CBD Gummies for Women's Health and Hormones: What Research Shows | PureCraft CBD
By PureCraft Editorial Team | PureCraft CBD | Updated October 2026
The endocannabinoid system and the female reproductive hormone axis are deeply interconnected — more so than most CBD discussions acknowledge. Estrogen directly upregulates FAAH expression (the enzyme that degrades anandamide), creating a cycle in which estrogen levels modulate endocannabinoid tone throughout the menstrual cycle, pregnancy, and menopause. CB1 and CB2 receptors are expressed in the uterus, ovaries, fallopian tubes, and endometrium — the ECS is not peripheral to female reproductive physiology, it is embedded in it. Prostaglandin-driven uterine cramping, endometrial CB1/CB2 dysregulation in endometriosis, androgen-ECS crosstalk in PCOS, and the HPA-estrogen axis in perimenopausal mood and sleep disruption all represent specific, mechanistically grounded targets for CBD. This article covers what research suggests about CBD gummies and women's health — with honest differentiation between the strong preclinical and mechanistic evidence and the areas where dedicated women's health RCT data is still emerging.
The Estrogen-ECS Axis: Why CBD Is Uniquely Relevant to Women's Health
Estrogen Regulates Endocannabinoid Tone
The most fundamental connection between female hormones and the ECS is estrogen's direct regulation of FAAH — the enzyme that degrades anandamide. High estrogen levels (late follicular phase, around ovulation) upregulate FAAH expression, accelerating anandamide breakdown and lowering endocannabinoid tone. Low estrogen levels (late luteal phase pre-menstruation, perimenopause, post-menopause) downregulate FAAH, allowing anandamide to accumulate — but this occurs against a background of increasing prostaglandin production (luteal phase) or declining overall sex hormone support (perimenopause).
This estrogen-FAAH dynamic has several practical implications: CBD's FAAH inhibition is most impactful during phases of high estrogen (high FAAH activity) — extending anandamide availability against an estrogen-driven degradation environment. The luteal phase (progesterone-dominant, pre-menstrual) is characterized by lower FAAH but higher prostaglandin production — CBD's anti-prostaglandin mechanism (via CB2/NF-κB reducing COX-2) becomes most relevant here. And in perimenopause, as estrogen declines, endocannabinoid tone itself fluctuates dramatically — creating the HPA dysregulation, sleep disruption, and mood volatility that CBD's 5-HT1A and HPA normalization mechanisms are well-positioned to address.
The Female Reproductive ECS: Uterus, Ovaries, and Endometrium
CB1 and CB2 receptors are expressed throughout female reproductive tissue. In the uterus, CB1 receptors on uterine smooth muscle cells modulate myometrial contractility — CB1 activation reduces uterine contractile force, providing the mechanistic basis for CBD's relevance to uterine cramping. CB2 receptors on uterine and endometrial immune cells regulate the inflammatory environment of the endometrium — the site of the prostaglandin-driven inflammation central to dysmenorrhea (menstrual cramps) and endometriosis. In the ovaries, CB1 and CB2 receptors modulate follicular development and corpus luteum function. Anandamide levels in follicular fluid correlate with oocyte quality. TRPV1 on uterine sensory nerves mediates the visceral pain signaling of cramping and endometriosis. The uterine ECS is not a discovered afterthought — it is an integral regulator of reproductive physiology that is dysregulated in multiple common women's health conditions.
Women's Health Conditions and CBD Mechanisms
| Condition | Core Biology | Primary CBD Mechanism | Evidence Level |
|---|---|---|---|
| Dysmenorrhea (menstrual cramps) | Prostaglandin PGF2α → uterine smooth muscle hypercontractility → ischemia → pain; TRPV1-sensitized uterine nociception | CB2/NF-κB → reduces COX-2/PGE2; CB1 (via AEA/FAAH) → reduces uterine contractility; TRPV1 desensitization → nociceptive modulation | Preclinical robust; survey data strong; human RCT emerging |
| PMS / PMDD | Luteal-phase HPA hyperreactivity; GABA-A sensitivity to allopregnanolone (progesterone metabolite); serotonin fluctuations; mood/anxiety/irritability | 5-HT1A → serotonin stabilization; HPA normalization → CRH/cortisol attenuation; GABA-A potentiation (indirect); CB2 → neuroinflammatory component of PMDD | Preclinical; mechanistic; survey data |
| Endometriosis | Ectopic endometrial lesions with CB1/CB2 downregulation; elevated PGE2/PGF2α; nerve fiber ingrowth; immune dysregulation; central sensitization | CB2/NF-κB → reduces lesion inflammation and PGE2; TRPV1 → nociceptive nerve sensitization; FAAH/AEA → restores CB1 signaling deficient in endometriotic tissue | Preclinical; mechanistic; limited human data |
| PCOS | Androgen excess; insulin resistance; chronic low-grade inflammation; hypothalamic GnRH pulse dysregulation; anxiety/mood comorbidity | CB2/NF-κB → reduces ovarian inflammation; PPARγ (CBG entourage) → insulin sensitivity; HPA normalization → stress-GnRH axis; 5-HT1A → mood/anxiety comorbidity | Preclinical; mechanistic; no dedicated RCT |
| Perimenopause / menopause | Estrogen decline → FAAH downregulation → ECS dysregulation; hot flashes (HPA/thermoregulation); sleep disruption; mood volatility; bone loss (osteoclast CB2); vaginal atrophy (local ECS) | HPA/5-HT1A → hot flash and mood support; sleep architecture (SWS/GH); CB2/bone ECS → osteoclast inhibition; TRPV1 → thermosensation in hot flashes; FAAH/AEA restoration of declining ECS tone | Mechanistic; survey data; limited perimenopause RCT |
Endometriosis and the ECS: A Specific Mechanistic Case
Endometriosis — a condition where endometrial-like tissue grows outside the uterus, primarily on the peritoneum, ovaries, and fallopian tubes — affects an estimated 10% of women of reproductive age and is one of the leading causes of chronic pelvic pain and infertility. The ECS connection to endometriosis is unusually specific and well-characterized for an understudied condition.
Research has consistently found that endometriotic lesions express significantly lower levels of CB1 and CB2 receptors compared to normal endometrium (Sanchez et al., 2016). This CB1/CB2 downregulation in ectopic lesions has two consequences: the lesions lose the normal CB1-mediated brake on myometrial contractility and cell migration (contributing to lesion progression), and they lose CB2-mediated anti-inflammatory restraint, allowing the intense local inflammatory environment (elevated PGE2, IL-8, TNF-α) that drives lesion growth and peritoneal inflammation. TRPV1 upregulation on sensory nerve fibers that grow into endometriotic lesions (nerve fiber ingrowth is a specific feature of endometriotic tissue) sensitizes the nociceptive signals from lesion tissue — accounting for the disproportionately severe pain in endometriosis relative to lesion size.
CBD's FAAH inhibition addresses the CB1 deficiency in endometriotic tissue by elevating anandamide — restoring some CB1 signaling in tissue where the receptor itself is downregulated. CBD's CB2/NF-κB mechanism reduces the local inflammatory cascade in endometriotic lesions. TRPV1 desensitization addresses the sensitized nociceptive nerve fibers in lesion tissue. In preclinical endometriosis models (rat and mouse), cannabinoids reduce lesion size and inflammatory markers — establishing mechanistic proof-of-concept. Human data for CBD specifically in endometriosis is extremely limited; dedicated clinical trials are needed. However, the mechanistic specificity of the ECS-endometriosis relationship makes this one of the most scientifically compelling women's health applications for CBD research.
Perimenopause and Menopause: The Estrogen-ECS Transition
The perimenopausal transition represents one of the most profound ECS disruptions in the female life cycle. As estrogen declines, the estrogen-FAAH regulatory relationship that has governed anandamide tone throughout reproductive life is removed — producing widespread ECS dysregulation that maps directly onto the symptom complex of perimenopause and menopause.
Hot Flashes and TRPV1/Thermoregulation
Hot flashes — vasomotor symptoms affecting 75–80% of perimenopausal women — are driven by estrogen withdrawal destabilizing the hypothalamic thermoregulatory set point. TRPV1 in the hypothalamic thermoregulatory center (the preoptic area) responds to anandamide, and the ECS modulates the thermoregulatory threshold. Low estrogen → reduced hypothalamic anandamide tone (through complex estrogen-AEA feedback) → narrowed thermoregulatory zone → lower threshold for heat-dissipation responses (sweating, vasodilation). CBD's FAAH inhibition elevating anandamide, and its direct TRPV1 desensitization in hypothalamic thermosensory circuits, provides a mechanistic basis for hot flash modulation. Survey data in perimenopausal women using CBD consistently shows hot flash frequency and severity reduction as among the most commonly reported benefits, alongside sleep improvement and mood support.
Perimenopausal Mood, Sleep, and HPA Dysregulation
Perimenopausal mood volatility, anxiety, and depression are driven by the intersection of estrogen withdrawal on serotonin synthesis and 5-HT receptor sensitivity, HPA hyperreactivity (estrogen has direct HPA-dampening effects; its withdrawal increases cortisol reactivity), and sleep disruption from vasomotor symptoms and progesterone withdrawal (progesterone has GABA-A positive allosteric modulator effects via its metabolite allopregnanolone — progesterone loss removes a natural anxiolytic). CBD's 5-HT1A mechanism addresses the serotonin component of perimenopausal mood disruption; the HPA normalization mechanism addresses the cortisol hyperreactivity; and the sleep architecture support addresses the cascade through which sleep disruption amplifies mood, cognitive, and vasomotor symptoms. The combination of CBD + CBN + melatonin is particularly well-suited to perimenopausal sleep disruption, which is driven by vasomotor symptoms interrupting sleep and by the circadian disruption that accompanies estrogen withdrawal.
Practical Protocol: CBD Gummies for Women's Health
Women's Health Protocol — CBD Gummies
Daily hormonal support foundation: Broad Spectrum CBD Gummies (25–50 mg) consistently each morning. The estrogen-FAAH dynamic means CBD's effects on endocannabinoid tone vary across the menstrual cycle — some women may find they respond differently at different cycle phases (more noticeable FAAH-inhibition effect in the follicular/high-estrogen phase when FAAH is highest; more prostaglandin-relevant effect in the luteal phase). Consistent daily dosing is the foundation for any hormonal application, as the HPA normalization and CB2 anti-inflammatory mechanisms benefit from sustained engagement. The Broad Spectrum CBD Oil sublingual provides acute rapid-onset coverage for menstrual cramp flares and acute PMS symptom peaks — 15–30 minute onset from nanoemulsion sublingual makes it useful as an add-on for breakthrough symptom episodes while the daily gummies provide baseline ECS support.
Full-spectrum hormonal entourage: Full Spectrum Berry Gummies bring the most therapeutically relevant entourage components for women's health: CBG's PPARγ/PPARα activity is relevant to both insulin sensitivity (important for PCOS) and the anti-inflammatory resolution of the uterine inflammatory environment; beta-caryophyllene as a direct CB2 agonist amplifies the anti-prostaglandin mechanism most relevant to dysmenorrhea and endometriosis; CBC's TRPA1/TRPV1 activity adds nociceptive coverage for visceral pelvic pain. For women managing endometriosis or dysmenorrhea primarily, the full-spectrum formulation provides more comprehensive ECS engagement for the CB2 and TRPV1 mechanisms central to pelvic pain. The Water Soluble CBD Softgels offer a convenient daily capsule format for women who prefer to take supplements with meals as part of a consistent wellness routine.
Perimenopausal and PMS sleep support: CBD+CBN+Melatonin Gummies 60–90 minutes before bed. Sleep disruption is a central symptom of both PMS/PMDD (progesterone/allopregnanolone withdrawal disrupts GABA-A in the late luteal phase) and perimenopause (vasomotor symptoms, progesterone decline). Melatonin's circadian support is complemented by CBN's SWS-deepening CB1 partial agonism and CBD's HPA normalization — the triple-mechanism sleep formulation addresses the multi-driver sleep disruption of hormonal transitions. For women in perimenopause specifically, melatonin secretion declines with age in addition to the estrogen-withdrawal effect, making exogenous melatonin support particularly relevant. The reduced overnight cortisol from CBD's HPA normalization also supports GH-mediated overnight tissue repair — relevant for the skin, bone, and connective tissue changes of perimenopause.
Antioxidant and immune support: CBD Elderberry Gummies provide anthocyanin antioxidant support alongside CBD. Elderberry's cyanidin-3-glucoside has documented anti-inflammatory and antiviral properties relevant to the immune-dysregulated state of endometriosis and the elevated oxidative stress of perimenopause. Anthocyanins have demonstrated some phytoestrogenic activity in cell models (weak estrogen receptor binding) — this is not sufficient to meaningfully replace estrogen, but the combined antioxidant and mild estrogen-receptor modulation may support the perimenopausal transition modestly. The Nrf2/HO-1 antioxidant induction from CBD complements elderberry's direct antioxidant activity for managing the oxidative stress associated with chronic inflammatory gynecological conditions.
Delta-8 note: Delta-8 Gummies are not recommended for women managing menstrual health, endometriosis, or perimenopause. CB1 agonism in reproductive tissue is involved in embryo implantation and uterine tone regulation — these are not well-characterized in the context of delta-8 specifically, but the caution is warranted for women in their reproductive years managing fertility-related conditions. Delta-8's REM suppression also counteracts the sleep quality objective central to perimenopausal management. CBD-dominant formulations are preferred for all women's health applications in this article.
Frequently Asked Questions
Can CBD gummies help with menstrual cramps and period pain?
Research suggests CBD gummies may help with menstrual cramps (dysmenorrhea) through mechanisms that directly address the prostaglandin-driven uterine cramping biology — and this is one of the most mechanistically well-grounded women's health applications for CBD. Primary dysmenorrhea (painful periods without underlying structural cause) is driven by excessive prostaglandin PGF2α and PGE2 production in the secretory endometrium during the late luteal phase. These prostaglandins trigger uterine smooth muscle hypercontractility, which compresses uterine blood vessels, causing transient uterine ischemia — the ischemic cramping produces the characteristic intense, wave-like pain. TRPV1 on uterine sensory nerve fibers amplifies the pain signaling from this ischemic cramping. CBD addresses dysmenorrhea at multiple points in this cascade: CB2/NF-κB inhibition reduces endometrial COX-2 expression (COX-2 is the enzyme that converts arachidonic acid to prostaglandins — the same enzyme NSAIDs block, but via a different mechanism); CB1 activation via FAAH-inhibited anandamide reduces uterine smooth muscle contractility directly; TRPV1 desensitization reduces the nociceptive amplification from uterine sensory nerves. The traditional use of cannabis for menstrual pain spans centuries — Queen Victoria's physician reportedly prescribed cannabis tincture for her menstrual cramps. Modern survey data: a 2019 Australian survey found 52% of women reporting cannabis use specifically for menstrual pain, with 96% of those reporting effective relief. Dedicated CBD RCT data for dysmenorrhea is limited; the mechanistic case is strong and consistent with the survey and historical use evidence. Starting CBD 1–2 days before expected menstrual onset (when COX-2 is being upregulated in the secretory endometrium) and continuing through the first 2 days of menstruation covers the peak prostaglandin production window.
Can CBD gummies help with PMS symptoms and mood changes?
Research suggests CBD gummies may help with PMS and PMDD symptoms through mechanisms addressing the serotonin, HPA, and GABA-A dysregulation that drives luteal-phase mood symptoms — while being clear that dedicated CBD PMS RCT evidence is very limited and most of the mechanistic rationale is inferred from CBD's established anxiolytic and HPA-modulatory effects. PMS and PMDD (premenstrual dysphoric disorder — the severe form with clinically significant mood disruption) are driven by abnormal central nervous system sensitivity to normal luteal-phase hormonal changes rather than hormone levels themselves being abnormal. Specifically: the progesterone metabolite allopregnanolone (which has GABA-A positive allosteric modulatory effects — natural sedative/anxiolytic activity) triggers a paradoxical dysphoric response in PMDD-susceptible women through poorly understood GABA-A subunit changes in the luteal phase. Serotonin levels fluctuate across the menstrual cycle (estrogen upregulates serotonin synthesis and receptor sensitivity; progesterone's effect is more complex); women with PMDD show reduced serotonin transporter binding in the luteal phase. HPA hyperreactivity is characteristic of PMDD — women with PMDD show exaggerated cortisol responses to stressors in the luteal phase, amplifying anxiety and irritability. CBD's 5-HT1A agonism provides serotonin-stabilizing effects independent of estrogen fluctuations; the HPA normalization mechanism directly attenuates luteal-phase cortisol hyperreactivity; GABA-A potentiation (a secondary CBD mechanism) complements the GABA-A disruption in PMDD. The combination of CBD's anxiolytic mechanisms covers the multi-system disruption of PMDD more comprehensively than single-target approaches. SSRIs (used for PMDD) are CYP2C19/2D6 substrates — CBD's CYP2C19 inhibition can raise SSRI levels; any combination with antidepressants for PMDD requires physician oversight.
Can CBD gummies help with perimenopause symptoms like hot flashes and mood changes?
Research suggests CBD gummies may help with perimenopausal symptoms through multiple mechanisms that directly map onto the biology of the menopausal transition — and perimenopause is increasingly being recognized as one of the most clinically relevant women's health applications for CBD. Perimenopause symptoms are driven by four overlapping biological disruptions: hypothalamic thermoregulatory instability (hot flashes — from estrogen-withdrawal destabilization of the GnRH pulse generator and hypothalamic thermosensory threshold); HPA hyperreactivity (mood volatility, anxiety, cortisol spikes — estrogen normally dampens the HPA axis, and its withdrawal increases cortisol reactivity to all stressors); serotonin system changes (estrogen upregulates 5-HT2A receptor sensitivity; withdrawal reduces serotonin's mood-stabilizing signaling); and sleep architecture disruption (progesterone withdrawal removes allopregnanolone/GABA-A support; vasomotor symptoms fragment SWS; melatonin secretion declines with age). CBD addresses each disruption: TRPV1 desensitization and FAAH/anandamide elevation in hypothalamic thermoregulatory circuits → hot flash frequency and intensity; 5-HT1A agonism → serotonin system support during estrogen-withdrawal serotonin fluctuations; HPA normalization via 5-HT1A/CRH → cortisol hyperreactivity attenuation; CBD+CBN+melatonin → multi-mechanism sleep architecture support. Survey data from perimenopausal women using CBD shows hot flash reduction, mood improvement, and sleep quality as the three most consistently reported benefits — aligned with the mechanistic predictions. Important context: CBD does not replace hormone therapy (HRT/MHT) for women with severe vasomotor symptoms or significant osteoporosis risk — it is a complementary support that addresses the neuroendocrine and quality-of-life dimensions of the menopausal transition. Women considering HRT should discuss that decision with their gynecologist; CBD can be used alongside HRT or as an alternative approach for women who prefer not to use hormonal therapy for mild-to-moderate symptoms.
Can CBD gummies interact with hormonal contraceptives or hormone therapy?
Yes — CBD gummies have important pharmacokinetic interactions with hormonal contraceptives and hormone therapy that women should be aware of before combining them. The central concern is CBD's CYP3A4 inhibition: most hormonal contraceptives (combined oral contraceptives containing ethinyl estradiol and progestins) are extensively metabolized by CYP3A4. CBD's CYP3A4 inhibition can raise ethinyl estradiol plasma levels — the clinical significance depends on the specific formulation, CBD dose, and individual variation. Elevated ethinyl estradiol from CYP3A4 inhibition could theoretically increase estrogen-related side effects (nausea, breast tenderness, headaches, thromboembolic risk at higher exposures). Practically: at typical CBD supplement doses (25–50 mg), the CYP3A4 inhibition from nanoemulsion CBD is likely modest; at higher therapeutic doses (100 mg+), the interaction becomes more clinically relevant. Progestins vary in CYP metabolism: norgestimate (in Ortho Tri-Cyclen) is primarily CYP3A4-metabolized; levonorgestrel is less dependent on CYP3A4. CBD does not affect contraceptive efficacy directly (contraceptive failure from drug interactions requires reduced hormone levels, not increased); the concern is elevated hormone levels, not reduced efficacy. For menopausal hormone therapy: estradiol patches and gels (transdermal) bypass first-pass hepatic CYP metabolism — the interaction risk is substantially lower than oral estradiol. Oral estradiol is CYP3A4-metabolized; CBD inhibition could modestly raise oral estradiol levels. Progesterone and synthetic progestins (medroxyprogesterone acetate — Provera) are CYP3A4 substrates with the same interaction concern. The practical guidance: women on hormonal contraceptives or HRT who add CBD should start at the lower end of the dose range (10–25 mg), discuss with their gynecologist particularly at higher CBD doses, and monitor for any changes in hormonal side effect profile.
Can CBD gummies help with endometriosis pain?
Research suggests CBD gummies may help with endometriosis-related pain through mechanisms that are unusually specific to endometriosis biology — making this one of the most mechanistically coherent applications for CBD in women's health, even while dedicated human clinical trial data remains very limited. Endometriosis pain has three distinct components that CBD addresses through different mechanisms: the ongoing inflammatory pain from endometriotic lesions (elevated PGE2/PGF2α, TNF-α, and IL-8 in peritoneal fluid and lesion tissue → CB2/NF-κB anti-inflammatory mechanism reduces the local inflammatory milieu); the visceral pelvic pain from nerve fiber ingrowth into lesions (TRPV1 upregulation on sensory neurons growing into endometriotic tissue → CBD's TRPV1 desensitization reduces sensitized nociception from this innervation); and the central sensitization component (chronic endometriosis pain produces central sensitization in the spinal cord and brain, amplifying all pelvic pain signals → CBD's CB1/AEA and HPA mechanisms address the central nervous system component of sensitized pain processing). The CB1/CB2 downregulation specifically documented in endometriotic lesions makes the FAAH-inhibition/anandamide-elevation mechanism particularly relevant: by elevating anandamide, CBD partially compensates for the reduced CB1/CB2 receptor density in the lesions themselves. Preclinical endometriosis animal models show cannabinoid treatment reducing lesion size, inflammatory markers, and pain behavior — but human endometriosis RCTs with CBD specifically are absent from the literature. An Australian survey (Armour et al., 2019) found self-management strategies for endometriosis included cannabis use in 13% of participants, with high reported effectiveness. Women with endometriosis should maintain their prescribed medical management (hormonal suppression therapy, surgery as indicated) and discuss CBD as a complementary pain management tool with their gynecologist or endometriosis specialist.
Can CBD gummies help with PCOS symptoms?
Research suggests CBD gummies may support symptom management in PCOS (polycystic ovary syndrome) through mechanisms addressing several of its overlapping biological drivers — while acknowledging that dedicated CBD PCOS clinical trials do not yet exist and most of the rationale is mechanistic. PCOS is a heterogeneous endocrine disorder characterized by androgen excess (producing hirsutism, acne, alopecia), ovulatory dysfunction (irregular cycles, anovulation), polycystic ovarian morphology on ultrasound, and frequently co-existing insulin resistance and chronic low-grade inflammation. CBD mechanisms relevant to PCOS: the CB2/NF-κB anti-inflammatory pathway reduces the chronic ovarian and systemic inflammation that is increasingly recognized as a driver of PCOS progression and insulin resistance; PPARγ activation (through CBG in the full-spectrum entourage) improves insulin sensitivity — PPARγ agonism is the mechanism of thiazolidinedione diabetes medications, and CBG's PPARγ activity may provide modest insulin-sensitizing support; HPA normalization is relevant because chronic stress and cortisol elevation worsen PCOS insulin resistance and androgen production through adrenal androgen pathways; 5-HT1A anxiety and mood support addresses the significant anxiety and depression comorbidity in PCOS (prevalence 2–3× higher than controls). CBD does not directly block androgen production or directly regulate GnRH pulsatility — it is not an anti-androgen in the pharmacological sense. The lifestyle and dietary interventions (weight management, low-glycemic diet, exercise) that improve PCOS outcomes share some metabolic overlap with CBD's PPARγ and HPA mechanisms, but lifestyle intervention remains the primary first-line approach. Women with PCOS using hormonal contraceptives, metformin, or spironolactone for PCOS management should review the drug interaction picture with their physician — metformin has minimal CYP interaction with CBD; spironolactone is a CYP3A4 substrate with modest interaction risk; oral contraceptives have the CYP3A4 interaction described in the FAQ above.
Related Articles
- → CBD Gummies for Stress and Anxiety
- → CBD Gummies for Sleep Quality and Deep Sleep
- → CBD Gummies for Skin Health and Anti-Aging
- → CBD Gummies for Bone Health and Osteoporosis
- → CBD Gummies for Mental Health and Depression
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Medical Disclaimer
This article is for informational and educational purposes only and does not constitute medical advice. CBD gummies are dietary supplements; these statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure, or prevent any disease or medical condition, including endometriosis, PCOS, PMS, PMDD, or menopause. CBD gummies are not a substitute for appropriate gynecological evaluation and treatment. Women who are pregnant or breastfeeding should not use CBD products. Women on hormonal contraceptives or hormone therapy should consult their physician before adding CBD due to potential drug interactions. Women with PCOS, endometriosis, or PMDD requiring prescription treatment should maintain their prescribed medical management.