Harvard Research Reveals: Don't Think Too Much, You Might Die Earlier
By Jiyoung Lee
We consider age a factor of intelligence during adolescence, implying that we’re better able to think and process information as our brains mature. It's assumed that older people who have lived longer are likely wiser and better informed of how the world works. However, this doesn’t actually correlate in respect to brain activity. Imaging studies reveal that older aged people have more intense and complex neuron activity when thinking over a cognitive concept than younger individuals. Although this may sound at first as if we gain deeper thinking abilities as we age, it actually indicates a decrease in neuronal efficiency; greater amount of neuron triggers are required to solve what might be a simple math problem due to decreased productivity of individual neurons. This concept alludes to the idea that quieter brains requiring fewer neuronal triggers when getting to a conclusion may be more favorable.
It’s been long known through extensive research that a protein called REST is crucial in regulating proper neuronal excitation by acting as a neuron repressive gene and preventing overexcitation. This protein is normally present at high levels in the brains of fetuses, then inactivated during childhood until it’s re-expressed as the brain begins to progressively age. People differ in the amount that REST is transcriptionally expressed when it turns back on, which is what causes variance in our individual neuronal excitation levels. Complete deletion of the protein is common in people with Alzhemier’s disease and dementia, highlighting REST as a vital factor in preventing neurodegeneration.
Bruce Yanker, a neurologist and geneticist at Harvard Medical School, claims that our gene patterns naturally and unrandomly alters our brains so that the young and the old can be easily distinguished by their transcriptional signatures. He led the study on brain aging by sequencing the RNA of over a hundred non-degenerative deceased brains. The transcriptional profiling revealed the key difference between the two groups that were separated by longevity: those who lived longer had fewer transcripts that coded for neural excitation. Furthermore, brain tissue analysis also revealed that people who lived over 100 years old all had noticeably very high amounts of REST in their brain nuclei. High expression of REST leads to lower excitation levels, which in return activates transcription factors stimulating the insulin/IGF1 pathway, known as the “longevity pathway.” Animal studies were done on worms and mice to pinpoint the correlation, and they all indicated that blocking REST expression led to increased neural activity and earlier mortality, while boosting its expression did the opposite.
All evidence points to conclude that aging comes with inevitable increased brain activity, and our longevity—if not affected by unforeseen accidents or illnesses—largely depends on whether our brain can effectively limit this natural increase. The key regulatory protein involved is REST—a suppressor of neural excitation by inhibiting excitatory synapses. Modes in effectively increasing REST levels would in return help limit unnecessary triggers and neurodegeneration. This conclusion took years to formulate and was only released to the public about a month ago due to it largely contradicting our general societal norm: exploit all that we can learn throughout life.
Through this discovery, new perspectives were enlightened from other previous research work; for example, it gave new insight on a study that revealed anticonvulsants and antidepressants as longevity extenders in a worm species. This brings into question whether the consumption of these brain activity inhibiting drugs are actually beneficial in promising a longer life for humans, and whether elderly should be actively encouraged to rely on these suppressants in hopes of a longer life. Certainly, wasting the final years of your life with stunted brain power isn’t very ideal and contradicts with our desire to maximize what we can experience in the world, but is it simply the cost we must pay to live a couple years more? For all we know though, we’re more likely to die from accidents and other illnesses, so why take the risk and live with a cloudy brain (jab at druggies)? I definitely would rather be living the last few years of my life using my brain’s full extent, even if it means I might live a few years less. This is what makes the research so bleak when applied in respect to our personal lives: no one would willingly compromise their brain power. How can you tell someone that it’s better for them to “dumb down”?
The answer to whether a medicative drug should be implemented in the elderly population is very controversial and pretty unreasonable; there are currently no drugs that allow lower neural triggering without compromising the brain’s efficiency and effectivity. In the long run, however, the study indicates that our hopes of manipulating human lifespan might not be so fictional after all. If the mechanisms of REST are more thoroughly understood and new drugs are developed accordingly, we might be able to target the protein specifically without causing harmful or detrimental effects. Furthermore, this study also provides promising research prospects in preventing age related neurological disorders such as Alzheimer’s, which currently has no cure.
To make it completely clear, this research isn’t encouraging us to stop all brain stimulating activities and to start drowning in anti-depressants. It does suggest, though, that you might want to maximize your brain power while you’re still young, since engaging in learning later in life might not be worth it if it means quicker mortality. Following advice from health instructors and psychiatrists, you might want to start working on meditation and yoga- after all, it’s now inferred it’ll increase your lifespan.
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