The ketogenic diet improves healthspan and memory in aging mice
A study by the Buck Institute and University of Chile found the ketogenic diet boosts memory in aging mice by enhancing synapse function through a new molecular pathway involving β-hydroxybutyrate. Future research will explore interventions for brain health.
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A study conducted by the Buck Institute for Research on Aging and the University of Chile has revealed that the ketogenic diet can improve memory in aging mice by enhancing synapse function through a new molecular signaling pathway. Published in Cell Reports Medicine, the research suggests that the diet's benefits on brain health and aging can be explained by these mechanisms. The study, led by Dr. Christian González-Billault and Dr. John Newman, showed that a ketogenic diet administered later in life can enhance memory in aging mice without the need for long-term dietary changes. The diet, high in fat and low in carbohydrates, activated the protein kinase A signaling pathway in synapses, particularly through the ketone body β-hydroxybutyrate (BHB). This finding opens up possibilities for targeted interventions to improve brain health and memory in aging individuals without the need for strict dietary adherence. Further research will focus on exploring the specific role of BHB and potential interventions targeting the protein kinase A pathway to replicate the memory-enhancing effects observed in the study.
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14 commentsKetogenic diets inhibit mitochondrial biogenesis and induce cardiac fibrosis (2021) (PMID: 33558457)
> increased β-OHB levels and SIRT7 expression, decreased mitochondrial biogenesis, and increased cardiac fibrosis were detected in human atrial fibrillation heart tissues. Our results highlighted the unknown detrimental effects of KDs
Ketogenic diet induces p53-dependent cellular senescence in multiple organs (2024) (PMID: 38758782)
> Mice on two different KDs and, at different ages, induce cellular senescence in multiple organs, including the heart and kidney. This effect is mediated through adenosine monophosphate-activated protein kinase (AMPK) and inactivation of mouse double minute 2 (MDM2) by caspase-2, leading to p53 accumulation and p21 induction. This was established using p53 and caspase-2 knockout mice and inhibitors to AMPK, p21, and caspase-2. In addition, senescence-associated secretory phenotype biomarkers were elevated in serum from mice on a KD and in plasma samples from patients on a KD clinical trial. Cellular senescence was eliminated by a senolytic and prevented by an intermittent KD.
As per PMC11100565, a cycled KD avoids the senescence issue:
> Both an alternate-day and an alternate-week IKD have been reported to improve health parameters over a continuous KD in different murine models (10, 64), while a third study using a 3-day/week IKD reported attenuated improvements relative to continuous KD (74).
High-fat diet, microbiome-gut-brain axis signaling, and anxiety-like behavior in male rats https://news.ycombinator.com/item?id=40801181
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