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Updated: Jul 5, 2025

Author Spotlight: Insights into Cardiometabolic Diseases with Subcutaneous Adipose Tissue Microvasculature Studies
Published on: April 5, 2024
Cardiometabolic disease in Black African and Caribbean populations: an ethnic divergence in pathophysiology?
Reuben M Reed1, Martin B Whyte2, Louise M Goff3
1Department of Nutritional Sciences, Faculty of Life Sciences & Medicine, King's College London, London SE1 9NH, UK.
Insights
Black African and Caribbean (BAC) populations face higher cardiometabolic disease risks than White Europeans (WE). This review explores ethnic differences in obesity, inflammation, and complement system activation contributing to these disparities.
Area of Science:
- Cardiology
- Genetics
- Immunology
Background:
- Black African and Caribbean (BAC) populations exhibit higher cardiometabolic disease (CMD) rates than White Europeans (WE).
- Obesity-induced visceral adipose tissue (VAT) and intrahepatic lipid (IHL) accumulation are linked to insulin resistance and inflammation, key CMD drivers.
- Current CMD theories inadequately explain the higher prevalence in BAC populations, who paradoxically show lower VAT/IHL and a more anti-inflammatory profile.
Purpose of the Study:
- To review current understanding of obesity's role in CMD.
- To highlight emerging evidence of ethnic divergence in CMD pathophysiology between BAC and WE populations.
- To investigate the potential role of complement system dysregulation in CMD disparities.
Main Methods:
- Literature review of existing studies on obesity, cardiometabolic disease, inflammation, and complement activation.
- Comparative analysis of pathophysiological mechanisms in Black African and Caribbean (BAC) versus White European (WE) populations.
- Exploration of ethnic differences in adipose tissue metabolism, inflammatory markers (TNF-α, IL-10), and complement system activity.
Main Results:
- BAC populations paradoxically present with lower VAT and intrahepatic lipid (IHL) despite higher CMD rates.
- BAC individuals may exhibit a more anti-inflammatory profile with lower TNF-α and higher IL-10.
- Recent findings indicate greater complement activation in BAC individuals compared to WE, suggesting its dysregulation is crucial.
Conclusions:
- Existing models of obesity-driven CMD do not fully account for ethnic differences observed in BAC populations.
- Complement system dysregulation emerges as a potential key factor driving higher CMD rates in BAC individuals.
- Further research into ethnic-specific pathophysiological mechanisms is essential for targeted CMD prevention and treatment.
Abstract:
In the UK, populations of Black African and Caribbean (BAC) ethnicity suffer higher rates of cardiometabolic disease than White Europeans (WE). Obesity, leading to increased visceral adipose tissue (VAT) and intrahepatic lipid (IHL), has long been associated with cardiometabolic risk, driving insulin resistance and defective fatty acid/lipoprotein metabolism. These defects are compounded by a state of chronic low-grade inflammation, driven by dysfunctional adipose tissue. Emerging evidence has highlighted associations between central complement system components and adipose tissue, fatty acid metabolism and inflammation; it may therefore sit at the intersection of various cardiometabolic disease risk factors. However, increasing evidence suggests an ethnic divergence in pathophysiology, whereby current theories fail to explain the high rates of cardiometabolic disease in BAC populations. Lower fasting and postprandial TAG has been reported in BAC, alongside lower VAT and IHL deposition, which are paradoxical to the high rates of cardiometabolic disease exhibited by this ethnic group. Furthermore, BAC have been shown to exhibit a more anti-inflammatory profile, with lower TNF-α and greater IL-10. In contrast, recent evidence has revealed greater complement activation in BAC compared to WE, suggesting its dysregulation may play a greater role in the high rates of cardiometabolic disease experienced by this population. This review outlines the current theories of how obesity is proposed to drive cardiometabolic disease, before discussing evidence for ethnic differences in disease pathophysiology between BAC and WE populations.
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