Reply to Ferreira et al.

Dear Editor:

We thank Ferreira et al. for their interest and commentary pertaining to our review (1). Ferreria et al. have raised some interesting and relevant points, which warrant further discussion.

We agree that the type of fat consumed can influence inflammatory markers. Rocha et al. (2) reviewed the evidence concerning dietary lipid intake and inflammatory gene expression, concluding that SFA consumption is correlated with many proinflammatory pathways, including the IL-1, IL-6, and TNF-α pathways, which were also of interest in our review. Conversely, mono- and polyunsaturated fatty acid dietary consumption produced an anti-inflammatory response compared to that of SFA. Further, increased SFA dietary intake has been independently correlated to elevated C-reactive protein (CRP) concentrations (3). As populations following vegetarian diets have lowered intakes of preformed DHA compared with omnivorous populations who consume fish and animal products (4), exploration of the omega-3 index and its relation to inflammation and immunity in these groups could be a focus for future research. This is of particular interest as the omega-3 index has been associated with favorable inflammation profiles (5).

Exploration of the relationship between dietary fat consumption and inflammatory and immune markers was outside of the scope of our review; however, we feel that future research exploring plant-based dietary patterns and inflammation should explicitly investigate lipid intakes and the relationship with inflammatory and immune markers. We hypothesize a stepwise trend, with vegetarian dietary groups consuming the most dietary SFA exhibiting the highest markers of inflammation.

We acknowledge that plant-based eating patterns are associated with a reduced risk of many chronic diseases, in which the nutritional components of plant foods, including fiber, phytochemicals, and an array of vitamins and minerals, can provide protection (6). Conversely, animal-dense eating patterns, particularly those with high intakes of red and processed meats, are associated with increased risks of some chronic diseases, including cardiovascular disease (CVD) and type 2 diabetes mellitus (7, 8). It appears that the observed protection among plant-based dietary groups are 2-fold, in that consumption of plant-based foods is protective, yet conversely, consumption of meat-based foods can be deleterious, with several mechanistic underpinnings being described (8).

One possible mechanism which Ferreira et al. highlight is trimethylamine N-oxide (TMAO), which has been linked to both CVD and low-grade systemic inflammation (9). Given that TMAO is metabolized from choline, betaine, ergothioneine, and carnitine, compounds predominately found in animal-based products, consideration of the role of this molecule is warranted. This is particularly true considering the differences in gut microbiota between individuals with vegetarian and those with nonvegetarian eating patterns, whereby production of trimethylamine (TMA) from l-carnitine in persons following a vegetarian eating pattern is substantially lessened when these groups are compared (10). Future exploration of plant-based dietary patterns and inflammation should contrast TMAO concentrations in the different vegetarian subclasses i.e., ovo-vegetarian, lacto-ovo vegetarian, vegan, and whole-food plant-based vegan.

While we too believe that there are diverse economic and cultural implications associated with the consumption of meat products, consideration of these factors was outside of the scope of the present review, in which we aimed to explore the effects of vegetarian-based dietary patterns on inflammatory and immune markers. Further consideration of these broader implications could be a topic for further research.

Notes

Author disclosures: JCC is the proprietor of “Purely Plants” and has an interest in advocating vegetarian-based diets to patients when appropriate. All other authors report no conflicts of interest.

All authors read and approved the final manuscript.

Abbreviations used: CRP, C-reactive protein; CVD, cardiovascular disease; TMA, trimethylamine; TMAO, trimethylamine N-oxide.