Life data

Snoring gets older faster! Studies have shown that after this treatment, it can be reversed

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Obstructive sleep apnea (OSA) can lead to the activation and transmission of oxidative stress and systemic inflammatory pathways, which is largely like mimicking the accelerated aging process.

Aging is a complex and time-dependent physiological process, accompanied by certain symptoms and death. In the process of aging, epigenetic changes continue to accelerate the accumulation, and show the characteristics of systematic or limited to specific tissue / cell types.

With the epigenetic clock becoming an important biological age prediction tool, scientists return the age of DNA methylation to the calendar age. Through the epigenetic clock, we can determine whether the acceleration of biological age occurs in some diseases or in the response to environmental factors.

Recently, studies by scientists from the United States and Spain have shown that the treatment of OSA with continuous positive airway pressure (CPAP) can slow down the aging process based on epigenetics.

The researchers conducted the study on a group of people who participated in the epiosa project (nct02131610). The age range of participants in this group was 28-58 years old. All individuals were non-smokers and underwent overnight laboratory polysomnography (PSG) assessment. The study selected patients who had been diagnosed with OSA at baseline by PSG evaluation and had insisted on CPAP treatment for 12 months (n = 16). The standard of fully adhering to the use of CPAP is > 4 hours per night. The non snoring control group members matched and included in the study had normal nocturnal polysomnography (PSG) (apnea hypopnea index (AHI) < 5 events / hour sleep) and were reassessed after 12 months (n = 8).

The study evaluated each participant at the initial visit (V1) and the second visit (V2) after 1 year. During this period, fasting blood samples after overnight PSG were collected, peripheral blood monocytes (PBMC) samples were isolated and stored at – 80 ℃ until use. C-reactive protein (CRP), total cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL)) and DNA methylation were analyzed in the laboratory.

In addition, the OSA group and the control group selected by the researchers were matched in race, age and gender, blood pressure was similar, body mass index (BMI) was slightly different, and the levels of AHI and high-sensitivity CRP in OSA subjects were significantly higher (Figure 1).

Figure 1 Demographic characteristics of OSA group and control group. *: T-test showed that the significant difference (P < 0.05) was in bold. #: Inclusion in the female control group did not change the results. BMI: body mass index; SBP: systolic blood pressure; DBP: diastolic blood pressure; AHI: apnea hypopnea index; HDL: high density lipoprotein. LDL: low density lipoprotein; IMT: intima-media thickness; CRP: C-reactive protein.

All OSA patients received CPAP treatment and showed good compliance (mean CPAP use: 6.03 ± 0.81 hours per night). There was no significant difference in blood cell composition inferred from DNA methylation map between OSA group and control group at V1 and V2, and there was no significant difference in V1 and V2 between OSA group and control group (P > 0.05; t-test). The epigenetic clock was determined by the DNA methylation map of PBMC in OSA group and control group. The scientists first assessed the epigenetic age changes of each participant in V1 and V2 (Figure 2).

Figure 2 The epigenetic age estimated by dnamage model was related to the biological age of OSA group and control group samples at V1 and V2.

Then the data were analyzed by principal component analysis (PCA). The results showed that (Fig. 3), OSA patients were clustered separately from the control group. Conversely, the post CPAP (V2) samples of OSA patients migrated and converged to the control group, while the control group did not change over time. The variable diagram (Figure 4) shows that the age accelerated residual (accresv2. V1) between two visits V1 and V2 is a variable that drags the sample distribution to the control sample. The increase of cardiovascular disease-related parameters (such as intima-media thickness, plaque, systolic blood pressure (SDP) and diastolic blood pressure (DBP)) and OSA related risk factors (i.e. AHI and BMI) makes the sample distribution migrate to the location of OSA samples.

Figure 3 Principal component analysis (PCA) plots used all output epigenetic clock variables and coexisting diseases to distinguish patients in OSA group and control group (red and blue shapes, respectively).

Figure 4 The graph shows the direction and contribution of each variable mentioned in Figure 3 in PCA analysis. Positive and negative variables point to the same or opposite side of the graph, respectively. The contribution to sample discrimination is color coded, showing a gradient from red (large contribution) to yellow and then to light blue (small contribution).

AccResV2. V1 is the variable with the highest discrimination between OSA group and control group among all output epigenetic clock variables (Fig. 5). It is worth noting that similar PCA results were obtained by applying different epigenetic clock estimates (data not shown).

Figure 5 Use accresv2 only PCA diagram of V1 as the output of epigenetic clock. It is the same as the OSA group and control group samples used in Figure 3.

Although the epigenetic age of the control group remained accelerated during the year between V1 and V2 (mean accresv2.v1 1.41 ± 1.96) (Fig. 6), patients in the OSA group showed a significantly reduced epigenetic acceleration index between visits (mean accresv2.v1 -1.03 ± 0.48; OSA and control: P = 5.5) × 10-4; F inspection). In addition, the average accresv2 in the control group and OSA group The percentage change in V1 was 62% and 5%, respectively (Figure 7). Therefore, the epigenetic age slowing changes observed in patients in the OSA group may be attributed to CPAP treatment. In addition, the V2 sample data of OSA patients with lower CRP levels (0.02-0.28 mg · DL-1) were more closely clustered with the control group than those with higher CRP levels (0.4-0.94 mg · DL-1) (Fig. 8). This suggests that the reduction of epigenetic aging observed in OSA patients treated with CPAP is weakened in patients with increased inflammation.

Figure 6 Mean value of age accelerated residuals between V1 and V2 in OSA group and control group (accresv2. V1). The difference between groups was statistically significant (P = 5.5) × 10-4; F-inspection). The error bar corresponds to the standard error of the average.

Figure 7 Percentage change in mean age accelerated residuals (accresv2. V1) between V1 and V2 in OSA and control groups.

Figure 8 Use accresv2 only PCA plot of V1 as an epigenetic clock output variable in OSA patients with high and low CRP levels. The V2 sample was closer to the control group in patients with low CRP OSA (right panel) than in patients with high CRP OSA (left panel), indicating that the rate of epigenetic age reduction decreased in patients with high inflammation.

In conclusion, OSA patients showed higher systemic epigenetic age acceleration than the control group. However, after 12 months of treatment with CPAP, which can normalize breathing and sleep patterns, the changes of epigenetic age in these patients with OAS slowed down, but the acceleration trend of epigenetic age in the control group did not change.

The results of this study show that the disturbance caused by OSA promotes the acceleration of biological age, but these processes are at least partially reversible when effective treatment of OSA is implemented. Although the cellular and molecular mechanisms behind accelerated biological aging are still unclear, this study provides a new framework for the management of OSA and its related incidence rate in adults. Assessing the accelerated changes in patients’ epigenetic age may provide new opportunities for molecular diagnosis and personalized clinical management.


[1] Cortese R, Sanz-Rubio D, Kheirandish-Gozal L, et al. Epigenetic age acceleration in obstructive sleep apnoea is reversible with adherent treatment. Eur Respir J 2022; 59: 2103042 [DOI: 10.1183/13993003.03042-2021].

From: biological Valley

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