Mechanism of hot flashes

Vilar-González, Santiago; Pérez-Rozos, A.; Cabanillas-Farpón, Ruben

doi:10.1007/s12094-011-0633-x

Cited by 9 publications

(3 citation statements)

References 40 publications

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“…Since HFs are thought to occur due to the changes in thermoregulation induced by oestrogen deprivation, with a consequent decrease in serotonin levels [19], the block of serotonin and norepinephrine receptors induced by SSRIs and SNRIs may oppose this imbalance.…”

Section: Management Of Vasomotor Menopausal Symptoms With Non-hormonamentioning

confidence: 99%

Non-hormonal strategies for managing menopausal symptoms in cancer survivors: an update

Biglia

Bounous

Seta

et al. 2019

ecancer

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Vasomotor symptoms, particularly hot flushes (HFs), are the most frequently reported symptom by menopausal women. In particular, for young women diagnosed with breast cancer, who experience premature ovarian failure due to cancer treatments, severe HFs are an unsolved problem that strongly impacts on quality of life. The optimal management of HFs requires a personalised approach to identify the treatment with the best benefit/risk profile for each woman. Hormonal replacement therapy (HRT) is effective in managing HFs but it is contraindicated in women with previous hormone-dependent cancer. Moreover, many healthy women are reluctant to take HRT and prefer to manage symptoms with non-hormonal strategies. In this narrative review, we provide an update on the current available non-oestrogenic strategies for HFs management for women who cannot, or do not wish to, take oestrogens. Since isoflavones have oestrogenic properties and it is not known if they can be safely consumed by women with previous hormone-dependent cancer, they were excluded. Selective serotonin reuptake inhibitors/selective serotonin-norepinephrine reuptake inhibitors, as well as other neuroactive agents, some herbal remedies and behavioural strategies are considered.

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Section: Management Of Vasomotor Menopausal Symptoms With Non-hormonamentioning

confidence: 99%

Non-hormonal strategies for managing menopausal symptoms in cancer survivors: an update

Biglia

Bounous

Seta

et al. 2019

ecancer

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“…Oestrogens modulate serotonin and noradrenalin activity in the brain and these neurotransmitters participate to the hypothalamic thermoregulation (Boulant ; Romanovsky ; Rossmanith & Ruebberdt ; Vilar‐González et al . ). Serum serotonin concentrations in post‐menopausal women are inversely related to the intensity of climacteric symptoms (Słopień et al .…”

Section: Discussionmentioning

confidence: 97%

Duloxetine and escitalopram for hot flushes: efficacy and compliance in breast cancer survivors

et al. 2016

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Selective serotonin reuptake inhibitors (SSRI) and serotonin-norepinephrine reuptake inhibitors (SNRI) might be an effective treatment for hot flushes (HFs) in breast cancer survivors (BCSs). This study aims to compare the efficacy and tolerability of duloxetine (SNRI) versus escitalopram (SSRI) in reducing frequency and severity of HFs in BCSs and to assess the effect on depression. Thirty-four symptomatic BCSs with emotional impairment received randomly duloxetine 60 mg daily or escitalopram 20 mg daily for 12 weeks. Patients were asked to record in a diary HF frequency and severity at baseline and after 4 and 12 weeks of treatment. Depression was evaluated through validated questionnaires (Beck Depression Inventory and Montgomery Asberg Depression Rating Scale) at baseline and after 4 and 12 weeks of treatment. Both drugs showed a significant reduction of HF frequency and severity after 12 weeks of treatment with no significant difference between the two groups. A significant improvement in depression symptoms was observed at the end of the study period within both the groups, without difference between the two drugs. In conclusion, escitalopram and duloxetine are both effective treatment for the relief of HFs in BCSs, with similar beneficial effect. A significant improvement of depression was obtained with no major side effects.

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“…Hot flashes underline complex endocrine, epigenetic and neuroendocrine mechanisms; kisspeptin, neurokinin B, noradrenaline, 5-hydroxytriptamine (5-HT), calcitonin gen-related peptide are involved (12)(13)(14). Estrogen deficiency uncouple the negative feedback with hypothalamus; dysfunction of hypothalamic thermoregulation consists in a exacerbated vasodilatory response to a small increase of body temperature (a narrowed window of thermoregulation) (12,14). Hypothalamic regulation of body temperature affects preoptic area where different neurotransmitters and their receptors play a role in heat resumption (15).…”

Section: Mechanisms Of Hot Flashesmentioning

confidence: 99%

Untitled

2021

Ro Med J.

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Hot flashes (HF), transitory episodes of erythema, heat sensation, anxiety followed by chills, are described in carcinoid syndrome, mastocytosis, medullary thyroid cancer, hyperthyroidism, pheochromocytoma, alcohol consumption, side effects of drugs, and infections. They are pivotal among menopause-related vasomotor symptoms beside genitourinary syndrome in addition to sleep disturbances (40-60% of females), and metabolic changes. HF affect 70% of women (20% of them have a severe impairment of life quality); they last for 4-7 years, starting 4-6 years before last menstruation. The main HF cause is ovarian-derivate estrogen deprivation which activates complex endocrine and neuroendocrine mechanisms involving noradrenaline, 5-hydroxytriptamine (5-HT), calcitonin gen-related peptide, orexin, kisspeptin, neurokinin B, and epigenetic elements like modulation of tachykinin receptor 3, accelerated epigenetic aging (as found in Women's Health Initiative Observational Study), expression of central serotonin transporters. Estrogen deficiency uncouples the negative feedback with preoptic area of hypothalamus, responsible for thermoregulation by inducing an exacerbated vasodilatory response to a small increase of body temperature. TRPV1 (transient receptor potential vanilloid 1) in preoptic hypothalamic area may play a role by NE-α2ADR (norepinephrine-activated α2-adrenergic receptors) activation. Higher expression of serotonin transporter SLC6A4 causes a lack of 5-HT at synapsis which is a trigger for presynaptic 5-HT receptor feedback, thus a release of serotonin amount prevents hot flashes. Kisspeptin and neurokinin B which are co-expressed in infundibular nucleus of hypothalamus are involved in central thermoregulation and gonadotropin releasing hormone anomalies. The NKR3 (neurokinin 3 receptor) antagonist receptor improves HF. Understanding the pivotal role of central neurotransmitters in hot flashes is the basis of new therapeutically researches because otherwise estrogen replacement has a long list of side effects, and it is contraindicated in breast cancer-related hypogonadism.

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Mechanism of hot flashes

Cited by 9 publications

References 40 publications

Non-hormonal strategies for managing menopausal symptoms in cancer survivors: an update

Non-hormonal strategies for managing menopausal symptoms in cancer survivors: an update

Duloxetine and escitalopram for hot flushes: efficacy and compliance in breast cancer survivors

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