A recent study has found that a strict ketogenic diet can reverse biological aging linked to obesity by more than six years. This breakthrough research sheds light on how weight loss through a very-low-calorie ketogenic diet (VLCKD) can slow or even reverse epigenetic aging.
The Connection Between Obesity and Epigenetic Aging
Obesity accelerates biological aging by causing oxidative stress, chronic inflammation, and mitochondrial dysfunction. These factors are common in both obesity and aging. Additionally, obesity can alter epigenetic patterns, speeding up the aging process at a molecular and cellular level.
The epigenetic clock, based on DNA methylation patterns, is a key tool for predicting biological age. Modern epigenetic clocks, such as Horvath, Hannum, and Levine’s models, can quantify the difference between biological age and chronological age, known as epigenetic acceleration (AgeAccel). Understanding the molecular mechanisms behind accelerated aging in obesity could lead to more targeted therapies for reversing or slowing this process.
Study Overview: Investigating VLCKD’s Effect on Aging
The study aimed to investigate whether a VLCKD could slow down the biological aging caused by obesity. Researchers used epigenetic clocks to measure biological age and compared it to participants’ chronological age. The difference between the two—AgeAccel—was used to assess the impact of obesity on biological aging.
The study involved 28 obese participants and 20 normal-weight participants. Additionally, a cohort of 10 obese individuals followed a VLCKD for six months to observe its effects. Blood samples were taken at the start, at day 30 when the participants entered nutritional ketosis, and at the end of the study at day 180 for epigenetic analysis.
Obesity Accelerates Biological Aging
The results showed that obese individuals had higher DNA methylation age (DNAmAge) compared to their normal-weight counterparts. This discrepancy between chronological age and DNAmAge was observed in both men and women.
Obese participants had an average AgeAccel of +4.4 years, while normal-weight participants had a deceleration of epigenetic age by -3.1 years. This suggests a clear relationship between higher body mass index (BMI) and accelerated biological aging, confirming the role of obesity in epigenetic aging.
How VLCKD Reverses Epigenetic Aging
For the obese individuals following a VLCKD, the results were striking. The VLCKD group showed a significant reduction in DNAmAge, indicating a slowdown in biological aging. By the end of the study, participants had lost an average of 9 kg by day 30 and 20 kg by day 180.
During the nutritional ketosis (NK) phase, the VLCKD group experienced an average deceleration in epigenetic age of -6.1 years, which was sustained throughout the study. This deceleration was consistent for both men and women and was linked to changes in BMI.
The study also found a strong negative correlation between AgeAccel and ketone levels, particularly β-hydroxybutyrate (β-OHB), in the VLCKD phase. This suggests that increased ketone activity could play a significant role in the observed deceleration of biological aging.
Additionally, improvements were seen in metabolic health markers, such as glucose, insulin, cholesterol, and triglyceride levels, in participants following the VLCKD.
Conclusion
The study highlights the potential of VLCKD in reversing the biological aging linked to obesity. By monitoring epigenetic clocks, researchers were able to observe a significant slowdown in biological age in obese individuals who followed a VLCKD. This process was closely associated with improvements in metabolic parameters, BMI, and ketone levels.
However, further research with larger sample sizes and longer follow-up periods is needed to confirm these findings and better understand the role of ketones in the epigenetic regulation of aging.
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