Our DNA is thought to hold the ultimate power in determining the lives we live. Whether it’s how we look, how we feel, or how we behave, everything is decided by a string of letters. Recently, genetic testing kits such as 23andMe and AncestryDNA have skyrocketed in popularity, giving users the chance to learn more about their ancestry and potentially any predisposition to certain diseases. After all, if we have no control in the matter, we might as well know and succumb to our fate, right? Perhaps not.

According to a study by researchers at Stanford University, learning that you have a genetic risk for something, such as obesity, changes your physiology to reflect symptoms characteristic of the disease – regardless of your actual genetic risk. In some cases, they even observed that the effects of a perceived genetic risk can be greater than the effects associated with an actual genetic risk. It’s an interesting case of the placebo effect, a phenomenon where our expectations actually influence our physiology. This landmark study showcases that DNA may not be as definitive in determining our health outcomes as we once believed, and that our thoughts could play a more important role in our health than we give them credit for.

How did the Stanford study determine this? Well, the premise of the study was to determine if simply receiving genetic risk information for obesity could change an individual’s actual risk of developing a disease. What role could the mindset we have about our genes play in affecting how certain physiological, psychological, or behavioural outcomes are expressed?

To find out, participants were genotyped for their actual genetic risk of obesity: high, moderate, or low. People in each group were then randomly assigned to one of two conditions: one group was told that they had a high genetic risk of developing obesity, and the other group was informed that they had a low risk of developing obesity.

With these participants, researchers conducted two experiments designed to examine outcomes related to obesity: exercise and diet habits. In the first experiment, participants were asked to run on a treadmill to measure cardiorespiratory physiology, running endurance, and how participants felt about their exercising experience. In the second experiment, they consumed a meal to measure satiety physiology and how participants felt as they ate. 

After taking initial measurements for these outcomes, forming the baseline of their study, the researchers told participants their supposed “genetic risk” regarding exercise and satiety genes. This set the stage for the next round of experiments (conducted one week later), creating the necessary mindset in participants to potentially influence their performance.

In Experiment 1, individuals who believed they carried the gene for poor exercise performance reported more worry and less control on their ability to exercise. These expectations were reflected in their cardiovascular physiology as they performed poorly in comparison to their baseline. Their ability to remove carbon dioxide from their body was reduced, as was the amount of air supplied to their lungs. They also had lower running endurance, giving up earlier than they did in their baseline session. Meanwhile, the only change in participants from the other group, who were told they had low genetic risk of developing obesity, was that they were able to run for a longer period of time. Clearly, participants’ exercise performance swayed in the direction they believed their genes would lead them.

In Experiment 2, individuals who were told that they were at high risk for obesity believed that it would take more food for them to feel full (poorer satiety). Once again, these expectations were reflected in their physiology. Here, a hormone that is released after meal intake to indicate fullness was used as a measure of satiety in this experiment. While the perceived high-risk group had no change in levels of this hormone, the perceived low-risk group’s levels had almost tripled. They believed they would feel full sooner, and this was indeed the case. Much like their exercise performance, the way participants’ hormones acted to influence feelings of fullness depended on how they felt about their genetic risk of obesity.

These experiments offer an interesting insight into the way we perceive our genes – they may be less influential than we believe, and it’s safe to say that DNA is not the only factor at play. The perception of our circumstances shapes our experiences, and there’s now compelling scientific evidence to back this up. Our mindset influences the way our brain communicates with our body, and this can have very real implications for shaping our health. It will be interesting to see what this means for healthcare going forward. Could believing we have a lower risk of developing certain diseases lower our actual risk? How could physicians and researchers use this placebo effect, if at all? While this entails further scientific inquiry and some serious ethical consideration, in the mean time we can be sure of one thing: when it comes to mind over matter, your mind does matter.

By: Pallavi Mathur

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