Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 08, 2025 8 hours, 7 minutes ago
Thailand Medical News: New Study Uncovers How a Low-Methionine Diet Can Improve Brain Health by Activating DNA Repair Genes
A groundbreaking new study by researchers from the Department of Physiology and the Department of Genetics, Physiology and Microbiology at the Complutense University of Madrid (UCM), Spain, reveals how restricting a single amino acid—methionine—can affect the body’s ability to repair DNA differently in the brain and liver.
Cutting Methionine Boosts Brain DNA Repair but Slows Liver Response
Methionine is an essential amino acid found in foods like red meat, eggs, and dairy. Scientists have long known that reducing methionine intake, without lowering overall calories, can extend lifespan in animals. However, how this specific dietary change protects our genes was unclear—until now. This
Thailand Medical News report uncovers how a 40% methionine-restricted diet impacts the expression of genes responsible for a critical DNA repair process known as base excision repair (BER), which is vital for protecting against age-related diseases.
Boosting Brain Defenses While Slowing Liver Repair
The study, conducted on male Wistar rats over seven weeks, found that methionine restriction increased the activity of key DNA repair genes—Ogg1 and Ape1—in the brain cortex. These genes are responsible for detecting and removing oxidative damage to DNA. Their upregulation means the brain may be better prepared to handle DNA damage that accumulates with age, possibly protecting against conditions like Alzheimer’s or Parkinson’s disease.
However, in a surprising twist, the same methionine-restricted diet caused a drop in the expression of multiple BER genes in the liver, including Neil2, Udg, Ogg1, and Ape1, as well as the mitochondrial DNA polymerase Polγ. This suggests that while the brain ramps up its repair systems, the liver may reduce its DNA repair activity, possibly because methionine restriction also reduces oxidative damage there—thus, less repair is needed.
Why This Matters for Aging and Longevity
Base excision repair is one of the body’s most important tools for fixing oxidative damage to DNA. Damage to DNA is a major driver of aging and degenerative diseases. By regulating how the body repairs DNA, methionine restriction might help slow the aging process—especially in the brain.
Interestingly, the liver’s lowered DNA repair activity might not be a bad sign. The researchers suggest that because methionine restriction leads to lower levels of mitochondrial oxidative stress in the liver, the need for DNA repair is reduced. Meanwhile, the brain, which is more vulnerable to damage and has limited cell regeneration, seems to activate its defenses more aggressively in response to methionine restriction.
Possible Role of Epigenetics and Future Applications
The researchers also believe that methionine restriction may be changing
gene activity by affecting DNA methylation—an epigenetic mechanism that turns genes on or off. Methionine is the precursor to molecules that control methylation, and cutting it from the diet may reshape how repair genes are regulated across different organs.
This opens up potential future therapies that could mimic the effects of methionine restriction, especially for neurodegenerative conditions or age-related cognitive decline. While methionine restriction is difficult to implement in human diets, understanding its molecular benefits brings science one step closer to targeted anti-aging solutions.
Final Thoughts
This study reveals a powerful connection between diet and the body's ability to protect its own DNA. By simply cutting methionine intake, the brain activates key repair genes while the liver, benefiting from reduced oxidative stress, slows its repair machinery. These findings support the growing belief that targeted dietary changes can have tissue-specific benefits and may be an achievable strategy to delay aging and prevent age-related diseases. Further research will be essential to determine whether these effects can be replicated in humans and how they may influence long-term health outcomes.
The study findings were published in the peer reviewed journal: Biomolecules
https://www.mdpi.com/2218-273X/15/7/969
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