Is laziness a personal choice or a genetic trait?

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November 02, 2019 – Is laziness a choice or genetic trait? At the age where genetics seems to explain everything, it is certainly interessant to learn that a seemingly personal choice such as laziness as such may loom somewhere in your genetic outfit. Perhaps, you can not escape your laziness behaviour, because it is part or your make-up, based on your very own genetic backing? If nothing else, this is at least a fascinating thought and would help to explain a lot of things, among them recurring lifestyle issues.


Regular physical activity is a crucial part of living a healthy lifestyle. However, a majority of adults spend their waking hours sitting, which leads to a variety of health issues such as obesity, cardiovascular disease and cancer. Recent research at the University of Missouri has identified a specific gene related to physical inactivity in rats that could potentially play a role in sedentary behavior in humans as well. Previously, research has shown that genes may play some role in physical inactivity of individuals. Since in humans, inactivity may lead to chronic disease, there has been for long time a quest for identifying genes involved in this phenomenon. Newest research has now discovered one such gene, namely the Protein Kinase Inhibitor Alpha gene (PKIA gene), that seems to play a significant role in the phenomenon of human laziness.

Thus, in a long term study since 2009, researchers took 80 male rats and bred them with 80 female rats. They then placed the rats in voluntary running wheels, similar to those sold in pet stores, and tracked which rats ran the most and least. Over the past decade, the researchers then selectively bred the highly active rats with each other as well as the “lazy” rats with each other to determine if there is a difference in their genetic makeup. The researchers found that the PKIA gene was significantly less present in the “lazy” rats. While this study was done in rats, it may nevertheless be rather relevant to humans to in that the PKIA gene in humans codes for exact the same molecular and physiological function as its homologue counterpart in rats.

Generally, common believe holds that physical inactivity in humans may contribute to more than 40 chronic diseases. Rather than focusing on ways to treat chronic diseases after they have already developed, understanding the contributing factors to physical inactivity, particularly genetic predispositions to it,  could help prevent those chronic diseases from occurring in the first place, in that individuals at risk for non-activity (i.e., seeming laziness) could be more specifically motivated to increase prophylactic physical activities without falsely accusing the patients for their (inborn) tendency for being lazy.

According to US government data, costs associated with physical inactivity total $138 billion and account for more than 11 percent of total health care expenditures. In addition to the financial benefits of a more physically active society a better understanding of genetic makeup could help public health officials see physical inactivity as a crucial priority to address. One difficulty of most chronic diseases is that they usually are not caused  by just one gene. For example, there are more than 150 gene variations involved in type 2 diabetes. The present study helps to identify other genes that might be involved in physical inactivity in humans as well and to identify additional factors that may help to prevent 0r at least reduce chronic disease development.

The study “Overexpression of Protein Kinase Inhibitor Alpha Reverses Rat Low Voluntary Running Behavior” was published in the Journal “Molecular Neurobiology”.

See here a short sequence on “laziness”:


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About the Author
thassodotcom Ph.D.; Professor in Pharmacology and Toxicology. Senior expert in theragenomic and personalized medicine and individualized drug safety. Senior expert in pharmaco- and toxicogenetics. Senior expert in human safety of drugs, chemicals, environmental pollutants, and dietary ingredients.

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