Hormonal
Genetic or pharmacological interventions that impair lipid synthesis (specifically ceramide and sphingolipid pathways) or enhance lipid hydrolysis (lysosomal lipases) extend lifespan in model organisms including nematodes and fruit flies.
Current research shows that modifying specific lipid pathways (like reducing ceramide synthesis or increasing certain lipases) extends lifespan in worms and flies. However, these are complex genetic or pharmacological interventions not yet available or safe for general human use. Focus on maintaining healthy lipid profiles through balanced nutrition rather than attempting unproven lipid-targeting supplements for longevity.
For example, the impairment of genes involved in ceramide and sphingolipid synthesis extends lifespan in both worms and flies. The overexpression of fatty acid amide hydrolase or lysosomal lipase prolongs life in Caenorhabditis elegans, while the overexpression of diacylglycerol lipase enhances longevity in both C. elegans and Drosophila melanogans.
Why this rating
Strong evidence in invertebrates and rodents, but human data is largely observational (biomarkers) rather than interventional.
Source
The role of lipid metabolism in aging, lifespan regulation, and age‐related disease
Adiv A. Johnson et al. · Aging Cell · 2019
DOI 10.1111/acel.13048
More from this paper
- Surgical removal of adipose tissue and specific genetic modifications (e.g., deletion of diacylglycerol acyltransferase 1) extend lifespan in rodents.Good
- Specific blood lipid profiles (e.g., levels of triglycerides, lysophosphatidylcholine, and apolipoprotein E alleles) correlate with human aging and exceptional longevity.Moderate
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