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Published in final edited form as: Am J Ophthalmol. 2024 Sep 5;268:368–377. doi: 10.1016/j.ajo.2024.08.041

Omega-3 Polyunsaturated Fatty Acids as a Protective Factor for Myopia

Can Can Xue 1,*, Hengtong Li 2,3,*, Xing-Xuan Dong 4, Marco Yu 1, Zhi Da Soh 1,3, Crystal Chun Yuen Chong 1, Chen Jiang 5, Helene Choquet 5, Nazlee Zebardast 6,7, Seyedeh Maryam Zekavat 6,7,8, Pirro G Hysi 9,10,11, Seang Mei Saw 1,3,12, Qiao Fan 13, Yih-Chung Tham 1,2,3,14, Chen-Wei Pan 4,, Ching-Yu Cheng 1,2,3,14,
PMCID: PMC11606739  NIHMSID: NIHMS2030692  PMID: 39244001

Abstract

Purpose:

Animal models suggest omega-3 polyunsaturated fatty acids (PUFAs) may protect against myopia by modulating choroidal blood perfusion, but clinical evidence is scarce and mixed. We aimed to determine the causality between omega-3 PUFAs and myopia using Mendelian randomization (MR) analysis.

Design:

Two-sample MR analysis.

Methods:

Exposures are genetically predicted plasma level of 18 fatty acids (FAs) related traits. Spherical equivalent refraction (SER) and axial length were used as measurements of myopia. Genome-wide association study summary data on plasma levels of 18 FAs related traits (n=115,006), refractive spherical equivalent (n=351,091), axial length (n=69,945) and choroidal thickness (n=44,823) were sourced from the UK Biobank, the Genetic Epidemiology Research on Adult Health and Aging cohort, and the Consortium for Refractive Error and Myopia Study. We used five MR models and considered results statistically significant if the Bonferroni-corrected P-value was ≤2.78 ×10−3 in at least 3 MR models. The beta represents the change in outcomes (SER in diopter; axial length in mm; choroidal thickness in standard deviation) per standard deviation unit increase in FAs levels.

Results:

At a Bonferroni-corrected significance, higher levels of omega-3 (Beta, 0.32–0.34), omega-3/total FAs ratio (Beta, 0.31–0.44), docosahexaenoic acid (DHA) (Beta, 0.36–0.46), DHA/total FAs ratio (Beta, 0.37–0.53), PUFAs/total FAs ratio (Beta, 0.07–1.003), and degree of unsaturation (Beta, 0.28–0.44) were associated with a more positive SER, suggesting a lower risk of myopia. Similar trends were observed for axial length albeit with borderline significance (P≤0.035 in ≥2 models). Higher levels of omega-3, DHA, DHA/total FAs ratio, PUFAs/total FAs ratio, PUFAs/monounsaturated FAs ratio, and degree of unsaturation were nominally associated with thicker choroidal thickness (Beta, 0.05–0.13; P≤0.045 in ≥2 models).

Conclusion:

Our multiple MR models suggest a protective effect of omega-3 and DHA on myopia, potentially through modulation of choroidal blood perfusion. Further randomized clinical trials are needed to confirm the effectiveness and determine the optimal dose and duration.

Keywords: Myopia, Axial length, Omega-3, Docosahexaenoic acid, Mendelian randomization

Table of Contents

Effective interventions for preventing or delaying myopia onset and progression are limited. Omega-3 polyunsaturated fatty acids had protective effects against myopia in animal models, but human studies are scarce and yield mixed results. Our Mendelian randomization study demonstrated that higher plasma omega-3 levels are causally linked to a lower myopia risk. Further randomized controlled trials are needed to validate whether omega-3 supplementation or diet enrichment can provide a convenient, manageable, and non-invasive intervention for myopia.

Introduction

Myopia primarily develops during childhood and early adulthood and has emerged as a major public health concern.1,2 It affects over 20% of the world population and 80–90% of young adults in some parts of East and Southeast Asia.24 By 2050, half of the world’s population are projected to be affected by myopia, with 10% developing high myopia.3 Although the blurred vison caused by myopia can be corrected with optical aids, a higher degree of myopia elevates risks of sight-threatening complications such as myopic macular degeneration, cataract, glaucoma and retinal detachment.5 These complications have a significant impact on lifelong development, imposing a considerable socioeconomic and healthcare burden.6 Therefore, it is crucial to prevent or delay the onset of myopia or slow its progression during childhood.

Omega-3 polyunsaturated fatty acids (PUFAs), primarily including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have demonstrated systemic and ocular health benefits.7,8 Experimental models have suggested the protective effects of omega-3 PUFAs on myopia.911 For example, daily administration of omega-3 PUFAs was found to effectively suppress myopic refractive changes and axial elongation in lens-induced or form-deprivation myopic guinea pigs and mice, possibly by enhancing choroidal blood perfusion.9,10 Moreover, EPA and its metabolites demonstrated associations with myopia suppression and inhibition of choroidal thinning,11 These findings suggested the potential role of dietary modification in managing myopia.

However, in humans, myopia is a more complex condition influenced by both environmental and genetic factors. Clinical studies assessing the role of fatty acids in myopia are limited and have shown mixed results.1215 Higher dietary intake of EPA has been reported to decrease high myopia risk in juveniles from the National Health and Nutrition Examination Survey (NHANES) database,14 and higher saturated fat intake was associated with longer axial length in Singapore schoolchildren.15 However, some studies reported no such association, and these discrepancy may be due to recall bias in dietary assessments and unaddressed confounders in observational studies.12,13

On the other hand, interventional studies in human, such as randomized controlled trials (RCTs) in this field face several challenges. These include, but are not limit to, the protracted time required to assess treatment efficacy of PUFAs, determining optimal does and duration of administration, and ensuring participants’ adherence to the study protocol.1618 Clarifying the association between omega-3 and myopia is essential to determine if further clinical trials are needed to assess the effectiveness of increasing omega-3 PUFAs intake as a convenient, manageable, and non-invasive treatment for myopia.

Therefore, our primary aim in this study was to determine the causal relationship between omega-3 PUFAs and myopia using two-sample mendelian randomization (MR) analyses. MR mimics traditional RCTs by leveraging natural randomization of germline genotypes, overcoming the limitations of observational studies. Our secondary aim was to assess the causal association between omega-3 PUFAs and choroidal thickness to examine whether the protective effect of omega-3 PUFAs is modulated through choroidal blood perfusion. Findings from this study may provide new insights into the role of omega-3 PUFAs in myopia.

Methods

Study design and ethics

This is a two-sample MR analysis. The de-identified genome-wide association study (GWAS) summary data were obtained from the UK Biobank, the Genetic Epidemiology Research on Adult Health and Aging (GERA) cohort, and the Consortium for Refractive Error and Myopia (CREAM) Study, where each of them was approved by the relevant institutional review boards and/or medical ethics committees. We report this MR study following the Strengthening the Reporting of Observational Studies in Epidemiology using MR guideline.19,20

Genome-wide association study summary dataset for fatty acids

For the exposure, we utilized the largest available GWAS summary data on 18 circulating fatty acids (FAs) related traits from 115,006 European descent participants in the UK Biobank (Figure 1).21 We included FAs ratio in the analyses as omega-6 and omega-3 PUFAs compete using the same desaturase and elongase enzymes in metabolism.22 The omega-6 to omega-3 ratio is a critical determinant of health, with a higher ratio reported to promote the pathogenesis of various diseases like cardiovascular disease, cancer, and inflammatory and autoimmune disorders, while higher omega-3 levels may have suppressive effects.23 The circulating FAs-related traits were quantified using targeted high-throughput nuclear magnetic resonance metabolomics, and were standardized using an inverse rank-based normalization method. The GWAS analyses employed the BOLT-LMM approach, adjusting for age, sex, fasting time, and genotyping chip.21

Figure 1. Genome wide association study summary data used for fatty acids, spherical equivalent refraction and axial length.

Figure 1.

MUFA: monounsaturated fatty acids, PUFA: polyunsaturated fatty acids, SFA: saturated fatty acids, LA: Linoleic acid, DHA: docosahexaenoic acid, GERA: Genetic Epidemiology Research on Adult Health and Aging cohort; CREAM: Consortium for Refractive Error and Myopia Study

The solid arrows indicate the measurements of fatty acids, while the dotted arrows indicate the fatty acids ratio

Genome-wide association study summary dataset for myopia.

For myopia, we used two measurements, spherical equivalent refraction (SER) and axial length (Figure 1). For myopic SER, we used a large GWAS meta-analysis included summary statistics from 351,091 European descent individuals, which were sourced from two separate cohorts from UK Biobank, the GERA cohort, and the CREAM Study.24 We generated the necessary data for MR analysis, including beta effect and standard error, following methodologies detailed in our previous publication.25 For axial length, we utilized GWAS data from the CREAM study (n=10,851),26 and the GERA cohort (n=59,094).27 The unit was myopic diopter for SER and was millimetres for axial length.

Genome-wide association study summary dataset for choroidal thickness

The GWAS data on choroidal blood perfusion is unavailable. Given the choroid’s vascular nature, and the well-established decrease in choroidal thickness during myopia development, which is likely attributable to changes in choroidal blood flow,28,29 we used choroidal thickness from UK Biobank as a surrogate for choroidal blood perfusion in this study. Nonmydriatic spectral domain OCT scans of the macula were obtained using Spectral Domain Topcon 3D OCT 1000 Mark II (Topcon GB, Newberry, Berkshire, UK). Choroidal thickness was calculated as the difference between the Burch’s membrane and choroid-scleral interface. The values were measured in μm and were standardized using an inverse rank-based normalization method. GWAS was performed employing a linear regression model adjusting for age, age2, sex, smoking, spherical equivalent, the first 10 principal components of genetic ancestry, and genotyping array. Analyses were restricted to 44,823 consenting unrelated European ancestry participants.30

Mendelian randomization analysis

The robustness of MR findings relies on three key assumptions: (1) the instrumental variable (IV) is associated with the exposure, (2) the IV is not associated with confounders, (no correlated pleiotropy), and (3) the IV is not associated with the outcome conditional on the exposure and confounders, (no uncorrelated pleiotropy).

To identify independent SNPs for each exposure, we conducted a clumping analysis utilizing the OpenGWAS Database API within the ieugwasr R package. The process was executed with specific parameters: a 500kb window, a P-value threshold of 5×10−8, and a linkage disequilibrium r2 threshold of 0.01. The SNPs selected through the clumping analysis were subsequently employed as IVs in the MR analysis. To ensure the independence of these IVs, we imposed an additional criterion that each IV must be separated by a minimum distance of 1Mb from any other IVs. To address potential existence of any pleiotropy, we strategically selected a set of MR models: random-effect inverse-variance weighted (RE-IVW),31 MR-Egger,32 weighted median,33 weighted mode,34 and MR pleiotropy residual sum and outlier (MR-PRESSO).35 Each model is characterized by its own set of strengths and constraints. RE-IVW required balanced pleiotropy, that is, the overall zero-pleiotropic effect. MR-Egger model is claimed to be robust under the instrument strength independent of direct effect assumption, which may be broadly defined as an absence of confounder effect and a bidirectional relationship of the exposure and the outcome.36,37 The weighted median and the weighted mode models could provide robust estimates, in particular, in the situation of existence of correlated pleiotropy due to unmeasured confounders. The MR-PRESSO model was applied to estimate causal effect after excluding invalid IVs arising from uncorrelated pleiotropy. All five models are applicable in situations where the third assumption may be breached by the existence of uncorrelated pleiotropy. Through the careful selection of IVs and strategic application of MR models, we are able to elucidate the causal relationship between fatty acid exposures and myopia related outcomes.

Additionally, to address the sample overlap arising from the inclusion of UK Biobank datasets (FAs, SER, choroidal thickness), we employed the MRlap model as the sensitivity test, which could provide unbiased estimate in the presence of sample overlap by adjusting the IVW causal effect and modifying the weak instrument bias and winner’ curse (Supplemental Text).38 The corrected IVW effect by MRlap model is preferred than RE-IVW effect when the significance test shows a difference between these two estimates (P<0.05).

For each FAs related trait, we considered a causal relationship to be statistically significant if P-value meet the Bonferroni-corrected threshold (2.78×10−3 = 0.05/18) in at least three MR models. For all models, the beta represents the change in SER (in diopter), axial length (in mm) and choroidal thickness (in SD) per SD unit increase in FAs related traits.21

Results

The GWAS summary data and analyses framework for our study are provided in Figure 1. Detailed information about the IVs used in each MR analysis are provided in Supplemental Table 1. We selected between 18 to 52 FA-associated SNPs as instruments for the analyses of SER, 20 to 55 SNPs for analyses of axial length, and 22 to 60 SNPs for the analyses of choroidal thickness, collectively explaining between 1.23% and 9.49 % of the variation in exposures.

Causal relationship between fatty acids and myopia

Figure 2 and Supplemental Table 2 show the association between FAs and SER. A high level of omega-3 PUFAs (Beta, 0.32 to 0.34 per SD increase in omega-3 PUFAs for different MR models; P≤6.09×10−7 in three models), and a higher omega-3 PUFAs/total FAs ratio (Beta, 0.31 to 0.44; P≤4.23×10−4 in four models) were associated with a more positive SER, suggesting a lower risk of myopia. Likewise, a higher level of DHA (Beta, 0.36 to 0.46; P≤4.62×10−8 in three models), a higher DHA/total FAs ratio (Beta, 0.37 to 0.53; P≤6.82×10−9 in three models), a higher PUFAs/total FAs ratio (Beta, 0.07 to 1.003; P≤5.0×10−5 in five models), and a higher degree of unsaturation (Beta, 0.28 to 0.44; P ≤2.93×10−4 in five models) were all associated with a lower risk of myopia. In contrast, a higher omega-6/omega-3 ratio (Beta, −0.31 to −0.29; P≤8.44×10−7 in four models) and a higher MUFAs/total FAs ratio (Beta, −0.50 to −0.36; P≤3.0×10−6 in three models) were associated with a more negative SER, indicating an increased risk of myopia (Supplemental Table 2, Figure 2).

Figure 2. Causal association between fatty acids and spherical equivalent refraction.

Figure 2.

MR models are represented in different colors. The circular dots indicate the association effect estimates of fatty acids traits on spherical equivalent refraction. The lines represent the 95% confidence intervals for each estimate after Bonferroni correction.

MR: mendelian randomization; RE-IVW: random-effect inverse-variance weighted model; MR-PRESSO: MR pleiotropy residual sum and outlier

To address the sample overlapping issue arising from the inclusion of UK Biobank samples in both FAs and SER datasets, we used the MRlap model to provide unbiased corrected IVW effect. There was no significant difference between the RE-IVW effect and MRlap corrected IVW effect, except for the PUFAs/total FAs ratio (P=0.024). However, the significance and direction of the association between the PUFAs/total FAs ratio and SER remained unchanged after correction (MRlap corrected-IVW: Beta, 0.070; 95% CI, 0.04 to 0.104; P=4.92×10−5) (Supplemental Table 2).

We found consistent results using axial length as the outcome. Increased levels of omega-3 PUFAs (Beta, −0.08 to −0.06 per SD increase; P≤0.035 in two models), DHA (Beta, −0.10 to −0.08; P≤8.75×10−3 in two models), a higher DHA/total FAs ratio (Beta, −0.13 to −0.08; P≤0.035 in three models), and a higher degree of unsaturation (Beta, −0.10 to −0.08; P≤7.32×10−3 in four models) were nominally associated with a shorter axial length, suggesting a lower risk of myopia. Conversely, a higher level (per SD) of omega-6/omega-3 ratio (Beta, 0.07 to 0.10; P≤0.014 in three models), a higher Linoleic acid/total fatty acids ratio (Beta, 0.12 to 0.13, P≤0.018 in four models), and a higher MUFAs/total FAs ratio (Beta, 0.08 to 0.12; P≤0.039 in two models) were nominally associated with a longer axial length, indicating an increased risk of myopia (Supplemental Table 3, Figure 3)

Figure 3. Causal association between fatty acids and axial length.

Figure 3.

MR models are represented in different colors. The circular dots indicate the association effect estimates of fatty acids traits on axial length. The lines represent the 95% confidence intervals for each estimate after Bonferroni correction.

MR: mendelian randomization; RE-IVW: random-effect inverse-variance weighted model; MR-PRESSO: MR pleiotropy residual sum and outlier

Causal relationship between fatty acids and choroidal thickness

We observed nominally significant associations between thicker choroidal thickness and higher levels of omega-3 (Beta, 0.05; P≤0.029 in two models) and DHA (Beta, 0.05 to 0.06, P≤0.031 in three models). Moreover, higher ratios of DHA/total FAs (Beta, 0.06 to 0.07; P≤0.041 in three models), PUFA/total FA (Beta, 0.12 to 0.13; P≤0.02 in two models) and PUFA/MUFA (Beta, 0.07 to 0.10; P≤0.045 in three models) and a higher degree of unsaturation (Beta, 0.05; P≤0.02) were also nominally associated with thicker choroidal thickness. Conversely, higher ratios of omega-6/omega-3 (Beta, −0.05 to −0.04; P≤0.029 in two models), linoleic acid/total FAs (Beta, −0.09 to −0.06; P≤0.024 in two models) and MUFAs/total FAs (Beta, −0.10 to −0.06; P≤0.033 in three models) were nominally associated with thinner choroidal thickness. No significant difference was observed between the RE-IVW effect and MRlap corrected IVW effect (all P>0.05) (Supplemental Table 4).

Discussion

Myopia and its complications impose a significant socioeconomic and healthcare burden. Preventing or delaying its onset or progression is crucial. Our results indicate that higher levels and ratios of omega-3 and DHA, as well as higher PUFAs/total FAs ratios and degree of unsaturation, were causally associated with a more positive SER, indicating their protective effects on myopia. Supporting findings were obtained when using axial length as the outcome. Our research supports further clinical trials to test the feasibility of increasing omega-3 PUFAs intake through dietary modification as a convenient, manageable, and non-invasive treatment for myopia.

The health benefits of PUFAs, specifically, omega-3 PUFAs, have been observed in both systemic and ocular diseases.3942 Diets rich in long-chain omega-3 PUFAs may to provide long-term benefits for dry eye disease and age related macular degeneration.39,40,43 Previous studies on myopia and omega-3 PUFAs, mainly using animal models, suggested a potential therapeutic benefits.9,10 Pan et al. found that the daily gavage of omega-3 PUFAs (300 mg DHA plus 60 mg EPA) significantly attenuated the formation and development of myopia in guinea pigs and mice.9 Similarly, intake of omega-3 PUFAs was reported to effectively suppress myopic refractive changes and axial elongation when compared to omega-6 group in lens-induced myopic murine.10 Human studies on association between omega-3 and myopia are limited and have yield mixed results.1215 Findings from the NHNES showed that a higher EPA intake (>11 mg/1,000 Kcal) correlated with reduced high myopia risk but not low myopia in juveniles, while no associations was found with DHA intake.14 However, the findings from this study may be biased due to the small proportion of high myopic eyes (41 eyes).14 In contrast, no association was found between myopia and PUFAs in Singapore schoolchildren.12,13,15 The discrepancy among studies may be attributed to recall bias in dietary assessment using questionnaires and unaddressed confounders in observational studies.12 Furthermore, some studies only examine PUFAs intake without specifically considering the omega-3 subgroup, which could also contribute to the inconsistent findings.12,13,15

The mechanism underlying the therapeutic effect of omega-3 PUFAs against myopia remains to be elucidated. During myopia development, choroid thinning and reduced choroidal blood perfusion were observed in both animal models and humans,28,4446 which are hypothesized to cause local retinal and scleral hypoxia.28,44,47,48 The scleral hypoxia affects extracellular matrix remodeling, potentially biomechanically weakening and thinning the sclera, leading to axial elongation.47 Decreased DHA and EPA levels have been observed in sclera, retina, and serum during the early stage of form-deprivation myopia,9 and in serum of myopic children and adolescents.49 DHA or EPA could antagonize hypoxia-induced myofibroblast trans-differentiation in cultured human scleral fibroblasts.9 In animal models, both choroidal thickness and choroidal blood perfusion decrease during myopia development,28 and omega-3 PUFAs can inhibit this reduction.9 However, in young human adults, near work only reduced the choroidal vascularity index but not choroidal thickness, and omega-3 PUFAs supplements attenuated the choroidal vascularity index reduction.9 This may be because choroidal thickness is less sensitive to near work than the choroidal vascularity index. Our study found a potentially causal relationship between higher Omega-3 and DHA levels with thicker subfoveal choroid. Our study, combined with previous research, indicates that omega-3 PUFAs may mitigate myopia progression by modulating the choroidal blood perfusion. However, further clinical studies in humans are needed to verify these results.

Existing studies yield inconsistent results as to which components of omega-3 PUFAs (ie. DHA or EPA) play the major role in protecting against myopia. We found that higher DHA levels and higher DHA/total FAs ratios were associated with more hyperopia and shorter axial length. The effect of EPA on myopia was not tested in our study due to the insufficient IVs. Consistent with our findings, Pan et al. found that despite that both the DHA and EPA levels in serum, sclera, and retina were dysregulated during the early stage of form-deprivation in guinea pigs, gavage of omega-3 PUFAs only elevated the scleral DHA levels but not EPA levels.9 Correspondingly, peribulbar injection of DHA, but not EPA, showed inhibitory effects on form deprivation-induced reduction of choroidal thickness and blood perfusion, as well as myopia progression.9 However, another study reported that EPA and its metabolites were associated with inhibition of choroidal thinning and myopia progression in mice.11 Nevertheless, this study may be limited by its small sample size as only 4 mice were included in the case and control groups.11

We also found that a higher omega-6 to omega-3 ratio and a higher MUFAs to total FAs ratio may increase the risk of myopia. An unbalanced omega-6 to omega-3 ratio in favor of omega-6 PUFAs has been linked to prothrombotic and proinflammatory conditions,50,51 and may contribute to its detrimental role in myopia as inflammation could potentially promote myopia progression.52,53 The physiological effect of MUFAs varies with carbon chains length and sources. Long chain MUFAs (16:1n-7 and 18:1n-9) has been inversely associated with mortality, while very long chain MUFAs (20:1n-9, 22:1n-9 and 24:1n-9) showed a positive association with mortality among coronary artery disease patients.54 A prospective study in the U.S. found that higher plant-based MUFAs intake was associated with lower total mortality, while animal-based MUFAs intake was associated with higher mortality.55 Therefore, additional genetic data on MUFAs and its subtypes are needed to elucidate their effect on myopia.

Our study has several strengths. First, we used genetically determined plasma FAs levels as exposures, which offers a more objective measurement of omage-3 intake and metabolism compared to dietary assessment. This approach facilitates the causal relationships establishment. Second, we employed two measurements of myopia, including SER and axial length, and obtained consistent findings. Third, we employed a total of five main MR analysis methods to ensure the consistency of causality assessment. However, our study also has limitations. First, due to the inclusion of the UK Biobank study, there is an overlap between datasets for FAs and SER. To address this limitation, we used the MRlap model, which was specifically designed to address the sample overlapping issue.38 For most of our analyses, there were no significant difference between RE-IVW estimates and MRlap corrected IVW effects. Moreover, we obtained supporting results using axial length from independent datasets. Second, due to the unavailability of GWAS summary data on choroidal blood perfusion, we used choroidal thickness measurement as a surrogate. Third, we only used European-sourced data in our analyses due to data availability. The applicability of our findings to other ethnicities requires verification. Our results warrant further validation through more comprehensive GWAS summary data from diverse ethnic groups and RCTs of dietary intervention.

In conclusion, our study suggests a protective effect of omega-3 and DHA on myopia, possibly through the modulation of choroidal blood perfusion. The results suggest a promising, non-invasive, and scalable intervention for myopia through nutritional supplements. Further clinical trials are warranted to confirm the effectiveness, as well as to determine the optimal dose and duration.

Supplementary Material

1
2

Highlights.

  • Animal models suggest omega-3 polyunsaturated fatty acids may protect against myopia

  • Clinical evidence of omega-3’s protective effect on myopia is scarce and faces challenges

  • Higher omega-3 levels causally linked to lower myopia risk in Mendelian randomization analysis

Acknowledgments:

Funding:

Prof. Ching-Yu Cheng was supported by the National Medical Research Council of Singapore (NMRC/MOH/CSASI22jul-0002). Prof. Chen-Wei Pan was supported by the National Natural Science Foundation of China (82122059). Genotyping of the Genetic Epidemiology Research on Adult Health and Aging cohort was supported by the National Institute on Aging, National Institute of Mental Health, and National Institute of Health Common Fund (RC2AG036607). Helene Choquet was supported by the National Eye Institute (NEI) (R01EY027004).

Role of funders:

The funder of the study had no role in study design, data collection, data analysis, data interpretation, or writing of the report.

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

Conflicts of interests: None

Supplemental Material available at AJO.com.

Declaration of interests

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Data and data sharing:

The genome-wide association study summary data for fatty acids and refractive spherical equivalent used for this study are publicly available (https://www.ebi.ac.uk/gwas/). The genome-wide association study summary data for axial length from Genetic Epidemiology Research on Adult Health and Aging cohort are avaibale on reasonable request from Helene Choquet (Helene.Choquet@kp.org). The genome-wide association study summary data on choroidal thickness from UK Biobank are available on reasonable request from Nazlee Zebardast (Nazlee_Zebardast@MEEI.HARVARD.EDU).

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

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Data Availability Statement

The genome-wide association study summary data for fatty acids and refractive spherical equivalent used for this study are publicly available (https://www.ebi.ac.uk/gwas/). The genome-wide association study summary data for axial length from Genetic Epidemiology Research on Adult Health and Aging cohort are avaibale on reasonable request from Helene Choquet (Helene.Choquet@kp.org). The genome-wide association study summary data on choroidal thickness from UK Biobank are available on reasonable request from Nazlee Zebardast (Nazlee_Zebardast@MEEI.HARVARD.EDU).

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