is that obesity and overweight initially were largely considered as a preventable disease but has evolved into a global burden. Since the 1960s, worldwide obesity has nearly tripled and reached epidemic proportions. Recently published data show that there is a gradual increase in the global prevalence of overweight adults (Figure 2.6) and that overweight and obesity, and its associated comorbidities cause over four million deaths yearly, worldwide (Grundy 2016; G. B. D. Obesity Collaborators et al. 2017).
Figure 2.6 Graphical representations showing how ecology and urbanisation have impacted obesity and cardiometabolic syndrome with years (d) cardio‐metabolic disease (CMD) per 100 000 population (WHO) is congruent with the data for (a) global temperature abnormalities (NOAA 2013), (b) global prevalence of overweight adults (‘Our World in Data: Obesity’ 2017), and (c) percentage of global urban population (‘The World Bank’ 2013) through a span of almost last 50 years.
Obesity is fundamentally caused by an imbalance in dietary and nutritional intake (Hruby and Hu 2015). The disproportion of the calories consumed and calories expended, along with higher intake of energy‐dense foods which are high in fat and sugars poses a major burden to chronic diseases and health complications such as insulin resistance, type 2 diabetes, inflammation, cardiometabolic syndrome, coronary heart disease (CHD), CVD, liver disease, cancer, and neurodegeneration (Figure 2.7) (Saltiel and Olefsky 2017).
Figure 2.7 Individual suffering from obesity leads to insulin resistance, glucose intolerance, visceral adiposity, diabetes, hyperinsulinemia which are the major causes for cardiometabolic syndrome.
Source: Based on Saltiel and Olefsky (2017).
It is also known that a high BMI is a major risk factor for non‐communicable diseases such as CVD (mainly heart disease and stroke), which were the leading cause of death in 2012, diabetes, musculoskeletal disorders, especially osteoarthritis, and cancers including endometrial, breast, ovarian, prostate, liver, gallbladder, kidney, and colon. As the BMI increases, the risk of the cardiometabolic syndrome greatly increases. There is huge evidence of the sharp increase in the obesity‐associated cardiometabolic risks and morbidities. These findings have led to an increase in studies that link and relate the fundamental reasons and risk factors in obesity and their mode of action which lead to these diseases (Table 2.1).
Table 2.1 Obesity‐induced risk factors and associated comorbidities.
| Risk factors due to obesity | Mode of action | Associated morbidities | References |
|---|---|---|---|
| Chronic low‐level inflammation and oxidative stress | Causes DNA damage, affects growth‐promoting cytokines, and immune modulation | Chronic local inflammation which is a result of gastroesophageal reflux disease is a probable cause of oesophageal adenocarcinoma | Berger (2014); Fruh (2017); Gregor and Hotamisligil (2011); Bishayee (2014); Randi et al. (2006) |
| Gallbladder inflammation is a strong risk factor for gallbladder cancer | |||
| Chronic ulcerative colitis, hepatitis are risk factors for different types of liver cancer | |||
| Atherosclerosis formation, impaired fibrinolysis, increased risk for CVD, including stroke and venous thromboembolism | |||
| Increased blood levels of insulin and insulin‐like growth factor‐1 (IGF‐1) (hyperinsulinemia or insulin resistance) | Cause cells to divide more than usual which increases the chances of cancer cells being made | Promotes the development of colon, kidney, prostate, and endometrial cancers, type 2 diabetes | Roberts et al. (2010); Gallagher and LeRoith (2015); Dey and Senapati (2021b) |
| Adipokines, hormones produced by fat cells | Stimulate or inhibit cell growth, induce cell proliferation | Example: Leptin, an adipokine is linked to the pathophysiology of breast cancer, obesity‐induced hypertension, neurodegenerative diseases including Alzheimer's disease | Modzelewska et al. (2019); Ray (2018) |
| Fat cells may also have direct and indirect effects on other cell growth regulators | Dysregulation of rapamycin, mTOR pathway, and AMP‐activated protein kinase | Cancer, diabetes, cardiovascular disease, neurodevelopmental, and neurodegenerative disorders | Saxton and Sabatini (2017); Takei and Nawa (2014) |
2.5.6 The Impact of Urbanisation on Epidemiology of Obesity and Overweight in Relation to Cardiometabolic Syndrome
It is reported that excessive weight gain or obesity is not the result of a single cause, such as genetic tendency or the socioeconomic level of living as they do not justify the rapid increases in obesity in the nineteenth century. A number of other research suggested that urbanisation is one of the most important factors of an obesogenic environment as it entails an environment that promotes gaining weight and contributes to obesity (Swinburn et al. 1999) (Figure 2.6). There are various factors in the model of urbanisation which has led to the increased prevalence of overweight and obesity in the world over the last 50 years (Pinchoff et al. 2020). Several other factors include residential environment, cultural structure, social relationships, and extent of surrounding areas that changed during the phase of urbanisation and industrialisation. These are considered as some of the most important environmental factors impacting nutrition intake and physical activity which is a major cause of obesity. Industrialisation, a product of urbanisation in the UK and the United States of America (USA) from the start of the nineteenth century though made life easier but lead to a directly associated increase in the frequency of obesity in society (Congdon 2019).
After the association of the increasing trend of urban population and obese people in the developed countries, obesity epidemic spread in low‐ and middle‐income economies were also linked to the lifestyle changes and a decrease in physical activity due to the sedentary
