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Bipolar disorder linked to accelerated cellular aging in young adults
In a study on 130 individuals with bipolar disorder, most showed a characteristic pattern of accelerated cellular aging.
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Bipolar disorder (BD) is one of the major psychiatric disorders affecting at least 1% of the general population. The occurrence of BD has been associated with a 10-15 years decrease in life expectancy. One reason behind this is an increased prevalence of suicide, but multiple comorbid diseases also play a role, including cardiovascular and metabolic disorders. Another hypothesis is accelerated aging in individuals with BD.
To validate this hypothesis, several markers were studied, such as telomere length (TL) and the copy number of mitochondrial DNA (mtDNAcn). mtDNAcn is a measure of the number of mitochondrial DNA per cell, which is used to characterize mitochondrial function. Age-related decay of mitochondrial function leads to a decrease in mtDNAcn. In most available studies, TL is significantly reduced in individuals with BD compared to the healthy control. mtDNAcn is much less studied in BD, and the results remain inconsistent. Moreover, most aging markers in BD studies were performed in small samples (less than a hundred participants) and included patients with different mood states during inclusion (euthymic, depressed, and manic).
Spano et al. investigated TL and mtDNAcn in a homogenous cohort of 130 individuals with BD compared to healthy control. The sample included individuals of Caucasian origin, aged over 18 years, and euthymic (tranquil mental state without any major mood episodes) for at least three months. For all participants, data on age, sex, body mass index, smoking status, depression, and manic scale scores were obtained at inclusion. Blood samples were collected from each participant as well.
The authors employed various statistical methods to analyze the collected data, including regression and cluster analysis. Significantly lower TL and mtDNAcn (26.5% and 35.8%) were observed in the BD group compared to the control. Significant albeit moderate correlation was found between TL and mtDNAcn in the BD group, suggesting that both markers are involved in accelerated cellular aging and may influence one another. Cluster analysis additionally revealed several subgroups with different rates of aging. Though a small BD subgroup showed the profile of “synchronous” cellular aging (corresponding to chronological age), most individuals with BD formed a particular subgroup with a characteristic pattern of accelerated cellular aging.
Spano et al. hypothesize that such aging patterns may be present at a young age and even precede the BD onset. To address this, more research is needed, which will include data on somatic comorbidities and other psychiatric conditions (such as anxiety disorders). In their further research, the authors also intend to include a larger range of biomarkers, including epigenetic age, inflammatory biomarkers, markers of metabolic imbalance, or oxidative stress. These biomarkers have already shown a significant connection with aging in other mental disorders, particularly major depressive disorder and schizophrenia.
Source nature.com
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Bipolar disorder (BD) is one of the major psychiatric disorders affecting at least 1% of the general population. The occurrence of BD has been associated with a 10-15 years decrease in life expectancy. One reason behind this is an increased prevalence of suicide, but multiple comorbid diseases also play a role, including cardiovascular and metabolic disorders. Another hypothesis is accelerated aging in individuals with BD.
To validate this hypothesis, several markers were studied, such as telomere length (TL) and the copy number of mitochondrial DNA (mtDNAcn). mtDNAcn is a measure of the number of mitochondrial DNA per cell, which is used to characterize mitochondrial function. Age-related decay of mitochondrial function leads to a decrease in mtDNAcn. In most available studies, TL is significantly reduced in individuals with BD compared to the healthy control. mtDNAcn is much less studied in BD, and the results remain inconsistent. Moreover, most aging markers in BD studies were performed in small samples (less than a hundred participants) and included patients with different mood states during inclusion (euthymic, depressed, and manic).
Spano et al. investigated TL and mtDNAcn in a homogenous cohort of 130 individuals with BD compared to healthy control. The sample included individuals of Caucasian origin, aged over 18 years, and euthymic (tranquil mental state without any major mood episodes) for at least three months. For all participants, data on age, sex, body mass index, smoking status, depression, and manic scale scores were obtained at inclusion. Blood samples were collected from each participant as well.
The authors employed various statistical methods to analyze the collected data, including regression and cluster analysis. Significantly lower TL and mtDNAcn (26.5% and 35.8%) were observed in the BD group compared to the control. Significant albeit moderate correlation was found between TL and mtDNAcn in the BD group, suggesting that both markers are involved in accelerated cellular aging and may influence one another. Cluster analysis additionally revealed several subgroups with different rates of aging. Though a small BD subgroup showed the profile of “synchronous” cellular aging (corresponding to chronological age), most individuals with BD formed a particular subgroup with a characteristic pattern of accelerated cellular aging.
Spano et al. hypothesize that such aging patterns may be present at a young age and even precede the BD onset. To address this, more research is needed, which will include data on somatic comorbidities and other psychiatric conditions (such as anxiety disorders). In their further research, the authors also intend to include a larger range of biomarkers, including epigenetic age, inflammatory biomarkers, markers of metabolic imbalance, or oxidative stress. These biomarkers have already shown a significant connection with aging in other mental disorders, particularly major depressive disorder and schizophrenia.
Source nature.com
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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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