As humans, the ability to adapt to our environment is what has allowed us to exist from the beginning of time to present day. One way we have been able to survive all these years is by regulating our core temperature to ensure that we do not fry ourselves from the inside out or freeze to death. Unfortunately, this is not the case for some people; like many systems in the world today, technical difficulties arise from thin air, and the human body is no different.
When it comes to the inability to regulate our body temperature, specifically through perspiration, some people will develop a case called anhidrosis. Anhidrosis is a condition where the body’s ability to sweat becomes inefficient. This can be affected anywhere between your unconscious brain all the way to the eccrine sweat glands, where sweat is produced and transported to the surface of our skin (Science Direct).
Anhidrosis is caused by the genetic mutation of human tropomyosin kinase A, which inhibits the nerve growth factor in nociceptive sensory neurons and sympathetic autonomic neurons. This ultimately leads to the mutated development of the somatic sensory system. In English, this genetic mutation disables the nerves that send signals to our brain when we feel pain or heat, so for the sake of sweating, our eccrine sweat glands don’t allow perspiration to occur, since the body can’t tell if it needs cooling or heating to maintain homeostasis. Along with the disablement of these nerves, the eccrine glands won’t even have nerves in them to begin with due to the maldevelopment of the autonomic sympathetic nervous system (Mughal, 2021). The sympathetic nervous system is responsible for the fight or flight response in the body, so this includes the increase in sweat production, and increased heart rate.
Interesting enough, a lot of case studies found that individuals develop congenital insensitivity to pain and anhidrosis (CIPA); anhidrosis doesn’t seem to occur on its own. The conjunction of these two diagnoses is interesting but makes sense because the ability to sense pain and heat is under the same jurisdiction of the somatic sensory system. As congenital insensitivity to pain states in its name, an individual with this mutation doesn’t feel pain (Mughal, 2021).
To not feel pain is dangerous for survival purposes, but the behavior of subjects with CIPA is alarming as well. Subjects in other studies were found to self-mutilate, but images gathered from this study showed the self-mutilation of subjects that were selected to draw blood samples from them for genetic analysis. The findings in the genetic analysis were able to give scientists a better understanding of CIPA and can pinpoint where the genetic mutations occur. This is a big step for further studies to develop a remedy for the maldevelopment of nerves in the skin and eccrine sweat glands (Geng, 2018).
For my STEAM project, my sister and I are performing a contemporary dance routine; the dance is a representation between the tribulations we face in life and the love siblings have for one another. During the routine, observe the costumes we used in our routine and the environment we performed the routine in. The day we recorded this was a very hot day with clear skies, and we didn’t dress appropriately for the environment we were dancing in. Think about the adaptability of the sympathetic nervous system as we begin to perform movement, how the sympathetic nervous system kicks the eccrine sweat glands into gear and how our nervous system allowed us to adapt to our environment to be able to perform at a high intensity. In contrast, think about the complications of anhidrosis and how the genetic mutation would affect our ability to perform this routine.
Geng X, Liu Y, et. al. Novel NTRKI Mutations in Chinese Patients with Congenital Insensitivity to
Pain and Anhidrosis. Molecular Pain. 2018; 14: 1-11.
Mughal S, Farhat A. Case Study of a Rare Genetic Disorder: Congenital Insensitivity to Pain with
Anhidrosis. Cureus. 2021; 13(1).
Palma J, Kaufmann L, et. al. Disorders of the Autonomic Nervous System: Autonomic
Dysfunction in Pediatric Practice. Pediatric Neurology. 2017; 6: 1173 – 1183.