A neurobiological link between transportation noise exposure and metabolic disease in humans

Osborne, Michael T.; Naddaf, Nicki; Abohashem, Shady; Radfar, Azar; Ghoneem, Ahmed; Dar, Tawseef; Wang, Ying; Patrich, Tomas; Oberfeld, Blake; Tung, Brian; Pitman, Roger K.; Mehta, Nehal N.; Shin, Lisa M.; Lo, Janet; Rajagopalan, Sanjay; Grinspoon, Steven; Fayad, Zahi A.; Tawakol, Ahmed

doi:10.1016/j.psyneuen.2021.105331

Cited by 13 publications

(8 citation statements)

References 38 publications

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“…Clinical studies confirmed that long-term exposure to air pollution links to the increased risk of both CVD and T2D [29][30][31][32][33]. [29][30][31][32][33] And increased transportation noise and e-noise exposures are associated with a greater risk of T2D [34][35][36]. Early growth status (short length and / or thinness at birth and during infancy) also links to T2D [37].…”

Section: Eth Ics Statementmentioning

confidence: 85%

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A novel comprehensive program combining optimal medical treatment with lifestyle for type 2 diabetes

Tkebuchava²,

Wu³

2023

Preprint

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This article introduces briefly current status in type 2 diabetes (T2D) and an updated classical standardized comprehensive program which combines optimal medical treatment (OMT) with lifestyle modification, that is, intervention of RT-ABCDEFG (iRT-ABCDEFG) for control and prevention of T2D, and discusses its advantages and prospects. Here, G means goals, F follow-up, E examination, D disease & risk factors control, C changing unhealthy lifestyle & Chinese medicine or control the source of infection & cutting genetic or spreading pathways, B biohazard control, and A antagonistic treatment, such as anti-diabetic agents, the glucagon-like peptide-1 receptor (GLPR) agonists, the sodium-glucose cotransporter 2 (SGLT2) inhibitors, and the ultralong-acting, once-daily basal insulin. As an effective comprehensive program and strategy for Interventions of diabetes, this program can be used as a Reverse, Right, and Routine Treatment (iRT). Several pivotal goals which include less major adverse cardiocerebrovascular events (MACCE) and diabetic complications, less medical costs, longer life expectancy, lower morbidity and mortality, and higher quality of life, will be realized by consistently practicing this program due to early diagnosis, OMT, and lifestyle modification for overall prevention. Herein, this iRT-ABCDEFG program is worthy of recommending for clinical professional management and health care of T2D due to better cost-effectiveness.

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Section: Eth Ics Statementmentioning

confidence: 85%

“…intensive body weight management [2]. Moreover, healthy lifestyle included five core elements -"environment-sleep-emotion-exercise-diet" intervention [E(e)SEEDi] [27,28] may achieve better goals in control and prevention of T2D (Table 2) [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43].…”

mentioning

confidence: 99%

A novel comprehensive program combining optimal medical treatment with lifestyle for type 2 diabetes

Tkebuchava²,

Wu³

2023

Preprint

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“…DHE staining images were reused from (Kroller-Schon et al, 2018) with permission. Hahad et al, 2021a;Osborne et al, 2021). Noisemediated inflammation in mice was also prevented by genetic Nox2 deletion as shown by two independent preclinical studies (Kroller-Schon et al, 2018;Eckrich et al, 2021) and antioxidant pharmacological activation/induction of the Nrf2-HO1-axis (Bayo Jimenez et al, 2021).…”

Section: Noise Causes Activation Of the Phagocytic Nadph Oxidase With Subsequent Redox Activation Of Inflammatory Cellsmentioning

confidence: 87%

“…Evidence that stress responses are a key component in the appearance and exacerbation of cardiovascular risk factors has been both explicitly and tangentially explored. Enhanced glutaminergic signaling in the amygdala of rats ( Singewald et al, 2000 ) and amygdalar activation in humans ( Osborne et al, 2020 ; Hahad et al, 2021a ; Osborne et al, 2021 ) demonstrates a stress-induced arousal in response to noise. Activation of the HPA axis is evident in the increased plasma corticosterone of noise-exposed rats and increases in plasma cortisol in noise-exposed mice aligns with readouts of sympathetic activation, adrenaline and noradrenaline, increased in plasma and kidney of noise-exposed mice ( Munzel et al, 2017 ) and rats ( Gannouni et al, 2013 ).…”

Section: Animal Research On Noise-induced Cardiovascular and Neuronal Dysregulationmentioning

confidence: 99%

“…It may be also speculated that noise-induced ROS formation promotes an inflammatory phenotype in the heart, vessels and the brain as central mediators of inflammatory reactions such as the NLR family pyrin domain containing 3 (NLRP3) inflammasome and high-mobility group box 1 protein (HMGB1) are activated under oxidative stress conditions via redox switches as well as redox-sensitive transcription factors such as nuclear factor kappa B (NFκB) ( Wenzel et al, 2017 ; Steven et al, 2019 ). This is probably the reason, aside from stress hormone-dependent activation and infiltration of immune cells into the vasculature, for the observed noise-triggered inflammation in exposed mice ( Munzel et al, 2017 ; Kroller-Schon et al, 2018 ; Steven et al, 2020 ; Eckrich et al, 2021 ; Frenis et al, 2021 ) but also the shift to a pro-atherothrombotic phenotype of the plasma proteome of train noise-exposed healthy human subjects ( Herzog et al, 2019 ), epigenetic changes that promote immune cell activation and expression of CRP ( Cai et al, 2017 ; Eze et al, 2020 ) and amygdala activation driven coronary atherosclerosis ( Osborne et al, 2020 ; Hahad et al, 2021a ; Osborne et al, 2021 ). Noise-mediated inflammation in mice was also prevented by genetic Nox2 deletion as shown by two independent preclinical studies ( Kroller-Schon et al, 2018 ; Eckrich et al, 2021 ) and antioxidant pharmacological activation/induction of the Nrf2-HO1-axis ( Bayo Jimenez et al, 2021 ).…”

Section: Redox Switches Activated By Noise Exposurementioning

confidence: 99%

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Redox Switches in Noise-Induced Cardiovascular and Neuronal Dysregulation

Frenis

Kuntic

Hahad

et al. 2021

Front. Mol. Biosci.

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Environmental exposures represent a significant health hazard, which cumulatively may be responsible for up to 2/3 of all chronic non-communicable disease and associated mortality (Global Burden of Disease Study and The Lancet Commission on Pollution and Health), which has given rise to a new concept of the exposome: the sum of environmental factors in every individual’s experience. Noise is part of the exposome and is increasingly being investigated as a health risk factor impacting neurological, cardiometabolic, endocrine, and immune health. Beyond the well-characterized effects of high-intensity noise on cochlear damage, noise is relatively well-studied in the cardiovascular field, where evidence is emerging from both human and translational experiments that noise from traffic-related sources could represent a risk factor for hypertension, ischemic heart disease, diabetes, and atherosclerosis. In the present review, we comprehensively discuss the current state of knowledge in the field of noise research. We give a brief survey of the literature documenting experiments in noise exposure in both humans and animals with a focus on cardiovascular disease. We also discuss the mechanisms that have been uncovered in recent years that describe how exposure to noise affects physiological homeostasis, leading to aberrant redox signaling resulting in metabolic and immune consequences, both of which have considerable impact on cardiovascular health. Additionally, we discuss the molecular pathways of redox involvement in the stress responses to noise and how they manifest in disruptions of the circadian rhythm, inflammatory signaling, gut microbiome composition, epigenetic landscape and vessel function.

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