Why does lactose intolerance occur?
Lactase production by the bowel cells begins in the eighth week of foetal development and reaches its apex at birth, as part of Nature’s plan to prepare the infant for its first diet. The majority of mammals, including humans, lose the capacity to produce lactase within a few months of birth. The incidence of lactose intolerance varies with age, location, ethnicity, and race, and can be either congenital or acquired.
According to the underlying causes, the heading is broken down into three subtypes:
Lactose intolerance, primary:
This explains why lactase production typically decreases from childhood to maturity in the majority of Asian and African communities. Rarely do symptoms appear before the age of six. Different racial and mammalian communities and species exhibit distinct age gradients. Lactase deficiency is observed in 2% of the population of Northern Europe. The graph rises considerably to an estimated 50-80% for Hispanic individuals. Nearly 80 to 100 percent of African and Asian adults develop primary lactose intolerance. The study of ancient DNA suggests that our ancestors also experienced lactase hypo production following withdrawal. This indicates that it is inherent and inherent throughout generations. However, the population of northern Europe deviates from this pattern by continuing to produce lactase into maturity. There is a paradoxical relationship between the concepts of evolution and natural selection that is baffling. The geographical variation is attributed to the beginning of dairy production in that region 10,000 years ago. Those whose diet consisted primarily of milk evolved a trait that causes them to produce lactase continuously throughout their lives. People with a generational history of a diet devoid of substantial milk proportions, on the other hand, did not need the evolutionary change to produce lactase significantly and can therefore get by with primary levels of lactase production. They develop lactose intolerance if they consume an excessive amount of lactose because their bodies are not equipped to handle it. Their DNA contains a specific genetic polymorphism that is responsible for this trait. At the molecular level, we lack more information, but it appears that both environmental and genetic factors are at play here. Based on the presented evidence, it is possible to hypothesise that adult mammals are not designed to consume milk. According to this research, lactase persistence is a mutation, not hypolactasia, as suggested by the subsequent theory.
The second theory contends that mammals naturally produce lactase and that the decades-long commercialization of milk and dairy products has resulted in engineered forms that lack or contain non-natural components. Our bodies have adapted to these aberrant forms by mutating the lactase gene so that it is no longer expressed once we reach adulthood. This theory is not well supported by ancient DNA research and comparative analysis of other mammals. It is quite a paradoxical approach to view this age-old issue.
