Summary: Fiber digestion produces short-chain fatty acids like propionate and butyrate, which directly alter gene expression with anti-cancer effects, according to new research. The study found that these fatty acids influence genes involved in cell proliferation, differentiation, and apoptosis, key processes that control tumor growth.
Researchers demonstrated these epigenetic changes in human cells and mouse models, highlighting fiber’s systemic impact on health. With less than 10% of Americans meeting fiber intake guidelines, this study underscores fiber’s critical role in cancer prevention.
Key Facts
- Anti-Cancer Effects: Short-chain fatty acids from fiber digestion directly modulate genes that regulate cell growth, differentiation, and apoptosis.
- Global Mechanism: These fatty acids circulate throughout the body, suggesting fiber’s widespread influence on gene function.
- Diet Deficiency: Less than 10% of Americans consume the recommended daily fiber intake, limiting these protective benefits.
Source: Stanford
Fiber is well known to be an important part of a healthy diet, yet less than 10% of Americans eat the minimum recommended amount.
A new study from Stanford Medicine might finally convince us to fill our plates with beans, nuts, cruciferous veggies, avocados and other fiber-rich foods.
The research, which will be published in Nature Metabolism on Jan. 9 identified the direct epigenetic effects of two common byproducts of fiber digestion and found that some of the alterations in gene expression had anti-cancer actions.
When we eat fiber, the gut microbiome produces short-chain fatty acids. These compounds are more than just an energy source for us: They have long been suspected to indirectly affect gene function.
The researchers traced how the two most common short-chain fatty acids in our gut, propionate and butyrate, altered gene expression in healthy human cells, in treated and untreated human colon cancer cells, and in mouse intestines.
They found direct epigenetic changes at specific genes that regulate cell proliferation and differentiation, along with apoptosis, or pre-programmed cell death processes — all of which are important for disrupting or controlling the unchecked cell growth that underlies cancer.
“We found a direct link between eating fiber and modulation of gene function that has anti-cancer effects, and we think this is likely a global mechanism because the short-chain fatty acids that result from fiber digestion can travel all over the body,” said Michael Snyder, PhD, Stanford W. Ascherman, MD, FACS Professor in Genetics.
“It is generally the case that people’s diet is very fiber poor, and that means their microbiome is not being fed properly and cannot make as many short-chain fatty acids as it should. This is not doing our health any favors.”
Given the worrying rates of colon cancer in younger adults, the study findings could also spur conversation and research about the possible synergistic effects of diet and cancer treatment.
“By identifying the gene targets of these important molecules we can understand how fiber exerts its beneficial effects and what goes wrong during cancer,” Snyder added.
About this diet, cancer, and genetics research news
Author: Lisa Kim
Source: Stanford
Contact: Lisa Kim – Stanford
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Short-chain fatty acid metabolites propionate and butyrate are unique epigenetic regulatory elements linking diet, metabolism and gene expression” by Michael Snyder et al. Nature Metabolism
Abstract
Short-chain fatty acid metabolites propionate and butyrate are unique epigenetic regulatory elements linking diet, metabolism and gene expression
The short-chain fatty acids (SCFAs) propionate and butyrate have beneficial health effects, are produced in large amounts by microbial metabolism and have been identified as unique acyl lysine histone marks.
To better understand the function of these modifications, we used chromatin immunoprecipitation followed by sequencing to map the genome-wide location of four short-chain acyl histone marks, H3K18pr, H3K18bu, H4K12pr and H4K12bu, in treated and untreated colorectal cancer (CRC) and normal cells as well as in mouse intestines in vivo.
We correlate these marks with open chromatin regions and gene expression to access the function of the target regions. Our data demonstrate that propionate and butyrate bind and act as promoters of genes involved in growth, differentiation and ion transport.
We propose a mechanism involving direct modification of specific genomic regions by SCFAs resulting in increased chromatin accessibility and, in the case of butyrate, opposing effects on the proliferation of normal versus CRC cells.
