Healthy diets link to longer life regardless of longevity genes, large study finds

By Priyanjana Pramanik, MSc.Reviewed by Susha Cheriyedath, M.Sc.Feb 16 2026

A major cohort study suggests that consistent adherence to established healthy eating patterns may add years to life, even after accounting for genetic predisposition.

Study: Healthy dietary patterns, longevity genes, and life expectancy: A prospective cohort study. Image Credit: Pacorpi / Shutterstock

In a recent study published in Science Advances, researchers investigated the impact of adherence to five established healthy dietary patterns on life expectancy and mortality, examining whether these associations differed by genetic predisposition to longevity rather than susceptibility to shorter lifespan. Greater adherence to all five dietary patterns was linked to lower mortality and longer life expectancy. These benefits were associated with dietary adherence regardless of genetic predisposition to longevity.

Life expectancy growth has begun to stagnate despite decades of improvement, highlighting the need for effective strategies to reduce premature mortality. Unhealthy diets are a leading global cause of death, making dietary modification a cost-effective and scalable intervention.

Rather than focusing on individual nutrients, contemporary research emphasizes overall dietary patterns, which better capture antagonistic or synergistic effects among foods. Several a priori dietary indices, such as the Diabetes Risk Reduction Diet (DDRD), Alternate Mediterranean Diet (AMED), Alternate Healthy Eating Index-2010 (AHEI-2010), Dietary Approaches to Stop Hypertension (DASH), and healthful Plant-based Diet Index (hPDI), have been associated with lower risks of mortality and multiple chronic diseases.

However, relatively few analyses have translated these associations into absolute measures such as life expectancy, which are more relevant for public health messaging and policy decisions than relative risk estimates. Additionally, genetic factors contribute to longevity, and emerging evidence suggests interactions between genetic predisposition and lifestyle exposures, including diet. Yet, the combined effects of dietary quality and genetic predisposition to longevity on life expectancy remain unclear.

UK Biobank Cohort, Dietary Scores, and Genetic Analysis

This prospective cohort study used data from the UK Biobank, which recruited over 500,000 adults aged 40–69 years between 2006 and 2010 across the United Kingdom. Dietary intake was assessed using a validated 24-hour recall questionnaire administered on up to five occasions between 2009 and 2012. Participants completing at least two dietary assessments and free from cardiovascular disease or cancer at baseline were included (n = 103,649). Those with implausible energy intake were excluded.

Five dietary pattern scores were calculated: AHEI-2010, AMED, hPDI, DASH, and DRRD, using predefined scoring systems that reflect adherence to healthy eating principles. Average intake across assessments was used. Covariates included demographic factors, socioeconomic status, smoking, physical activity, body mass index (BMI), energy intake, alcohol consumption, with additional alcohol adjustment applied specifically to dietary scores that did not include alcohol components, and baseline chronic conditions.

Mortality data were obtained from national registries through November 2022. Cox proportional hazards models estimated hazard ratios (HRs) for all-cause and cause-specific mortality across quintiles of dietary scores. Life expectancy at age 45 was estimated using life-table methods that integrated UK population mortality rates and adjusted HRs; these estimates were model-derived rather than directly observed survival differences. A polygenic risk score (PRS) for longevity was used to assess gene–diet interactions. Sensitivity analyses were conducted to test robustness across multiple assumptions and subgroups.

Mortality Risk Reductions and Absolute Life Expectancy Gains

Over a median follow-up of 10.6 years, resulting in 1,094,467 person-years, 4,314 deaths occurred. Higher adherence to all five dietary patterns was correlated with lower all-cause mortality after multivariable adjustment. When the highest and lowest quintiles were compared, adjusted HRs ranged from 0.76 (DDRD) to 0.82 (hPDI), indicating an 18–24% lower risk of death. Significant inverse associations were also observed for several cause-specific outcomes, particularly cancer, respiratory, and other-cause mortality.

Life expectancy analyses showed meaningful absolute differences. At age 45, men in the highest versus lowest quintile gained 1.9 to 3.0 years of life, while women gained 1.5 to 2.3 years. The largest gain for men was observed with DDRD, whereas AMED showed the longest gain for women.

Higher longevity PRS was independently associated with lower mortality, 15% lower risk in the highest versus the lowest tertile. Joint analyses indicated that individuals with both high PRS and high dietary scores had the greatest life expectancy. However, no significant additive or multiplicative interactions were detected for most dietary scores, suggesting that healthy dietary patterns are associated with survival benefits regardless of genetic predisposition. An exception was DDRD, which showed a stronger inverse association with mortality among individuals with lower longevity PRS. Sensitivity analyses confirmed the robustness of findings across multiple adjustments and restrictions.

Public Health Implications and Study Limitations

This large prospective study demonstrated that greater adherence to five healthy dietary patterns is consistently associated with reduced mortality and extended life expectancy, independent of genetic predisposition to longevity. Absolute gains of up to three additional years at age 45 underscore the public health relevance of sustained dietary quality. DDRD showed slightly stronger associations, although the study did not directly test biological mechanisms and proposed explanations, such as improved glycemic control, remain speculative.

Strengths include a large sample size, repeated dietary assessments, comprehensive adjustment for confounders, integration of genetic data, and the use of life-table methods to estimate absolute life-expectancy differences. However, limitations include reliance on 24-hour recalls, potential residual confounding, limited ethnic diversity in genetic analyses, and possible overestimation of genetic effects due to sample overlap. Dietary changes over time were not fully captured. In addition, UK Biobank participants may not fully represent the general population, which could affect the generalizability of the findings.

In conclusion, adherence to established healthy dietary patterns is associated with longer life expectancy, regardless of genetic predisposition to longevity. These findings support public health recommendations promoting high-quality diets as a flexible and accessible strategy for extending life span, while recognizing that observational studies cannot establish causality and should be interpreted accordingly.