Researchers find evidence of a link between high fat diets, gut bacteria, and bowel cancer

September 1, 2014 by Bob Yirka, Medical Xpress report
Cancer — Histopathologic image of colonic carcinoid. Credit: Wikipedia/CC BY-SA 3.0

(Medical Xpress)—A large team of researchers, with members primarily from Germany, has found evidence that implicates high fat diets as a cause of bowel cancer due to a link with gut bacteria. In their paper published in the journal Nature, the team describes the results of research they conducted using mice that have a gene associated with the onset of bowel cancer.

Medical scientist have known for some time that there is a link between high fat diets and various cancers of the bowels, but until now were not able to explain why such a connection exists. Some have suggested that it's tied to obesity, or other side-effects that occur when a person eats a high in fat. In this new effort, the researchers have found evidence that exonerates obesity and instead implicates .

To learn more about the onset of , the researchers obtained mice with a to the disease—they fed some of them on high fat diets and others on normal fat diets. They also took fecal samples to note the makeup of the microbial community in the gut, initially and then periodically thereafter. In so doing, they noted a shift in composition of the gut microbe composition over time in the mice on the high fat diet—there were more of some bugs, and less of others. The result they noted was a reduced immunity defense against bowel cancers with an associated increase in the rates of cancers observed.

To further bolster the evidence of the impact of gut biota in fighting off bowel cancer, the team killed off the biota community completely in some mice (with a predisposition to bowel cancer) and found the incidence of bowel cancers decreased. They also found that transferring samples of gut biota from predisposed mice that had bowel tumors to tumor-free (but still predisposed) —they too exhibited a higher rate of developing tumors than those that did not receive the transfer. These experiments, the researchers claim, indicate a very strong link between a , gut biota and bowel cancer.

The research also suggests that in addition to modifying diet to reduce bowel cancers, there may be a way to lower the chances of getting bowel cancers by reestablishing normal gut biota in people who continue to eat diets high in fat.

Explore further: Chronic intake of Western diet kills mice

More information: High-fat-diet-mediated dysbiosis promotes intestinal carcinogenesis independently of obesity, Nature (2014) DOI: 10.1038/nature13398

Several features common to a Western lifestyle, including obesity and low levels of physical activity, are known risk factors for gastrointestinal cancers. There is substantial evidence suggesting that diet markedly affects the composition of the intestinal microbiota. Moreover, there is now unequivocal evidence linking dysbiosis to cancer development3. However, the mechanisms by which high-fat diet (HFD)-mediated changes in the microbial community affect the severity of tumorigenesis in the gut remain to be determined. Here we demonstrate that an HFD promotes tumour progression in the small intestine of genetically susceptible, K-rasG12Dint, mice independently of obesity. HFD consumption, in conjunction with K-ras mutation, mediated a shift in the composition of the gut microbiota, and this shift was associated with a decrease in Paneth-cell-mediated antimicrobial host defence that compromised dendritic cell recruitment and MHC class II molecule presentation in the gut-associated lymphoid tissues. When butyrate was administered to HFD-fed K-rasG12Dint mice, dendritic cell recruitment in the gut-associated lymphoid tissues was normalized, and tumour progression was attenuated. Importantly, deficiency in MYD88, a signalling adaptor for pattern recognition receptors and Toll-like receptors, blocked tumour progression. The transfer of faecal samples from HFD-fed mice with intestinal tumours to healthy adult K-rasG12Dint mice was sufficient to transmit disease in the absence of an HFD. Furthermore, treatment with antibiotics completely blocked HFD-induced tumour progression, suggesting that distinct shifts in the microbiota have a pivotal role in aggravating disease. Collectively, these data underscore the importance of the reciprocal interaction between host and environmental factors in selecting a microbiota that favours carcinogenesis, and they suggest that tumorigenesis is transmissible among genetically predisposed individuals.

Related Stories

Chronic intake of Western diet kills mice

June 19, 2014
(Medical Xpress)—When Cornell researchers fed high-fat Western diets to mice engineered without key immune system receptors to recognize pathogens, the mice died from lethal lung damage.

Gut microbes turn carbs into colorectal cancer

July 17, 2014
Colorectal cancer has been linked to carbohydrate-rich western diets, but the underlying mechanisms have been unclear. A study published by Cell Press July 17th in the journal Cell shows that gut microbes metabolize carbohydrates ...

Gut microbes spur development of bowel cancer

March 3, 2014
It is not only genetics that predispose to bowel cancer; microbes living in the gut help drive the development of intestinal tumors, according to new research in mice published in the March issue of The Journal of Experimental ...

New research links bad diet to loss of smell

July 21, 2014
Could stuffing yourself full of high-fat foods cause you to lose your sense of smell?

Scientists uncover stem cell behavior of human bowel for the first time

August 7, 2014
For the first time, scientists have uncovered new information on how stem cells in the human bowel behave, revealing vital clues about the earliest stages in bowel cancer development and how we may begin to prevent it.

Scientists discover how iron levels and a faulty gene cause bowel cancer

August 9, 2012
High levels of iron could raise the risk of bowel cancer by switching on a key pathway in people with faults in a critical anti-cancer gene, according to a study published in Cell Reports today.

Recommended for you

Cancer comes back all jacked up on stem cells

March 19, 2018
After a biopsy or surgery, doctors often get a molecular snapshot of a patient's tumor. This snapshot is important - knowing the genetics that cause a cancer can help match a patient with a genetically-targeted treatment. ...

A small, daily dose of Viagra may reduce colorectal cancer risk

March 19, 2018
A small, daily dose of Viagra significantly reduces colorectal cancer risk in an animal model that is genetically predetermined to have the third leading cause of cancer death, scientists report.

Researchers create a drug to extend the lives of men with prostate cancer

March 16, 2018
Fifteen years ago, Michael Jung was already an eminent scientist when his wife asked him a question that would change his career, and extend the lives of many men with a particularly lethal form of prostate cancer.

Machine-learning algorithm used to identify specific types of brain tumors

March 15, 2018
An international team of researchers has used methylation fingerprinting data as input to a machine-learning algorithm to identify different types of brain tumors. In their paper published in the journal Nature, the team ...

Higher doses of radiation don't improve survival in prostate cancer

March 15, 2018
A new study shows that higher doses of radiation do not improve survival for many patients with prostate cancer, compared with the standard radiation treatment. The analysis, which included 104 radiation therapy oncology ...

Joint supplement speeds melanoma cell growth

March 15, 2018
Chondroitin sulfate, a dietary supplement taken to strengthen joints, can speed the growth of a type of melanoma, according to experiments conducted in cell culture and mouse models.


Adjust slider to filter visible comments by rank

Display comments: newest first

1 / 5 (2) Sep 01, 2014
The ecological origin of all biological laws is apparent 1) in the context of systems biology [91]; 2) in the context of the metabolism of nutrients by microbes [157]; and 3) in the context of how the metabolism of nutrients results in species-specific pheromones that control the physiology of reproduction [158].


157. Kohl, K. D., Diversity and function of the avian gut microbiota. J Comp Physiol B 2012, 182 (5), 591-602. doi: 10.1007/s00360-012-0645-z
1 / 5 (2) Sep 01, 2014
"The mRNA that encodes the histone demethylase JMJD1A is a direct target of miR-627. " http://www.ncbi.n...3722307/

That fact makes it clear that the conserved molecular mechanisms of nutrient-dependent pheromone-controlled ecological adaptations are as important to human cell type differentiation as they are in any other population of any other species on this planet.

The microRNA/messenger RNA balance typically leads from nutrient-uptake and the metabolism of nutrients by gut microbes to species-specific pheromones that control the physiology of reproduction, which is how amino acid substitutions that stabilize DNA in organized genomes are fixed.

Mutations that perturb protein-folding can lead to genetic predispositions, but there is no such thing as an 'evolutionary event' that links mutations to the increasing organismal complexity and biodiversity manifested in the morphological and behavioral phenotypes of any species.
4 / 5 (4) Sep 01, 2014
@JVK, for someone who claims that you don't use the term "mutations", you sure seem to introduce it into threads a lot.

Do you admit that you use the term 'mutations', and that your earlier claim was thus false?
1 / 5 (2) Sep 01, 2014
A nucleotide change could initiate fragile X syndrome http://medicalxpr...ome.html

Is this an example of a mutation that you think leads to the evolution of increasing organismal complexity? If not, provide an example for comparison to what I have detailed in the context of the microRNA/messenger RNA balance and amino acid substitutions that differentiate cell types in species from microbes to man.
3.7 / 5 (3) Sep 01, 2014
amino acid substitutions that stabilize DNA

If those substitutions take place post-transcriptionally, then they have nothing to do with the DNA. Are you talking about splicing making these substitutions?
4 / 5 (4) Sep 01, 2014
You didn't answer the question, JVK.
Here it is again: For someone who claims that you don't use the term "mutations", you sure seem to introduce it into threads a lot.

Do you admit that you use the term 'mutations', and that your earlier claim was thus false?
1 / 5 (2) Sep 01, 2014
Experimental evidence needed to demonstrate inter- and trans-generational effects of ancestral experiences in mammals http://onlinelibr...105/full
4 / 5 (4) Sep 01, 2014
@JVK, You have ADMITTED that you throw out results that show evidence of mutations contributing to evolution. It seems to be broader than that - you appear to ignore anything that shows that you are wrong.

Or do you have the honesty to admit that you use the term 'mutations', and that your earlier claim was thus false?
1 / 5 (2) Sep 01, 2014
The Body's Ecosystem

Research on the human microbiome is booming, and scientists have moved from simply taking stock of gut flora to understanding the influence of microbes throughout the body.

By The Scientist Staff | August 1, 2014

3.7 / 5 (3) Sep 02, 2014
First JVK, this article has nothing to do with the biology of reproduction. Or are you claiming causation between pheromones and obesity now? That's just ridiculous.

Second, humans have no genetic pathways to allow pheromone control of anything. None of the studies you linked to support it. In fact, none of them even mention the word pheromone at all (except - drum roll - your own article!)

You just add this bit to dress up your bogus pheromone perfume snake oil. Spammer James V Kohl, stop your scamming!

PS: I know what you're doing. But SEO works both ways: Now you have your name associated with "scam" on Google page 1 results, and it's only going to get worse as you keep spamming this board:

1 / 5 (1) Sep 05, 2014
The de novo Creation of new cell types via nutrient-dependent amino acid substitutions links the epigenetic landscape to the physical landscape of DNA in the organized genomes of species from microbes to man. The de novo Creation of new cell types must be controlled by the metabolism of nutrients to species-specific pheromones, which control the physiology of reproduction. That fact seems to have never occurred to evolutionary theorists.

When theorists only think in terms of mutations, natural selection and the evolution of biodiversity, they cannot link biologically-based cause and effect from ecological variation to ecological adaptations via conserved molecular mechanisms. Instead, serious scientists must provide experimental evidence that continue to support refutations of the theorist's pseudoscientific nonsense.

See for examples:


2.3 / 5 (3) Sep 05, 2014
When theorists only think in terms of mutations...

For someone who claims not to use the term "mutations", you sure use it a lot.

In spite of this additional evidence that you DO use the term 'mutations', you will probably continue to ignore the evidence that your claim was false, just as you ignore the evidence that nature does use actual mutations in natural selection.

When theorists only think in terms of mutations...

But essentially no one in biology these days think ONLY in terms of mutations. It has been known for decades that they are just one part of the complex interaction of genes, epigenetic modifications, histone modifications, regulatory RNAs, etc.

It is YOU who thinks only in terms of one mechanism, your THEORY (with no experimental evidence) that ALL adaptation is due to nutrient-dependent, pheromone-controlled amino acid substitutions. And you IGNORE the experimental evidence AGAINST your theory - so you are a failed narrow-minded THEORIST.
1.5 / 5 (2) Oct 18, 2014
I am concerned about the chow fed to the mice. If it was manufactured in the US, being it is for mice, it most likely contains gmo grains and the HFD will have glyphosate residue. The glyphosate residue is sufficient to cause the dysbiosis all by itself.
1 / 5 (1) Oct 18, 2014
Arrival of the Fittest: Solving Evolution's Greatest Puzzle

Puts together a great deal of information on the microbiome and metabolism to link RNA-mediated amino acid substitutions to cell type differentiation.
1 / 5 (1) Oct 18, 2014

Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.