While the phenotype of social aging in humans is unique, evidence suggests similarities with chimpanzees. This article focuses on the APOE/TOMM40 gene. While the lifespan of human beings is not fully understood, we can speculate about its role. However, genetics is not the only factor determining lifespan. Various lifestyle factors also affect the human lifespan. We can also investigate whether a specific gene causes aging.
Despite the long life span of human beings, some close relatives live for just half that. The research team from the Institute of Evolutionary Biology in Spain has now identified a new set of genes that may explain the difference between human life expectancy and that of other primates. Nowadays, there are people who are also curious to know about lifespan of idiots as well. Their findings are published in the journal Molecular Biology and Evolution. And the study is featured on the front cover of the journal! But why is this so?
Previous studies have shown that common genetic variation contributes to longevity. The researchers used a case/control method to find out which polymorphisms are responsible for long life in different populations. In the former, they found that sibship reconstruction was significantly associated with long life expectancy compared with a younger population. However, when considering the age-old population, they found that the influence of genetics increased with age.
Life span is one of the major factors influencing a species’ survival, and this is especially true in humans. While aging and harshness are both factors influencing a species’ longevity, the length of a life span is also affected by the environment. Extreme conditions, such as severe climates, increase the likelihood of dying from predation or starvation, while predictable conditions are favorable for longevity. This theory provides insight into the evolution of the human life span.
The hypothesis of variability selection posits that life-history traits are strongly influenced by the environment. It emphasizes that Homo was not limited to one type of environment, but had the ability to adapt to a wide variety of environments. This is a key component of adaptation and the variability selection hypothesis addresses this question. The variability selection hypothesis also assumes that human traits evolved over time in response to varying environmental conditions.
Lifestyle evolution of the human lifespan has many influences, including genetics and the environment. In the distant past, mortality rates were extremely high, with the average lifespan of children of fifteen years only reaching thirty years. This rate remained high even after civilization developed, and life expectancies in the 19th century reached thirty years. In developed nations, however, improvements in nutrition and medicine led to an increase in life expectancy, with youth mortality decreasing to one percent or less in most countries. The increase in life expectancy set the stage for the further evolution of longevity.
Moreover, if we take into consideration the fact that humans are physically fitter than chimpanzees, we might see an even greater increase in the average lifespan. In the Bronze and Iron Ages, humans had a LEB of only twenty-six years, and the average lifespan of non-industrial farming societies was seventy-two years. This suggests that our current lean body mass is a factor in increasing human longevity.
The APOE/TOMM40 gene has been implicated in human longevity, but how long the human lifespan has been the same is a mystery. Many hypotheses have been advanced on this question, but the answer is still far from clear. Stanford, Sapolsky, and Finch argued that human lifespan evolution is linked to an interaction between genotype and diet. They found that carriers of the e4 allele of the APOE gene accumulate more cholesterol and atherosclerotic plaques in the arteries than other carriers. They also observed an increased risk of stroke and cardiovascular disease.
Using the LD region of TOMM40 and APOE3, the researchers uncovered polymorphisms in the gene and associated age at disease onset. Using this method, the authors were able to link the APOE gene to the poly-T allele, which was associated with LOAD. The results suggest that the poly-T allele is codominant, with two inherited 523 alleles determining age at disease onset. Further study will be necessary to determine whether the poly-T alleles have a linear relationship to age at disease onset. Moreover, you may also know to stay connected to the facts related blogs to explore such topics.