Certain Fatty Acids May Worsen Inflammation in Crohn’s Disease

Certain Fatty Acids May Worsen Inflammation in Crohn’s Disease
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A number of previously published studies suggest intake of omega-3 fatty acids can help alleviate the inflammation that drives Crohn’s disease. A recently published study by scientists at Duke School of Medicine caution, however, that while supplementing with fatty acids can be beneficial in this condition and in overall health, certain fatty acids may actually be detrimental to Crohn’s disease. The study is available in the September 15 issue of the journal Genome Biology, and utilized cutting-edge research software that helps form associations between seemingly unrelated diseases and traits. The study is entitled “CPAG: software for leveraging pleiotropy in GWAS to reveal similarity between human traits links plasma fatty acids and intestinal inflammation“.

“Dietary therapies for Crohn’s disease should be examined more systematically, and this study provides a good first step,” said in a news release the study’s senior author Dr. Dennis Ko, an assistant professor of molecular genetics and microbiology in the Duke School of Medicine.

While food intake rich in fat content has been associated with Crohn’s disease, this nutritional factor has never been linked to the disease from the point of view of shared genetics. According to research, there are sets of very particular genetic modifications that have been associated with higher concentrations of fatty acids circulating in the bloodstream. This new study was able to pinpoint these genetic overlaps between palmitoleic acid, a subtype of omega-7 fatty acid, and Crohn’s disease thanks to a novel software called CPAG (“SEE-PAG”; short for Cross-Phenotype Analysis of GWAS), which allowed the researchers to note similarities between 1,400 genome-wide association studies (GWAS) that have been published in the past.

“The basis of the approach is simply to ask, ‘Is the [genetic] overlap between the two diseases or traits more than you’d expect just by chance?’” said Dr. Ko, who is also a member of the Duke Center for Host-Microbial Interactions.

To help shed light on the exact cause and effect relationship between levels of circulating fatty acids and Crohn’s disease, the Duke researchers examined a model of the disease using zebrafish, previously created by Stefan Oehlers, a post-doctoral fellow in David Tobin’s team at Duke. Surprisingly, researchers found that palmitoleic acid (omega-7) was not responsible for driving inflammation, and instead identified that its counterpart in saturated fat, palmitic acid, did. They also discovered that linoleic acid – a type of omega-6 fatty acid – helped lessen inflammation in the zebrafish. Interestingly, omega-6 levels have been noted to be reduced in patients with Crohn’s disease.

Dr. Ko clarified that while these findings may seem groundbreaking, further studies would have to be conducted to strengthen the results before physicians and patients begin implementing dietary modifications to help alleviate Crohn’s disease symptoms. “If we can deepen our understanding of lipid imbalance in Crohn’s disease and the consequences of having too much or too little of any one lipid in particular, then we might eventually be able to develop new strategies for managing Crohn’s disease and other inflammatory disorders,” concluded the study’s co-author Dr. John Rawls, an associate professor of molecular genetics and microbiology in the Duke School of Medicine.

Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Técnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.
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Margarida graduated with a BS in Health Sciences from the University of Lisbon and a MSc in Biotechnology from Instituto Superior Técnico (IST-UL). She worked as a molecular biologist research associate at a Cambridge UK-based biotech company that discovers and develops therapeutic, fully human monoclonal antibodies.
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