Mechanisms of thermal dysregulation in primary hyperhidrosis and hypohidrosis

Thermal regulation in humans is achieved through behavioural and autonomic thermoeffectors (Schlader and Vargas 2019). Autonomic thermoeffectors are involuntary changes to heat exchange mechanisms. They affect change by varying skin blood flow, encouraging heat loss through sweating, or augmenting metabolic heat production (Schlader and Vargas 2019). Behavioural thermoeffectors are voluntary behaviours which promote thermal homeostasis (Schlader and Vargas 2019). For example, when a person is hot, they may engage in cool-seeking behaviour such as taking off a piece of clothing or altering their exercise rate (Schlader and Vargas 2019). The integumentary system has a significant role in autonomic thermoregulation. Most notably, the skin is responsible for the secretion of sweat, a mechanism through which heat is dissipated from the body into the environment (Nawrocki and Cha 2019a). The skin has three sweat-secreting glands: eccrine, apocrine and apoeccrine (Nawrocki and Cha 2019a). When stimulated, these glands secrete an isotonic solution which progressively becomes hypotonic as electrolytes are reabsorbed within the duct of the gland (Schlader and Vargas 2019). Eventually, this liquid reaches the surface of the skin, where it promotes heat loss. This is thought to occur predominantly through an autonomically regulated process known as evaporative cooling, wherein the high heat capacity of water allows sweat droplets to absorb a large amount of heat energy from the body and effectively release it into the environment through evaporation (Schlader and Vargas 2019). This process is more effective in low-humidity climates where there is less water vapour pressure and consequently more efficient evaporation of sweat droplets (Schlader and Vargas 2019). Dysfunction in cutaneous sweat secretion with no known underlying medical or pharmaceutical cause may result in a diagnosis of primary hyperhidrosis or hypohidrosis. When the skin produces an excess amount of sweat beyond the thermoregulatory requirements of the person, this is known as hyperhidrosis (Nawrocki and Cha 2019b). Correspondingly, when the skin has deficient sweat production, this is known as hypohidrosis (Chia and Tey 2012). These two sweating disorders have been clinically acknowledged in terms of the autonomic role of sweat in evaporative cooling. However, new evidence reported by Vargas et al. (2020) indicates that sweat may have a greater role in behavioural thermoregulation, which may have implications for patients with primary hyperhidrosis and primary hypohidrosis. The present study by Vargas et al. (2020) tested the hypothesis that increases in skin wetness enhance cool-seeking behaviour when passive heat stress is applied. Twelve participants wore a suit circulating 34°C water and completed two trials. Core and mean skin temperatures were fixed across both trials whereas the ambient humidity was manipulated in order to evoke two diverse skin-wetness profiles, with increased skin wetness in the high-humidity condition. When the water temperature in the suit progressively increased (passive heat stress), causing elevated levels of skin wetness, intentional engagement in cool-seeking behaviour increased to a greater degree in the high-humidity condition, when compared with the low-humidity condition. This was illustrated by greater reductions in neck device temperature, a greater time spent receiving cooling, greater reductions in neck skin temperature, and a greater amount of continuous button presses to obtain cooling. Additionally, the mean skin temperature at which subjects initiated thermal behaviour was lower than when skin wetness was elevated. These findings support the hypothesis that elevated levels of skin wetness augment cool-seeking behaviour throughout passive heat stress, independent of variations in core and skin temperature. This study was the first to investigate the role of skin wetness in promoting cool-seeking behaviour independently of body temperature (Vargas et al. 2020). Prior literature has frequently established the role of sweat in lowering internal body temperature through a process known as evaporative cooling (Schlader and Vargas 2019). The results of this study provide evidence for a greater role of sweat in behavioural thermoregulation. The evidence reported by Vargas et al. (2020) suggests that sweat may increase cool-seeking behaviour in addition to propagating heat transfer from the skin to air. This has implications for the specialty of dermatology and the management of primary hyperhidrosis and hypohidrosis. During the HIGH trial, the ambient humidity was raised to increase skin wetness (Vargas et al. 2020). This simulates the pathophysiological conditions experienced by patients with primary hyperhidrosis, where patients have increased rates of sweat production that exceed their thermoregulatory needs (Nawrocki and Cha 2019a). The results of the study suggest that an increased rate of sweating may provide additional disadvantages to patients when they experience heat stress by potentially increasing the perception of thermal discomfort, and subsequently increasing their cool-seeking behaviour (Vargas et al. 2020). Cool-seeking behaviour includes actions such as moving to a colder room or environment, generalized or localized cooling techniques like removing clothing or taking a bath, and deliberate changes in exercise workload (Schlader and Vargas 2019). This may be disadvantageous when performing activities with high metabolic demands, which produce heat energy as a by-product and trigger excessive sweating. Patients with hyperhidrosis engaging in these activities may have to pause exercise prematurely or may avoid initiating these activities altogether in an attempt to feel cool (Schlader and Vargas 2019). This may make it more difficult for these patients to engage in these activities. As such, dermatologists may counsel patients with hyperhidrosis to wear clothing which effectively absorbs sweat to limit the role of skin wetness in promoting exercise intolerance. They may also counsel patients to exercise in low-humidity environments to increase the rate of sweat evaporation and decrease skin wetness. Correspondingly, this has implications for patients who suffer from hypohidrosis. Patients with hypohidrosis have been observed to suffer adverse outcomes such as hyperthermia, heat exhaustion and death (Chia and Tey 2012). This was previously thought to occur due to the lack of evaporative cooling, resulting in decreased dissipation of body heat into the environment. The results reported by Vargas et al. (2020) suggest that these adverse events may also occur due to decreased skin wetness resulting in less awareness of thermal discomfort and subsequently less cool-seeking behaviour. However, it is unclear how clinically significant this effect is, given that there are alternative mechanisms for the perception of thermal discomfort (Schlader and Vargas 2019). Nonetheless, due to the lack of treatments available, it may be worthwhile to explore the role of decreased cool-seeking behaviour in generating hyperthermic adverse events (Chia and Tey 2012). The current mainstay of treatment for patients with hypohidrosis is the avoidance of triggers (Chia and Tey 2012). However, given the findings of Vargas et al (2020), dermatologists may also consider counselling patients to intermittently monitor the environment and their body's activity level and augment their cool-seeking behaviour consciously according to these factors. For example, patients may consider limiting exercise or pausing at prespecified intervals to ensure that they are allowing their body to cool down. They may also consider having scheduled cooling breaks when exposed to heat stress, so as to replicate the role of skin wetness in stimulating cool-seeking behaviour. Vargas et al. (2020) used sound research methodology in their study. Firstly, the use of blinding for study participants and a cross-over study design was imperative to the rigour of the study. This ensured that participant perceptions of thermal discomfort were not influenced by the knowledge of the intervention used. The cross-over design also ensured that personal differences in heat tolerance did not confound the amount of time receiving cooling, as subjects and controls were the same participants. However, Vargas et al. (2020) only performed this examination on females when they were in the first 10 days of their menstrual cycle, or in the first seven days of their hormonal birth control placebo phase. Although this was important to ensure that the body temperature increases associated with the elevation of progesterone levels did not confound thermoregulatory behaviour, this restricted inclusion criterion limits the generalizability of the study results in pre-menopausal adult women. Future studies may consider including women in all stages of the menstrual cycle to identify whether these results are still applicable. Future studies may also replicate this study using a larger sample size to increase the power of the study results. In conclusion, Vargas et al. (2020) identified the role of skin wetness in promoting cool-seeking behaviour independently of skin and body temperature. This has implications for the field of dermatology and the management of primary hyperhidrosis and hypohidrosis. Primarily, it suggests that patients with hyperhidrosis may perform more cool-seeking behaviour such as regulating the amount of exercise or high metabolic demand activities they participate in. To prevent this, patients may consider managing their skin wetness by wearing clothing which keeps them dry. Correspondingly, patients with hypohidrosis may not engage in enough cool-seeking behaviour due to their decreased skin wetness. As a result, it may be helpful for patients with hypohidrosis to consciously monitor their cool-seeking behaviour and augment them according to their thermoregulatory requirements. None. All authors have contributed equally to the work presented. None.

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