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Heavy water intake might prevent age-related hearing loss
Recent research shows that D2O (heavy water) supplementation might decrease oxidative stress production, and therefore grant resistance to age-related hearing loss.
Age-related hearing loss (ARHL) is the third most common age-related disease, and its incidence rate has been gradually increasing. Patients with ARHL are shown to develop progressive slow bilateral high-frequency hearing loss, which affects their speech recognition and sound source localization. It increases the risk of Alzheimer's disease and reduces the quality of life.
So far, there is no treatment to prevent or reverse ARHL effectively. Therefore, preventing ARHL through environmental intervention or nutrient uptake is an exciting approach worth exploring, even though the underlying mechanisms are not yet completely understood. Oxidative stress and metabolic deterioration go in pair with the aging of the auditory organs. ARHL is accompanied by an imbalance of reactive oxygen species (ROS) and a metabolism decline in the inner ear. Deregulated ROS production has been associated with ARHL in humans and mice.
In a recent article using mouse models of ARHL, Hou et al. reported the effect of deuterated oxygen (D), also known as "heavy water" . They found that supplementation can slow the pace of metabolism and reduce endogenous oxidative stress in the cochlea. It was proven by reduced activation of the Nrf2/HO-1/glutathione axis, which plays a crucial role in oxidative stress regulation.
Three strains of mice have been used in the research. The first model for ARHL research was DBA/2J mice with mutations in cadherin 23 (CDH23) and fascin-2. The onset of progressive hearing loss in these is early and is already detectable at the age of one month. For comparison, they examined C57BL/6J mice exhibiting high-frequency hearing loss by the age of 3–6 months with a profound impairment by 15 months due to the mutation in CDH23. The third was the CBA/CaJ strain, often used as wildtype control for good hearing, which does not have a predisposing CDH23 variant and remains resistant to ARHL until 15 months of age or beyond.
In all three mouse models with different deafness mechanisms and genetic backgrounds, D2O granted resistance to ARHL by decreasing oxidative stress production. Such results were observed after supplementing the typical mouse diet with 10% D2O from 4 to 9 weeks of age. The main observations of the research prove that dietary D2O supplementation:
- alleviates ARHL in DBA/2J mice and protects cochlear hair cells
- decreases endogenous oxidative stress in the cochlea
- slows down catabolic reactions and may delay the metabolic deterioration related to aging
- ameliorates ARHL in C57BL/6J and CBA/CaJ mouse models and decreases endogenous oxidative stress in the cochlea
To summarize, D2O supplementation can delay ARHL progression in mice by reducing the pace of metabolism and lowering endogenous oxidative stress production in the cochlea. These results give hope for protecting the cochlea from oxidative stress and regulating metabolism to prevent ARHL. Nevertheless, the D2O supplementation still needs to be closely investigated.
Source: Hou, Shule, et al. "Dietary intake of deuterium oxide decreases cochlear metabolism and oxidative stress levels in a mouse model of age-related hearing loss." Redox Biology (2022): 102472. https://doi.org/10.1016/j.redox.2022.102472
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Age-related hearing loss (ARHL) is the third most common age-related disease, and its incidence rate has been gradually increasing. Patients with ARHL are shown to develop progressive slow bilateral high-frequency hearing loss, which affects their speech recognition and sound source localization. It increases the risk of Alzheimer's disease and reduces the quality of life.
So far, there is no treatment to prevent or reverse ARHL effectively. Therefore, preventing ARHL through environmental intervention or nutrient uptake is an exciting approach worth exploring, even though the underlying mechanisms are not yet completely understood. Oxidative stress and metabolic deterioration go in pair with the aging of the auditory organs. ARHL is accompanied by an imbalance of reactive oxygen species (ROS) and a metabolism decline in the inner ear. Deregulated ROS production has been associated with ARHL in humans and mice.
In a recent article using mouse models of ARHL, Hou et al. reported the effect of deuterated oxygen (D), also known as "heavy water" . They found that supplementation can slow the pace of metabolism and reduce endogenous oxidative stress in the cochlea. It was proven by reduced activation of the Nrf2/HO-1/glutathione axis, which plays a crucial role in oxidative stress regulation.
Three strains of mice have been used in the research. The first model for ARHL research was DBA/2J mice with mutations in cadherin 23 (CDH23) and fascin-2. The onset of progressive hearing loss in these is early and is already detectable at the age of one month. For comparison, they examined C57BL/6J mice exhibiting high-frequency hearing loss by the age of 3–6 months with a profound impairment by 15 months due to the mutation in CDH23. The third was the CBA/CaJ strain, often used as wildtype control for good hearing, which does not have a predisposing CDH23 variant and remains resistant to ARHL until 15 months of age or beyond.
In all three mouse models with different deafness mechanisms and genetic backgrounds, D2O granted resistance to ARHL by decreasing oxidative stress production. Such results were observed after supplementing the typical mouse diet with 10% D2O from 4 to 9 weeks of age. The main observations of the research prove that dietary D2O supplementation:
- alleviates ARHL in DBA/2J mice and protects cochlear hair cells
- decreases endogenous oxidative stress in the cochlea
- slows down catabolic reactions and may delay the metabolic deterioration related to aging
- ameliorates ARHL in C57BL/6J and CBA/CaJ mouse models and decreases endogenous oxidative stress in the cochlea
To summarize, D2O supplementation can delay ARHL progression in mice by reducing the pace of metabolism and lowering endogenous oxidative stress production in the cochlea. These results give hope for protecting the cochlea from oxidative stress and regulating metabolism to prevent ARHL. Nevertheless, the D2O supplementation still needs to be closely investigated.
Source: Hou, Shule, et al. "Dietary intake of deuterium oxide decreases cochlear metabolism and oxidative stress levels in a mouse model of age-related hearing loss." Redox Biology (2022): 102472. https://doi.org/10.1016/j.redox.2022.102472
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
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Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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