Trans Fat Consumption and Aggression

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DOI: 10.1371/journal.pone.0032175 · Source: PubMed
Abstract
Background Dietary trans fatty acids (dTFA) are primarily synthetic compounds that have been introduced only recently; little is known about their behavioral effects. dTFA inhibit production of omega-3 fatty acids, which experimentally have been shown to reduce aggression. Potential behavioral effects of dTFA merit investigation. We sought to determine whether dTFA are associated with aggression/irritability. Methodolgy/Prinicpal Findings We capitalized on baseline dietary and behavioral assessments in an existing clinical trial to analyze the relationship of dTFA to aggression. Of 1,018 broadly sampled baseline subjects, the 945 adult men and women who brought a completed dietary survey to their baseline visit are the target of this analysis. Subjects (seen 1999–2004) were not on lipid medications, and were without LDL-cholesterol extremes, diabetes, HIV, cancer or heart disease. Outcomes assessed adverse behaviors with impact on others: Overt Aggression Scale Modified-aggression subscale (primary behavioral endpoint); Life History of Aggression; Conflict Tactics Scale; and self-rated impatience and irritability. The association of dTFA to aggression was analyzed via regression and ordinal logit, unadjusted and adjusted for potential confounders (sex, age, education, alcohol, and smoking). Additional analyses stratified on sex, age, and ethnicity, and examined the prospective association. Greater dTFA were strongly significantly associated with greater aggression, with dTFA more consistently predictive than other assessed aggression predictors. The relationship was upheld with adjustment for confounders, was preserved across sex, age, and ethnicity strata, and held cross-sectionally and prospectively. Conclusions/Significance This study provides the first evidence linking dTFA with behavioral irritability and aggression. While confounding is always a concern in observational studies, factors including strength and consistency of association, biological gradient, temporality, and biological plausibility add weight to the prospect of a causal connection. Our results may have relevance to public policy determinations regarding dietary trans fats. Clinicaltrials.gov # NCT00330980
Trans Fat Consumption and Aggression
Beatrice A. Golomb
1,2
*, Marcella A. Evans
, Halbert L. White
3
, Joel E. Dimsdale
4
1 Department of Medicine, University of California San Diego, San Diego, California, United States of America, 2 Department of Family and Preventive Medicine, University
of California San Diego, San Diego, California, United States of America, 3 Department of Economics, University of California San Diego, California, United States of
America, 4 Department of Psychiatry, University of California San Diego, California, United States of America
Abstract
Background:
Dietary trans fatty acids (dTFA) are primarily synthetic compounds that have been introduced only recently;
little is known about their behavioral effects. dTFA inhibit production of omega-3 fatty acids, which experimentally have
been shown to reduce aggression. Potential behavioral effects of dTFA merit investigation.
We sought to determine
whether dTFA are associated with aggression/irritability.
Methodolgy/Prinicpal Findings:
We capitalized on bas eline dietary and behavioral assessments in an existi ng clinical trial
to analyze the relationship of dTF A to aggression. Of 1,018 broadly sampled baseline subjects, the 945 adult men and
women who brought a completed dietary survey to their baseline visit are the target of this analysis. Subjects (seen 1999–
2004) were not on lipid medications, and were without LDL-cholest erol ex tremes, diabetes, HIV, cancer or heart disease.
Outcomes assessed adverse behaviors with impact on others: Overt Aggression Scale Modified-aggression subscale
(primary behavioral endpoint); Life History of Aggression; Conflic t Tactics Scale; and self -rated impatience and irritability.
The association of dTFA to agg ression was analyzed via regression and or dinal logit, unadjusted and adjusted for potential
confounders (sex, age, education, alcoh ol, and smoking). Additional analyses stra tified on sex, age, and ethnicity, and
examin ed the prospec tive association. Greater dTFA were strongly significantly associate d with greater aggression, with
dTFA more consistently pred ictive than other assessed aggression predictors. The relationship was upheld with
adjustment for confounders, was preserved a cross sex, age, and ethnicity strata, and held cross-sectionally and
prospectively.
Conclusions/Significance:
This study provides the first evidence linking dTFA with behavioral irritability and aggression.
While confounding is always a concern in observational studies, factors including strength and consistency of association,
biological gradient, temporality, and biological plausibility add weight to the prospect of a causal connection. Our results
may have relevance to public policy determinations regarding dietary trans fats.
Clinicaltrials.gov # NCT00330980
Citation: Golomb BA, Evans MA, White HL, Dimsdale JE (2012) Trans Fat Consumption and Aggression. PLoS ONE 7(3): e32175. doi:10.1371/journal.pone.0032175
Editor: Thomas Langmann, University of Regensburg, Germany
Received August 19, 2011; Accepted January 22, 2012; Published March 5, 2012
Copyright: ß 2012 Golomb et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This research was supported by a grant from the National Institutes of Health (NHLBI RO1 HL63055-05). The funder had no role in the study design,
data collection and analysis, decision to publish or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: bgolomb@ucsd.edu
¤ Current address: Department of Anatomy and Neurobiology, University of California Irvine, Irvine, California, United States of America
Introduction
Dietary trans fatty acids (dTFA) are primarily products of
hydrogenation, a chemical process that makes (unsaturated) oils
solid at room temperature [1]. They are present at high levels in
margarines, shortenings, and prepared foods [2–4]. Adverse health
effects of dTFA have been identified on lipids, metabolic function,
insulin resistance, oxidation, inflammation, and cardiac and
general health [5–20]. Advantageous associations of another class
of fatty acids, long chain omega-3 fatty acids (n3FA), to behavioral
outcomes have been previously reported [21–23].
Due to the range of their deleterious biological effects, including
inhibition by dTFA of n3FA production (by inhibition of delta-6
desaturase activity) [24,25], we theorized that dTFA may be
associated with greater aggression and irritability.
Methods
Subjects
Of 1018 male and female adults, minimum age 20 years,
screened for participation in a clinical trial of lipid-lowering
therapy in a primary prevention setting (the UCSD Statin Study)
[26], 945 had completed a dietary assessment prior to a baseline
visit and were the target of the present assessment. Subjects were
broadly sampled, however persons on lipid medications, or with
very low or high LDL (,115 mg/dL or .190 mg/dL), known
diabetes, cardiovascular disease, HIV, or cancer were excluded
[26].
The study protocol was approved by the University of
California, San Diego Human Research Protections Program.
All subjects gave written informed consent.
PLoS ONE | www.plosone.org 1 March 2012 | Volume 7 | Issue 3 | e32175
Dietary Trans Fatty Acid Estimation
Nutrient data were collected using a food frequency question-
naire developed by the Nutrition Assessment Shared Resource of
the Fred Hutchinson Cancer Research Center [27]. Consumption
frequency and portion size are queried, for a series of food
categories, each in turn defined by a series of foods or beverages.
Additional questions relating to food preparation and purchasing
further refine nutrient calculations (http://www.fhcrc.org/
science/shared_resources/nutrition/ffq/).
Nutrient calculations were performed using the Nutrient Data
System for Research software version 4.03, developed by the
Nutrition Coordinating Center, University of Minnesota Food and
Nutrient Database (version 31, released November 2000), which
added trans fatty acid values in 1998. ‘‘Trans-fatty acid values were
determined for all foods in the database (0% missing) and include
individual contributions of 16:1 trans (trans-hexadecenoic acid);
18:1 trans (trans-octadecenoic acid); and 18:2 trans (trans-octadeca-
dienoic acid), which encompasses cis-trans, trans-cis, and trans-trans
forms; as well as total trans-fatty acids. The USDA table ‘‘Fat and
Fatty Acid Content of Selected Foods Containing Trans-Fatty
Acids’’… was the primary source of trans-fatty acid information for
assignment of values to foods in the database. Additional data
sources included other nutrient databases and articles in the
scientific literature containing trans-fatty acid values for US foods,
using appropriate methodologies’’ [28].
The study period (1999–2004) was advantageous because dTFA
values were available in the nutrient database, while trans fat
composition in foods was relatively stable (USFDA trans fat
labeling requirements were implemented later, Jan 1 2006 [29]).
Behavioral Endpoints
The following validated instruments were used:
N
Overt Aggression Scale Modified Aggression sub-
scale (OASMa) [30–34]. the primary designated aggression
measure, it inquires about actual aggressive behavioral actions
in the prior week.
N
Life History of Aggression (LHA) [35]. examines
behavioral aggression over the subject’s lifetime, generally
excluding childhood violence.
N
Conflict Tactics Scale (CTS) [36–38]. examines tactics,
including aggressive ones, employed by (or against) the subject
(behavioral hostility or hostile attribution) in the prior 2 weeks.
We employed the portion eliciting behaviors by the subject.
N
Impatience. measures self-report of subjective impatience,
asking subjects to rate their impatience on a scale of 0 (not
present) to 10 (maximally present).
N
Irritability. measures self-report of subjective irritability,
asking subjects to rate their irritability on a scale of 0 (not
present) to 10 (maximally present).
The latter two instruments have been validated in this study
(construct, convergent, predictive validity; information available
on request).
Covariates
Potential confounders of relevance to aggression assessments
(and related behaviors) included age and sex [39], education,
alcohol [39,40], and smoking [40]. Exercise was examined by two
measures: self-rated activity relative to others your age (5 point
Likert scale from much less active through about the same to much
more active in models that also adjust for age); and the number
of times in a week exercised vigorously for at least 20 minutes.
Analyses
The association of dTFA to aggression was assessed cross-
sectionally at baseline, prior to any study-related treatment. An
additional prospective analysis capitalized on subsequent assess-
ments of aggression in the placebo group. Regression analyses
were performed for each behavior/aggression outcome, unadjust-
ed and adjusted. The ‘‘full’’ model for each (using heteroskedas-
ticity-independent robust standard errors, aka ‘‘White’’ standard
errors [41]) adjusted for reported aggression predictors (age, sex,
education, alcohol, smoking) and dTFA, allowing for contrast of
consistency of impact of different aggression predictors, including
dTFA. Both least squares regression and ordinal logit were
performed for each outcome, assessing the robustness to regression
approach (including for outcomes where either regression
approach could be justified and, purely for illustration
of robustness, those for which one specification was concep-
tually preferred). Exercise variables were evaluated as potential
confounders.
Additional analyses examined impact of stratification by sex,
ethnicity and age on the relationship between dTFA and OASMa
(the primary aggression endpoint).
Prospective prediction was also assessed, restricted to the
placebo group for simplicity of interpretation (averting concerns
that the intervention could modify the results though results of
analysis including the total sample are also provided). dTFA at
baseline were examined relative to OASMa at follow-up (6 months
after baseline), adjusting for baseline OASMa.
A prior study looked at trans and saturated fats on depression;
we added this combined analysis (and also examined depression).
Trans fat consumption relates strongly to linoleic acid consump-
tion; we evaluated the effect of each after removing the
contribution by the other; and also examined a model adjusting
simultaneously for the joint trans-saturated variable and the
linoleic variable.
Results
Baseline characteristics are shown in Table 1.
Strongly significant interrelations among the behavioral end-
points (p,0.001) but modest correlation coefficients affirm that the
aggression measures we employed tapped related but distinct
constructs (Table S1 and S2).
Regression analysis showed a strong association between dTFA
and each aggression-related outcome. This association was
retained after adjustment for other predictors, and was more
Table 1. Baseline Subject Characteristics (N = 945)*.
Sample Mean (SD) or %
Age (years) 57.2 (12.0)
Male 68.3%
Caucasian 80.1%
Education (scaled 1–9){ 5.82 (1.50)
Current Smoker 7.94%
Alcohol (g/day) 9.64 (14.9)
Trans fat Consumption (g/day) 3.49 (2.47)
*Subjects with trans fat measurement, out of 1,016 subjects appearing for
baseline participation in a clinical trial.
{Education was scored on a 9-point scale, with 1 = grade school or less,
9 = doctoral degree.
doi:10.1371/journal.pone.0032175.t001
Trans Fats & Aggression
PLoS ONE | www.plosone.org 2 March 2012 | Volume 7 | Issue 3 | e32175
consistently predictive other assessed aggression predictors
(Table 2 and Table 3). Coefficients were similar for men and
women (except for irritability) though significance was greater for
men, who were twice as numerous in the sample. Significance was
upheld across age and ethnicity strata. Regression coefficients for
dTFA as a predictor of OASMa by age were: b = 0.53 p = 0.003
(age 20–40); b = 0.27 p = 0.003 (age 40–60); b = 0.27 p = 0.008
(age.60); by ethnicity: b = 0.30 p,0.001 (Caucasian); b = 0.31
p = 0.037 (non-Caucasian).
dTFA significantly predicted future aggression, in adjusted
prospective analysis confined to the placebo group. This was true
even after also adjusting for aggression at time of dTFA assessment
(factoring out the association of baseline aggression with dTFA):
b = 0.15 p = 0.041. This contrasted with other predictors, for
which the impact on aggression at baseline largely accounted for
the impact at follow-up. (The central follow-up analysis presented
here was in the untreated placebo group. However dTFA also
prospectively preedicted aggression in the statin group: b = 0.25,
p = 0.032; and in the total sample, adjusted for active treatment, as
well as baseline and on-treatment cholesterol: b = 0.21 p = 0.009.)
Regarding other potential lifestyle confounders, exercise variables
(62) had no relationship to aggression variables (65) with one
exception: vigorous activity for 20 minutes predicted CTS (one of
10 tested pairings), but the trans fat relationship retained its potent
prediction of aggression with additional adjustment for this
(p = 0.001). Linoleic acid (pfa18:2) was collinear with trans fats,
but the residual transfat contribution, after separating out the
shared contribution with pfa18:2 remained strong, 0.23, and
significant, p = 0.002. Others have considered trans and saturated
fat variables together for mood associations. A fused trans-
saturated fat variable bore a smaller coefficient consistent with the
lower saturated fat coefficient; significance remained strong
(p = 0.001). The pfa18:2 coefficient lost significance (and the
coefficient was negative), when both the trans-saturated variable
and the pfa18:2 variable were included in the model.
Discussion
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 [42]
has been previously reported [43]. Of note, dTFA variably obstruct
production of docosahexaenoic acid, a long chain n3FA that has
protected against aggression-related outcomes in some observation-
al and experimental studies [21–23]. In one animal study the effect
of dTFA on n3FA themselves did not extend to the brain [44].
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 [45–
47]. Indeed, dTFA mechanisms that could have implications for
aggression include cell energy alterations [18], oxidative stress [15]
and inflammatory effects [10,11]. 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
[48]. 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, observa-
Table 2. Dietary Trans Fat is Significantly Linked to Aggression Measures.
Aggression Measure
Dietary Trans Fats
Relation to That Measure*
Variable Mean Value ± SD
Dietary Trans Fats (grams/day)
P-value
b SE
OASMa 2.50±4.72 0.296 0.092 0.001
Conflict Tactics Scale 1.08±1.70 0.101 0.031 0.001
Life History of Aggression 10.1±6.93 0.277 0.106 0.009
Impatience 1.87±2.12 0.0953 0.0372 0.011
Irritability 1.30±1.83 0.084 0.031 0.007
OASMa: Overt Agg ression Scale Modified aggression subscale.
*In regression with robust standard errors, adjusted for age, sex, education, alcohol and smoking.
doi:10.1371/journal.pone.0032175.t002
Table 3. Significance of Dietary Trans Fats Along with Other
Potential Aggression Predictors in Multivariable Adjustment{.
Predictor
Aggression Measures
OASMa LHA CTS Impatience Irritability
Age **/** **/** */2 */* **/**
Male 2/2 **/** 2/22/22/2
Education */** +/* 2/22/22/*
Smoking 2/22/22/2 */++/2
Alcohol 2/2 **/** 2/2 **/* */*
Trans Fats
*/** **/* **/** */* **/**
OASMa: Overt Aggression Scale Modified aggression subscale.
LHA: Life History of Aggression. CTS: Conflict Tactics Scale.
2 No significant or borderline association.
+ 0.05,p, 0.1 (borderline significant).
*0.01,p,0.05 (significant).
**p,0.01 (highly significant).
{Significance levels shown are results (respectively) of linear regression/ordinal
logit analyses (both with robust standard errors [41]). Analyses for each
aggression outcome are adjusted for each predictor variable.
doi:10.1371/journal.pone.0032175.t003
Trans Fats & Aggression
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tional 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 [49], or plasma
phospholipid trans fats [50], and future studies should seek to
employ these measures to establish whether the relationship is
upheld. Use of these as biomarkers of dTFA [51], 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 [20,52–54] (analogous to the
observation that n3FA may serve as a common protection against
both [43]).
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.
Supporting Information
Table S1 OASMa: Overt Aggression Scale Modified aggres-
sion subscale. LHA: Life History of Aggression. CTS: Conflict
Tactics Scale. * P,0.0001 for all correlations.
(DOC)
Table S2 OASMa: Overt Aggression Scale Modified - aggres-
sion subscale. LHA: Life History of Aggression. CTS: Conflict
Tactics Scale. Power was greater for men, who represented 68% of
the sample (about twice as many men as women). * Significant
change in aggression shown in bold (P,0.05).
(DOC)
Acknowledgments
We thank Julie Denenberg MS for data management; Michael Criqui MD
MPH, Janis Ritchie BSN, Diana King BA, and all study personnel for their
efforts; Julie Broadwin PhD MPH for early editorial assistance; Sabrina
Koperski, BS for editorial and administrative assistance.
Author Contributions
Conceived and designed the experiments: BG JD. Performed the
experiments: BG. Analyzed the data: BG ME HW. Wrote the paper:
BG. Critical revision of the manuscript for important intellectual content:
BG ME HW JD. Final approval of the manuscript version to be published:
BG ME HW JD.
References
1. Stender S, Dyerberg J, Holmer G, Ovesen L, Sandstrom B (1995) The influence
of trans fatty acids on health: a report from the Danish Nutrition Council [see
comments]. Clin Sci (Colch) 88: 375–392.
2. Innis SM, King DJ (1999) trans Fatty acids in human milk are inversely
associated with concentrations of essential all-cis n-6 and n-3 fatty acids and
determine trans, but not n-6 and n-3, fatty acids in plasma lipids of breast-fed
infants. Am J Clin Nutr 70: 383–390.
3. Larque E, Zamora S, Gil A (2001) Dietary trans fatty acids in early life: a review.
Early Hum Dev 65 Suppl: S31–41.
4. Elias SL, Innis SM (2002) Bakery foods are the major dietary source of trans-
fatty acids among pregnant women with diets providing 30 percent energy from
fat. J Am Diet Assoc 102: 46–51.
5. Mensink RP, Katan MB (1989) Effect of a diet enriched with monounsaturated or
polyunsaturated fatty acids on levels of low-density and high-density lipoprotein
cholesterol levels in healthy women and men. N Engl J Med 321: 436–441.
6. Mensink RP, Katan MB (1990) Effect of dietary trans fatty acids on high-density
and low-density lipoprotein cholesterol levels in healthy subjects [see comments].
N Engl J Med 323: 439–445.
7. Mensink RP, Katan MB (1993) Trans monounsaturated fatty acids in nutrition
and their impact on serum lipoprotein levels in man. Prog Lipid Res 32:
111–122.
8. Mensink RP, Temme EH, Hornstra G (1994) Dietary saturated and trans fatty
acids and lipoprotein metabolism. Ann Med 26: 461–464.
9. Hill EG, Johnson SB, Holman RT (1979) Intensification of essential fatty acid
deficiency in the rat by dietary trans fatty acids. J Nutr 109: 1759–1765.
10. Mozaffarian D, Pischon T, Hankinson SE, Rifai N, Joshipura K, et al. (2004)
Dietary intake of trans fatty acids and systemic inflammation in women.
Am J Clin Nutr 79: 606–612.
11. Mozaffarian D, Rimm EB, King IB, Lawler RL, McDonald GB, et al. (2004) trans
fatty acids and systemic inflammation in heart failure. Am J Clin Nutr 80: 1521–1525.
12. Sundram K, Ismail A, Hayes KC, Jeyamalar R, Pathmanathan R (1997) Trans
(elaidic) fatty acids adversely affect the lipoprotein profile relative to specific
saturated fatty acids in humans. J Nutr 127: 514S–520S.
13. Sundram K, Karupaiah T, Hayes K (2007) Stearic acid-rich interesterified fat
and trans-rich fat raise the LDL/HDL ratio and plasma glucose relative to palm
olein in humans. Nutr Metab (Lond) 4: 3.
14. Dyerberg J, Christensen JH, Eskesen D, Astrup A, Stender S (2006) Trans, and
n-3 polyunsaturated fatty acids and vascular function-a yin yang situation?
Atheroscler Suppl 7: 33–35.
15. Cassagno N, Palos-Pinto A, Costet P, Breilh D, Darmon M, et al. (2005) Low
amounts of trans 18:1 fatty acids elevate plasma triacylglycerols but not cholesterol
and alter the cellular defence to oxidative stress in mice. Br J Nutr 94: 346–352.
16. Mensink RP (2005) Metabolic and health effects of isomeric fatty acids. Curr
Opin Lipidol 16: 27–30.
17. Ibrahim A, Natrajan S, Ghafoorunissa R (2005) Dietary trans-fatty acids alter
adipocyte plasma membrane fatty acid composition and insulin sensitivity in
rats. Metabolism 54: 240–246.
18. Natarajan S, Ibrahim A (2005) Dietary trans fatty acids alter diaphragm
phospholipid fatty acid composition, triacylglycerol content and glucose
transport in rats. Br J Nutr 93: 829–833.
Trans Fats & Aggression
PLoS ONE | www.plosone.org 4 March 2012 | Volume 7 | Issue 3 | e32175
19. Corcoran MP, Lamon-Fava S, Fielding RA (2007) Skeletal muscle lipid
deposition and insulin resistance: effect of dietary fatty acids and exercise.
Am J Clin Nutr 85: 662–677.
20. Albuquerque KT, Sardinha FL, Telles MM, Watanabe RL, Nascimento CM,
et al. (2006) Intake of trans fatty acid-rich hydrogenated fat during pregnancy
and lactation inhibits the hypophagic effect of central insulin in the adult
offspring. Nutrition 22: 820–829.
21. Iribarren C, Markovitz JH, Jacobs DR, Jr., Schreiner PJ, Daviglus M , et al.
(2004) Dietary intake of n-3, n-6 fatty acids and fish: relationship with hostility in
young adults–the CARDIA study. Eur J Clin Nutr 58: 24–31.
22. Conklin SM, Harris JI, Manuck SB, Yao JK, Hibbeln JR, et al. (2007) Serum
omega-3 fatty acids are associated with variation in mood, personality and
behavior in hypercholesterolemic community volunteers. Psychiatry Res 152:
1–10.
23. Fontani G, C orradeschi F, Felici A, Alfatti F, Migliorini S, et al. (2005) Cognitive
and physiological effects of Omega-3 polyunsaturated fatty acid supplementation
in healthy subjects. Eur J Clin Invest 35: 691–699.
24. De Schrijver R, Privett OS (1982) Interrelati onship between dietary trans Fatty
acids and the 6- and 9-desaturases in the rat. Lipids 17: 27–34.
25. Kurata N, Privett OS (1980) Effects of dietary trans acids on the biosynt hesis of
arachidonic acid in rat liver microsomes. Lipids 15: 1029–1036.
26. Golomb BA, Criqui MH, White HL, Dimsdale JE (2004) The UCSD Statin
Study: a randomized controlled trial assessing the impact of statins on selected
noncardiac outcomes. Control Clin Trials 25: 178–202.
27. Schakel SF (1997) Procedures for estimating nutrient values f or food
composition databases. J Food Comp and Anal 10: 102–114.
28. Harnack L, Lee S, Schakel SF, Duval S, Luepker RV, et al. (2003) Trends in the
trans-fatty acid composition of the diet in a metropolitan area: the Minnesota
Heart Survey. J Am Diet Assoc 103: 1160–1166.
29. US Food and Drug Administration (2003) FDA acts to provide better
information to consumers on trans fats. Available: http://wwwfdagov/oc/
initiatives/transfat. Accessed: 2007 March 30.
30. Chukwujekwu DC, Stanley PC (2008) The Modified Overt Aggression Scale:
how valid in this environment? Niger J Med 17: 153–155.
31. Margari F, Matarazzo R, Casacchia M, Roncone R, Dieci M, et al. (2005)
Italian validation of MOAS and NOSIE: a useful package for psychiatric
assessment and monitoring of aggressive behaviours. Int J Methods Psychiatr
Res 14: 109–118.
32. Endicott J, Tracy K, Burt D, Olson E, Coccaro EF (2002) A novel approach to
assess inter-rater reliability in the use of the Overt Aggression Scale-Modified.
Psychiatry Res 112: 153–159.
33. Silver JM, Yudofsky SC (1991) The Overt Aggression Scale: overview and
guiding principles. J Neuropsychiatry Clin Neurosci 3: S22–29.
34. Sorgi P, Ratey J, Knoedler DW, Markert RJ, Reichman M (1991) Rating
aggression in the clinical setting. A retrospective adaptation of the Overt
Aggression Scale: preliminary results. J Neuropsychiatry Clin Neurosci 3:
S52–56.
35. Coccaro EF, Berman ME, Kavoussi RJ (1997) Assessment of life history of
aggression: development and psychometric characteristics. Psychiatry Research
73: 147–157.
36. Straus MA (1979) Measuring intrafamily conflict and violence: The Conflict
Tactics Scales. J Marriage Fam 41: 75–88.
37. Morse BJ (1995) Beyond the Conflict Tactics Scale: assessing gender differences
in partner violence. Violence Vict 10: 251–272.
38. Schafer J, Caetano R, Clark CL (1998) Rates of intimate partner violence in the
United States. Am J Public Health 88: 1702–1704.
39. Golomb BA, Stattin H, Mednick S (2000) Low cholesterol and violent crime.
J Psychiatr Res 34: 301–309.
40. Vartiainen E, Puska P, Pekkanen J, Tuomilehto J, Lonnqvist J, et al. (1994)
Serum cholesterol concentration and mortality from accidents, suicide, and
other violent causes. BMJ 309: 445–447.
41. White H (1980) A heteroskedasticity-consistent covariance matrix estimator and
a direct test for heteroskedasticity. Econometrica 48: 817–838.
42. Liu J, Raine A, Venables PH, Mednick SA (2004) Malnutrition at age 3 years
and externalizing behavior problems at ages 8, 11, and 17 years. Am J Psychiatry
161: 2005–2013.
43. Hibbeln JR, Ferguson TA, Blasbalg TL (2006) Omega-3 fatty acid deficiencies
in neurodevelopment, aggression and autonomic dysregulation: opportunities
for intervention. Int Rev Psychiatry 18: 107–118.
44. Larque E, Perez-Llamas F, Puerta V, Giron MD, Suarez MD, et al. (2000)
Dietary trans fatty acids affect docosahexaenoic acid concentrations in plasma
and liver but not brain of pregnant and fetal rats. Pediatr Res 47: 278–283.
45. Ribeiro L (1990) [Prostaglandins and omega-3 acids in the prevention of
atherosclerosis]. Arq Bras Cardiol 54: 279–281.
46. Knapp HR (1989) Omega-3 fatty acids, endogenous prostaglandins, and blood
pressure regulation in humans. Nutr Rev 47: 301–313.
47. Engblom D, Ek M, Saha S, Ericsson-Dahlstrand A, Jakobsson PJ, et al. (2002)
Prostaglandins as inflamm atory messengers across the blood-brain barrier. J Mol
Med 80: 5–15.
48. Sanchez-Villegas A, Verberne L, De Irala J, Ruiz-Canela M, Toledo E, et al.
(2011) Dietary fat intake and the risk of depressio n: the SUN Project. PLoS One
6: e16268.
49. Lemaitre RN, King IB, Mozaffarian D, Sotoodehnia N, Siscovick DS (2006)
Trans-fatty acids and sudden cardiac death. Atheroscler Suppl 7: 13–15.
50. Lemaitre RN, King IB, Mozaffarian D, Sotoodehnia N, Rea TD, et al. (2006)
Plasma phospholipid trans fatty acids, fatal ischemic heart disease, and sudden
cardiac death in older adults: the cardiovascular health study. Circulation 114:
209–215.
51. Lemaitre RN, King IB, Raghunathan TE, Pearce RM, Weinmann S, et al.
(2002) Cell membrane trans-fatty acids and the risk of primary cardiac arrest.
Circulation 105: 697–701.
52. Kawachi I, Sparrow D, Spiro A, 3rd, Vokonas P, Weiss ST (1996) A prospective
study of anger and coronary heart disease. The Normative Aging Study.
Circulation 94: 2090–2095.
53. Ascherio A, Willett W (1995) Metabolic and atherogenic effects of trans fatty
acids. Journal of Internal Medicine 238: 93–96.
54. Kris-Etherton PM, Harris WS, Appel LJ (2002) Fish consumpti on, fish oil,
omega-3 fatty acids, and cardiovascular disease. Circulation 106: 2747–2757.
Trans Fats & Aggression
PLoS ONE | www.plosone.org 5 March 2012 | Volume 7 | Issue 3 | e32175
    • "Our results extend these observations, suggesting that one of the culprits in Western diets may be trans fatty acid intakes in regard to both positive and negative affective state. In addition to evidence linking trans fatty acids to depression [18], some data suggest an association between trans fatty acids and behavioral irritability and aggression [46]. The potential role of trans fatty acids appears to be independent of the source of the fat. "
    [Show abstract] [Hide abstract] ABSTRACT: Trans fatty acids in Western diets increase health risks, and have been associated with the risk of depression. We hypothesized that intakes of trans fatty acids (primarily from margarines and baked goods) were inversely associated with positive affect and positively associated with negative affect in a longitudinal study. Church attendees residing in North America completed a food frequency questionnaire in 2002-6 as part of the Adventist Health Study-2. A subset in which we excluded participants with established cardiovascular disease (n=8,771) completed the Positive and Negative Affect Schedule (PANAS) in 2006-7. The associations between dietary intakes of fatty acids to positive and negative affect were tested with linear regression analysis controlling for age, gender, ethnicity, education, body mass index, exercise, sleep, sleep squared, Mediterranean diet, total energy intake and alcohol. Intakes of trans fatty acids were inversely associated with positive affect (β=-0.06, B=-0.27 [95% CI -0.37, -0.17], p<.001) and positively associated with negative affect (β=0.05, B=0.21 [95% CI 0.11, 0.31], p<.001). In comparison, we found no association between n-3 polyunsatured fatty acids (PUFA) intakes with affect. The n-6:n-3 PUFA ratio was inversely associated with positive affect (β=-0.03, B=-0.34 [95% CI -0.58, -0.10], p=0.006). The findings suggest that a lower dietary trans fatty acid intake has beneficial effects on emotional affect while the n-6: n-3 ratio is detrimental to positive affect.
    Article · Jan 2016
    • "These findings, in which greater dTFA consumption is linked to worse word memory in adults during years of high productivity, adults age <45, add to evidence for unfavorable health correlates of trans fat consumption. They extend findings to a third pillar of central nervous system function, cognition—complementing evidence for adverse dTFA relations to behavior (aggres- sion/irritability)[28] and mood[29]. Findings comport with recent FDA moves to rescind the designation as " generally recognized as safe " for dTFAs[65]; and add support to similar efforts in other nations. "
    [Show abstract] [Hide abstract] ABSTRACT: We sought to assess the relation of dietary trans fatty acid (dTFA) consumption to word-memory. We analyzed cross-sectional data from the 1999-2005 UCSD Statin Study. Participants were 1018 adult men and non-procreative women age ≥20 without diagnosed diabetes, CVD, or extreme LDL-cholesterol. Primary analyses focused on men, as only men (N = 694) were effectively represented in younger adult ages. "Recurrent words" assessed word memory. dTFA (grams/day) estimates were calculated from the Fred Hutchinson Food Frequency Questionnaire. Regression, stratified at age 45, assessed the relation between memory and dTFA in various adjustment models. Major findings were replicated in the full sample (including women). Potential mediators were examined. An age-by-dTFA interaction was significant. dTFA adversely predicted memory in younger adults (only), robust to adjustment model. Each gram/day dTFA was associated with an estimated 0.76 fewer words recalled (full model) (SE = 0.27, 95%CI = 0.22,1.3, P = 0.006). Adjustment for systolic blood pressure, waist circumference and BMI (but not lipid or glycemic variables) attenuated the relationship, consistent with mediation by factors involving, relating to, or concurrently influencing, these factors. Greater dTFA was significantly associated with worse word recall in younger adults. Prooxidant and energetic detriments of dTFA and triangulation with other evidence offer prospects for causality.
    Full-text · Article · Jun 2015
    • "Intake of fat has also been linked with proclivity for aggression, both positively and negatively. Consumption of a diet containing high quantities of n-6 polyunsaturated fats increased aggression in mice and rats [5], and dietary trans-fatty acids (originating from the hydrogenation of an unsaturated fat during food processing) associated, for example, with a decrease in n-3 fatty acids and inflammation have been linked with irritability and aggression in humans [6]. Further, increased aggression has been associated with low concentrations of n-3 polyunsaturated fat and low plasma cholesterol in dogs [7] and a high intake of n-3 polyunsaturated fat has been associated with less hostility in humans [8]. "
    [Show abstract] [Hide abstract] ABSTRACT: High fat, low carbohydrate diets have become popular, as short-term studies show that such diets are effective for reducing body weight, and lowering the risk of diabetes and cardiovascular disease. There is growing evidence from both humans and other animals that diet affects behaviour and intake of fat has been linked, positively and negatively, with traits such as exploration, social interaction, anxiety and fear. Animal models with high translational value can help provide relevant and important information in elucidating potential effects of high fat, low carbohydrate diets on human behaviour. Twenty four young, male Göttingen minipigs were fed either a high fat/cholesterol, low carbohydrate diet or a low fat, high carbohydrate/sucrose diet in contrast to a standard low fat, high carbohydrate minipig diet. Spontaneous behaviour was observed through video recordings of home pens and test-related behaviours were recorded during tests involving animal-human contact and reaction towards a novel object. We showed that the minipigs fed a high fat/cholesterol, low carbohydrate diet were less aggressive, showed more non-agonistic social contact and had fewer and less severe skin lesions and were less fearful of a novel object than minipigs fed low fat, high carbohydrate diets. These results found in a porcine model could have important implications for general health and wellbeing of humans and show the potential for using dietary manipulations to reduce aggression in human society.
    Full-text · Article · Apr 2014
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