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.

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