Sweat Gland Function Research Articles

Infrared thermal imaging for assessing human perspiration and evaluating antiperspirant product efficacy

In humans, perspiration regulates core body temperature. Therefore, objectively evaluating it is essential for studying sweat gland function and mechanisms, particularly in antiperspirant efficacy studies. Various approaches have been developed for measuring human perspiration and evaluating antiperspirant efficacy, but are unsuitable for robust and routine clinical testing applications. This paper shows how infrared thermography, utilizing both high- and low-resolution modes, functions as a multiscale imaging modality. The high-resolution mode extracts physiological parameters (respiratory ~ 0.3 Hz and heart rate ~ 1.0 Hz) and visualizes the reduction of the sweat pore radii (from 359 ± 155 μm to 161 ± 47 μm) after antiperspirant application, consistent with known mechanisms of pore plugging and constriction induced by aluminum salts. The low-resolution mode quantitatively maps sweat retention in underarm clothing. All study participants in a clinical trial showed reduced sweat retention on their T-shirts due to antiperspirants, with reductions ranging from approximately 37–97% and an average reduction of 77.7 ± 22.1% using the developed methodology and tested antiperspirant. Overall, this non-invasive technique presents significant potential for clinical and personal care product evaluations, particularly in the early stages of product development.

Sweat Gland‐Like Fabric for Personal Thermal‐Wet Comfort Management

AbstractThe sweat evaporation strategy has shown great potential for passive cooling of the human body. However, the accumulation of sweat at the skin resulting from the hindrance by traditional fabrics increases the heat load and causes the clothing to stick to the skin. Sweat evaporation cooling textiles that perform the sweat‐wicking function of sweat glands are thus highly desirable. Here, a sweat gland‐like (Sg‐like) fabric is proposed for personal thermal‐wet comfort management. The Sg‐like channels formed in the fabric through spraying and ultrasonic welding processes can pull liquid water from the skin and spread it out over the outer layer of the fabric for rapid evaporation. The Sg‐like design principle is also well‐validated based on colored fabrics. In artificial sweating skin demonstrations, the temperature of skin covered with the Sg‐like fabric is comparable to that of bare skin and lower than that of skin covered with commercial textiles. In human body tests, a temperature reduction of ≈2 °C is observed in sweating for skin coated with the Sg‐like fabric compare with skin‐coated cotton. It is expected this work offers promising guidelines for developing a sweat‐evaporation cooling textile to meet the thermal‐wet comfort requirements of the human body.

Pretreatment of microneedles enhances passive transdermal administration of pilocarpine and pilocarpine-induced sweat production in humans

The development of an effective transdermal drug delivery protocol to eccrine sweat glands is important for the advancement of research on the human sweating response. We investigated whether microneedle treatment prior to the application of pilocarpine, a hydrophilic and sudorific agent that does not induce sweating due to a limited percutaneous passive diffusion by skin application alone, augments sweat production. We applied three microneedle arrays to forearm skin sites simultaneously (n = 20). Upon removal of the microneedles, 1 % pilocarpine was applied to each site for 5-, 15-, and 30-min for the assessment of sweat gland function. In parallel, pilocarpine was administered by transdermal iontophoresis (5-min) at a separate site. Sweat rate was assessed continuously via the ventilated capsule technique. Pilocarpine augmented sweat rate at the 15- and 30-min periods as compared to the application at 5-min. The sweating responses induced by the 15- and 30-min application of pilocarpine were equivalent to ∼ 80 % of that measured at the iontophoretically treated sites. Notably, we observed a correlation in sweat rate between these two transdermal drug delivery methods. Altogether, our findings show that pre-treatment of microneedle arrays can enhance transdermal delivery efficiency of pilocarpine to human eccrine sweat glands.

Discovery of a C-S lyase inhibitor for the prevention of human body malodor formation: tannic acid inhibits the thioalcohol production in Staphylococcus hominis.

Human body odor is a result of the bacterial biotransformation of odorless precursor molecules secreted by the underarm sweat glands. In the human axilla, Staphylococcus hominis is the predominant bacterial species responsible for the biotransformation process of the odorless precursor molecule into the malodorous 3M3SH by two enzymes, a dipeptidase and a specific C-S lyase. The current solutions for malodor, such as deodorants and antiperspirants are known to block the apocrine glands or disrupt the skin microbiota. Additionally, these chemicals endanger both the environment and human health, and their long-term use can influence the function of sweat glands. Therefore, there is a need for the development of alternative, environmentally friendly, and natural solutions for the prevention of human body malodor. In this study, a library of secondary metabolites from various plants was screened to inhibit the C-S lyase, which metabolizes the odorless precursor sweat molecules, through molecular docking and molecular dynamics (MD) simulation. In silico studies revealed that tannic acid had the strongest affinity towards C-S lyase and was stably maintained in the binding pocket of the enzyme during 100-ns MD simulation. We found in the in vitro biotransformation assays that 1 mM tannic acid not only exhibited a significant reduction in malodor formation but also had quite low growth inhibition in S. hominis, indicating the minimum inhibitory effect of tannic acid on the skin microflora. This study paved the way for the development of a promising natural C-S lyase inhibitor to eliminate human body odor and can be used as a natural deodorizing molecule after further in vivo analysis.

Altered Sweat Composition Due to Changes in Tight Junction Expression of Sweat Glands in Cholinergic Urticaria Patients.

In cholinergic urticaria (CholU), small, itchy wheals are induced by exercise or passive warming and reduced sweating has been reported. Despite the described reduced muscarinic receptor expression, sweat duct obstruction, or sweat allergy, the underlying pathomechanisms are not well understood. To gain further insights, we collected skin biopsies before and after pulse-controlled ergometry and sweat after sauna provocation from CholU patients as well as healthy controls. CholU patients displayed partially severely reduced local sweating, yet total sweat volume was unaltered. However, sweat electrolyte composition was altered, with increased K+ concentration in CholU patients. Formalin-fixed, paraffin-embedded biopsies were stained to explore sweat leakage and tight junction protein expression. Dermcidin staining was not found outside the sweat glands. In the secretory coils of sweat glands, the distribution of claudin-3 and -10b as well as occludin was altered, but the zonula occludens-1 location was unchanged. In all, dermcidin and tight junction protein staining suggests an intact barrier with reduced sweat production capability in CholU patients. For future studies, an ex vivo skin model for quantification of sweat secretion was established, in which sweat secretion could be pharmacologically stimulated or blocked. This ex vivo model will be used to further investigate sweat gland function in CholU patients and decipher the underlying pathomechanism(s).

Early Detection of Peripheral Neuropathy by Assessment of Sudomotor Function

Chronic hyperglycemia in both type 1 and type 2 diabetes commonly lead to diabetic peripheral neuropathy (DPN) which commonly affects small nerve fibers, including autonomic sudomotor nerves, of the lower limbs. DPN results from nerve damage leading to gradual onset of foot pain, tingling, numbness, muscle weakness, extreme sensitivity to touch, and heat intolerance. Peripheral neuropathy is associated with increased all-cause mortality and morbidities such as foot ulcers, poor wound healing, local and systemic infection, limb amputation, and painful neuropathic symptoms. DPN is also typically diagnosed during later stages when disease progression has already led to irreversible nerve damage and associated severe symptoms. As such, early detection of peripheral neuropathy is important in implementing early interventions and can help preserve nerve function and prevent serious complications of DPN. Non-invasive methods of testing for early DPN rely on assessment of sudomotor nerve function. One method includes quantitative sudomotor axon reflex test (QSART) which measures postganglionic sympathetic function via iontophoresis which allows quantification of sweat production, and by extension, autonomic function. In general, QSART provides a non-invasive, reproducible, and precise evaluation of autonomic function in both controls and diabetics. It can be used to evaluate a large number of autonomic diseases, and the quantitative data it generates provides a measure of the extent and location of the peripheral neuropathy in each individual. Another assessment method includes the sympathetic skin response (SSR) test which measures the change in electrical potential of the skin which itself comes from activated eccrine sweat glands. The SSR test has a well-established protocol, and the results are easily-measured, and the results are quantifiable. It can be used reliably in the diagnosis of numerous autonomic disorders including DPN where a diminished or absent response correlate with sudomotor nerve damage. SudoCheck by VitalScan is an FDA-cleared, non-invasive autonomic sdomotor assessment tool that combines QSART, SSR, BIA, and EIS to provide rapid results with a specificity of 95% and a sensitivity of 80%. It was created to enable a precise evaluation of sweat gland function, and by extension, the presence and progression of diabetic peripheral neuropathy including early sub-clinical disease

Onset of an Active Charcot Foot in a Person with Longstanding Type 1 Diabetes and Normal Vibration Perception Threshold-A Case Report.

Charcot neuro-osteoarthropathy (CNO), or Charcot foot, is a disabling complication of diabetes, which is poorly understood and frequently overlooked. We describe an atypical presentation of an active Charcot foot in a woman with a long-standing type 1 diabetes who did not exhibit loss of protective sensation (sensate to a 10-gram monofilament) or loss of vibration sensation. These standard measures of large nerve fibre function ruled out "classical" neuropathy. However, additional testing showed reduced sweat gland function most likely related to degeneration of c-fibres (small fibre neuropathy). This case raises the awareness that in addition to the "textbook" description, in diabetes, Charcot foot can develop in individuals with "minimal" or "no signs" of clinical neuropathy. The onset of active Charcot foot should be suspected in every person with diabetes and history of trauma even when foot and ankle x-rays are normal. Offloading should be initiated until the diagnosis is proven otherwise.

Electrodermal activity and heart rate variability for detection of peripheral abnormalities in type 2 diabetes: A review.

Modern medicine exhibits an upward trend towards non-invasive methods for early detection of disease and long-term monitoring of patients' health. Diabetes mellitus and its complications are a promising area for implementation of new medical diagnostic devices. One of the most serious complications of diabetes is diabetic foot ulcer. The main causes responsible for diabetic foot ulcer are ischemia caused by peripheral artery disease and diabetic neuropathy caused by polyol pathway-induced oxidative stress. Autonomic neuropathy impairs function of sweat glands, which can be measured by electrodermal activity. On the other hand, autonomic neuropathy leads to changes in heart rate variability, which is used to assess autonomic regulation of the sinoatrial node. Both methods are enough sensitive to detect pathological changes caused by autonomic neuropathy and are promising screening methods for early diagnosis of diabetic neuropathy, which could prevent the onset of diabetic ulcer.

Effects of the bovine SLICK1 mutation in PRLR on sweat gland area, FOXA1 abundance, and global gene expression in skin.

The SLICK1 mutation in the prolactin receptor (PRLR) results in a short-hair coat and increased ability to regulate body temperature during heat stress. It is unclear whether the mutation affects capacity for sweating. The objective of this observational study was to evaluate whether the SLICK1 mutation in PRLR alters characteristics of skin related to sweat gland abundance or function. Skin biopsies from 31 Holstein heifers, including 14 wild-type (SL-/-) and 17 heterozygous slick (SL+/-), were subjected to histological analysis to determine the percent of the surface area of skin sections that are occupied by sweat glands. We detected no effect of genotype on this variable. Immunohistochemical analysis of the forkhead transcription factor A1 (FOXA1), a protein essential for sweating in mice, from 6 SL-/- and 6 SL+/- heifers indicated twice as much FOXA1 in sweat glandular epithelia of SL+/- heifers as in SL-/- heifers. Results from RNA sequencing of skin biopsies from 5 SL-/- and 7 SL+/- heifers revealed few genes that were differentially expressed and none that have been associated with sweat gland development or function. In conclusion, results do not support the idea that the SLICK1 mutation changes the abundance of sweat glands in skin, but do show that functional properties of sweat glands, as indicated by increased abundance of immunoreactive FOXA1, are modified by inheritance of the mutation in PRLR.

How Important Is Local Skin Temperature On Sweat Gland Function?

How Important Is Local Skin Temperature On Sweat Gland Function?

Biomimetic small exosome with outstanding surgical applications for rapid large-scale wound healing and functional sweat gland restoration

The realization of coordinated infiltration of dermal and epidermal cell types, and the rapid deposition of extracellular matrix are the prerequisites for improved healing quality of large skin defects. However, presently used materials are limited for wound healing due to the inherent poor histocompatibility, low permeability, poor mechanical property and cytotoxicity. It is challenging to develop new therapeutic agents that enable timely and efficient wound healing and meanwhile there are minimal side effects to avoid chronic wounds, wound adhesions, and large scarring. Herein, we fabricated biomimetic exosomes (EMs) that enriched transforming growth factor β1 (TGF-β1) for the rapid healing of large-scale cutaneous wounds. The EM encapsulation allowed well-managed dosing of the TGF-β1 to effectively promote the wound healing process by endowing epidermal keratinocytes with a migratory feature, enhancing their stem cell properties, and resulting in accelerated in vivo wound re-epithelization. Specifically, the EMs could fast restore the function of sweat glands in a thermally injured mice model. Our work provides a promising strategy for improving the healing speed and healing quality for patients with large wounds.

Revisiting regional variation in the age-related reduction insweat rate during passive heat stress.

Aging is associated with attenuated sweat gland function, which has been suggested to occur in a peripheral‐to‐central manner. However, evidence supporting this hypothesis remains equivocal. We revisited this hypothesis by evaluating the sweat rate across the limbs and trunk in young and older men during whole‐body, passive heating. A water‐perfused suit was used to raise and clamp esophageal temperature at 0.6°C (low‐heat strain) and 1.2°C (moderate‐heat strain) above baseline in 14 young (24 (SD 5) years) and 15 older (69 (4) years) men. Sweat rate was measured at multiple sites on the trunk (chest, abdomen) and limbs (biceps, forearm, quadriceps, calf) using ventilated capsules (3.8 cm2). Sweat rates, expressed as the average of 5 min of stable sweating at low‐ and moderate‐heat strain, were compared between groups (young, older) and regions (trunk, limbs) within each level of heat strain using a linear mixed‐effects model with nested intercepts (sites nested within region nested within participant). At low‐heat strain, the age‐related reduction in sweat rate (older‐young values) was greater at the trunk (0.65 mg/cm2/min [95% CI 0.44, 0.86]) compared to the limbs (0.42 mg/cm2/min [0.22, 0.62]; interaction: p = 0.010). At moderate‐heat strain, sweat rate was lower in older compared to young (main effect: p = 0.025), albeit that reduction did not differ between regions (interaction: p = 0.888). We conclude that, contrary to previous suggestions, the age‐related decline in sweat rate was greater at the trunk compared to the limbs at low‐heat strain, with no evidence of regional variation in that age‐related decline at moderate‐heat strain.

The Early Prostehtic Management Of Hypohidrotic And Anhidrotic Ectodermal Dysplasia: About Two Clinical Cases

Ectodermal dysplasia is a hereditary disorder. Patients with ectodermal dysplasia have ectodermally-derived organs disorders which can affect teeth, nails, hair and sweat glands. Disorders of sweat gland function can be classified into two major groups: hypohidrotic or anhidrotic. Oral findings in patients with ectodermal dysplasia (ED) include markedly reduction in number of teeth (oligodontia or hypodontia), malformed and widely spaced conical-shaped teeth, and underdeveloped alveolar ridges. Other dominant clinical features can be found like very thin hair. The goal of the article is to present the prosthetic management particularities of two patient with hereditary ectodermal dysplasia.

Research advances on signaling pathways affecting sweat gland development and their involvement in the reconstitution of sweat adenoid cells in vitro

The damage of sweat glands in patients with extensive deep burns results in the loss of thermoregulation, which seriously affects the quality of life of patients. At present, there are many researches on the repair of sweat gland function, but the mechanism of human sweat gland development has not been fully clarified. More and more studies have shown that the cascaded pathways of Wnt/β-catenin, ecto- dysplasin A/ectodysplasin A receptor/nuclear factor-κB, sonic hedgehog, and forkhead box transcription factor jointly affect the development of sweat glands, and it has been reported that the cascaded signaling pathways can be used to achieve the reconstruction of sweat adenoid cells in vitro. This article reviews the signaling pathways that affect the development of sweat glands and their involvement in the reconstruction of sweat adenoid cells in vitro.

Personalized medicine with drugs targeting the underlying protein defect in cystic fibrosis: is monitoring of treatment response necessary?

Cystic fibrosis (CF) is caused by two mutations in the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene. In the last years, drugs targeting the underlying protein defect like lumacaftor/ivacaftor (LUM/IVA) or tezacaftor/ivacaftor (TEZ/IVA) and more recently elexacaftor/tezacaftor/ivacaftor (ELX/TEZ/IVA) were admitted. Outcome parameters evaluating therapy response like forced expiratory pressure in 1 s (FEV1), body mass index (BMI) or the efficacy of CFTR function in sweat glands showed improvement in several cases. Other, CFTR biomarkers were analysed rarely. This prospective observational study was aimed at evaluating CFTR function in patients treated with different CFTR modulators together with common valid clinical outcome parameters at standardized appointments (day 0, week 2, 4, 16). We followed four patients with the same mutation (F508del-CFTR), sex, age and disease severity. Monitoring focused on lung function, gastrointestinal aspects and CFTR function of sweat glands, nasal and intestinal epithelium. Sweat tests were performed by pilocarpine iontophoresis. Nasal potential difference (NPD) measured transepithelial voltage in vivo and potential increased when CFTR function improved. Rectal biopsies were obtained for intestinal current measurements (ICM) ex vivo. Intestinal CFTR function was assessed by stimulating chloride secretion with different reagents. Response to CFTR modulators regarding clinical outcome parameters was rather variable. A sweat chloride reduction of 35.3 mmol/L, nasal CFTR rescue of 4.4% and fivefold higher CFTR function in the intestine was seen at week 16 post-LUM/IVA. Due to our monitoring, we identified a non-responder to LUM/IVA and TEZ/IVA. In case of ELX/TEZ/IVA, clinical parameters and CFTR bioassays improved and were concordant. Although our cohort is small, results emphasize that non-responders exist and conclusions could not be drawn if patients were not monitored. Data on CFTR function can confirm or disprove ongoing CFTR dysfunction and might be helpful selectively. Non-responders need other alternative therapy options as demonstrated with ELX/TEZ/IVA.

Ion Channel and Ubiquitin Differential Expression during Erythromycin-Induced Anhidrosis in Foals.

Simple SummaryMacrolide treatment for Rhodococcus equi infections can result in severe adverse effects including hyperthermia and temporary anhidrosis. Despite these potentially lethal side effects, and a lack of understanding of the mechanisms causing them, macrolide drugs remain the recommended treatment for R. equi infections in foals. To better understand the molecular biology behind these adverse effects, we performed a differential gene expression study of skin biopsies of six healthy macrolide-treated foals experiencing anhidrosis. In total, 132 transcripts were significantly differentially expressed, and these genes belonged to functional ontologies relevant to sweat function. Genes involved in ubiquitination and ion-channel function were upregulated during the anhidrotic timepoint. These biological mechanisms play an important role in equine idiopathic anhidrosis and sweat gland function and warrant further investigation as potential targets for avoiding macrolide-induced temporary anhidrosis.Macrolide drugs are the treatment of choice for Rhodococcus equi infections, despite severe side-effects temporary anhidrosis as a. To better understand the molecular biology leading to macrolide induced anhidrosis, we performed skin biopsies and Quantitative Intradermal Terbutaline Sweat Tests (QITSTs) in six healthy pony-cross foals for three different timepoints during erythromycin administration—pre-treatment (baseline), during anhidrosis and post-recovery. RNA sequencing of biopsies followed by differential gene expression analysis compared both pre and post normal sweating timepoints to the erythromycin induced anhidrosis episode. After Bonferroni correction for multiple testing, 132 gene transcripts were significantly differentially expressed during the anhidrotic timepoint. Gene ontology analysis of the full differentially expressed gene set identified over-represented biological functions for ubiquitination and ion-channel function, both biologically relevant to sweat production. These same mechanisms were previously implicated in heritable equine idiopathic anhidrosis and sweat gland function and their involvement in macrolide-induced temporary anhidrosis warrants further investigation.

The effect of seasonal acclimatization on whole body heat loss response during exercise in a hot humid environment with different air velocity.

Seasonal acclimatization from winter to summer is known to enhance thermoeffector responses in hot-dry environments during exercise whereas its impact on sweat evaporation and core temperature (Tcore) responses in hot-humid environments remains unknown. We, therefore, sought to determine whether seasonal acclimatization is able to modulate whole body sweat rate (WBSR), evaporated sweat rate, sweating efficiency, and thermoregulatory function during cycling exercise in a hot-humid environment (32°C, 75% RH). We also determined whether the increase in air velocity could enhance evaporated sweat rate and sweating efficiency before and after seasonal acclimatization. Twelve males cycled for 1 h at 40% V̇o2max in winter (preacclimatization) and repeated the trial again in summer (after acclimatization). For the last 20 min of cycling at a steady-state of Tcore, air velocity increased from 0.2 (0.04) m/s to 1.1 (0.02) m/s by using an electric fan located in front of the participant. Seasonal acclimatization enhanced WBSR, unevaporated sweat rate, local sweat rate and mean skin temperature compared with preacclimatization state (all P < 0.05) whereas sweating efficiency was lower (P < 0.01) until 55 min of exercise. Tcore and evaporated sweat rate were unaltered by acclimatization status (all P > 0.70). In conclusion, seasonal acclimatization enhances thermoeffector responses but does not attenuate Tcore during exercise in a hot-humid environment. Furthermore, increasing air velocity enhances evaporated sweat rate and sweating efficiency irrespective of acclimated state. NEW & NOTEWORTHY Seasonal acclimatization to humid heat enhances eccrine sweat gland function and thus results in a higher local and whole body sweat rate but does not attenuate Tcore during exercise in a hot-humid environment. Sweating efficiency is lower after seasonal acclimatization to humid heat compared with preacclimatization with and without the increase of air velocity. However, having a lower sweating efficiency does not mitigate the Tcore response during exercise in a hot-humid environment.

Methods for the Administration of EDAR Pathway Modulators in Mice.

Genetic deficiency of ectodysplasin A (EDA) causes X-linked hypohidrotic ectodermal dysplasia, a congenital condition characterized by the absence or abnormal formation of sweat glands, teeth, and several skin appendages. Stimulation of the EDA receptor (EDAR) with agonists in the form of recombinant EDA or anti-EDAR antibodies can compensate for the absence of Eda in a mouse model of Eda deficiency, provided that agonists are administered in a timely manner during fetal development. Here we provide detailed protocols for the administration of EDAR agonists or antagonists, or other proteins, by the intravenous, intraperitoneal, and intra-amniotic routes as well as protocols to collect blood, to visualize sweat gland function, and to prepare skulls in mice.

The stiffness of hydrogel-based bioink impacts mesenchymal stem cells differentiation toward sweat glands in 3D-bioprinted matrix.

Mechanical aspects of printable hydrogels can impact cell behavior in 3D-bioprinted constructs, and in this context the stiffness of hydrogel-based bioink can serve as an important physical cue in regulating cell differentiation. Here we bioprinted mesenchymal stem cells (MSCs) by the commonly used bioink alginate-gelatin (Alg-Gel) blends and investigated the influence of stiffness on MSC differentiation toward sweat glands. Mechanical properties were assessed through compression testing and it was found that higher compressive modulus was associated with the higher Alg-Gel concentrations. Using these Alg-Gel blends for bioprinting, we demonstrated that stiffness variance cannot cause differences in cell spreading, adhesion and viability. However, MSCs bioprinted by stiffer hydrogels were found to further upregulate the protein and gene expression of sweat gland cell phenotype, function and development of signaling pathways. Furthermore, we found that the increased Yes-associated protein (YAP) localization of nuclei in MSCs when bioprinted by stiffer hydrogels. These results illustrated that the stiffness of Alg-Gel blends is a potent regulator of MSC differentiation, which was possibly achieved through a YAP-dependent mechanotransduction mechanism.

Randomized controlled three-arm study of NADA acupuncture for alcohol addiction

IntroductionAlcohol addiction compromises cardiovascular health, possibly due to impaired control of the heart and vasculature by the autonomic nervous system. We aimed to assess the effects of National Acupuncture Detoxification Association (NADA) acupuncture on cardiovascular autonomic functions, psychiatric comorbidities and abstinence in patients addicted to alcohol. Material and methodsA randomized sham controlled three-arm study was undertaken in 72 patients (nine females, aged 43.7 ± 9.2 years, mean ± SD) undergoing in-patient rehabilitation for alcohol addiction. Patients were randomly allocated (1:1:1) to receive twenty 30-minute NADA or sham acupuncture sessions within six weeks or no intervention. They were evaluated for craving, depression, anxiety and autonomic control of the heart (heart rate variability, HRV), vasculature (laser Doppler flowmetry) and sweat glands (sympathetic skin response). Testing was performed at baseline, immediately post intervention (sham intervention or control period, respectively) and another four weeks later. Abstinence was assessed one year after study completion. ResultsPatients in the NADA arm displayed increased HRV immediately post-intervention compared to baseline (SDNN: 72.8 ms ± 34.2 ms vs. 57.9 ms ± 31.2 ms, p = 0.001). This increase was sustained four weeks later (66.2 ms ± 32.4 ms, p = 0.015). HRV remained unaltered following sham or no acupuncture (p = n.s.). Autonomic function of vasculature and sweat glands, psychiatric comorbidities and one-year abstinence did not differ between study arms. ConclusionsNADA acupuncture may improve autonomic cardiac function. However, this improvement appears not to translate into alleviation of psychiatric comorbidities or sustained abstinence.