Pathogenesis of (smoking-related) non-communicable diseases—Evidence for a common underlying pathophysiological pattern

Abstract

Non-communicable diseases, like diabetes, cardiovascular diseases, cancer, stroke, chronic obstructive pulmonary disease, osteoporosis, arthritis, Alzheimer’s disease and other more are a leading cause of death in almost all countries. Lifestyle factors, especially poor diet and tobacco consumption, are considered to be the most important influencing factors in the development of these diseases. The Western diet has been shown to cause a significant distortion of normal physiology, characterized by dysregulation of the sympathetic nervous system, renin-angiotensin aldosterone system, and immune system, as well as disruption of physiological insulin and oxidant/antioxidant homeostasis, all of which play critical roles in the development of these diseases. This paper addresses the question of whether the development of smoking-related non-communicable diseases follows the same pathophysiological pattern. The evidence presented shows that exposure to cigarette smoke and/or nicotine causes the same complex dysregulation of physiology as described above, it further shows that the factors involved are strongly interrelated, and that all of these factors play a key role in the development of a broad spectrum of smoking-related diseases. Since not all smokers develop one or more of these diseases, it is proposed that this disruption of normal physiological balance represents a kind of pathogenetic “basic toolkit” for the potential development of a range of non-communicable diseases, and that the decision of whether and what disease will develop in an individual is determined by other, individual factors (“determinants”), such as the genome, epigenome, exposome, microbiome, and others. The common pathophysiological pattern underlying these diseases may provide an explanation for the often poorly understood links between non-communicable diseases and disease comorbidities. The proposed pathophysiological process offers new insights into the development of non-communicable diseases and may influence the direction of future research in both prevention and therapy.

Relationships between Serum Biomarkers of Oxidative Stress and Tobacco Smoke Exposure in Patients with Mental Disorders

“…It is acknowledged that lifetime smoking rates are higher in patients who are diagnosed with major depression disorder (59%), bipolar disorder (83%), or schizophrenia and other mental disorders (90%), compared to 32% among adults with no mental illness [ 25 ]. Studies have indicated that exposure to cigarette smoke and/or nicotine, through active and passive smoking, causes a complex dysregulation of the sympathetic nervous system and immune system, as well as disruption of physiological oxidant/antioxidant homeostasis, all of which play a key role in the aggravation of a broad spectrum of diseases, including mental disorders [ 12 , 13 , 16 , 26 ].…”

“…New data highlight the negative consequences of smoking or nicotine addiction specifically in subjects with mental disorders, beyond the inflammation and oxidative stress which could be a common characteristic for all smokers [ 14 , 15 ]. This relationship is very complex, as smokers can also develop a broad spectrum of non-communicable diseases [ 16 ]. Although this risk is influenced by other individual determinants such as the genome, epigenome, exposome, microbiome, and others, smokers with serious mental illness have an increased risk of dying from cancer, lung disease, and cardiovascular disease, and account for more than 200,000 out of the 520,000 tobacco-related deaths each year [ 16 , 17 , 18 ].…”

“…This relationship is very complex, as smokers can also develop a broad spectrum of non-communicable diseases [ 16 ]. Although this risk is influenced by other individual determinants such as the genome, epigenome, exposome, microbiome, and others, smokers with serious mental illness have an increased risk of dying from cancer, lung disease, and cardiovascular disease, and account for more than 200,000 out of the 520,000 tobacco-related deaths each year [ 16 , 17 , 18 ]. Individuals with serious mental diseases die about 15 years earlier than individuals without serious mental diseases who never smoke [ 19 ].…”

Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation

“…Tobacco smoking is one of the major preventable causes of premature deaths globally and is a potentially acquired risk factor for cardiovascular diseases (CVDs), chronic obstructive pulmonary disease, and cancer [ 1 – 3 ]. The scientific literature suggests tobacco smoking to be a causative agent for CVDs and cancers [ 2 ]. According to the World Health Organization, tobacco kills more than 8 million people each year worldwide, including around 1.3 million people who do not smoke but are exposed to second-hand smoke.…”

A systematic review of preclinical studies evaluating the association between nicotine and the initiation and progression of cancer

“…Indeed, it is unclear what role nicotine plays, if any, in the carcinogenicity of tobacco smoke. Although some in vitro studies have shown that nicotine may lead to cellular changes associated with cancer initiation and progression ( 20 - 25 ), it is unclear whether these cellular changes are associated with cancer development in vivo in animals, or in humans.…”