The Study
Epigenetic Age Acceleration and Cardiometabolic Biomarkers in Response to Weight‐Loss Dietary Interventions Among Obese Individuals: The MACRO Trial
This study is like a controlled experiment where people were randomly assigned to eat either low-carb or low-fat food for a year. It found that eating better made their blood markers improve—but it didn't find that their 'biological age' (measured by DNA changes) caused those improvements. So we know diet helps, but we don't know if the DNA clock is the reason.
Analysis score
Maximum 90 for a randomized controlled trial.
Where the score came from
Scientists measured a biological aging clock in obese people before and after they lost weight by eating less carbs or fat.
Where does this study sit?
Reviews of RCTs (Meta-analyses)
Max 100Randomized Trials
Max 90Reviews of Cohort Studies
Max 85Cohort Studies
Max 72Reviews of Case-Control Studies
Max 63Case-Control Studies
Max 58Cross-Sectional & Case Series
Max 50Expert Opinion
Max 563 / 100
Quality score
Participants are randomly assigned to treatment or control groups, minimizing bias. The gold standard for testing whether an intervention causes an effect.
Key takeaways
Summary
Based on the study abstract and findings.
- 1Even though people got healthier (lower blood sugar, less inflammation), their biological aging clock didn't move — meaning the clock may reflect long-term damage, not short-term fixes.
- 2Before weight loss, the aging clock (DunedinPACE) matched bad health markers like high insulin and inflammation.
- 3After 12 months of weight loss, health improved — but the aging clock didn't change.
Score breakdown, methodology, conflicts of interest, evidence analysis & raw study data
Publication
Journal
Aging Cell
Year
2025
Authors
Minghao Kou, Xiang Li, Yoriko Heianza, Kirsten Dorans, Lydia A. Bazzano, Lu Qi
Related Content
Claims (5)
Weight loss improves insulin resistance, inflammation, and lipid levels in obese adults over 12 months, but these improvements are not caused by changes in DNA methylation patterns measured by epigenetic aging clocks.
In obese adults, a faster epigenetic aging rate measured by DunedinPACE at the start of the study is linked to higher levels of insulin, inflammation markers, and lower levels of beneficial metabolic hormones, but changes in this aging rate over 12 months do not match changes in these metabolic markers.
When obese adults lose weight through diet over 12 months, their insulin, HOMA-IR, CRP, and adiponectin levels improve, but their DunedinPACE epigenetic aging score does not change.
In obese adults, DunedinPACE is more closely linked to key metabolic health markers at the start of the study than two other epigenetic clocks, and none of the three clocks show significant changes after 12 months of weight loss.
In obese adults, weight loss reduces the connection between the rate of epigenetic aging (DunedinPACE) and most cardiometabolic biomarkers, but a link remains with CRP and adiponectin, suggesting that epigenetic aging captures long-term physiological changes rather than short-term metabolic fluctuations.
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.