A recent study published in Nutrients explores the relationship between obesity and the acceleration of biological aging through epigenetic mechanisms, highlighting the potential of a very-low-calorie ketogenic diet (VLCKD) to reverse this process. The study delves into how obesity influences epigenetic patterns of aging and investigates how VLCKD can modulate biological aging, potentially offering a pathway to decelerate or even reverse some of the adverse effects of obesity on aging.
Obesity and Epigenetic Aging
Obesity is commonly linked to a range of health issues, including oxidative stress, chronic low-grade inflammation, and mitochondrial dysfunction. These factors are not only characteristic of obesity but are also seen in the aging process. Research has shown that obesity can influence epigenetic aging, accelerating this process at the molecular and cellular levels. Epigenetic changes, particularly DNA methylation patterns, play a critical role in the aging process, with epigenetic clocks providing an accurate measure of biological age.
The epigenetic clock, a tool based on DNA methylation patterns, has become one of the most precise ways to estimate biological age. First developed by researchers Horvath and Hannum, these clocks have been refined to include more advanced models, such as the PhenoAge, which quantifies differences between chronological age (ChronoAge) and biological age (DNAmAge). Understanding the molecular mechanisms linking obesity and accelerated aging could lead to the development of more personalized therapies that help slow down or even reverse biological aging.
About the Study
The study aimed to investigate whether following a VLCKD could decelerate the biological aging associated with obesity. The researchers utilized Horvath, Hannum, and Levine’s epigenetic clocks to measure biological age across different groups of participants. The study focused on the relationship between body mass index (BMI), other metabolic parameters, and epigenetic age.
The study participants were divided into three groups: an obesity group (28 participants), a normal-weight group (20 participants), and a longitudinal cohort of 10 obese participants who followed a VLCKD for six months. Blood samples were collected at three points: baseline (BL), day 30 (designated as nutritional ketosis or NK), and day 180 (the endpoint or EP) to assess changes in epigenetic markers.
Obesity Accelerates Epigenetic Aging
The study revealed that obese individuals exhibited higher levels of DNAmAge compared to those with normal weight, confirming that obesity accelerates biological aging. The average AgeAccel (the difference between ChronoAge and DNAmAge) was significantly higher in the obese group, with a positive correlation between BMI and AgeAccel. In contrast, the normal-weight group showed a deceleration of biological aging, with an average AgeAccel of -3.1 years, while the obese group experienced a +4.4 years AgeAccel.
These findings suggest that obesity not only accelerates biological aging but also provides an important biomarker for predicting the health risks associated with obesity, as epigenetic clocks can help quantify this accelerated aging.
How VLCKD Reverses Epigenetic Aging
A key aspect of this study was exploring how following a VLCKD could reverse obesity-induced epigenetic aging. The results showed that, after following the VLCKD, the obese participants experienced a significant reduction in DNAmAge, suggesting a deceleration of biological aging. This effect was observed in both the NK phase (30 days) and the EP phase (180 days).
On average, participants in the VLCKD group lost 9 kg by the NK phase and 20 kg by the EP phase, with this weight loss closely correlating with the deceleration of biological age. During the NK phase, participants experienced an average reduction in epigenetic age of -6.1 years, which persisted at -6.2 years by the EP phase. This partial reversal of epigenetic aging was observed consistently across both men and women.
The study also found a significant negative correlation between the levels of β-hydroxybutyrate (β-OHB) — a key ketone body produced during ketosis — and AgeAccel. This suggests that increased ketonemia might play a role in reversing epigenetic aging, further supporting the idea that ketone bodies could be involved in modulating the epigenetic regulation of aging.
Additionally, improvements in metabolic parameters such as glucose, insulin, cholesterol, and triglycerides were observed in the VLCKD group. These metabolic benefits, alongside the deceleration of epigenetic aging, highlight the potential of VLCKD as a therapeutic approach for obesity, offering not just weight loss but also metabolic, anti-inflammatory, and antioxidant benefits.
Conclusions
The findings of this study underscore the important role of epigenetic clocks in tracking the acceleration of biological aging associated with obesity. The results suggest that VLCKD may offer a powerful tool for reversing epigenetic aging, particularly by improving metabolic health and reducing the inflammatory and oxidative stress associated with obesity.
However, the researchers note that further studies with larger sample sizes and longer follow-up times are needed to confirm these findings. More research is also required to better understand the precise mechanisms through which ketone bodies influence epigenetic aging and to determine the long-term impacts of VLCKD on overall health and aging.
In conclusion, this study suggests that VLCKD has the potential to reverse obesity-linked biological aging by over six years, making it a promising avenue for future therapeutic strategies aimed at mitigating the aging process in obese individuals.
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