I Get By With A Little Help From My Friends

Vegetables lend our body a helping hand. Image Credit: Public domain

Everyone has their “sick food,” that staple cure-all of childhood, one whose guarded family recipe has been passed through the generations. But in order to extract all the helpful nutrients from these typically veggie-laden foods, our digestive system needs a helping hand. Our gastrointestinal tracts not only digest and absorb nutrients from the food we eat, but also play host to millions of benign microorganisms, collectively known as the “gut microbiome.” They feed as we eat, and in turn assist in digestion and release molecules that affect our bodies. Such secretions, including different types of fatty acids, have been found to specifically impact the immune system. So it’s no wonder that scientists have probed into how these fatty acids affect human health and disease.

Cells in the immune system can take on many different functions, two of which are “inflammatory” and “suppressive.” Inflammatory cells promote the attack of foreign, or perceived foreign, invaders, while suppressive ones keep the body’s defenses at bay. Maintaining a balance between these two is critical, and disequilibrium can lead to disease. In the case of multiple sclerosis (MS), the scales are tipped in favor of an inflammatory immune response. This leads to an “overactive” immune system that attacks the patient’s own nervous system. Since the fatty acids released by our microbiome affect our immune system, and an immune imbalance is thought to contribute to the development of MS, Dr. Aiden Haghikia and his team wondered if our gut residents’ secretions could impact MS directly [1].

To test their hypothesis, the researchers first looked at naive T cells, cells from the immune system that have yet to decide their function. They treated the cells with two different types of fatty acids: short chain and long chain. While naive T cells exposed to short chain fatty acids became suppressive, those given long chain fatty acids were more inflammatory. Dr. Haghikia and his colleagues then asked if they could apply these findings to a disease model in mice. Would treatment with short chain fatty acids be both preventative and therapeutic, fixing the imbalanced immune system by promoting suppressive T cells? As it turns out, these secretions do have a beneficial effect, but only before disease onset. Mice that had been fed short chain fatty acids prior to MS induction had generally less trouble walking and had more balanced immune systems than untreated mice – that is, they had more suppressive immune cells. However, when mice started receiving short chain fatty acids after their MS became apparent, they saw none of these benefits.

We are only just discovering the effects of short chain fatty acids on the immune system. Here, researchers were able to show that, in the context of MS, these molecules may have preemptive beneficial effects. If you recall, fatty acids can be secreted by our little friends in the gut. And what type of diet results in our gut microbiome producing short chain fatty acids? A vegetable-heavy one.

Megan G. Massa (@MegMassa)

Guest Contributor, Signal to Noise

First year PhD student, UCLA Neuroscience Interdepartmental Program with a focus in neuroendocrinology

References:                   

[1] Haghikia, A. et al. Dietary Fatty Acids Directly Impact Central Nervous System Autoimmunity via the Small Intestine. Immunity 43, 817–829 (2015).

Biases in Science News: Tracking Down the Source of Exaggerations

Image Credit: Public domain

How often have you seen a news headline about a study on the benefits of red wine or dark chocolate only to hear later about a new study that contradicts the first one? While many science stories have strong data and evidence to back their claims, other news headlines come from the type of data that can’t provide a definitive proof of cause-and-effect. [1]. A recent study [2] looked at how journalists write science stories and how these stories can end up as misleading headline science.

The authors determined how statements made in press releases influenced the presence of exaggerations in news stories. An example would be saying that “eating dark chocolate causes fewer heart attacks” instead of indicating that there was a correlation between a group that ate more dark chocolate and the number of heart attacks occurring in that group. This study would only demonstrate a correlation between heart attacks and eating dark chocolate and does not prove that eating dark chocolate was the cause for fewer heart attacks. Researchers looked through 534 press releases prepared by research journals and the corresponding 582 news articles, then identified any statements or advice not included in the manuscript.

Results show that 25% of the press releases included more explicit advice compared to the original paper. 20% of the press releases also misinterpreted a correlation study as a study that presented a cause-and-effect relationship. The results also demonstrated that journalists would not tend to include over-exaggerations if the exaggerations were not part of the original press release.

This paper shows how exaggerations in press releases can create misleading headlines in science news stories. Since journalists may not have the expertise or time to fact-check statements from a press release, any information included in a press release should be precise, and any claims made should not be exaggerated from the original study. Headline news is crucial for communicating science, but if the stories are inaccurate or over-exaggerated, it can erode people’s trust in the scientific method.   

- Erica K. Brockmeier
Toxicology post-doc / Aspiring science writer
@EKBrockmeier

References:
[1] Aschwanden, C. Science Isn’t Broken. Five Thirty Eight Science and Health (2015, Aug 19). Accessed on 2017, Feb 24. https://fivethirtyeight.com/features/science-isnt-broken

[2] Sumner, P. et al. Exaggerations and Caveats in Press Releases and Health-Related Science News. PLoS ONE 11(12), e0168217. doi:10.1371/journal.pone.0168217 (2016).