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2.1 An overview of the various factors that are responsible for urbanisation and climate change finally leading to cardiometabolic syndrome.
2.2 Overview of Cardiometabolic Syndromes
Cardiometabolic syndrome is a cluster of insulin resistance and restricted high cholesterol responsiveness, elevated fasting, and epilepsy, which are all factors that influence glucose metabolism characterised by metabolic dysfunction. Often a list of cardiometabolic syndrome threats for individuals arises with glucose sensitivity. Individuals having cardiometabolic syndrome are substantially more likely to suffer from metabolic syndrome and twice as likely to have a sudden cardiac arrest (World Heart Federation 2015). The manufacturing and livestock revolutions in history produced more cholesterol‐rich crops and carbs for intake than humanity needs (Miles et al. 2019). The addition of processed carbs, an abundance of saturated fats, and the shift from predator to civilised people have all led to the growth of obesity. According to the Global Burden of Disease report, India's adult cardiometabolic syndrome disease burden of 272 per 100 000 population was higher than the global average (Prabhakaran et al. 2016).
2.3 Pathophysiology of Cardiometabolic Syndromes
A multitude of pathophysiological cardiometabolic variables have been correlated with the severity of cardiovascular events. The variance of fat cells is a critical aspect of cardiometabolic risk. The cardiac syndrome's most prominent interpretation is abdominal obesity. Adipose tissue is also an endocrine organ that expels adipokines which make a contribution to the atherogenic/diabetic physiological risk level attributed to hyperlipidaemia. A mismatch between energy consumption and expenditure contributes to abdominal fat. The pathogenicity of hyperglycaemia and hyperlipidaemia correlated with the cardiometabolic syndrome is probably triggered by variations in free fatty acid metabolism. It is a metabolically active tissue that metabolises a number of up‐regulation and thrombogenic immune cells. Elevated plasma unsaturated fatty acid accumulation and inordinate release of lipids from adipocytes can hinder the ability of insulin to stimulate muscle glucose metabolism and suppress hepatic glucose production (Figure 2.2) (Kirk and Klein 2009). In juveniles, insulin tolerance tends to be related to a decline in the mitochondrial to nuclear DNA ratio. Elevated secretion of lipids from adipocytes is attributed to insulin sensitivity leading to a decline in glucose transmission through the muscles (Gill et al. 2005). Hyperinsulinemia has been reported as a significant prognostic factor in broad prospective epidemiologic trials. In conclusion, there is considerable proof that the most prevalent forms of the metabolic syndrome are correlated to abdominal obesity, especially when it is followed by abdominal adipocytes accumulation.
Figure 2.2 Dysregulation of sugar metabolism leads to cardiometabolic syndrome.
Source: Based on Kirk and Klein (2009).
2.4 Urbanisation as a Factor to Increase Cardiometabolic and Cardiovascular Disorders
2.4.1 The Driving Development of Urbanisation and Its Implications on Cardiovascular Syndrome in the Twenty‐First Century
The birth of the metropolis has been a recent development in the latest generations. Backwoods regions have previously been urbanised; along with that many people have migrated to urban areas. In recent studies, it has been observed that the various risks of cardiometabolic and CVD begin in premature conditions of pregnant mothers, or at the time of birth. The risk increases more due to many factors like lack of physical activity, unhealthy diet, consumption of alcohol and tobacco, smoking, etc. Many of these exposures have increased due to the negative impacts of urbanisation. Although urbanisation has brought major improvements in the economy and many lifestyle opportunities like working variations, diversity to education, fast internet, and social world development and political mobilisation, but this poses a great obstruction towards maintaining a healthy lifestyle and behaviour (Figure 2.3). Taking into consideration man‐made landscapes, often in certain cases, industrialisation has occurred way too fast, leading to many defects in the construction of living places. As a result, a person has started to live in insubstantial conditions starting from cardboard boxes to pavements, under bridges, near streets, slums, sidewalks tents, etc. Individuals living in such conditions have low nutritious diets and less opportunities for medication and other daily exercises. People living in extremely well‐maintained houses are forced to sedentary behaviour due to lack of physical activity, less active in playing outside environment, not only that but much more addiction towards drinking and smoking. As a result, people residing in crowded places have a high risk to develop rheumatic heart disease (RHD), which causes damage to the heart muscle and heart valves. On the other hand, it has been said that children may suffer obesity due to maternal obesity during pregnancy; however, there is less proof to this statement (Castro et al. 2003). Individuals of low middle economic status are more open to street and cheap foods since they are easily available like open vendors as they have limited budget and less choice. Moreover, it has been noticed that people living in well‐maintained conditions are also at threat of developing cardiometabolic syndrome often seen due to much addiction in the social world (Münzel et al. 2017a). In addition to that smoking rate, consumption of drugs, alcohol among youth has increased rapidly which is ultimately leading them to stress, depression, anxiety, obesity, and early‐stage diabetes.
Figure 2.3 Complex urban planning and its impact on cardiometabolic syndrome.
2.4.2 Mutualistic Relationship Between Urbanisation and Ecosystem
Industrialisation has been one of the most prominent causes of population changes in recent years, which is propelled by a multitude of societal, financial, and ecological mechanisms. Through the development of towns, communities, and infrastructure upgrades, urbanisation altered natural and previous rural habitats (Miller and Hutchins 2017). Smart employee population levels, expanded rough areas (e.g. roads and buildings), enhanced toxicity (e.g. air quality, light, soil), and high temperature are all characteristics of the novel, human urban setting. The urban sprawl resonance is a form in which cities are hotter than non‐urban areas due to the increased impermeable surfaces (e.g. gravel and mortar) and significantly lower tree cover. The trend and intensity of the interaction between urbanisation and ecological consequences can differ and evolve with present, based on the geographic, societal, and financial factors as well as progress trajectories, according to emerging evidence (Bai et al. 2017). Poor air quality is a dynamic combination of airborne pollutants emitted by a wide range of sources, including factories, residential gasification heating systems, automobiles, and industrialisation. Domestic air emissions and urban chemical fumes are the third and ninth leading causes of death and disease, respectively. The latter two are contributing for 6.6 million deaths and 7.6% of global, with pollutants accounting for 3.5% of global disease burden (Münzel et al. 2017a).
CVD is also known to be the leading cause of mortality (Dey et al. 2020). Air contamination containing fine particulate matter with a diameter of less than 2.5 μm (PM2.5) is the world's leading cause of death rates. Rigorous disposal of pollutants from urban centres, combined with an increase in impermeable surfaces as a result of urbanisation, will lead to a steady decline in the health of urban aquatic habitats, defined as the urban stream syndrome (Bai et al. 2017). Pollution from faecal matter and microbial pathogens, as well as antimicrobial agents, is common in urban environments, particularly urban aquatic environments. Toxins from marine ecosystems can be exported to lands through