Ravi Misra |
The incidence and prevalence of IBD varies throughout the world, with the highest incidence seen in industrialised regions of North America and Europe [1]. Within Europe an East–West gradient has been demonstrated, with Western centres showing almost twice the incidence observed in Eastern centres [2].
The general trend in migration is from lower and middle income countries to higher income countries in Western Europe and North America.
The estimated number of international migrants has increased over the past five decades. The total number of people living in a country other than that of their birth was estimated to be 281 million in 2020, which was 128 million more than in 1990 and over three times the estimated number in 1970 [3].
When populations move from an area with a low IBD incidence to one with a high IBD incidence, they adopt the incidence of the host country and their offspring have a similarly high incidence compared to non-immigrants [4–6]. Also, a fascinating study by Hammer et al. showed the reverse effect: The Faroe Islands has the highest reported IBD incidence in the world; however, among immigrants from the Faroe Islands to Denmark, the excess Ulcerative Colitis (UC) risk was found to normalise over one generation in men and over two generations in women [7].
These observations have clear implications for disease pathogenesis, highlighting the impact of environmental change as a key driver of disease expression in populations with a genetic predisposition. Diet, early-life microbiota exposure, changing hygiene status, pollution and socioeconomic status are all associated with changes in microbiota which may potentiate the risk of developing IBD [8].
The impact of urbanisation has been demonstrated in the city of Guangzhou, China. Over a 30-year period the incidence of IBD has increased 20-fold, mirroring a rapid rise in urbanisation and a population explosion from 2.5 million people to 15 million [9].
Identifying which environmental factors are most important is difficult and a precise mechanism of action remains to be elucidated.
Not only have changes in disease incidence and prevalence been demonstrated, but a clear difference in disease phenotype has been identified between populations of different ethnicities. For example, a study of 33,157 UC patients participating in the UK biobank showed pancolitis to be significantly more prevalent among South Asians than among Caucasians [10].
If the epidemiology and phenotype differ, how does this correspond to treatment response? More studies are needed to examine different treatment responses in different ethnic groups. Trials should reflect different ethnicities and be more generalisable to different populations in order to reflect the global world in which we live.