2003
DOI: 10.1016/s0378-5122(02)00317-1
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Kava–Kava administration reduces anxiety in perimenopausal women

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Cited by 48 publications
(36 citation statements)
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“…These studies showed kava's therapeutic potential both as a monotherapy for patients with anxiety disorder [48], GAD [43,44,49], elevated generalized anxiety [47] and those being tapered off of benzodiazepines [45], as well as in combination with calcium for perimenopausal women [46]. …”
Section: Resultsmentioning
confidence: 99%
“…These studies showed kava's therapeutic potential both as a monotherapy for patients with anxiety disorder [48], GAD [43,44,49], elevated generalized anxiety [47] and those being tapered off of benzodiazepines [45], as well as in combination with calcium for perimenopausal women [46]. …”
Section: Resultsmentioning
confidence: 99%
“…Two small RCTs evaluated the effects of kava extract on anxiety symptoms in peri-70 and postmenopausal women 71 ; the efficacy of kava extract plus calcium supplementation in reducing anxiety symptoms was superior than calcium supplementation only (control group). 70 The combination of kava extract 1 hormone therapy was more efficacious than hormone alone to alleviate anxiety symptoms in 40 postmenopausal women and this effect was maintained after 6 months of treatment. 71 Although preliminary, these findings suggest that kava extract may be a useful option in the management of anxiety during menopausal transition and the postmenopausal years.…”
Section: Managing Anxiety During Midlifementioning
confidence: 96%
“…In addition to being used to treat mild or moderate anxiety, kava preparations are used for insomnia, stress, menopause, and muscle fatigue. Experiments with animal models and epidemiological data have shown that kava has a wide spectrum of therapeutic properties, such as sedative, anxiolytic, analgesic, and neuroprotective effects (Jamieson and Duffield, 1990;Martin et al, 2000;Wheatley, 2001;Singh and Singh, 2002;Cagnacci et al, 2003). It has been postulated that these activities are achieved through multiple mechanisms, such as blockade of voltage-gated sodium channels (Schirrmacher et al, 1999), enhanced interactions between ligand and corresponding receptors (e.g., aminobutyric acid type A receptor) (Davies et al, 1992), modulation on neurotransmitter release (Baum et al, 1998), inhibition of enzyme activity (e.g., cyclooxygenase-2) (Wu et al, 2002), and decrease in cytokine release (e.g., tumor necrosis factor-␣; TNF-␣) (Hashimoto et al, 2003).…”
mentioning
confidence: 99%