An international research team led by Prof. Dr Frank Bosmanbs (Vrije Universiteit Brussel) has discovered a major genetic cause of hyperhidrosis (chronic and excessive sweating). The study, published in the scientific journal *Science Advances* , provides strong evidence that a genetically determined form of hyperhidrosis arises from overstimulation of the nerves that control the sweat glands. The discovery removes the stigma surrounding the condition and paves the way for targeted treatments using existing medicines.
Excessive sweating affects an estimated 2 to 5 per cent of the population. The symptoms are far more severe than mere ‘awkward discomfort’. Patients sweat so profusely that they have to change their clothes several times a day. The impact on daily life is enormous. Many patients avoid social contact, feel deeply ashamed and develop depression. Yet the condition is still too often dismissed as a superficial skin problem, meaning patients encounter a lack of understanding and do not receive the right care.
An overactive ‘thermostat’ in the nerves
Bosmans’ team spent ten years searching for answers to this problem, in collaboration with Johns Hopkins University. By analysing the DNA of more than 180 patients, they discovered defects in a specific protein channel in our nerves: the Nav1.8 ion channel. This channel normally functions as a biological gate that regulates electrical signals in the nervous system. In patients with hyperhidrosis, this gate is left too wide open due to a genetic predisposition. As a result, the nervous system that controls the sweat glands is constantly overstimulated. The nerves are constantly in a state of activity, resulting in excessive sweating. This is consistent with the clinical picture in which sweating is often triggered by emotional or stress-related stimuli, without the condition being of psychological origin.
Strong evidence from experimental models
To substantiate the theory, the researchers developed an experimental model. As mice only sweat from their paws, the team spent two years developing a microscopic measurement method to count sweat droplets using an iodine-starch mixture. Mice with the same genetic defect were indeed found to sweat excessively. As soon as the researchers administered a substance that blocked the overactive nerve signals, sweating decreased significantly and reversibly in the mouse model.
The genetic reality is, however, complex. The team also discovered a patient who had actually inherited an ‘inhibitory’ nerve mutation, but who nevertheless sweated excessively due to an additional, unique mutation in a local water channel within the sweat gland itself. This proves that hyperhidrosis is a condition in which different biological pathways can lead to the same overstimulation that becomes visible on the skin.
Hope for targeted therapy without unnecessarily invasive procedures
The discovery offers the prospect of better, more targeted treatments. Today, severe forms of hyperhidrosis are sometimes treated with procedures that sever the sympathetic nerve pathways in the chest. Such treatments can be effective, but they are invasive, not suitable for everyone and can cause unwanted side effects. By gaining a better understanding of the biological cause, in-depth genetic and functional research may, in the long term, help to better predict in advance which patients are likely to benefit most from localised treatment of the sweat glands, systemic medication or nerve-targeted therapies.
A second important avenue is drug repurposing : the targeted re-evaluation of existing medicines based on the new mechanism. In the mouse model, several clinically relevant agents reduced excessive sweating, including treatments that act on cholinergic signalling – a way in which nerve cells communicate with one another – or on the excitability of nerve cells. This also provides a biological context for patient reports regarding cannabis products, as some cannabinoids can influence sodium channels. This does not mean that these agents can already be recommended as standard treatment, but it does mean that the research lays a rational foundation for controlled clinical trials. In this way, the management of hyperhidrosis is shifting from symptomatic treatment towards a more mechanism-based approach.
Broader implications for the autonomic nervous system
The study places hyperhidrosis within a broader context of autonomic nervous system disorders. Sweating is a visible function of the autonomic nervous system and can therefore serve as a measurable indicator of biological dysregulation. Whether similar ion channel mechanisms also contribute to other forms of dysautonomia, for example following infections, requires further investigation.
For patients, the message is clear: primary hyperhidrosis is not merely a cosmetic problem or a matter of stress; for at least some patients, it is a genuine, biological and potentially treatable disorder of the nerves and sweat glands.
Reference:
Suguru Yamauchi, Jolien Vander Cruyssen, Michele Cervellera et al. (2026) A Neurocutaneous NaV1.8 Channelopathy Underlies a Genetic Subtype of Primary Idiopathic Hyperhidrosis. Science Advances. DOI: 10.1126/sciadv.aed3221
Science Advances
A Neurocutaneous NaV1.8 Channelopathy Underlies a Genetic Subtype of Primary Idiopathic Hyperhidrosis
17-Jul-2026