When Your Period Goes Quiet: Understanding Hypothalamic Amenorrhoea
Your missing period isn't something to push through or ignore; it's your body speaking. Here's how to truly listen, and how to bring it back, holistically.
There is a particular kind of confusion, and quiet worry, that comes with losing your period when you're not pregnant. No big warning. No dramatic explanation. It simply stops. Or becomes so sporadic and faint that it barely counts at all. If this resonates, you may be dealing with Hypothalamic Amenorrhoea (HA), one of the most under-recognised and mismanaged hormonal presentations I see in clinic.
The good news? HA is almost always reversible. The hard truth? It requires genuine investigation, not just a prescription, and a willingness to look honestly at the lifestyle factors that may be driving it. Let's walk through everything you need to know.
"Your menstrual cycle is not a luxury; it is a vital sign. When it disappears, your body is telling you something important about its internal environment."
What Is Hypothalamic Amenorrhoea?
Hypothalamic Amenorrhoea is the absence of menstruation for three or more consecutive months in a previously cycling woman, resulting from suppression of the hypothalamic-pituitary-ovarian (HPO) axis, not from a structural abnormality or primary ovarian failure.
To understand HA, we need to briefly revisit how ovulation is orchestrated. The hypothalamus, a small but extraordinarily intelligent region of the brain, releases GnRH (gonadotrophin-
releasing hormone) in precise, rhythmic pulses. This signals the pituitary to release LH (luteinising hormone) and FSH (follicle- stimulating hormone), which travel to the ovaries and drive follicle maturation, oestrogen production, and ultimately ovulation.
In HA, this pulsatile GnRH secretion is disrupted or suppressed entirely. The hypothalamus, perceiving the body to be in a state of threat, whether from energy deficit, psychological stress, or systemic inflammation, essentially turns off the reproductive signal. This is an adaptive survival mechanism: in biological terms, it is not safe to reproduce when resources are scarce.
HA vs. PCOS — A Critical Distinction
These two conditions can look identical on the surface, both present with absent or irregular periods and can show polycystic- appearing ovaries on ultrasound. The distinction matters enormously, because the treatment approach is near-opposite.
HA: Low or low-normal FSH & LH, low oestrogen, low to absent GnRH pulsatility. Often thin/lean presentation. Ovaries may appear polycystic due to arrested follicle development.
PCOS: Elevated LH:FSH ratio, normal to elevated oestrogen, elevated androgens, insulin resistance common. Often (but not always) associated with weight changes.
The overlap: Both can show multiple antral follicles on ultrasound. Without proper hormonal testing, misdiagnosis is common and consequential.
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The Primary Drivers of HA
HA is almost always driven by one or more of three core stressors. These are known in the research as the "functional triad", and they work synergistically, meaning you don't necessarily need all three to suppress ovulation.
1. Energy Deficiency (Low Energy Availability)
This is the most foundational driver. Energy availability (EA) refers to the amount of energy left over for physiological function after accounting for exercise expenditure. Research by Dr. Anne Loucks established that GnRH pulsatility becomes significantly disrupted when EA falls below approximately 30 kcal per kg of fat-free mass per day, a threshold that can be crossed without overt starvation.
Critically, this doesn't require severe restriction. Cutting carbohydrates aggressively, skipping meals, under-eating relative to training load, or even inadequate dietary fat, all create the metabolic signal of scarcity that tells the hypothalamus to shut down reproduction. The body is extraordinarily sensitive to fuel availability.
2. Psychological & Emotional Stress
Chronic stress activates the HPA (hypothalamic-pituitary-adrenal) axis, leading to sustained elevation of cortisol and CRH (corticotropin-
releasing hormone). CRH directly suppresses GnRH release and has been shown to blunt LH pulsatility. This is why profound life stressors such as grief, relationship breakdown, perfectionism, overwork, burnout — can independently trigger HA even in the absence of dietary restriction.
The nervous system and the reproductive system share resources and wiring. When the body is in threat mode, ovulation is not a priority.
3. Excessive Exercise
Exercise is a powerful stressor, hormonally speaking. While moderate, restorative exercise supports cycle health, high-volume or high-intensity training without adequate caloric compensation raises cortisol, lowers leptin, and depletes the metabolic fuel required for HPO axis function. This is particularly prevalent in endurance athletes, competitive dancers, gymnasts, and those training extensively in strength sports.
Additional Contributing Factors
Low body fat percentage: Adipose tissue is an endocrine organ, essential for oestrogen synthesis via aromatisation. Very low body fat compromises oestrogen production directly.
Sudden or significant weight loss: Even in women who are currently at a "normal" weight, rapid loss triggers HA risk.
Disordered eating patterns: Including orthorexia, chronic dieting, or compulsive clean eating without overt restriction.
Post-pill HA: The oral contraceptive pill suppresses the HPO
The Role of Lifestyle & Diet: More Than You Think
In clinical practice, the conversation about lifestyle in HA is often the most important, and the most delicate. Many women I see have been operating under the belief that their diet and exercise habits are genuinely healthy. Often, they are. But healthy choices for one woman's body, biology, and stress load may be profoundly dysregulating for another.
Macronutrient Restriction
Low-carbohydrate and ketogenic dietary patterns have become prevalent, particularly in women interested in metabolic health. For a subset of women, particularly those with pre-existing HPO axis
sensitivity, aggressive carbohydrate restriction is a meaningful driver of HA. Carbohydrates are preferential fuel for the hypothalamus, and their absence communicates scarcity. Reintroducing adequate carbohydrate (particularly starchy, nourishing sources) is often one of the first steps toward period recovery.
Fat restriction is equally important to address. Cholesterol is the backbone of all steroid hormones, oestrogen, progesterone, testosterone, and cortisol all derive from it. A diet too low in dietary fat creates a substrate deficit for hormone synthesis.
The Role of Leptin
Leptin, a hormone produced by adipose tissue, is a critical permissive signal for GnRH release. When body fat and caloric intake are adequate, leptin levels are sufficient to signal "safety" to the hypothalamus. In energy-deficient or very lean states, leptin plummets. Research has demonstrated that leptin deficiency alone can suppress LH pulsatility and halt ovulation. Eating adequate dietary fat and overall calories is the most direct way to restore leptin sensitivity.
Exercise Modifcation
This is genuinely hard for many women to hear, but exercise load often needs to be reduced, at least temporarily, to allow the HPO axis to recover. This doesn't necessarily mean stopping movement entirely, but transitioning from high-intensity training to more restorative practices like walking, gentle yoga, swimming, and Pilates during the
recovery phase can be profoundly supportive. The goal is to shift the nervous system from a sympathetically dominant state toward parasympathetic recovery.
Stress Load & the Nervous System
Stress is not always psychological. Physiological stressors, including over-exercise, dietary restriction, poor sleep, and gut inflammation, all activate the HPA axis and compound the cortisol burden. Addressing sleep quality, building genuine rest into the day, and exploring tools like breathwork, meditation, and therapy (particularly for perfectionist or overachiever tendencies often seen in HA) are essential parts of recovery, not optional add-ons.
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The Gut-Hormone Axis: How an Infamed Gut Can Steal Your Period
This is perhaps the most underappreciated dimension of HA, and one that I find particularly fascinating clinically. Gut health and hormonal health are intimately connected, and an inflamed, compromised gut environment can meaningfully contribute to period loss through multiple pathways.
The Estrobolome
The estrobolome refers to the collection of gut bacteria responsible for metabolising and recirculating oestrogen. These bacteria produce an enzyme called beta-glucuronidase, which deconjugates oestrogen in the gut, allowing it to be reabsorbed and recirculated. When the estrobolome is disrupted through dysbiosis, antibiotic use, or poor dietary diversity, oestrogen metabolism becomes impaired. This can contribute to oestrogen excess in some women, and oestrogen deficiency in others, depending on the direction of imbalance.
Gut-Derived Inflammation & the HPA Axis
Intestinal permeability (often referred to as "leaky gut") allows bacterial endotoxins, particularly lipopolysaccharides (LPS), to enter systemic circulation. LPS is a potent inflammatory stimulus that activates the innate immune system and drives sustained elevation of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α). These cytokines directly suppress the HPO axis by inhibiting GnRH pulsatility and blunting pituitary LH release. Gut inflammation is, neurologically and hormonally speaking, a stressor, and the hypothalamus responds accordingly.
Gut Microbiome & Serotonin
Approximately 90–95% of the body's serotonin is produced in the gut. Serotonin not only influences mood and cognition, but plays a role in GnRH regulation. Disrupted gut microbiota, particularly depletion of Lactobacillus and Bifidobacterium species, impairs serotonin synthesis, which can contribute to the mood dysregulation and HPO axis suppression seen in HA.
Malabsorption & Nutrient De!ciency
A chronically inflamed gut is a poorly absorbing gut. Even if a woman is eating adequately on paper, conditions such as SIBO, dysbiosis, or intestinal permeability can impair absorption of the nutrients most critical to reproductive function, including zinc, magnesium, B vitamins, vitamin D, and essential fatty acids. Addressing the gut is therefore not a separate clinical priority from addressing HA, it is often part of the same root-cause investigation.
Gut Flags to Watch for in an HA Presentation
History of antibiotic use, recurrent infections, or long-term OCP use (all disrupt the microbiome)
Bloating, abdominal distension, altered bowel habits, particularly in those following restrictive diets
Low stool fat (steatorrhoea), incomplete digestion
Food sensitivities or reactivity, often a sign of intestinal permeability
History of gastroenteritis or traveller's diarrhoea (SIBO trigger)
Skin conditions such as acne or eczema, often reflect gut- immune dysregulation
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Testing: What to Investigate & Why
HA is a diagnosis of exclusion, meaning other causes of amenorrhoea must be ruled out before attributing the presentation to hypothalamic suppression. Thorough investigation is non-negotiable. Here is the framework I work through in clinic.
Testing: What It Tells Us
FSH, LH & LH:FSH ratio
In HA: both are typically low-normal or low, with a flat or reversed LH:FSH ratio. Elevated FSH suggests premature ovarian insufficiency. Elevated LH:FSH (>2:1) points toward PCOS.
Oestradiol (E2)
Usually low in HA, often below 100 pmol/L. Low oestradiol explains bone density loss risk, vaginal dryness, and poor mucus production.
Progesterone (Day 21)
Confirms whether ovulation has occurred. A result below 16 nmol/L on day 21 of a 28-day cycle suggests anovulation.
Total & free testosterone, DHEA-S, androstenedione
Androgen panel rules out PCOS and adrenal androgen excess (CAH). Androgens are typically normal-low in HA.
Prolactin
Hyperprolactinaemia suppresses GnRH independently. A significantly elevated prolactin warrants MRI of the pituitary to exclude prolactinoma.
Full thyroid panel (TSH, Free T3, Free T4, antibodies).
Subclinical hypothyroidism and Hashimoto's thyroiditis can both suppress ovulation and must be excluded.
Fasting insulin & glucose / HOMA-IR
Differentiates HA from insulin-resistant PCOS. In HA, insulin tends to be low-normal. HOMA-IR ≥2.5 suggests insulin resistance.
AMH (Anti- Müllerian Hormone)
Reflects ovarian reserve. Very low AMH may suggest premature ovarian insufficiency. Elevated AMH is more consistent with PCOS.
Full blood count & iron studies (ferritin)
Iron deficiency is extremely common and suppresses ovulation independently. Ferritin below 30 μg/L impairs thyroid peroxidase function and mitochondrial energy production.
Vitamin D (25- OH)
Vitamin D receptors are present throughout the HPO axis. Deficiency is independently associated with anovulation and impaired folliculogenesis.
Zinc & magnesium (serum or RBC)
Both are critical cofactors for GnRH release, progesterone synthesis, and LH receptor sensitivity.
hs-CRP & ESR
Systemic inflammatory markers. Elevated levels can point toward gut-mediated or autoimmune inflammatory load suppressing the HPO axis.
DUTCH Complete (urine hormone panel)
Provides a comprehensive map of sex hormones, metabolites, cortisol diurnal curve (CAR), cortisone, DHEA, and melatonin. Invaluable for understanding HPA axis function and the full oestrogen metabolism picture. Best used once basal bloods have been reviewed.
Gut microbiome mapping (stool analysis)
Assesses estrobolome composition, dysbiosis, inflammatory markers (calprotectin), secretory IgA, beta-glucuronidase activity, and gut permeability markers. Recommended where gut symptoms are present or where HA is resistant to initial treatment.
Pelvic Ultrasound
Rules out structural pathology; assesses antral follicle ultrasound count and ovarian morphology to differentiate HA from PCOS.
Bringing the Period Back: A Holistic Recovery Framework
Recovery from HA is possible. and in my clinical experience, it is often remarkable how quickly the body responds when the right conditions are created. The pathway is not quick-fix oriented. It is layered, intentional, and asks something meaningful of the woman undertaking it. But it works.
Step One: Nourish
The single most impactful intervention is eating more, particularly more carbohydrates and dietary fat, and more calories overall. This is not negotiable. The hypothalamus needs to receive consistent, reliable signals of energy abundance before it will reinstate reproductive function. Practically, this means:
markers. Recommended where gut symptoms are present or where HA is resistant to initial treatment.
Nutritional Priorities in HA Recovery
Caloric adequacy: Work with a naturopath or dietitian to establish a realistic energy target that accounts for activity level. Under-eating "a little" still counts as under-eating.
Reintroduce carbohydrates: Prioritise nourishing, whole-food sources, sweet potato, root vegetables, legumes, wholegrains, rice, fruit. These fuel the hypothalamus and restore leptin.
Increase dietary fat: Avocado, olive oil, fatty fish, nuts, seeds, pasture-raised eggs, full-fat dairy (if tolerated). These provide the cholesterol substrate for steroid hormone synthesis.
Protein for building: 1.4–1.8 g/kg bodyweight from diverse sources including animal protein where appropriate, as amino acids support LH receptor function and progesterone synthesis.
Eat regular meals: Avoid prolonged fasting. Three structured meals with adequate snacks maintain steady glucose and leptin signalling.
Anti-inflammatory foundation: Oily fish (omega-3 fatty acids), colourful vegetables, herbs, spices, reducing systemic inflammatory load is supportive of HPO axis recovery.
Step Two: Rest & Restore
This is where many women find the greatest resistance, because rest doesn't feel productive. But this is precisely the period where the body needs permission to redirect energy toward reproduction. Practically, this involves reducing training volume and intensity, prioritising 7–9 hours of quality sleep nightly, building in genuine downtime (not scrolling, not planning, actual stillness), and exploring somatic tools like yoga nidra, restorative yoga, and diaphragmatic breathwork to shift the NS toward parasympathetic dominance.
Step Three: Address the Gut
Where gut dysbiosis, intestinal permeability, or SIBO is suspected or confirmed, targeted gut restoration is prioritised in parallel with hormonal recovery. The 5R framework — Remove, Replace, Reinoculate, Repair, Rebalance, provides the clinical scaffold for this work.
Naturopathic Herbal & Nutrient Support for Ovulation Recovery
Once the foundational lifestyle work is underway, a well-designed naturopathic protocol can provide meaningful support for HPO axis recovery, stress resilience, gut repair, and ovulation induction. The following is an overview of the key herbs and nutrients I draw on clinically for HA presentations — always individualised to the specific hormonal picture and underlying drivers.
Chaste Tree
Acts on the pituitary to support LH pulsatility and normalise the LH:FSH ratio. Supports the mid- cycle LH surge and subsequent progesterone production in the luteal phase. Best used where there is evidence of anovulation and insufficient luteal phase rather than severe hypothalamic suppression alone.
Shatavari
A deeply nourishing Ayurvedic adaptogen with affinity for the female reproductive system. Phyto-oestrogenic activity supports oestrogen production in low-oestrogen states. Supports endometrial integrity, cervical mucus quality, and overall reproductive resilience. Also nourishes the nervous system and adrenal response.
Withania
A premier HPA axis adaptogen — modulates cortisol response without sedation. Research demonstrates meaningful reductions in cortisol, improvement in thyroid hormone levels, and improved reproductive hormone profiles with consistent use. Particularly valuable in HA driven by chronic psychological stress and burnout.
Rhodiola
Adaptogenic and anti-fatigue. Supports adrenal resilience, mental clarity, and recovery from overtraining. Has preliminary evidence for supporting hormonal balance in stress-related amenorrhoea through cortisol and catecholamine modulation.
Licorice Root
Supports cortisol by inhibiting the enzyme that converts active cortisol to inactive cortisone, prolonging its availability. Supportive of HPA axis regulation and adrenal recovery in states of low cortisol output. Also mildly anti-androgenic, making it useful where there is adrenal androgen overlap.
Tribulus
Traditionally used as an ovulation-stimulating herb, with evidence suggesting effects on FSH receptor sensitivity and LH pulsatility. May support follicular development and oestrogen production in anovulatory women. Best combined with other reproductive tonics.
Gymnema
Where there is concurrent blood sugar dysregulation or insulin resistance overlap, Gymnema supports glucose tolerance and reduces sweet cravings, relevant where restriction patterns have emerged around carbohydrate fear.
Paeonia
Contains paeoniflorin, which modulates LH pulsatility and reduces ovarian androgen synthesis. Particularly valuable where HA overlaps with a PCOS-type or post-pill androgenic picture. The classic Paeonia + Licorice combination supports follicular development and oestrogen/androgen balance.
Schisandra
A liver and adrenal tonic. Supports hepatic oestrogen metabolism, reduces oxidative stress, and provides adaptogenic nervous system support. Useful in presentations with emotional stress, liver congestion, and disrupted hormone clearance.
Key Nutritional Supplements
Zinc (glycinate or picolinate)
Essential for GnRH synthesis, LH receptor function, follicle development, and progesterone production. Commonly depleted in restrictive diets and OCP users. Dose: 25–45 mg elemental zinc, with food.
Magnesium (glycinate orbisglycinate)
Critical for HPA axis regulation, sleep quality, and GnRH release. Magnesium blunts the cortisol response to stress. Also supports insulin sensitivity. Dose: 300–500 mg elemental magnesium, evening dosing preferred.
Vitamin D3
Vitamin D acts as a hormone, with receptors throughout the HPO axis and ovaries. Deficiency independently impairs folliculogenesis and LH release. Repletion requires testing, typical therapeutic dosing 2,000–5,000 IU depending on baseline levels.
Active B Complex (methylated)
B6 (P5P) supports progesterone synthesis and prolactin regulation. Folate (methylfolate) and B12 are essential for methylation, critical for oestrogen detoxification via the COMT and MTHFR pathways. B5 supports adrenal function and cortisol synthesis.
Iron (bisglycinate)
Low ferritin is extremely common in HA, particularly in those with heavy prior bleed history or dietary restriction. Ferritin below 50 μg/L impairs ovulation, thyroid peroxidase activity, and mitochondrial energy. Retest at 8–12 weeks.
Omega-3 Fatty Acids (EPA/DHA)
Anti-inflammatory, supports prostaglandin balance, improves cell membrane fluidity, and reduces hypothalamic inflammatory load. Also supports mood regulation via serotonin pathway support, relevant given the nervous system component of HA. Dose: 2–3 g combined EPA/DHA daily.
Inositol (Myo-inositol)
Supports FSH signal transduction and follicular sensitivity. Also improves insulin sensitivity and is clinically useful where HA and PCOS-type patterns overlap. Dose: 2–4 g daily.
Probiotics & Gut-Specific Support
Targeted probiotic blends (including Lactobacillus rhamnosus, L. acidophilus, Bifidobacterium longum) to restore estrobolome function, reduce gut-derived inflammatory load, and support serotonin synthesis. Combine with gut-healing nutrients: L- glutamine, zinc carnosine, and collagen where intestinal permeability is suspected.
A Note on Protocol Sequencing
In clinical practice, the order matters. Attempting to stimulate ovulation with herbs like Vitex or Tribulus without first addressing the energy deficit, cortisol load, and nutrient repletion is unlikely to succeed, and can occasionally worsen the picture. The foundational work must come first. A practitioner-guided, staged approach is always preferable to a supplement-first strategy.
What You Can Expect on the Recovery Journey
Recovery timelines vary, and this is important to hold with honesty. For some women, restoring adequate nutrition and reducing exercise load will see a period return within 1–3 months. For others, particularly where there has been long-standing suppression, significant gut dysbiosis, or deep HPA axis dysregulation, the process may take 6– 12 months of consistent, supported work.
This is not a reason for despair. It is a reason for genuine, compassionate, sustained investment. The women I see who recover fully and go on to conceive naturally are often those who commit most fully to the lifestyle shifts, not just the supplement protocol. The body responds to being truly, deeply nourished.
What I can say with confidence: your period returning is possible. The HPO axis is remarkably resilient when given the right conditions. And the process of recovering from HA, learning to eat enough, to rest without guilt, to address the chronic stressors that stole your cycle, is often one of the most transformative journeys a woman can undertake.
Ready to Get to the Root of Your Missing Period?
If you're navigating a missing or irregular cycle and want expert, evidence-informed naturopathic support, I'd love to work with you. Consultations are available in-clinic in Ascot, Brisbane, or via telehealth nationally.
References
Loucks AB, Verdun M, Heath EM. Low energy availability, not stress of exercise, alters LH pulsatility in exercising women. Journal of Applied Physiology. 1998;84(1):37–46.
Gordon CM. Functional hypothalamic amenorrhea. New England Journal of Medicine. 2010;363(4):365–371.
Meczekalski B, Katulski K, Czyzyk A, Podfigurna-Stopa A, Maciejewska-Jeske M. Functional hypothalamic amenorrhea and its influence on women's health. Journal of Endocrinological Investigation. 2014;37(11):1049–1056.
Misra M, Klibanski A. Endocrine consequences of anorexia nervosa. The Lancet Diabetes & Endocrinology. 2014;2(7):581–592.
Berga SL, Loucks TL. The diagnosis and treatment of stress-induced anovulation. Minerva Ginecologica. 2005;57(1):45–54.
De Souza MJ, Nattiv A, Joy E, et al. 2014 Female Athlete Triad Coalition consensus statement on treatment and return to play of the female athlete triad. British Journal of Sports Medicine. 2014;48(4):289.
Shabir I, Ganie MA, Zargar MA, et al. Prevalence of hypothalamic amenorrhoea: pathogenesis, diagnosis and treatment approach. International Journal of Reproduction, Contraception, Obstetrics and Gynecology. 2017;6(10):4249–4257.
Cano Sokoloff N, Eguiguren ML, Wargo K, et al. Bone parameters in relation to attitudes and feelings associated with disordered eating in oligo-amenorrheic athletes, eumenorrheic athletes, and nonathletes. International Journal of Eating Disorders. 2015;48(5):522–526.
Baker ER. Body weight and the initiation of puberty. Clinical Obstetrics and Gynecology. 1985;28(3):573–579.
Brotman RM, Shardell MD, Gajer P, et al. Association between the vaginal microbiota, menopause status, and signs of vulvovaginal atrophy. Menopause. 2014;21(5):450–458.
Baker JM, Al-Nakkash L, Herbst-Kralovetz MM. Estrogen-gut microbiome axis: physiological and clinical implications. Maturitas. 2017;103:45–53.
Plottel CS, Blaser MJ. Microbiome and malignancy. Cell Host & Microbe. 2011;10(4):324– 335. [Estrobolome concept]
Yamano E, Sugimoto M, Hirayama A, et al. Index markers of chronic fatigue syndrome with dysfunction of TCA and urea cycles. Scientific Reports. 2016;6:34990. [LPS/gut- HPA axis inflammatory signalling]
Carabotti M, Scirocco A, Maselli MA, Severi C. The gut-brain axis: interactions between enteric microbiota, central and enteric nervous systems. Annals of Gastroenterology. 2015;28(2):203–209.
Tata B, Mimouni NEH, Barbotin AL, et al. Elevated prenatal anti-Müllerian hormone reprograms the fetus and induces polycystic ovary syndrome in adulthood. Nature Medicine. 2018;24(6):834–846.
Santoro N, Worsley R, Miller KK, et al. Role of estrogens and estrogen deficiency in the practice of medicine. Endocrine Reviews. 2019;40(6):1370–1430.
Whirledge S, Cidlowski JA. Glucocorticoids, stress, and fertility. Minerva Endocrinologica. 2010;35(2):109–125.
Podfigurna A, Meczekalski B. Functional hypothalamic amenorrhea — a stress-based disease. Endocrines. 2021;2(3):203–211.
Chavarro JE, Rich-Edwards JW, Rosner BA, Willett WC. Diet and lifestyle in the prevention of ovulatory disorder infertility. Obstetrics & Gynecology. 2007;110(5):1050– 1058.
Murray M, Pizzorno J. The Encyclopedia of Natural Medicine. 3rd ed. Atria Books; 2012. [Herbal and nutritional support for reproductive health]
Arentz S, Abbott JA, Smith CA, Bensoussan A. Herbal medicine for the management of polycystic ovary syndrome (PCOS) and associated oligo/amenorrhoea and hyperandrogenism: a review of the laboratory evidence for effects with corroborating pharmacology. Reproductive Biology and Endocrinology. 2014;12:87.
Rao A, Steels E, Beccaria G, Inder WJ, Vitetta L. Influence of a Rhodiola rosea extract on the physical and mental performance of athletes: a randomized double-blind trial. Phytotherapy Research. 2013;27(12):1882–1892. [Adaptogenic and HPA effects]
Pratte MA, Nanavati KB, Young V, Morley CP. An alternative treatment for anxiety: a systematic review of human trial results reported for the Ayurvedic herb ashwagandha (Withania somnifera). Journal of Alternative and Complementary Medicine. 2014;20(12):901–908.
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This blog is for educational purposes only and does not constitute medical advice. Please consult a qualified practitioner for individualised health guidance.