Genome-wide single nucleotide polymorphism (SNP) data are now quickly and inexpensively acquired, raising the prospect of creating personalized dietary recommendations based on an individual’s genetic variability at multiple SNPs. However, relatively little is known about most specific gene–diet interactions, and many molecular and clinical phenotypes of interest (e.g., body mass index [BMI]) involve multiple genes. In this review, we discuss direct to consumer genetic testing (DTC-GT) and the current potential for precision nutrition based on an individual’s genetic data. We review important issues such as dietary exposure and genetic architecture addressing the concepts of penetrance, pleiotropy, epistasis, polygenicity, and epigenetics. More specifically, we discuss how they complicate using genotypic data to predict phenotypes as well as response to dietary interventions. Then, several examples (including caffeine sensitivity, alcohol dependence, non-alcoholic fatty liver disease, obesity/appetite, cardiovascular, Alzheimer’s disease, folate metabolism, long-chain fatty acid biosynthesis, and vitamin D metabolism) are provided illustrating how genotypic information could be used to inform nutritional recommendations. We conclude by examining ethical considerations and practical applications for using genetic information to inform dietary choices and the future role genetics may play in adopting changes beyond population-wide healthy eating guidelines.

There are limited studies on neuroprotection from repeated subconcussive head impacts (RSHI) following docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) supplementation in contact sports athletes. We performed a randomized, placebo-controlled, double-blinded, parallel-group design trial to determine the impact of 26 weeks of DHA+EPA supplementation (n = 12) vs. placebo (high-oleic safflower oil) (n = 17) on serum concentrations of neurofilament light (NfL), a biomarker of axonal injury, and inflammatory cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a)) in National Collegiate Athletic Association Division I American football athletes. DHA+EPA supplementation increased (p < 0.01) plasma DHA and EPA concentrations throughout the treatment period. NfL concentrations increased from baseline to week 26 in both groups (treatment (<0.001); placebo (p < 0.05)), with starting players (vs. non-starters) showing significant higher circulating concentrations at week 26 (p < 0.01). Fish oil (DHA+EPA) supplementation did not mitigate the adverse effects of RSHI, as measured by NfL levels; however, participants with the highest plasma DHA+EPA concentrations tended to have lower NfL levels. DHA+EPA supplementation had no effects on inflammatory cytokine levels at any of the timepoints tested. These findings emphasize the need for effective strategies to protect American football participants from the effects of RSHI.

This study characterized body composition profiles of elite American heptathletes and cross-validated skinfold (SKF) and bioelectrical impedance analysis (BIA) field method equations for estimation of percent body fat (%Fat) using dual energy x-ray absorptiometry (DXA) as the criterion. Weight, height, fat mass (FM), fat-free mass (FFM), bone mineral density (BMD), and %Fat were measured in 19 heptathletes using standard measurement protocols for DXA, SKFs and BIA. The ages, heights, and weights were respectively 25.5 +/- 3.5 years, 175.0 +/- 6.6 cm, 67.3 +/- 7.1 kg. DXA estimates of mean +/- SD values for body composition variables were 57.2 +/- 6.1 kg FFM, 10.1 +/- 2.6 kg FM, 114 +/- 7% BMD for age/racial reference group, and 15 +/- 3.0 %Fat. Ranges of bias values for %Fat (DXA minus SKF or BIA) were, respectively, -0.5 to 1.6% and -5.5 to -1.2%. Ranges for standard errors of estimate and total errors were, respectively, SKF 2.4-2.5%, 2.4 - 2.8% and BIA 3.0%, 5.0-6.5%. Regression analyses of the field methods on DXA were significant (p < .05) for all SKF equations but not BIA equations. This study demonstrates that elite American heptathletes are lean, have high levels of BMD, and that SKF equations provide more accurate estimates of %Fat relative to DXA than estimates from BIA equations.

and Brinton RD ( ) E ects of docosahexaenoic acid and eicosapentaoic acid supplementation on white matter integrity after repetitive sub-concussive head impacts during American football: Exploratory neuroimaging findings from a pilot RCT.

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BackgroundRepetitive sub‐concussive head impacts (RSHIs) are common in American football, result in changes to white matter microstructural integrity, and are suggested as a potential risk factor for neurodegenerative diseases, including Alzheimer’s disease. RSHI‐induced white matter degradation may accelerate neurodegenerative processes, necessitating effective preventative and therapeutic approaches in this population. Prior studies indicate potential neuroprotective and remyelinating effects of docosahexaenoic acid (DHA). Here, we conducted a double‐blind, randomized, placebo‐controlled trial to assess the effects DHA supplementation during a National Collegiate Athletic Association football season on neuroimaging measures of white matter integrity.MethodThirty‐eight participants were randomized to treatment (6g DHA/EPA) or placebo (6g oleic/linoleic acid) group for seven months of five‐times‐per‐week supplementation. 27 participants completed the trial and had complete neuroimaging datasets (n = 16 placebo; n = 11 treatment). White matter integrity changes from preseason to immediately post‐season were quantified using voxel‐wise fractional anisotropy and diffusivity (mean, axial, radial) as well as deterministic tractography using quantitative anisotropy (QA). Gray matter volume as well as intra‐regional, edge‐wise, and network level functional connectivity were obtained as secondary measures along with serum neurofilament light (NfL) as a peripheral biomarker of axonal damage.ResultThere were no voxel‐wise, between‐group differences in voxel‐wise DTI analyses. Compared to placebo, the treatment group had increased QA in ascending corticostriatal fibers and decreased QA in long association and commissural fibers. Increased mean (ρ = 0.47), axial (ρ = 0.44), and radial (ρ = 0.51) diffusivity and decreased QA (ρ = ‐0.52) in the corpus callosum and bilateral corona radiata were correlated with increasing NfL levels during the season irrespective of treatment group. Default mode/frontoparietal network connectivity (g = 0.96, p = 0.024) was greater in the treatment group.ConclusionIn‐season DHA supplementation was insufficient to prevent or protect against axonal damage as it occurred during the season. However, there may be neuroprotective effects on functional connectivity despite structural damage. If RSHIs are a risk factor for future neurodegeneration, then alternative therapeutic merit further investigation. These present outcomes do not support the use of in‐season DHA supplementation as a preventive strategy to reduce brain injury resulting from collegiate football.AcknowledgementStudy funded by the Center for Innovation in Brain Science, University of Arizona. DHA provided by Pharmavite

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Participation in American football has been associated with repeated head impacts (RHI) and an increase in risk of concussive injury also called mild traumatic brain injury (mTBI). Elevated neurofilament light (NfL), a biomarker of axonal injury, has been shown to be a sensitive marker for both mTBI and sub‐concussive brain injury in contact sports. Omega‐3 polyunsaturated fatty acids, including docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), have been reported to reduce inflammation, protecting against nerve damage, stimulating neuronal growth, and promoting recovery following head injury. Here we performed a randomized, placebo‐controlled, double‐blinded, parallel group design trial to determine the potential impact of DHA/EPA supplementation on serum NfL in National Collegiate Athletic Association (NCAA) Division I American football athletes (n=38). Players (both starters and nonstarters) were assigned to either 3.0 g/d DHA/EPA or placebo groups, and blood was sampled at baseline and throughout the football season from no contact conditioning to the last in‐season scheduled game. DHA/EPA supplementation markedly increased plasma DHA levels from baseline at four time points (p<0.000001 at time point (T) 2; p<0.0001 at T3; p<0.001 at T4; and p<0.01 at T5). Additionally, serum NfL increased in all participants (starters and nonstarters) during conditioning and early season (p<0.001), and this upward trend continued in starters throughout the season (p<.05). There was no impact of DHA/EPA supplementation on serum NfL levels in either group tested. This study confirms results from previous studies which show an increased circulating NfL level in players who spent the greatest amount of time on the field in games (starters). However, it did not corroborate previous findings that DHA/EPA supplementation attenuates the increase in NfL levels in either group. Important limitations of this study include the small sample size and heterogeneous group of football players. This study supports the need for effective strategy to protect American football participants from brain injury.