The Predictive Role of ADRA2A rs1800544 and HTR3B rs3758987 Polymorphisms in Motion Sickness Susceptibility.

Motion sickness is a common central nervous system response, the primary sign of which is vomiting. Its susceptibility varies between individuals. To find predictive factors, we investigated the association of ADRA2A rs1800544 and HTR3B rs3758987 with motion sickness susceptibility and examined their mRNA changes during actual voyages. A total of 315 healthy college students were enrolled for SNP genotyping by the PCR-RFLP method. Blood samples were collected from another 42 subjects during two separate voyages to detect their mRNA expression changes at three time points. The frequency of the rs1800544 GG genotype in the susceptibility group was significantly higher (52.26%), and allele G increased the risk of motion sickness (OR = 1.585, 95% CI = 1.136-2.208). In the logistic regression model, the rs3758987 CC+TC genotype and rs1800544 GG genotype increased the risk of motion sickness-induced vomiting (OR = 2.105, 95% CI = 1.112-3.984; OR = 1.992, 95% CI = 1.114-3.571). The ADRA2A mRNA baseline was lower in the GG carriers and the HTR3B mRNA baseline was lower in the TC/CC carriers before sailing, then increased significantly within 24 h and then decreased after a long-term voyage. People carrying the rs1800544 GG genotype seem more susceptible to motion sickness. In combination with the incidence of vomiting during the actual-voyage experiments, our results indicate the involvement of rs1800544 and rs3758987 in motion sickness-induced vomiting.

Genetic Analysis of a Large Family with Migraine, Vertigo, and Motion Sickness.

BACKGROUND: Migraine is a common disorder most typically presenting as headache and often associated with vertigo and motion sickness. It is a genetically complex condition with multiple genes ultimately contributing to the predisposition and development of this episodic neurological disorder. We identified a large American family of 29 individuals of which 17 members suffered from at least one of these disorders, migraine, vertigo, or motion sickness. Many of these individuals suffered from several simultaneously. We hypothesized that vertigo and motion sickness may involve genes that are independent to those directly contributing to migraine susceptibility. METHODS: Genome-wide linkage analysis performed using 400 microsatellite repeat markers spaced at 10 cM throughout the genome. The members of this family were phenotyped for each condition, migraine, vertigo, and motion sickness and analyzed separately. Statistical analysis was performed using two-point and multipoint linkage analysis employing a number of models including autosomal recessive or dominant patterns of inheritance with high and low genetic penetrance. RESULTS: We identified a novel locus for migraine, 9q13-q22 (maximum two-point logarithm of odds [LOD] score-2.51). In addition, there are suggestive LOD scores that localize to different chromosomes for each phenotype; vertigo (chromosome 18, LOD score of 1.82) and motion sickness (chromosome 4, LOD score of 2.09). CONCLUSIONS: Our analysis supports our hypothesis that the migraine-associated vertigo and motion sickness may involve distinct susceptibility genes.

Analyse génétique d'une famille étendue dont les membres souffrent de migraines, de vertiges et du mal des transports. Contexte : La migraine est un trouble courant qui entraîne habituellement des maux de tête et qui est souvent associé à des vertiges et au mal des transports. Il s'agit aussi d'une condition génétique complexe en vertu de laquelle de nombreux gènes contribuent à terme à cette prédisposition et au développement de ce trouble neurologique périodique. À cet égard, nous avons identifié une famille étendue américaine comptant 29 membres. De ce nombre, 17 d'entre eux avaient souffert d'au moins un de ces troubles : des migraines, des vertiges ou le mal des transports. À noter que plusieurs d'entre eux avaient souffert de ces troubles en même temps. Nous avons émis l'hypothèse que les vertiges et le mal des transports pourraient impliquer des gènes qui sont indépendants de ceux contribuant directement à la propension aux migraines. Méthodes : Nous avons effectué une analyse de liaison au moyen de 400 marqueurs microsatellites répétés et espacés à tous les 10 cm au sein de l'ensemble du génome des membres de cette famille. Les membres de cette famille ont été « phénotypés ¼ pour chaque type de trouble (les migraines, les vertiges et le mal des transports) et ont été ensuite analysés de façon séparée. Nous avons effectué une analyse statistique au moyen de l'analyse de liaison multipoint et à deux points, utilisant pour ce faire un certain nombre de modèles, par exemple le modèle autosomique récessif ou des patterns dominants de transmission avec une pénétrance génétique élevée ou faible. Résultats : Nous avons été en mesure d'identifier un nouveau locus dans le cas de la migraine : 9q13-q22 (maximum 2-points ; score au logarithme des probabilités ou LOD : - 2,51). De plus, il est des scores révélateurs au logarithme des probabilités qui permettent de localiser divers chromosomes pour chaque phénotype : vertiges (chromosome 18 ; score au logarithme des probabilités ou LOD : 1,82) et mal des transports (chromosome 4 ; score au logarithme des probabilités ou LOD : 2,09). Conclusions : Notre analyse confirme ainsi notre hypothèse initiale, à savoir que les cas de migraine auxquels sont associés des vertiges et le mal des transports pourraient très bien impliquer différents gènes de susceptibilité.

Targeting TRPV1 to relieve motion sickness symptoms in mice by electroacupuncture and gene deletion.

Motion sickness (MS) is an acute disorder that occurs in healthy individuals worldwide regardless of gender, age, or ethnicity. Our study used a mouse model to rule out the effects of any psychological factors related to MS and EA. Subjects were randomly separated into four groups, namely the control group (Con), motion sickness inducing group (MS), mentioning sickness inducing with electroacupuncture treatment group (EA) and motion sickness inducing only in TRPV1 knockout mice group (TRPV1-/-). The consumption of kaolin, a non-nutrient substance, was measured as a behavior observed response of an emetic reflex in a murine model. This behavior is referred to as pica behavior. Our results showed that pica behavior was observed in the MS group. Moreover, kaolin consumption in the EA group decreased to the average baseline of the control group. A similar result was observed in TRPV1 null mice. We also observed an increase of TRPV1 and related molecules in the thalamus, hypothalamic and brain stem after MS stimulation and a significant decrease in the EA and TRPV1 null groups. This is the first study to demonstrate that TRPV1 pathways are possibly associated with mechanisms of MS, and can be attended through EA or TRPV1 genetic manipulation.

Acupuncture relieves motion sickness via the IRß-ERK1/2-dependent insulin receptor signalling pathway.

OBJECTIVE: Acupuncture has been widely used for the treatment of motion sickness (MS), but the underlying mechanisms are unclear. The aim of this research was to study the mechanism of acupuncture in the treatment of MS. METHODS: To observe the effects of acupuncture in the treatment of MS, 80 rats were randomised into five groups that were subjected to acceleration and either remained untreated (CTRL), or received restraint (REST), scopolamine (SCOP) or acupuncture at SP4 (sham) or PC6+ST36 (verum) acupuncture points. To study the mechanism underlying the effects of acupuncture in the treatment of MS, 48 rats were randomised into three groups: acupuncture+extracellular regulated protein kinases (ERK) 1/2 inhibitor (ERKinh), acupuncture+insulin receptor (IR) antagonist (IRant), and acupuncture+vehicle (VEH). After acceleration, the MS index (MSI) and spontaneous activity (SA) of the rats were recorded. Serum stress hormones, Fos-positive cells, c-fos mRNA in the vestibular nucleus, and IRß-, p-IRß-, ERK1/2- and p-ERK1/2-positive cells in the dorsal motor nucleus of the vagus nerve (DMV) were detected. RESULTS: After acceleration, MS symptoms in the PC6+ST36 and SCOP groups were reduced compared with the CTRL, REST, and SP4 groups. The number of p-IRß- and p-ERK1/2-positive cells and insulin levels were higher in the PC6+ST36 group than in the CTRL, REST, and SP4 groups. After ERK1/2 inhibitor and IR antagonist treatment, MS symptoms in the VEH group were lower than in the ERKinh and IRant groups. CONCLUSIONS: Our study demonstrates that acupuncture significantly alleviates MS through the IRß-ERK1/2-dependent insulin receptor signalling pathway in the DMV.

Storage of passive motion pattern in hippocampal CA1 region depends on CaMKII/CREB signaling pathway in a motion sickness rodent model.

Sensory mismatch between actual motion information and anticipated sensory patterns (internal model) is the etiology of motion sickness (MS). Some evidence supports that hippocampus might involve the neural storage of the "internal model". This study established an "internal model" acquisition-retention behavioral model using a repeated habituation rotation training protocol. We tried to identify the hippocampal subregion involved in "internal model" retention using chemical lesion methods. Hippocampal kinases (CaMK, CaMKIV, CREB and ERK1/2) phosphorylation in the target subregion was assayed and the effects of kinase inhibitors (KN93 or U0126) on "internal model" retention were investigated. The activities of potential kinases (CaMKII and CREB) were also examined in otoliths deficit het/het mice. In habituated rats, CA1 lesion reproduced MS-related behavioral responses on "internal model" retention day. Habituation training increased CaMKII and CREB activity but had no effect on CaMKIV and ERK1/2 activity in the CA1, while inhibition of CaMKII but not ERK1/2 impaired "internal model" retention. In het/het mice, CaMKII and CREB were not activated in the CA1 on the retention day. These results suggested that CaMKII/CREB pathway might potentially contribute to the storage of the "internal model" in the hippocampal CA1 after motion sickness induced by vestibular stimulation.

Management of mal de debarquement syndrome as vestibular migraines.

OBJECTIVE: Mal de debarquement syndrome (MdDS) is a balance disorder that typically starts after an extended exposure to passive motion, such as a boat or plane ride. Management is typically supportive (e.g. physical therapy), and symptoms that persist beyond 6 months have been described as unlikely to remit. This study was conducted to evaluate the response of patients with MdDS to management with migraine prophylaxis, including lifestyle changes and medical therapy. STUDY DESIGN: Prospective review. SETTING: Ambulatory setting at a tertiary care medical center. METHODS: Clinical history, detailed questionnaires, and audiograms were used to diagnose patients with MdDS. Those patients with the diagnosis of the MdDS were placed on our institutional vestibular migraine management protocol. Treatment response was assessed with a quality-of-life (QOL) survey and visual analog scale. RESULTS: Fifteen patients were diagnosed with MdDS, with a predominance of females (73%) and a mean age of 50 ± 13 years. Eleven patients (73%) responded well to management with a vestibular migraine protocol, which included lifestyle changes, as well as pharmacotherapy with verapamil, nortriptyline, topiramate, or a combination thereof. In comparison, a retrospective control group of 17 patients demonstrated a lower rate of improvement when treated with vestibular rehabilitation and physical therapy. CONCLUSION: Management of MdDS as vestibular migraine can improve patients' symptoms and increase the QOL. Nearly all the patients suffering from MdDS had a personal or family history of migraine headaches or had signs or symptoms suggestive of atypical migraine. LEVEL OF EVIDENCE: 4 Laryngoscope, 127:1670-1675, 2017.

[23andMe and motion sickness]. / 23andMe et le mal des transports - Chroniques génomiques.

A Genome Wide Association Study on propensity to motion sickness published by 23andMe gives interesting results, shows validity for self-reported phenotypic information and underlines the value of the model developed by the company for customer participation in genetic studies.

Motion Sickness: Current Knowledge and Recent Advance.

Motion sickness (MS) is a common physiological response to real or virtual motion. Numerous studies have investigated the neurobiological mechanism and the control measures of MS. This review summarizes the current knowledge about pathogenesis and pathophysiology, prediction, evaluation, and countermeasures of MS. The sensory conflict hypothesis is the most widely accepted theory for MS. Both the hippocampus and vestibular cortex might play a role in forming internal model. The pathophysiology focuses on the visceral afference, thermoregulation and MS-related neuroendocrine. Single-nucleotide polymorphisms (SNPs) in some genes and epigenetic modulation might contribute to MS susceptibility and habituation. Questionnaires, heart rate variability (HRV) and electrogastrogram (EGG) are useful for diagnosing and evaluating MS. We also list MS medications to guide clinical practice. Repeated real motion exposure and combined visual-vestibular interaction training accelerate the progress of habituation. Behavioral and dietary countermeasures, as well as physiotherapy, are also effective in alleviating MS symptoms.

AVP modulation of the vestibular nucleus via V1b receptors potentially contributes to the development of motion sickness in rat.

BACKGROUND: Arginine vasopressin (AVP) is considered to be an etiologic hormone in motion sickness (MS). The present study was designed to investigate whether individual differences in AVP expression in the paraventricular nucleus (PVN) and in modulation on the vestibular nucleus (VN) are involved in MS. Systemic application or microinjection of AVP into rat VN and rotatory stimulus were used to induce conditioned taste aversion (CTA) to 0.15 % saccharin sodium solution as a model of MS. RESULTS: Intra-VN use of SSR149415, an antagonist of V1b receptors (V1bRs), blunted CTA. AVP inhibited Ca(2+) influxes through L-type Ca(2+) channels and NMDA receptor channels in cultured VN neurones, but antagonised by SSR149415. More AVP and V1bRs were expressed respectively in the PVN and VN after rotatory stimulus, especially in rats susceptible to MS. In the VN, AVP content was low, the AVP mRNA was less expressed, a few AVP-positive fibres were sparsely distributed, and fewer AVP/synaptophysin-positive terminals were identified. Almost no fluoro-ruby-labelled AVP-positive neurones in the PVN were found with retrograde tracing from the VN. SNP analysis of the reported 9 sites of the AVP gene showed significant difference between the groups susceptible and insusceptible to MS at the site rs105235842 in the allele frequencies and genotypes. However, there was not any difference between these two groups in the SNP of the reported 38 sites of V1bR gene. CONCLUSIONS: AVP, through its modulatory, possibly humoral action on the VN neurones via the mediation of V1bR, may contribute to the development of motion sickness in rats; AVP gene polymorphisms may contribute to the individual difference in the responsive expression of AVP in the PVN; and higher expressions of AVP in the PVN and V1bRs in the VN may contribute to the development of motion sickness in rats after vestibular stimulation.

2000 CDC or 2007 WHO – What is the most sensitive anthropometric reference for determination of overweight and cardio-metabolic risk in children aged 6–10 years?

Objective To compare the two anthropometric standards for screening of overweight and cardio-metabolic risk in 6–10-year-old children.Subjects and methods This cross-sectional study included 175 subjects attending the Referral Center for the Treatment of Children and Adolescents in Campos, Rio de Janeiro. They were classified according to CDC and WHO BMI z scores as normal-weight (z-score > –1 and < 1), overweight (z-score ≥ 1 and < 2) or obese (z-score ≥ 2). Sensitivities and specificities in predicting systolic (SBP), diastolic (DBP) blood pressure and homeostatic model assessment insulin resistance index (HOMA-IR) alterations were calculated.Results There was a major difference in 11 children who rated overweight by the CDC but were reclassified as obese by the WHO. Their mean z-scores for SBP (1.71 ± 1.54), DBP (2.64 ± 1.83) and HOMA-IR (1.84 ± 0.98) were higher than those classified as overweight by both references (SBP = 0.49 ± 1.34, p < 0.023, DBP = 1.45 ± 0.97, p < 0.04 and HOMA = 1.24 ± 0.67, p < 0.04), but were similar to those classified as obese by both criteria (SBP = 1.25 ± 2.04, p = 0.60, DBP = 1.94 ± 1.19, p = 0.50 and HOMA = 2.09 ± 1.12, p = 0.76).Conclusion the 2007 WHO reference was the most sensitive in screening for overweight and alterations in blood pressure and HOMA-IR in 6–10-year-old children. Arch Endocrinol Metab. 2015;59(3):220-5.

Differential Gene Expression Profile in the Rat Caudal Vestibular Nucleus is Associated with Individual Differences in Motion Sickness Susceptibility.

OBJECTIVE: To identify differentially expressed genes associated with motion sickness (MS) susceptibility in the rat caudal vestibular nucleus. METHODS: We identified MS susceptible (MSS) and insusceptible (inMSS) rats by quantifying rotation-induced MS symptoms: defecation and spontaneous locomotion activity. Microarray analysis was used to screen differentially expressed genes in the caudal vestibular nucleus (CVN) after rotation. Plasma stress hormones were identified by radioimmunoassay. Candidate genes were selected by bioinformatics analysis and the microarray results were verified by real-time quantitative-PCR (RT-qPCR) methods. By using Elvax implantation, receptor antagonists or recombinant adenovirus targeting the candidate genes were applied to the CVN to evaluate their contribution to MS susceptibility variability. Validity of gene expression manipulation was verified by RT-qPCR and western blot analysis. RESULTS: A total of 304 transcripts were differentially expressed in the MSS group compared with the inMSS group. RT-qPCR analysis verified the expression pattern of candidate genes, including nicotinic cholinergic receptor (nAchR) α3 subunit, 5-hydroxytryptamine receptor 4 (5-HT4R), tachykinin neurokinin-1 (NK1R), γ-aminobutyric acid A receptor (GABAAR) α6 subunit, olfactory receptor 81 (Olr81) and homology 2 domain-containing transforming protein 1 (Shc1). In MSS animals, the nAchR antagonist mecamylamine significantly alleviated rotation-induced MS symptoms and the plasma ß-endorphin response. The NK1R antagonist CP99994 and Olr81 knock-down were effective for the defecation response, while the 5-HT4R antagonist RS39604 and Shc1 over-expression showed no therapeutic effect. In inMSS animals, rotation-induced changes in spontaneous locomotion activity and the plasma ß-endorphin level occurred in the presence of the GABAAR antagonist gabazine. CONCLUSION: Our findings suggested that the variability of the CVN gene expression profile after motion stimulation might be a putative molecular basis for individual differences in MS susceptibility and provide information for the development of new therapeutic strategies for MSS individuals.

Motion sickness: an evolutionary and genetic basis for the negative reinforcement model.

It has been theorized that motion sickness evolved as a negative reinforcement system which terminates motion involving postural instability and/or sensory conflict. A hypothetical example is provided by a "thought experiment" whereby protohominids are in a tree looking for food. Selection pressure results when the organisms that have an aversion to motion-producing sensory conflict do not venture out too far on the tree limbs and therefore tend to survive. In order to support an evolutionary model for motion sickness there must be evidence for genetic and/or heritable predisposition. The present study involves a retrospective literature review which reveals abundant evidence for genetic/heritable factors in motion sickness. Examples include genetic polymorphism of the alpha-2-adrenergic receptor, which has been shown to increase susceptibility to motion sickness, examination of family trees revealing heritable motion sickness susceptibility, evidence indicating that Asians are hyper-susceptible to motion sickness, and twin studies, just to mention a few. Thus, the theory of heritable negative reinforcement as a basis for motion sickness is supported by extensive evidence in the medical literature. This theory is compared and contrasted with other theories. Further areas for research are suggested.

Musk shrews selectively bred for motion sickness display increased anesthesia-induced vomiting.

Susceptibility to motion sickness is a predictor of postoperative nausea and vomiting, and studies in humans suggest that genetic factors determine sensitivity to motion sickness. The aim of the current study was to determine if a preclinical model could be selectively bred for motion-induced emesis and to assess a potential relationship to anesthesia-induced emesis. Musk shrews were tested for motion-induced emesis using a shaker plate (10min, 1Hz, and 4cm of lateral displacement). Animals were rank ordered for motion-induced emesis and selectively bred to produce high and low response strains. Shrews were also tested with nicotine (5mg/kg, sc), copper sulfate (CuSO4; 120mg/kg, ig), and isoflurane anesthesia (10min; 3%) to measure responses to a panel of emetic stimuli. High response strain shrews demonstrated significantly more emetic episodes to motion exposure compared to low response strain animals in the F1 and F2 generations. In F2 animals, there were no significant differences in total emetic responses or emetic latency between strains after nicotine injection or CuSO4 gavage. However, isoflurane exposure stimulated more emesis in F1 and F2 high versus low strain animals, which suggests a relationship between vestibular- and inhalational anesthesia-induced emesis. Overall, these results indicate genetic determinants of motion sickness in a preclinical model and a potential common mechanism for motion sickness and inhalational anesthesia-induced emesis. Future work may include genetic mapping of potential "emetic sensitivity genes" to develop novel therapies or diagnostics for patients with high risk of nausea and vomiting.

Effects of hypergravity on histamine H1 receptor mRNA expression in hypothalamus and brainstem of rats: implications for development of motion sickness.

CONCLUSION: The study findings suggest that histamine was released from the axon terminals in the hypothalamus and brainstem and the released histamine activated post-synaptic H1 receptors there, resulting in the development of motion sickness. OBJECTIVES: We first examined which subtype of post-synaptic histaminergic receptor was responsible for the development of motion sickness. We then examined whether H1 receptors were up-regulated in various areas of the rat brain after 2 G hypergravity load, because the stimulation of H1 receptor was reported to up-regulate the level of H1 receptor protein expression through augmentation of H1 receptor mRNA expression. MATERIALS AND METHODS: For this purpose, we used an animal model of motion sickness, using pica (eating non-nutritive substances such as kaolin), as a behavioral index in rats. RESULTS: After 2 G hypergravity load, rats ate a significant amount of kaolin, indicating that they suffered from motion sickness. The hypergravity-induced kaolin intake was suppressed by mepyramine, but not by terfinadine or zolantizine. This finding indicates that cerebral post-synaptic H1 but not H2 or peripheral H1 receptors play an important role in the development of motion sickness. The expression of H1 receptor mRNA was up-regulated in the hypothalamus and brainstem, but not in the cerebral cortex after 2 G hypergravity load in rats.

Genetic influences on motion sickness susceptibility in adult women: a classical twin study.

BACKGROUND: Motion sickness is a common and potentially debilitating condition that characteristically occurs in situations of conflicting sensory input. While the precise stimuli that give rise to this trait are increasingly well characterized, the underlying determinants of individual susceptibility to motion sickness remain unclear. This study uses a classical twin design to assess the influence of genetic and environmental factors. METHODS: A postal survey was conducted in an age-matched sample of 3652 monozygotic (MZ) and dizygotic (DZ) adult female twins selected from the TwinsUK Registry. Study participants were asked to complete items from a validated questionnaire relating to their lifetime susceptibility to motion sickness. The relative contribution of genetic and environmental factors to motion sickness susceptibility was assessed using variance components analysis. RESULTS: The response rate to the questionnaire was 78%. Approximately 40% of respondents reported at least moderate susceptibility to motion sickness. The pattern of responses among twins indicated a significant genetic contribution with heritability for a motion sickness factor score estimated as 57% (95% CI: 51%, 63%). The heritability of recalled motion sickness was at its highest in childhood (70% [59%, 80%]) and declined through puberty and the early adult years. DISCUSSION AND CONCLUSIONS: The findings highlight the importance of genetic factors in determining an individual's underlying propensity to motion sickness and should stimulate the search for specific susceptibility genes.

[Construction of the subtracted cDNA library in hypothalamus of the seasickness adaptive rats].

OBJECTIVE: To construct subtracted cDNA library in hypothalamus of the seasickness adaptive rats for providing theoretical basis for effective adaptive training against seasickness. METHODS: Suppression subtract hybridization technique was used, and forward and reverse hybridization was performed on the hypothalamus of seasickness adaptive rats and that of normal rats so that to construct subtracted cDNA library. Dot blot was used for differential screening the subtracted library. RESULTS: 23 fragments of differentially expressed genes was obtained including 10 up-regulating and 13 down-regulating fragments. CONCLUSION: Many played role in adaptability formation to seasickness such as SAM, vasopressin, and heme oxygenase.

[The human alpha(2A)-AR gene and the genotype of site -1296 and the susceptibility to motion sickness].

The gene sequences of alpha(2A)-adrenergic receptor(alpha(2A)-AR) in 39 Chinese and 1 Englishman showed 13 differences of g or c insertion or deletion in its regulation region, coding region and 3' untranslated region, compared with that reported in GenBank. The gene sequences from all the samples respectively were identical except for 2 single nucleotide polymorphisms, including the sequence of sense and antisense strand sequenced. It was found that: (1) the frequency of gg genotype in Chinese and Japanese, who are high susceptible to motion sickness, were 5.8 and 7.8 fold higher than that in Englishmen; (2) g allele frequencies in Chinese and Japanese were higher than latter ( P 0.01 ); (3) gg genotype frequency in population susceptible to motion sickness was 1.6 fold higher than that in population unsusceptible to motion sickness, and g allele frequency was higher than latter ( P 0.01 ). All the populations were in Hardy-Weinberg equilibrium. The results suggested that gg genotype and g allele at site -1296 in alpha(2A)-AR gene could associate with the susceptibility to motion sickness.

Asian hypersusceptibility to motion sickness.

A rotating optokinetic drum was used in three laboratory studies to test the hypothesis that Asian subjects are hypersusceptible to motion sickness. The results of the first study showed that Chinese women compared to European-American and African-American women experienced significantly more severe symptoms of motion sickness and greater disturbance of normal gastric myoelectric activity. A second study yielded similar results using American-born children of Asian parents. The results of a third study using Chinese men and women were similar and showed a significant increase in vasopressin during rotation. Possible genetic mechanisms that may account for these results are discussed.