Human Evolution May Have Amped Up Our Fight-or-Flight Urges

Lower ADRA2C expression increases sympathetic nervous activity in Homo sapiens.

Posted Apr 23, 2018

 CataVic/Shutterstock
Source: CataVic/Shutterstock

Homo sapiens and chimpanzees evolved with a turbo-charged “fight-or-flight” response mechanism in comparison to other non-human primates, according to a new study published April 19 in the journal Plos Genetics. The paper, “Selection on the Regulation of Sympathetic Nervous Activity in Humans and Chimpanzees,” reports the first evidence that modern-day Homo sapiens and chimps display lower expression of a gene called ADRA2C.

Adrenergic α2C receptor (ADRA2C) is an inhibitory modulator of the sympathetic nervous system (SNS) that is directly linked to the intensity of fight-or-flight responses. For this study, an international research team analyzed the genomes, transcriptomes, and epigenomes of ADRA2C in humans as it compared to other non-human primates. 

This research was a collaborative effort between South Korean scientists in the OMICS Lab for Computational Biology and Medicine at KAIST (Korea Advanced Institute of Science and Technology) and researchers in the United States at Georgia Tech.

The authors, who include Jung Kyoon Choi of KAIST and Soojin Yi of Georgia Tech, speculate that one reason humans and chimpanzees are the only primates known to frequently engage in warfare may be linked to decreased ADRA2C expression. 

“If intergroup aggression has been an adaptive or pervasive behaviour during the evolution of humans and chimpanzees, then the fight-or-flight response must have played a critical role in increasing fitness with constant exposure to lethal conflicts. Our study on the evolution of ADRA2C regulatory regions in humans will shed light on this hypothesis," the authors said in their study's introduction. 

During their detailed analysis, the researchers were able to pinpoint how humans and chimpanzees acquired complex genetic and epigenetic changes that decrease ADRA2C expression. The researchers hypothesize that the correlation between lower ADRA2C expression and amped up fight-or-flight responses may have evolved as an adaptation to threats of war.

In their concluding statements, the authors sum up the significance of identifying decreased ADRA2C expression in humans and chimpanzees:

“Regardless of the underlying mechanism, our results suggest that there has been selective pressure for enhanced sympathetic nervous activity during the evolution of humans as well as chimpanzees. Humans and chimpanzees are the only primates that are known to engage in regular lethal aggression among neighbouring groups, in contrast to their closest relatives, bonobos. A recent study proposed that conspecific killing by chimpanzees is more the result of adaptive strategies than the response to human disturbances. This proposal could explain the evolutionary roots of warfare, which may be a pervasive feature throughout human history.”

Diaphragmatic Breathing Counterbalances Fight-or-Flight Urges

The empirical evidence showing us that humans evolved with more robust fight-or-flight mechanisms is a clarion call for the importance of diplomatic peace-making efforts. This study also reaffirms the neverending importance of living by the creed of seemingly outdated anti-war slogans such as "Make Love, Not War." Clearly, if we are hardwired for more aggression and warfare than our primate cousins, we must make a concerted effort to counteract these fight-or-flight urges on a daily basis. 

Despite the persistence of ongoing militarized conflicts around the globe, there is a reason for hopefulness that is within the locus of our individual control. The good news: Among all primates, each of us has the unique power to consciously hack our autonomic nervous systems and counteract runaway excitatory stress responses by engaging the "relaxation response" of the parasympathetic nervous system (PNS) on demand.

One of the simplest ways to hack your PNS is via heart rate variability biofeedback and diaphragmatic breathing, which stimulate the vagus nerve. Exhalation modulates the release of vagusstoff (also known as "vagus substance" or acetylcholine) which acts like a tranquilizer within the nervous system and slows heart rate in-between beats.

KieferPix/Shutterstock
Source: KieferPix/Shutterstock

Practicing an HRV-biofeedback technique called "Resonance Frequency Breathing"—which simply entails taking 6 breaths per minute (4-second inhalation; 6-second exhalation)—creates a frequency of .1 Hz which tames the sympathetic nervous system and instantaneously balances autonomic functions.

The vagus nerve is like a muscle that gets stronger with regular use. Daily lifestyle habits that stimulate vagus nerve activity (as indexed by higher HRV) provide immediate stress reduction and also help to optimize vagal tone (VT) for the long haul. Toning your vagus nerve facilitates emotion regulation, impulse control, wise reasoning, prosocial behaviors, and countless other biomarkers of well-being linked to reducing hyperactive fight-or-flight stress responses. 

Stay tuned for a future blog post with more details on the specifics of .1 Hz breathing and other ways to hack the autonomic nervous system. In the meantime, please see: “A Vagus Nerve Survival Guide to Combat Fight-or-Flight Urges.

References

Kang Seon Lee, Paramita Chatterjee, Eun-Young Choi, Min Kyung Sung, Jaeho Oh, Hyejung Won, Seong-Min Park, Youn-Jae Kim, Soojin V. Yi, Jung Kyoon Choi. "Selection on the regulation of sympathetic nervous activity in humans and chimpanzees." PLOS Genetics (Published: April 19, 2018) DOI: 10.1371/journal.pgen.1007311

Paul M. Lehrer and Richard Gevirtz. "Heart Rate Variability Biofeedback: How and Why Does It Work?" Frontiers in Psychology (Published online: July 21, 2014) DOI: 10.3389/fpsyg.2014.00756

Patrick R., Steffen, Tara Austin, Andrea DeBarros, and Tracy Brown. "The impact of resonance frequency breathing on measures of heart rate variability, blood pressure, and mood." Frontiers in Public Health (Published: August 25, 2017) DOI: 10.3389/fpubh.2017.00222