How can food influence the severity of menopausal hot flashes?

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In a recent review published in Nutrients, researchers reviewed scientific literature from the previous five years, especially genome-wide association studies (GWAS), to identify mechanisms and nutrients related to menopause hot flashes.

Study: Menopause Hot Flashes and Molecular Mechanisms Modulated by Food-Derived Nutrients. Image Credit: fizkes/Shutterstock.comStudy: Menopause Hot Flashes and Molecular Mechanisms Modulated by Food-Derived Nutrients. Image Credit: fizkes/Shutterstock.com

Background

The etiology of vasomotor symptoms (VMS), such as hot flashes, is unknown; however, they may be molecular and polygenic.

Food provides bioactive compounds and nutrients to the human body, digested via several enzymatic biological pathways. The compounds can stimulate molecular signaling pathways, which activate effector protein molecules controlling hot flashes experienced by menopausal women.

About the review

In the present review, researchers explored the biological mechanisms underlying menopause hot flashes and related food-derived nutrients.

Introduction

Menopause refers to a physiological process that affects women at 50 years of age, characterized by a year of amenorrhea with no additional pathological or physiological factors.

The menopausal transitional phase, occurring between irregular menstrual periods and menopause, precedes this one year.

Menopausal transition symptoms include monthly irregularities, hot flashes, sleeplessness, sweating, vertigo, palpitation, tinnitus, headache, memory issues, mood changes, lack of focus, skin changes, genitourinary atrophy, and body weight changes.

Hot flashes, a common menopausal transitional feature, may present with palpitations, night sweats, irritability, and anxiety and lasts two to four minutes.

Hot flashes might occur infrequently or at least once per hour and are frequently associated with worse life quality, decreased productivity, reduced mood, embarrassment, exhaustion, anxiety, sleep disruption, social isolation, and impaired memory performance.

Hormone therapies are highly effective in treating hot flashes but are not always feasible. Future studies on pathways underlying menopause hot flashes could aid in developing targeted therapies, as foods might alter the processes of menopause hot flashes and regulate their effects.

Nutritional compounds and pathways involved in menopause hot flashes

Several biochemical pathways and compounds cause hot flashes, a frequent symptom of menopause. These pathways differ from individual to individual and involve thermoregulatory processes controlled by the parasympathetic and sympathetic nervous systems.

Thermoregulatory processes, such as the upregulation of neuropeptides like kisspeptin and neurokinin B, help to dissipate heat during menopause.

Nutritional compounds that modulate signaling pathways, such as nutrients that modulate the kisspeptin-gonadotropin-releasing hormone (GnRH) pathway; nutrients that modulate the aryl hydrocarbon receptor (AHR) signaling; catechol estrogens and estrogen sulfotransferase; and nutrients that modulate the inflammatory-oxidative stress biomarker, may cause hot flashes.

Compounds linked to hot flashes include genistein, docosahexaenoic acid (DHA), polyunsaturated fatty acid (PUFA), saturated fatty acid (SFA), β-carotene, curcumin, folic acid (Pteroyl-L-glutamic acid), vitamin B12, high-fat diet components, tryptophan metabolites, apigenin, chrysin, epicatechin, quercetin, resveratrol, and vitamin E.

Genistein boosts GnRH production via regulating kisspeptin receptors, sirtuin 1 (SIRT1), protein kinase c γ (PKCγ), and makorin ring finger protein 3 (MKRN3). DHA, PUFA, and SFA promote GnRH mRNA expression.

Palmitate disrupts hypothalamic function in GnRH neurons by regulating spexin (SPX) and its receptors, galanin receptor 2 (GALR2) and galanin receptor 3 (GALR3), through pathways involving protein kinase C (PKC), mitogen-activated protein kinases (MAPKs), and Toll-like receptor 4 (TLR4).

β-carotene, curcumin, tryptophan metabolites, and high-fructose diet (HFD) components such as cholesterol, fructose, and palmitic acid activate aryl hydrocarbon receptors (AHR) and folic acid and vitamin B12 inhibit their transcriptional activity.

Vitamin E lowers hot flashes over the week and enhances antioxidant status by boosting total antioxidant capacity (TAC). Higher ghrelin levels are associated with an increased risk of hot flashes in women in the early and late stages of menopause.

Hot flashes are associated with insulin resistance in postmenopausal women, and the relationship between the two depends on the leptin-adiponectin interaction.

Low estrogen activation of glucose transporter 1 (GLUT) may cause hot flashes, a frequent central nervous system symptom. Studies have demonstrated significant connections between SNPs in numerous genes, including aryl hydrocarbon receptor (AHR), aryl hydrocarbon receptor repressor (AHRR), aryl hydrocarbon receptor nuclear translocator (ARNT), catechol-O-methyltransferase (COMT), and cytochrome P450 (CYP) enzymes such as CYP1 A2, CYP3A4, and CYP19 A1.

These symptoms are most prevalent among African American women, Asian women, and white women of Hispanic and non-Hispanic heritage in the United States.

Conclusion

To conclude, based on the review findings, several variables, including food-derived nutrients and molecular pathways, impact hot flashes, a frequent symptom of menopause.

These symptoms are a primary concern for women, and understanding the underlying causes is critical. Modifying these processes may help relieve hot flash symptoms.

Hot flashes may be associated with lower estrogen levels, hypothalamic processes, adipocyte-derived hormones, the kisspeptin-GnRH pathway, aryl hydrocarbon receptor signaling, glucose availability, inflammatory-oxidative stress, catechol estrogens, and estrogen sulfotransferase.

Journal reference:
Pooja Toshniwal Paharia

Written by

Pooja Toshniwal Paharia

Dr. based clinical-radiological diagnosis and management of oral lesions and conditions and associated maxillofacial disorders.

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