79:123