gallbladder, liver, ovaries (epithelial), and advanced prostate cancer, as well as leukaemia (Esposito et al. 2012). The complex relation between all three can be mediated by several factors including diet, physical activity and hormonal signalling (insulin‐like growth factor signalling), oxidative stress (Dara Hope and Derek 2012). Pro‐inflammatory cytokines predominantly secreted by immune cells and also other cell types like endothelial and adipocytes affect all tissues and organ systems including the vasculature system (Dinarello and Pomerantz 2001). The aetiology of cardiometabolic syndrome involves accumulation of visceral fat. This promotes the synthesis and release of pro‐inflammatory cytokines leading to enhanced oxidative stress. Infiltration of immune cells particularly inflammatory macrophages in the adipose tissues further enhance the cytokine burden causing chronic inflammation (DeMarco et al. 2010). Pro‐inflammatory cytokines produced within adipose tissues are also found to be elevated in the serum of obese people. Inflammatory cytokines such as IL‐6, TNF‐α, leptin have been extensively associated with obesity, CVD (upto 20%), and cancer (Grivennikov and Karin 2011; Bielecka‐Dabrowa et al. 2007). Therefore, IL‐6 and TNF‐α and other potential pro‐inflammatory cytokines are probably the factors linking cardiometabolic syndrome, obesity, and cancer together, and pose as potential targets for the treatment of these associated pathologies (Figure 2.8). Therefore, it has been established that a major cause of cancer is metabolic imbalance conditions including hypercholesterolemia, diabetes, hypertension, specific drug use. Effective interventions to reduce their prevalence could potentially reduce cancer risk
2.6 Conclusion
The book chapter covered the evidence that changes in the urban lifestyle is one of the major causes leading to obesity and associated chronic diseases including cardiometabolic syndrome, metabolic dysregulations, and also cancer. It is important to formulate strategies on public health based on bearable lifestyle changes and sustainable urbanisation to curb obesity in the population and risk of cardiometabolic syndrome and associated cancer. Lifestyle interventions, weight management, and low‐calorie food intake are crucial to mitigate increasing global burden of obesity, cardiovascular, and metabolic risk factors. Along with this improvement of medical and research facilities to develop anti‐hypertensive and cardio‐protective compounds is a crucial step towards treatment (Kundu et al. 2021a, 2021b). Individual sensitisation and choices are crucial in the case of nutritional intake and the promotion of healthy lifestyle. Government, private, technical, financial, and institutional capacities have to work together for the implementation of adequate land‐use planning, well‐governed cities, and more sustainable infrastructure and environment with open and recreational spaces to mitigate impacts of climate change and unhealthy lifestyles on health. The World Health Organisation has provided a global strategy and action plan to strengthen initiatives for the prevention and control of noncommunicable diseases. Similarly, to curb these life‐threatening disorders individual alertness and population‐based collective approach is the need of the hour.
Paths for bicycling, walking, etc. are also essential. Instead of junk foods, balanced diets can be promoted for regular intake by the children and individuals with genetic backgrounds of developing metabolic syndromes. More research should be commenced urgently to decipher the underlying molecular mechanisms connecting metabolic syndrome with other environmental and societal factors to generate sustainable strategies to develop a better world for the future.
Acknowledgements
All authors of the book chapter would like to acknowledge the Dr. B.R. Ambedkar Center for Biomedical Research (ACBR), University of Delhi, India for various help to complete the current work. Sanjay Kumar Dey acknowledges the University of Delhi, Institute of Eminence grant (IoE/2021/12/FRP).
Authors also acknowledge the use of the academic user license of BioRender (https://biorender.com) for preparing few of the figures shown in the current book chapter.
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