Meditations of an oncology geek

Experimental Obesity Contributes to Cancer

with 3 comments

24 October 2012

Overweight people get certain types of cancer more frequently; It’s been known from epidemiological association studies for a long time (1). However, that alone does not necessarily mean that obesity causes cancer. The media frequently conflates correlation and causation. Just because the mean ocean temperature and the number of pirate attacks have both increased in the last decade does not mean that warmer water is causing more piracy, or that pirates are making the earth warm. It could be that obesity causes cancer, or that there is something in the environment that causes both cancer and obesity.

Without causation studies (i.e. experimental research) it’s impossible to know if obesity causes cancer. The CDC reports that more than 35% of U.S. adults are obese, and that this rate is rising! (2) Given this alarming health trend, it’s a startling hypothesis that this already detrimental chronic health condition could influence another deadly health epidemic: cancer.

This morning I came across a paper by Mikhail G. Kolonin and colleagues that caught my attention. (3)

The authors used a strain of mice that are genetically “identical”. I.e. the mice have been inbred to the point where genetic differences in phenotypes of individual mice will be minimal. The authors then induced obesity in mice environmentally by feeding a test group a high fat diet (HFD) while a control cohort of mice was fed a regular diet. The authors then took the test mice off the HFD, and proceeded to implant mouse tumor cells into the breast of both groups of mice.

The result? The tumor cells implanted into the obese group of mice developed tumors that grew more than twice as fast! The authors analyzed the tumors and found that the increased white adipose tissue (fat) of the host allowed for the tumors to recruit more adipose stromal cells (non tumor cells from the host) to help the tumors form new blood vessels to help the tumors hijack energy and resources from the bloodstream.

Tumors are not a solid mass of tumor cells. They consist of blood vessels recruited from the host, and stromal (non-tumor cells) that are recruited from surrounding tissues that are normally used to do things like heal wounds and repair tissue. It appears that, at least in this model of tumor growth, that the physiological environment associated with obesity can promote tumor growth.

One part of this study that I really liked was the fact that both sets of mice had the same diet during the phase of tumor growth. If we are to extrapolate these findings to humans, it would indicate that a diet intervention of already diagnosed cancer patients might not be effective. I.e. it’s not the fat in the diet itself and the greater availability of fat resources in the blood that’s fueling the cancer growth; it’s the effects of the stored fat in tissues that’s making the tumors grow faster. I also liked the fact that the same strain of mice had obesity induced experimentally to rule out confounding genetic influences on the process: environmental influences lead to a chronically obese condition, and the physiological changes accompanying the obese condition are what allowed tumor cells to grow faster.

Cancer is not a single disease, but a blanket classification used to describe many diseases with similar properties; cancer is a very heterogeneous disease. No two people’s cancer is exactly alike on a molecular scale. It’s important to note that these studies were done with one cancer cell line, and performed in mice. The same mechanisms might or might not exist in humans, or all types of human cancers for that matter.

Nonetheless, this paper provides fresh evidence to the causation hypothesis (obesity increases cancer risk) and that the two conditions are perhaps not caused by a third, unknown confounding factor.

It is in the opinion of this scientific apprentice that the mechanism presented needs to be further analyzed by other scientific groups (isn’t that what scientists always say?). But, it is one more piece of understanding about the world that we can use to better our lives and those around us. It comes back to a similar theme: the United States (and many other first world countries) are facing a dire health epidemic stemming from metabolic syndrome. The good news is that the influences of metabolic syndrome and the result (obesity, and perhaps some cancers) are environmental, and as opposed to our genes, these are things we can control. That is not to say it is easy‚Ķ

If you or a friend are overweight or obese, it is my hope that this article will be a little bit of motivation to make positive health choices.

Peace and Health!
Ryon

note: I’ve also written about the positive effects of exercise on reducing cancer risk as well: http://ryongraf.com/2012/03/can-exercise-help-prevent-cancer/

References:
1) http://www.nature.com/nrc/journal/v4/n8/full/nrc1408.html
2) http://www.cdc.gov/nchs/data/databriefs/db82.pdf
3) http://cancerres.aacrjournals.org/content/72/20/5198

Written by Ryon

October 24th, 2012 at 9:37 am

Posted in Science Blog

3 Responses to 'Experimental Obesity Contributes to Cancer'

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  1. A high fat diet causes obesity? What type of fat was in the diet. Was it regular chow with added vegetable oil?

    Jill

    25 Oct 12 at 12:50 pm

  2. Jill,

    Thanks for writing in. The materials and methods section pointed me to this chow used: http://www.taconic.com/user-assets/Documents/Taconic_D12492.pdf

    The low fat diet had 10% of kcal from fat, and the high fat diet had 60% kcal from fat. It appears that most of the fat in the mouse diet came from lard. Of notice is the significant sucrose and maltodextrin component of the chow as well. Being aware of Dr. Attia’s significant legwork and research, I have to wonder if the significant sugar component is a contributor to the experimentally induced obesity. However, the low-dat fiet has roughly 1/3 of calories from sucrose and 1/3 from corn starch, and perhaps a much higher glycemic load than the high fat chow mice.

    I am not sure if this model of induced obesity due to fat would translate to humans, or all humans for that matter. Dr. Attia has compiled some compelling evidence to suggest otherwise, which I won’t go into because I’m assuming you’re already aware of it?

    It is very plausible that mice and humans would react differently to the same diet. While both species are omnivores, I have seen evidence to suggest that humans require a certain amount of fat for brain development that mice do not. Biological anthropologists have speculated that the ability to hunt and get high quality fat in our evolutionary past made advanced cognitive development possible. It would not surprise me in the least if we could all subsist on more %fat than we actually do.

    Ryon

    Ryon

    25 Oct 12 at 6:12 pm

  3. Very interesting. Thank you Ryon. Personally, my appetite is quickly satisfied if I eat fat. Dr Richard K Bernstein said he tried to increase the weight of one of his patients with added fat. After six months, there was no difference. I think, if I remember correctly, he said he had to give him insulin.

    Jill

    25 Nov 12 at 12:12 pm

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