PMS & PMDD: Symptoms of Hormonal Imbalance?

Premenstrual symptoms are incredibly common, but the line between feeling a bit irritable and experiencing debilitating mental health distress is critical. Premenstrual Syndrome (PMS) and its severe counterpart, Premenstrual Dysphoric Disorder (PMDD), both occur during the luteal phase of your cycle. They are not psychological flaws; they are the result of a profound biological sensitivity to your cycling hormones.

This article outlines the difference between PMS and PMDD. We’ll also explain how our Advanced At-Home Hormone and Fertility Test can uncover the root causes of your symptoms.

If you need urgent help for your mental health, you can contact the Samaritans 24/7 helpline (116 123), or access Mind’s crisis resources (https://www.mind.org.uk/need-urgent-help/using-this-tool/).

Quick facts:

• Premenstrual Syndrome (PMS) affects around 90% of people who menstruate.
• Premenstrual Dysphoric Disorder (PMDD) is a more severe form of PMS, affecting around 3-8% of people.
• Both conditions are caused by an altered sensitivity to the normal hormonal changes that occur during the luteal phase.
• Tracking your cycle and testing your hormones are essential steps toward getting to the root cause.

What is PMS and PMDD?

Both PMS and PMDD are cyclical conditions linked entirely to the luteal phase of the menstrual cycle, the time between ovulation and your period.

Premenstrual Syndrome (PMS)

PMS is a cluster of physical and mental symptoms experienced in the week or two leading up to your period (NHS, 2024). It is super common, with up to 90% of women and people who menstruate experiencing it at some point.

Common PMS symptoms include:

• Mood swings, anxiety, or irritability.
• Physical symptoms like fatigue, trouble sleeping, bloating, and abdominal pain.
• Skin changes like acne flare-ups or oily skin.
• Food cravings and changes in appetite.

Premenstrual Dysphoric Disorder (PMDD)

PMDD is a severe, chronic form of premenstrual distress that has a significant impact on daily function, relationships, and work (NHS, 2024). Symptoms tend to be far more exaggerated, with emotional symptoms dominating the presentation, and they generally resolve entirely once the period begins.

PMDD symptoms often include:

• Severe mood swings, debilitating depression, or feelings of hopelessness.
• Marked anxiety or tension, or feeling constantly ‘on edge’.
• Intense irritability or anger, often leading to conflict.
• Difficulty concentrating, lethargy, or a marked lack of energy.
• In the most severe cases, some people may experience suicidal ideation or suicidal thoughts.

The Hormonal Cause: A Sensitivity Disorder

The exact cause of PMDD is not a hormonal deficiency or excess in the traditional sense, but a genetic and biological vulnerability to the normal hormonal changes that occur after ovulation. This makes it a disorder of sensitivity.

• The Neuroactive Steroid Link: Following ovulation, the corpus luteum releases progesterone, which is metabolised into a powerful neuroactive steroid called allopregnanolone. Allopregnanolone acts on the brain’s GABA receptors, which are responsible for relaxation and calm.
• Altered Sensitivity: Research suggests that women with PMDD have an altered sensitivity to allopregnanolone in the brain’s circuits. This means that instead of feeling calm and stable, the sharp rise or, more critically, the rapid withdrawal of this neurosteroid in the late luteal phase provokes profound anxiety, irritability, and depression (Hantsoo et al., 2015).
• Oestradiol and SHBG: Studies also point to differences in how the body handles oestrogen. Women with PMDD have been observed to have lower levels of free oestradiol and higher levels of SHBG compared to controls (Thys-Jacobs et al., 2008). Since oestradiol supports mood, low levels of active oestradiol in the luteal phase may contribute to greater symptom severity.

Other Contributing Hormones

While the oestrogen/progesterone axis is key, other hormones can modulate severity or flag underlying conditions:

• Androgens (Testosterone, DHEAS): Some research suggests elevated free testosterone levels may be linked to increased premenstrual irritability and dysphoria in susceptible individuals (Eriksson et al., 1992).
• Thyroid Hormones (TSH, Free Thyroxine): Thyroid dysfunction (hypothyroidism or hyperthyroidism) frequently causes mood swings and anxiety that can exacerbate or be confused with premenstrual symptoms.

Possible Contributing Factors: Genetic variations (particularly on the oestrogen receptor alpha gene), trauma, stress, and smoking are also linked to increased sensitivity or worsening PMDD symptoms.

Getting to the Root Cause

If you suspect you are suffering from severe PMS or PMDD, the first step is always to speak to a professional. However, gaining hormonal clarity can be vital for diagnosis and treatment planning.

• Tracking: Start by tracking your symptoms daily against your cycle. Symptoms must be present in the luteal phase and disappear shortly after the onset of your period to meet the clinical diagnostic criteria for PMDD.

💡 Is your cycle secretly impacting your mood?

Take our Advanced At-Home Hormone and Fertility Test to investigate the underlying hormonal patterns contributing to your mood shifts, including free oestradiol and androgen activity.

Treatment Pathways

The primary goal of treating PMDD is to dampen the body’s adverse reaction to the cyclical hormonal changes.

1. Hormonal Interventions: Hormonal contraceptives, particularly those taken without a break, can halt ovulation, which stabilises the fluctuation of oestradiol and progesterone, helping to lessen symptoms. Suppressing the ovarian cycle is highly effective in treating PMDD symptoms.
2. Psychotropic Agents: Selective Serotonin Reuptake Inhibitors (SSRIs) are the first-line medical treatment for PMDD. They work quickly (within days) in PMDD, often administered just during the luteal phase, supporting the evidence for a key link between serotonin dysfunction and this condition.
3. Therapy and Lifestyle: Cognitive Behavioural Therapy (CBT) is considered an effective psychological treatment. Further, lifestyle adjustments – diet, exercise, and stress reduction – are proven to have a positive impact on the severity of PMS symptoms (Hantsoo et al., 2015).

What Your Personalised Results Can Tell You

Testing a full panel of personalised hormones provides essential diagnostic data needed to find the root cause, tailored to your symptoms and concerns.

1. Assess Sensitivity Markers: We can assess SHBG and oestradiol to check for markers of altered hormonal binding that may increase your vulnerability to mood shifts.
2. Rule out comorbid conditions: The panel checks TSH and free thyroxine to rule out thyroid dysfunction, and measures testosterone/AMH to check for PCOS, both of which can cause mood instability that can mimic or worsen PMDD.
3. Guide Hormonal Treatment: Understanding your baseline hormone levels is essential for clinicians to determine treatment path.

💡 Find clarity on your mental health

If your emotional symptoms are severe and regularly affecting your wellbeing, don’t suffer in silence. Take our Advanced At-Home Hormone and Fertility Test to gain clarity and take control of your health.

References 

• https://www.nhs.uk/conditions/pre-menstrual-syndrome/ 
• https://www.mind.org.uk/information-support/types-of-mental-health-problems/premenstrual-dysphoric-disorder-pmdd/about-pmdd/ 
• Eriksson, E., Sundblad, C., Lisjö, P., Modigh, K., & Andersch, B. (1992). Serum levels of androgens are higher in women with premenstrual irritability and dysphoria than in controls. Psychoneuroendocrinology, 17(2-3), 195–204. https://doi.org/10.1016/0306-4530(92)90058-f 
• Hantsoo, L., Epperson, C.N. (2015). Premenstrual Dysphoric Disorder: Epidemiology and Treatment. Curr Psychiatry Rep 17, 87. https://doi.org/10.1007/s11920-015-0628-3 

Thys-Jacobs, S, McMahon, D, Bilezikian, JP. (2008). Differences in Free Estradiol and Sex Hormone-Binding Globulin in Women with and without Premenstrual Dysphoric Disorder. The Journal of Clinical Endocrinology & Metabolism. 93(1):96–102, https://doi.org/10.1210/jc.2007-1726