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

September 1, 2014 by Bob Yirka 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

Abstract
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.

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15 comments

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JVK
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].

http://figshare.c...s/994281

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
JVK
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.
RealScience
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.
(see http://phys.org/n...es.html)

Do you admit that you use the term 'mutations', and that your earlier claim was thus false?
JVK
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.
anonymous_9001
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?
RealScience
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?
JVK
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
RealScience
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?
JVK
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

http://www.the-sc...osystem/
animah
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:

https://www.googl...s+v+kohl
JVK
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:

http://www.nature...150.html

http://link.sprin...4-1558-7
RealScience
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.
dcmckee1947
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.
JVK
1 / 5 (1) Oct 18, 2014
Arrival of the Fittest: Solving Evolution's Greatest Puzzle
http://www.amazon..._title_0

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

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