dTFA showed a significant association to behaviors that have unfavorable repercussions to others – indeed dTFA were more consistently predictive than that of other assessed and recognized aggression predictors. The effect was robust to adjustment for potential confounders like age, education, smoking, and alcohol. This is the first study to show a connection of dTFA to aggression.
A role for nutrition and specifically fatty acids in behavior 
has been previously reported 
. Of note, dTFA variably obstruct production of docosahexaenoic acid, a long chain n3FA that has protected against aggression-related outcomes in some observational and experimental studies 
. In one animal study the effect of dTFA on n3FA themselves did not extend to the brain 
. However, it is unknown whether n3FA behavioral benefits reflect purely direct effects of n3FA on the brain or indirect effects – e.g. through effects on prostaglandins and oxidative and inflammatory mediators that may themselves cross the blood-brain-barrier 
. Indeed, dTFA mechanisms that could have implications for aggression include cell energy alterations 
, oxidative stress 
and inflammatory effects 
. n3FA have also been linked to lower depression risk, and analogous reasoning might yield the hypothesis that trans fats may adversely affect depression. Indeed, a relation of dTFA and saturated fats to depression has been reported 
. The association to depression was evident in our sample as well (based on the Center for Epidemiologic Studies Depression Scale); but our focus is on the aggression association, which, in our sample, is considerably stronger. Of note, n3FA intake was not significantly related to aggression in our sample.
As with all observational studies, there are limitations including the potential for unmeasured confounding. However, observational data will likely be central to exploring this issue as human intervention studies with randomized dietary trans fat allocation are unlikely to be pursued due to ethical concerns, given evidence of other adverse health effects of dTFA.
This study did not employ objective markers of trans fatty acids such as red blood cell membrane trans fats 
, or plasma phospholipid trans fats 
, and future studies should seek to employ these measures to establish whether the relationship is upheld. Use of these as biomarkers of dTFA 
, may correlate imperfectly to dTFA. However, while serum markers are “objective,” they also have limitations relative to dTFA. (Other factors may affect serum level and outcomes, creating an apparent connection that need not have anything to do with actions of the nutrient. For illustration, low serum levels of iron may be linked to colon cancer death, or death from exsanguination, but it is neither low iron intake nor low iron levels that produce
these. Rather, colon cancer may cause GI bleed and low measured iron at a given iron intake level
, producing the appearance of a connection.) Since one can intervene upon diet, the association of specifically dTFA to behavior remains of independent importance.
Trans fat consumption was estimated from dietary recall. Not all foods that go by the same label have the same trans fat content. However, provided the misclassification is nondifferential, this would be expected to produce bias toward the null and could not explain strong and significant findings. Moreover, this study was done during a period of relative stability of trans fat content in foods (1999–2004) prior to more recent efforts to restrict dTFA – a comparative strength of this investigation.
Trans fat consumption could serve as a marker for other untoward behaviors and practices that could in turn be linked to aggression. This concern is somewhat mitigated as our finding emerged in a clinical trial sample and was preserved with adjustment for other adverse health behaviors such as smoking and alcohol. Triangulating evidence and other studies will be required to more confidently establish whether the association is causal.
This work also has important strengths. The premise (and results) are original but rest on a biological foundation. Factors including the strength of association, consistency, temporality (prospective prediction), biological gradient (“dose response”), biological plausibility, and coherence with other literature – factors such as those in Hill's presumptive criteria for causality with observational data – were evident in our findings, and add weight to the possibility that the association we identify could have a causal basis; but confounding cannot be excluded. If the association is causal, the findings provide one further potential explanation for the recognized association between hostile/aggressive behaviors and heart disease. Trans fats could serve as common cause for both outcomes 
(analogous to the observation that n3FA may serve as a common protection against both 
If the association is determined to be causal, then the detrimental effects of trans fats may extend beyond the person who consumes them to affect others with whom that person interacts. Should that prove to be the case, the inclusion of synthetic trans fats in diets may bear reexamination – with implications to public policy and regulation.