Are breastfeeding women more prone to persistent nipple pain if they have other skin conditions?
Breastfeeding women with pre-existing skin conditions may be at increased risk of nipple pain
It seems likely that some women who are already prone to the experience of sensitive skin, or to skin conditions such as atopic dermatitis or psorhiasis, may have increased vulnerability to nipple epidermis inflammation and pain. (However, this would not translate into an increased risk of nipple wounds, which are always an indicator of nipple and breast tissue drag.) In women with pre-existing skin conditions, prevention or very early intervention for fit and hold problems which result in high levels of mechanical microtrauma is essential.
I hypothesise that once these women's nipple epidermis becomes inflamed due to nipple and breast tissue drag, epidermal inflammation is unable to resolve because of a heightened inflammatory response to repetitive mechanical tensile forces of even normal breastfeeding. Perhaps the epidermis is tipped into a pro-inflammatory state by the initial problem. It's also possible that for a small number of women with pre-existing skin vulnerability, even normal breastfeeding without nipple and breast tissue drag triggers painful inflammatory responses.
For a long time, the breastfeeding woman and baby have been blamed (by applying various pathological diagnoses), avoiding the need for breastfeeding support professionals to develop the clinical art of helping her minimise conflicting vectors of force inside her baby's mouth. There is a danger that this hypothesis of a sensitised inflammatory response, which may apply to very small numbers of breastfeeding women with pre-existing skin conditions, is taken up as a new diagnosis, which by-passes the fundamental and ongoing efforts of a clinician to help a woman eliminate nipple and breast tissue drag when she is experiencing nipple pain, or persistent nipple pain.
Sensitive skin
The skin is a target organ for many hormones, and its aging processes are tightly controlled by neuroendocrine axes, modulated by growth factors, growth hormone, oestrogens, retinoids, and melatonin. The skin also functions as an endocrine organ itself.
"Sensitive skin is a condition characterized by the perception of skin discomfort following mild stimuli, frequently without objective signs of skin irritation. This skin condition has been shown to be highly prevalent in the Western World but, despite extensive research in the past years, no consensus on its definition and pathomechanisms has been reached." (Richters et al 2017)
Richters et al 2017 found that the stratum corneum of subjects with sensitive skin is more vulnerable to chemical and mechanical stimuli than the stratum corneum of subjects with non-sensitive skin, suggesting an impaired barrier. However, sensitive skin is not a subclinical form of atopic dermatitis and the skin barrier is not impaired re stratum corneum thickness, water content, and other content.
For this reason, treatments of sensitive skin based on hydration and ceramides supplementation don't correspond with the research. The authors propose that research should be directed at unravelling the role of the cutaneous nervous system. They suggest that in addition to other mechanisms, further sensitive skin investigations need to include the role of an altered immune response and intercorneocyte adhesion.
Hormonally induced skin sensitivity
Skin physiology has been shown to vary within the menstrual cycle. Hormonal fluctuations significantly impact skin sensitivity and various dermatological conditions. The skin's response to irritants and its overall health are influenced by hormonal status, with menopausal hormone therapy users showing enhanced barrier responses but also elevated inflammatory cell counts after irritant challenge. These findings underscore the complex interplay between hormones and skin health.
-
Falcone et al 2017 analysed the digital survey responses of 278 women, and found that
-
About 42% premenopausal women reported increased skin sensitivity just before and during menstruation
-
Almost 32% of peri- and postmenopausal women reported increased skin sensitivity.
-
The authors concluded that the prevalence of the perceived effects of fluctuating hormone levels on self-assessed sensitive skin in women is high.
-
Ma et al 2023 investigated 197 Chinese women aged 18-35 years. They concluded that "based on the associations among hormones, skin physiological parameters and skin microbiota, it is possible that the skin physiological parameters, as well as the skin microbial diversity and composition, change with hormonal fluctuations during the menstrual cycle."
-
Hormone therapy, while beneficial for some skin parameters like collagen content and dermal thickness, is also associated with a higher risk of conditions such as psoriasis. The skin's response to irritants and its overall health are influenced by hormonal status, with HRT users showing enhanced barrier responses but also elevated inflammatory cell counts after irritant challenge. A literature review highlights that oestrogen treatment in postmenopausal women consistently increases collagen content, dermal thickness, and elasticity, and shows promising data for skin water content. Physiological studies also suggest a beneficial role for hormone replacement therapy (HRT) in cutaneous injury repair.
Atopic dermatitis
Atopic dermatitis is a systemic disease with elevated levels of multiple inflammatory mediators. The mechanisms by which stress may exacerbate atopic dermatitis likely involves alterations in the neuroendrocrine-immuno-cutaneous system. This study showed a greater tendency of those with atopic dermatitis to respond to stressful circumstances with increased worry.
Acute stress is associated with decreased pain responsiveness. Stress-induced analgesia, mediated by the descending inhibitory pain pathway, can be influenced by age, gender, and prior experience.
Psorhiasis and other autoimmune skin diseases
Psoriasis is a chronic autoimmune skin condition in which immune system T-cells mistakenly attack healthy skin cells. This attack causes skin cells to mature and rise to the surface much faster than the normal three or four week cycle, resulting in a buildup of cells which form thick, scaly, often itchy or painful red patches known as plaques. While the exact cause is unknown, genetics make some people more susceptible to psorhiasis, and environmental factors like stress, certain infections, or skin trauma can trigger flare-ups.
Naslund-Koch et al 2025 studied over 100,000 Danish people for almost ten years, and found that low-grade systemic inflammation, as measured by the pro-inflammatory markers of systemic immune-inflammation index, neutrophil-to-lyphocyte ratios, and C-reactive protein levels, was an independent risk factor for psoriasis, especially moderate-to-severe disease. These findings support the hypothesis that low-grade systemic inflammation may contributes to the pathogenesis of psoriasis rather than simply being a consequence of the disease.
Oestrogen has immunomodulatory properties. A Tainwanese study of health records from over eight million women showed that women using hormone therapy had increased risk of developing psoriasis.
-
In those of reproductive age (50 years or younger) the risk was twice as high as overall results
-
The risk was higher again among those who used hormone therapy continuosly.
-
The risk in postmenopausal women was increased but slightly lower than in younger women.
Other autoimmune skin diseases
"Pregnancy, menopause, contraceptive use, hormone replacement therapy, and breast cancer treatment drugs result in substantial shifts in hormone levels. Additionally, hormone levels are altered by aromatase inhibitors and anti-estrogen medications. These fluctuations can modulate mechanisms influencing autoimmune skin abnormalities." Gomes et al 2024
Recommended resources
Persistent lactation-related nipple pain: aetiology and management
Selected references
Falcone D, Richters RJ, Uzunbajakava NE. Sensitive skin and the influence of female hormone fluctuations: results from a cross-sectional digital survey in the Dutch population. European Journal of Dermatology. 2017;27(1):42-48 doi: 10.1684/ejd.2016.2913.
Gomes LL, Werth AJ, Thomas P. The impact of hormones in autoimmune cutaneous diseases. Journal of Dermatological Treatment. 2024;35(1):2312241 https://doi.org/2312210.2311080/09546634.09542024.02312241.
Hui-Wen Yang, Yi-Hsien Chen, Sheng-Yin To, Yuan-Liang Wen, Senyeong Kao, Liang-Hsuan Chen, Li-Ting Kao, Hormone therapy and increased risk of psoriasis in reproductive-age and postmenopausal women: a nationwide cohort study and target trial emulation, British Journal of Dermatology, Volume 193, Issue 2, August 2025, Pages 259–266, https://doi.org/10.1093/bjd/ljaf179
Kiss O, Bahir R, Watson REB. The impact of irritant challenge on the skin barrier and myeloid-resident immune cells in women who are postmenopausal is modulated by hormone replacement therapy. British Journal of Dermatology. 2024;191:746-759 https://doi.org/710.1093/bjd/ljae1226
Ma L, Jiang H, Han T. The menstrual cycle regularity and skin: irregular menstrual cycle affects skin physiological properties and skin bacterial microbiome in urban Chinese women. BMC Women's Health. 2023;23:292 https://doi.org/210.1186/s12905-12023-02395-z.
Naslund-Koch C, Kvist-Hansen A, Bojesen SE. Low-grade systemic inflammation is associated with risk of psoriasis in a general population study of more than 100,000 individuals. British Journal of Dermatology. 2025;193:250–258 https://doi.org/210.1093/bjd/ljaf1147.
Nguyen M-L, Nguyen S, Sood N. Physiological changes in women's skin during the menstrual cycle: a scoping review. Cureus. 2024;16(12):e75286. DOI 75210.77759/cureus.75286.
Richters R, Falcone D, Uzunbajakava NE. Sensitive skin: assessment of the skin barrier using confocal Raman Microspectroscopy. Skin Pharmacology and Physiology. 2017;30:1-12 DOI: 10.1159/000452152.
Tejos-Bravo M, Cid D, Espinoza F. Altered sensory and stress responses in atopic dermatiits: effects of acute stress on lesional and non-lesional skin. Experimental Dermatology. 2025;34:e70083 https://doi.org/70010.71111/exd.70083.