Effects of omega-3 supplementation on telomere length, inflammation, and oxidative stress in women with systemic lupus erythematosus: Protocol for a randomized double-blind placebo-controlled trial
Beatriz G. Carvalho, Eduardo F. Borba, Marcelo M. Rogero, Carolina F. Nicoletti
{"title":"Effects of omega-3 supplementation on telomere length, inflammation, and oxidative stress in women with systemic lupus erythematosus: Protocol for a randomized double-blind placebo-controlled trial","authors":"Beatriz G. Carvalho, Eduardo F. Borba, Marcelo M. Rogero, Carolina F. Nicoletti","doi":"10.1016/j.cnd.2026.08.072","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><div>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and accelerated cellular aging. Telomere shortening has been associated with disease progression and immunosenescence in SLE. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may exert anti-inflammatory and antioxidant effects; however, their impact on telomere biology in women with SLE remains unclear.</div></div><div>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and accelerated cellular aging. Telomere shortening has been associated with disease progression and immunosenescence in SLE. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may exert anti-inflammatory and antioxidant effects; however, their impact on telomere biology in women with SLE remains unclear.</div><div><h3>Objective</h3><div>To evaluate the effects of omega-3 supplementation on leukocyte telomere length, inflammatory pathways, and oxidative stress biomarkers in women with SLE in remission.</div></div><div>To evaluate the effects of omega-3 supplementation on leukocyte telomere length, inflammatory pathways, and oxidative stress biomarkers in women with SLE in remission.</div><div><h3>Methods</h3><div>This study is a randomized, double-blind, placebo-controlled, parallel-group clinical trial involving women aged 18–45 years with SLE in remission and healthy controls. Participants will be randomized (1:1) to receive either omega-3 supplementation (3,600<!--> <!-->mg/day EPA<!--> <!-->+<!--> <!-->DHA) or placebo for 12 weeks. The primary outcome is relative leukocyte telomere length, assessed by quantitative PCR using the telomere-to-single-copy gene (T/S) ratio. Secondary outcomes include inflammatory signaling pathways in peripheral blood mononuclear cells, oxidative stress biomarkers, antioxidant capacity, disease activity, anthropometric parameters, dietary intake, and physical activity. Outcomes will be assessed at baseline and after the intervention. The study was approved by the local Ethics Committee (CAAE: 92044025.6.0000.0068) and registered at ClinicalTrials.gov (<span><span>NCT07393399</span><svg><path></path></svg></span>).</div></div><div>This study is a randomized, double-blind, placebo-controlled, parallel-group clinical trial involving women aged 18–45 years with SLE in remission and healthy controls. Participants will be randomized (1:1) to receive either omega-3 supplementation (3,600<!--> <!-->mg/day EPA<!--> <!-->+<!--> <!-->DHA) or placebo for 12 weeks. The primary outcome is relative leukocyte telomere length, assessed by quantitative PCR using the telomere-to-single-copy gene (T/S) ratio. Secondary outcomes include inflammatory signaling pathways in peripheral blood mononuclear cells, oxidative stress biomarkers, antioxidant capacity, disease activity, anthropometric parameters, dietary intake, and physical activity. Outcomes will be assessed at baseline and after the intervention. The study was approved by the local Ethics Committee (CAAE: 92044025.6.0000.0068) and registered at ClinicalTrials.gov (<span><span>NCT07393399</span><svg><path></path></svg></span>).</div><div><h3>Preliminary results</h3><div>Before supplementation, women with SLE presented significantly shorter leukocyte telomere length than healthy controls (T/S ratio: 1.126<!--> <!-->±<!--> <!-->0.080 vs. 1.170<!--> <!-->±<!--> <!-->0.076; <em>P</em> <!-->=<!--> <!-->0.001). Baseline inflammatory markers were also elevated, with C-reactive protein of 5.87<!--> <!-->±<!--> <!-->9.03<!--> <!-->mg/dL versus 0.23<!--> <!-->±<!--> <!-->0.04<!--> <!-->mg/dL (<em>P</em> <!--><<!--> <!-->0.001) and erythrocyte sedimentation rate of 25.34<!--> <!-->±<!--> <!-->16.98 versus 6.25<!--> <!-->±<!--> <!-->1.09<!--> <!-->mm/h (<em>P</em> <!--><<!--> <!-->0.001). In contrast, baseline total oxidant status (TOS) was 2.32<!--> <!-->±<!--> <!-->1.38 vs. 2.58<!--> <!-->±<!--> <!-->1.096 (<em>P</em> <!--><<!--> <!-->0.001). Based on these findings, we expect that 12 weeks of omega-3 supplementation (3,600<!--> <!-->mg/day EPA<!--> <!-->+<!--> <!-->DHA) will improve inflammatory and oxidative stress biomarkers while preserving leukocyte telomere length compared with placebo.</div></div><div>Before supplementation, women with SLE presented significantly shorter leukocyte telomere length than healthy controls (T/S ratio: 1.126<!--> <!-->±<!--> <!-->0.080 vs. 1.170<!--> <!-->±<!--> <!-->0.076; <em>P</em> <!-->=<!--> <!-->0.001). Baseline inflammatory markers were also elevated, with C-reactive protein of 5.87<!--> <!-->±<!--> <!-->9.03<!--> <!-->mg/dL versus 0.23<!--> <!-->±<!--> <!-->0.04<!--> <!-->mg/dL (<em>P</em> <!--><<!--> <!-->0.001) and erythrocyte sedimentation rate of 25.34<!--> <!-->±<!--> <!-->16.98 versus 6.25<!--> <!-->±<!--> <!-->1.09<!--> <!-->mm/h (<em>P</em> <!--><<!--> <!-->0.001). In contrast, baseline total oxidant status (TOS) was 2.32<!--> <!-->±<!--> <!-->1.38 vs. 2.58<!--> <!-->±<!--> <!-->1.096 (<em>P</em> <!--><<!--> <!-->0.001). Based on these findings, we expect that 12 weeks of omega-3 supplementation (3,600<!--> <!-->mg/day EPA<!--> <!-->+<!--> <!-->DHA) will improve inflammatory and oxidative stress biomarkers while preserving leukocyte telomere length compared with placebo.</div><div><h3>Conclusion</h3><div>This trial may provide novel insights into the role of omega-3 supplementation as an adjunct nutritional strategy targeting inflammation, oxidative stress, and cellular aging in SLE.</div></div><div>This trial may provide novel insights into the role of omega-3 supplementation as an adjunct nutritional strategy targeting inflammation, oxidative stress, and cellular aging in SLE.</div>","PeriodicalId":43722,"journal":{"name":"CAHIERS DE NUTRITION ET DE DIETETIQUE","volume":"61 ","pages":"Pages e39-e40"},"PeriodicalIF":0.3000,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"CAHIERS DE NUTRITION ET DE DIETETIQUE","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0007996026001483","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/9/24 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
引用次数: 0
Abstract
Background
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and accelerated cellular aging. Telomere shortening has been associated with disease progression and immunosenescence in SLE. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may exert anti-inflammatory and antioxidant effects; however, their impact on telomere biology in women with SLE remains unclear.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and accelerated cellular aging. Telomere shortening has been associated with disease progression and immunosenescence in SLE. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may exert anti-inflammatory and antioxidant effects; however, their impact on telomere biology in women with SLE remains unclear.
Objective
To evaluate the effects of omega-3 supplementation on leukocyte telomere length, inflammatory pathways, and oxidative stress biomarkers in women with SLE in remission.
To evaluate the effects of omega-3 supplementation on leukocyte telomere length, inflammatory pathways, and oxidative stress biomarkers in women with SLE in remission.
Methods
This study is a randomized, double-blind, placebo-controlled, parallel-group clinical trial involving women aged 18–45 years with SLE in remission and healthy controls. Participants will be randomized (1:1) to receive either omega-3 supplementation (3,600 mg/day EPA + DHA) or placebo for 12 weeks. The primary outcome is relative leukocyte telomere length, assessed by quantitative PCR using the telomere-to-single-copy gene (T/S) ratio. Secondary outcomes include inflammatory signaling pathways in peripheral blood mononuclear cells, oxidative stress biomarkers, antioxidant capacity, disease activity, anthropometric parameters, dietary intake, and physical activity. Outcomes will be assessed at baseline and after the intervention. The study was approved by the local Ethics Committee (CAAE: 92044025.6.0000.0068) and registered at ClinicalTrials.gov (NCT07393399).
This study is a randomized, double-blind, placebo-controlled, parallel-group clinical trial involving women aged 18–45 years with SLE in remission and healthy controls. Participants will be randomized (1:1) to receive either omega-3 supplementation (3,600 mg/day EPA + DHA) or placebo for 12 weeks. The primary outcome is relative leukocyte telomere length, assessed by quantitative PCR using the telomere-to-single-copy gene (T/S) ratio. Secondary outcomes include inflammatory signaling pathways in peripheral blood mononuclear cells, oxidative stress biomarkers, antioxidant capacity, disease activity, anthropometric parameters, dietary intake, and physical activity. Outcomes will be assessed at baseline and after the intervention. The study was approved by the local Ethics Committee (CAAE: 92044025.6.0000.0068) and registered at ClinicalTrials.gov (NCT07393399).
Preliminary results
Before supplementation, women with SLE presented significantly shorter leukocyte telomere length than healthy controls (T/S ratio: 1.126 ± 0.080 vs. 1.170 ± 0.076; P = 0.001). Baseline inflammatory markers were also elevated, with C-reactive protein of 5.87 ± 9.03 mg/dL versus 0.23 ± 0.04 mg/dL (P < 0.001) and erythrocyte sedimentation rate of 25.34 ± 16.98 versus 6.25 ± 1.09 mm/h (P < 0.001). In contrast, baseline total oxidant status (TOS) was 2.32 ± 1.38 vs. 2.58 ± 1.096 (P < 0.001). Based on these findings, we expect that 12 weeks of omega-3 supplementation (3,600 mg/day EPA + DHA) will improve inflammatory and oxidative stress biomarkers while preserving leukocyte telomere length compared with placebo.
Before supplementation, women with SLE presented significantly shorter leukocyte telomere length than healthy controls (T/S ratio: 1.126 ± 0.080 vs. 1.170 ± 0.076; P = 0.001). Baseline inflammatory markers were also elevated, with C-reactive protein of 5.87 ± 9.03 mg/dL versus 0.23 ± 0.04 mg/dL (P < 0.001) and erythrocyte sedimentation rate of 25.34 ± 16.98 versus 6.25 ± 1.09 mm/h (P < 0.001). In contrast, baseline total oxidant status (TOS) was 2.32 ± 1.38 vs. 2.58 ± 1.096 (P < 0.001). Based on these findings, we expect that 12 weeks of omega-3 supplementation (3,600 mg/day EPA + DHA) will improve inflammatory and oxidative stress biomarkers while preserving leukocyte telomere length compared with placebo.
Conclusion
This trial may provide novel insights into the role of omega-3 supplementation as an adjunct nutritional strategy targeting inflammation, oxidative stress, and cellular aging in SLE.
This trial may provide novel insights into the role of omega-3 supplementation as an adjunct nutritional strategy targeting inflammation, oxidative stress, and cellular aging in SLE.
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