How to Calm Eczema Flares During Perimenopause

Why childhood eczema can return in your 40s, how changing hormones in perimenopause affect the skin barrier, and where nutrition can help.

This is the fully referenced version of this article, with the underlying research and citations behind every clinical claim. If you would prefer a shorter, more personal read on the same subject, you will find it over on my Substack, Escape the Eczema Trap, here.

I regularly hear from women whose eczema changes or even appears during perimenopause.

For some, childhood eczema returns after decades of quiet skin. For others, a previously manageable condition becomes more persistent, more reactive or less predictable. There are also women who develop eczematous symptoms for the first time during this stage of life.

In my practice, this is not an occasional or isolated presentation. It is something I see frequently. The timing naturally raises questions about hormones. Yet the clinical picture is not as simple as falling oestrogen causing eczema.

Perimenopause is characterised by hormonal fluctuation, rather than a smooth decline, and those fluctuations occur alongside changes in sleep, stress tolerance, menstrual patterns and many other aspects of health.

When I reviewed the published evidence, the first thing that stood out was how little direct research there is. The strongest findings relate to measurable changes in skin barrier function. The evidence relating specifically to eczema consists largely of one retrospective dermatology study and one survey of 12 women.

The published literature has not yet caught up with the pattern many women describe, and that I repeatedly see in practice. That doesn’t mean the relationship is not there. It means we need to distinguish carefully between what has been measured, what is being consistently reported and what is still untested.

There is enough here to take hormonal timing seriously. There is not enough to treat hormones as the complete explanation.

Skin barrier function and eczema are not the same outcome

Research into menopausal skin often focuses on the skin barrier. Eczema is then discussed as though a change in one barrier measurement automatically explains the inflammatory disease. That is too large a leap.

The skin barrier can be assessed in several ways. Two measurements are particularly relevant to the current evidence.

• Transepidermal water loss, usually shortened to TEWL, measures the amount of water passing out through the skin. It tells us how effectively the epidermis is limiting outward water loss.

• Stratum corneum hydration measures the amount of water held within the outermost layer of the epidermis.

These are related functions, but they are not interchangeable. Skin can be reasonably effective at limiting water loss while still containing too little water.

That distinction becomes particularly useful when looking at the menstrual cycle and menopause data.

Skin Barrier measurements change across the menstrual cycle

Nikoletić and colleagues measured TEWL and stratum corneum hydration in 36 women of reproductive age during two stages of the menstrual cycle. Measurements were taken during ovulation and again during the mid luteal phase. The researchers also assessed 45 postmenopausal women.¹

Among the women of reproductive age, TEWL was significantly higher during the mid luteal phase than it was around ovulation. Skin hydration showed the opposite pattern and was significantly lower during the mid luteal phase.¹

In other words, the barrier was losing more water and holding less water during the mid luteal phase.

The authors proposed that oestradiol has a protective effect on the barrier which is opposed by progesterone.¹ This is a reasonable interpretation of the pattern they observed, but it is not proof that progesterone directly damages the barrier. This is especially true because they didn’t observe oestradiol and progesterone independently. The study compared measurements taken at two points in the cycle, when several physiological changes were happening at once.

I also want to spend a moment being clear about the study cohort, the women in the reproductive group had a mean age of approximately 27 years. So, quite definitely not perimenopausal. The study didn’t include a distinct group of women in perimenopause and it did not measure eczema severity.¹

The clear outcome it was able to demonstrate is that barrier function is not static across the menstrual cycle.

A woman who consistently reports more dryness, itching or eczema before her period may therefore be describing a genuine physiological pattern. The study cannot tell us that the hormonal change caused her eczema flare, but it gives us a plausible reason not to dismiss the timing.

What changes after menopause?

The same study found no statistically significant difference in TEWL between the postmenopausal women and the women of reproductive age.¹

This finding has sometimes been interpreted as evidence that water loss eventually returns to normal or that the skin adapts to chronic oestrogen deficiency.

However, the study didn’t demonstrate either of those processes. It compared separate groups at one point in time. It did not follow the same women from the reproductive years, through perimenopause and into postmenopause. We therefore cannot say that TEWL initially deteriorated and then recovered.

Hydration produced a different finding. Skin hydration was significantly higher around ovulation than it was in the postmenopausal group. The postmenopausal women also reported more subjective itching. Greater dryness was associated with lower hydration and with greater itch.¹

This points to an important feature of menopausal skin. The amount of water escaping through the epidermis may not appear markedly different, yet the outer layer of the skin may still hold less water.

In other words, a barrier can be reasonably effective at not leaking while still being poorly hydrated.

The wider review by Kamp and colleagues also describes the effects of reduced oestrogen on the skin, including changes in water loss, dryness and dermal collagen.² These changes may affect the resilience and comfort of the skin. They should not, however, be treated as direct measures of eczema activity.

The evidence relating specifically to eczema

The eczema evidence is far less developed than the barrier research.

Aboobacker and colleagues reviewed the records of 8,156 women aged between 45 and 55 who attended a tertiary dermatology centre in South India.³

Eczematous disorders were the most frequently recorded category of skin disease, accounting for 23.6 per cent of the dermatoses seen. Urticaria accounted for 12.4 per cent and papulosquamous disorders for 10.7 per cent.³

This does not mean that 23.6 per cent of all perimenopausal women have eczema. Every woman who participated in the study was attending a dermatology centre with a skin issue.

The term “eczematous disorders” also covered more than one presentation. Allergic and photosensitive forms were among the most frequently recorded types.³ Atopic eczema, allergic contact dermatitis and photosensitive eczema should not be treated as interchangeable diagnoses simply because they can all produce red, inflamed and itchy skin.

The researchers suggested that the high frequency of eczema and urticaria may reflect an exaggerated response to external factors.³ That is clinically interesting, particularly where a woman reports that products, heat or environmental exposures she previously tolerated have begun to trigger symptoms.

It remains an interpretation. The study did not measure oestradiol, progesterone, follicle stimulating hormone or luteinising hormone. It cannot show that hormonal change caused the conditions recorded. Equally, it cannot show that hormonal change had no part in them.

What women with eczema have reported

The most direct evidence comes from a small survey presented at the 2024 British Association of Dermatologists annual meeting.⁴

Twelve women with eczema completed the survey. Eight reported that their eczema had flared with menopause. Four said their eczema deteriorated with or before menstruation. None reported that their eczema had improved.⁴

The symptoms described included dryness, irritation, contact allergy, sensitivity, skin thinning and a rash without a specific diagnosis.

The survey also included women whose eczema had appeared later in life. Three had been diagnosed between the ages of 49 and 53, while one reported developing eczema for the first time after menopause.⁴

These accounts matter because they reflect the pattern women describe in practice. It was, however, a small cohort and it does not tell us how common the pattern is.

A survey of 12 participants cannot provide a reliable population estimate. There was no comparison group, no prospective follow up and no reported use of a validated eczema severity measure. The findings also depended on women remembering what had happened to their skin and relating it to the timing of menopause.

The frequently quoted figure of 67 per cent should therefore be read as eight women in this particular survey, not as evidence that two thirds of all women will have eczema that deteriorates during menopause.

It is enough to justify more research. It is not enough to establish causation.

What I see in clinical practice

The published evidence is limited, but the pattern I see in practice is considerably clearer than the literature might suggest.

I regularly work with women whose childhood eczema has returned during perimenopause after many years of settled skin. Others describe an existing condition becoming more persistent, spreading to new areas or reacting to exposures that they had previously tolerated without difficulty.

In many cases, the timing can be mapped against changes in the menstrual cycle.

A flare may repeatedly appear during the week before a period. It may become more pronounced as cycles shorten, lengthen or become less predictable. Some women can identify the point at which their skin changed alongside the first clear signs of perimenopause.

Cycle mapping isn’t perfect, particularly as perimenopause progresses and ovulation becomes less consistent. It can still reveal repeated associations that are clinically useful. When the same pattern appears over several cycles, I do not think it should be dismissed simply because the research has not yet captured it in a sufficiently large prospective trial.

Clinical observation cannot establish causation. I would not use it to claim that oestrogen fluctuation is the only factor involved. But the pattern is too consistent to ignore.

Women are not describing a pattern that research has disproved. They are describing one that research has barely investigated.

Does oestrogen replacement improve the barrier?

A small pilot study published in 1995 investigated skin barrier measurements in 30 menopausal women.⁵

Fifteen were receiving transdermal oestrogen and 15 were untreated. The researchers measured skin capacitance and TEWL, including the response to an occlusion stress test.

The women using transdermal oestrogen showed a significant increase in the capacity of the stratum corneum to hold water at the stress test site.⁵ This supports the view that oestrogen can influence the skin’s capacity to retain water.

The study did not assess eczema. It cannot tell us whether improved water holding capacity reduced inflammation, itching, flare frequency or eczema severity.

That boundary is important. An intervention may improve a physical property of the barrier but still not resolve an established inflammatory skin condition. Both statements can be true.

Is HRT an eczema solution?

The only direct information about HRT and eczema comes from the survey of 12 women discussed above.⁴ Most of the women taking HRT reported no noticeable change in their eczema.

This finding is interesting, but the study was far too small to confirm or deny anything. The abstract did not provide sufficient detail about HRT formulation, dose, route, duration or adherence. There was no control group and eczema severity was not assessed using a validated scale.

We cannot conclude from this survey that HRT does not help eczema.

We also can’t use the barrier studies to claim that HRT will improve eczema. The transdermal oestrogen pilot measured the skin’s capacity to hold water, not inflammatory skin disease.⁵

HRT may be appropriate for many women and for many reasons. Its use should be discussed with an appropriately qualified medical practitioner and considered in the context of the woman’s overall symptoms, medical history, risks and preferences.

Based on the evidence currently available, it shouldn’t be presented as a reliable solution for eczema.

What can reasonably be concluded?

Reproductive hormones influence the physiology of the skin.

Barrier measurements vary across the menstrual cycle. In the study by Nikoletić and colleagues, TEWL was higher and hydration lower during the mid luteal phase than during ovulation.¹

Postmenopausal skin also showed lower hydration than skin measured around ovulation, even though TEWL was not significantly different between the groups.¹

Transdermal oestrogen has been associated with an improved capacity to hold water in menopausal skin.⁵

The evidence relating to eczema is more tentative. Eczematous disorders were common within a large population of perimenopausal women attending a dermatology centre, while a very small survey found that several women experienced worsening or newly developed eczema around menopause.³,⁴

These findings do not prove that oestrogen fluctuation or decline triggers eczema.

My clinical interpretation is that hormonal fluctuation can materially alter the skin’s resilience and the threshold at which eczema flares. Reduced hydration or changing barrier function may make the skin less able to tolerate irritants, allergens, heat, friction or other inflammatory pressures.

For some women, hormonal change appears to expose a vulnerability that was already present. This may help to explain the return of childhood eczema after decades of remission. For others, it may modify an existing condition, making it harder to control without being the only reason it continues.

That leaves room for hormones to matter, sometimes considerably, without letting them be the explanation for everything.

Implications for clinical practice

A change in eczema during midlife should not be dismissed as “just dry skin”.

Nor should a new or changing rash automatically be labelled as hormonal eczema.

Persistent eyelid or hand eczema, photosensitivity, a marked change in the distribution of a rash, pain, weeping, crusting or recurrent infection may require medical or dermatological assessment. Allergic contact dermatitis, irritant dermatitis and other inflammatory skin conditions may resemble or coexist with atopic eczema.

Menstrual and menopause history can add useful context. It is reasonable to ask whether symptoms follow a cycle, whether the pattern changed as periods became less predictable and whether the onset coincided with other features of the menopausal transition.

In my view, mapping eczema activity alongside the menstrual cycle can be particularly useful during the earlier stages of perimenopause. It may identify repeated windows of vulnerability and provide a clearer picture of how the condition is changing.

Where nutritional therapy fits

The five studies reviewed here were designed to examine hormones, skin barrier measurements and eczema. They were not designed to test nutritional interventions, so they cannot tell us which nutritional strategies will be most effective.

That does not make nutrition peripheral to the conversation.

Skin is living, metabolically active tissue that is continually being broken down, repaired and renewed. It needs sufficient energy, protein, essential fats, vitamins and minerals to produce healthy skin cells, maintain the lipid structure of the barrier and support repair.

Hormone production, conversion and clearance also rely on an adequate supply of energy, fats, protein and micronutrients. Nutrition cannot prevent the hormonal fluctuations of perimenopause, but it can influence the wider physiological environment in which those fluctuations are taking place.

This becomes particularly important when the skin is already under pressure.

In practice, I am rarely looking at hormones or nutrition in isolation. I am looking at how the timing of the eczema relates to the menstrual cycle, whether the diet is providing the raw materials needed for barrier repair, whether meals are supporting stable energy and blood glucose, and whether digestive symptoms, alcohol, histamine reactivity, sleep or stress are adding to the overall burden.

For one woman, the priority may be increasing protein, essential fats and nutrient density. For another, it may be rebuilding dietary variety after years of unnecessary restriction. Someone else may need a structured investigation of a suspected food reaction, rather than continuing to remove foods without a clear method.

I also look at what has changed alongside the eczema. A woman may be eating the same foods she has eaten for years, but her hormonal environment, sleep, stress tolerance, digestion and inflammatory threshold may no longer be the same. A food or exposure that appears to have become problematic may therefore be one part of a much wider shift.

This is why I do not use a single “eczema diet”. Nutritional therapy allows me to assess the pattern, identify where the diet may be falling short and decide which areas deserve attention first.

It is also why I created a dedicated Hormones protocol within Escape the Eczema Trap®. The purpose is not to promise that food can “balance” perimenopausal hormones. It is to help women understand how hormonal change may be interacting with their skin, nutrition, blood glucose, stress, sleep, histamine response and inflammatory load, and to give them practical ways to support the areas they can influence.

Building skin resilience from within

If hormonal fluctuation is lowering the threshold at which the skin flares, the answer is not necessarily to focus on the hormone alone.

The skin still needs to be built and repaired. The immune response still needs to be regulated. The body still needs to manage inflammation, produce energy and recover from stress.

These processes depend upon nutritional input.

This does not mean that an isolated nutrient deficiency is responsible for every case of perimenopausal eczema. It means that nutritional adequacy matters more, not less, when the skin is becoming drier, more reactive and less resilient.

My assessment considers the foundations first. Is the client eating enough overall? Is there sufficient protein across the day? Are essential fats regularly included? Is the diet varied enough to provide a broad range of micronutrients and plant compounds? Have multiple exclusions created gaps that could be affecting the skin or the wider hormone picture?

From there, I consider the individual pattern. This may include digestive function, bowel regularity, suspected food reactions, alcohol intake, meal timing, blood glucose stability and symptoms that might make histamine more relevant.

The aim is not to find one food to blame. It is to improve the conditions in which the skin is trying to function.

When referral for nutritional therapy may be useful

Nutritional therapy may be particularly useful when eczema appears, returns or changes during perimenopause and the hormonal timing does not fully explain why the skin remains inflamed.

A referral may be appropriate when the client reports a clear cyclical pattern, has experienced the return of childhood eczema, has developed new food or histamine concerns, or feels that previously tolerated triggers have become more difficult to manage.

It may also be helpful when the diet has become restricted, when the client is unsure whether they are meeting their nutritional needs, or when digestive symptoms, variable energy, disrupted meal patterns or suspected food reactions are present alongside the eczema.

My role is to bring these different strands together. I assess the eczema history, hormonal timing, diet, digestion, symptoms, lifestyle and previous interventions, then identify the areas most likely to offer useful and realistic change.

I work alongside the client’s GP, dermatologist, menopause practitioner and other healthcare professionals. I do not advise on topical medication or alter prescribed treatment. Nutritional therapy adds another layer of assessment, addressing the internal foundations of skin health while medical and dermatological care continue.

Find out more about how I work

Clinical conclusion

The current evidence confirms that reproductive hormones influence skin barrier physiology.

TEWL and hydration vary across the menstrual cycle. Postmenopausal skin appears to hold less water, and transdermal oestrogen may improve the skin’s water holding capacity.¹,⁵

The direct eczema research is much smaller, but its findings follow the same direction as the pattern I repeatedly see in practice. Women report established eczema becoming more difficult to control, childhood eczema returning after years of remission and, in some cases, eczema appearing for the first time in midlife.³,⁴

The existing studies cannot prove that fluctuating or falling oestrogen directly causes eczema. They also provide no basis for dismissing the relationship.

My clinical interpretation is that hormonal fluctuation can change the skin’s resilience and lower the threshold at which eczema flares. For some women, it appears to uncover a vulnerability that has been quiet since childhood. For others, it makes an existing condition more reactive and less predictable.

Nutrition provides the raw materials for the skin barrier, hormone pathways, immune regulation and repair. It therefore gives us a meaningful and practical place to work, even when the hormonal transition itself cannot be controlled.

The hormonal timing deserves to be taken seriously. It can help us understand why the skin has changed. The next step is to identify what the skin needs now.

Referrals and professional enquiries

I accept referrals for adults whose eczema or dermatitis has appeared, returned or become more difficult to manage during perimenopause and menopause.

My nutritional assessment considers the relationship between hormonal timing and skin symptoms alongside nutritional adequacy, barrier support, blood glucose regulation, digestive function, histamine reactivity, suspected food triggers and previous dietary restriction.

I provide evidence informed nutritional therapy alongside the client’s existing medical and dermatological care. With the client’s consent, I can share my assessment and recommendations with the referring practitioner.

Adults who would like to explore their own pattern can complete the Escape the Eczema Trap® quiz. The quiz helps identify which area, including the Hormones strand, may offer the most appropriate place to begin.

For a more personal exploration of eczema and perimenopause, visit my Substack, Escape the Eczema Trap®.

References

The clinical claims in this piece are drawn from the following peer-reviewed papers.

1. Nikoletić ĐC, Ivanov D, Levakov O, et al. Menopause, menstrual cycle, and skin barrier function. Skin Research and Technology. 2025.
2. Piérard-Franchimont C, Letawe C, Goffin V, Piérard G. Skin water-holding capacity and transdermal estrogen therapy for menopause: a pilot study. Maturitas. 1995.
3. Aboobacker S, Saritha M, Karthikeyan K. A retrospective analysis of dermatoses in the perimenopausal population attending a tertiary care centre in South India. Journal of Mid-Life Health. 2015.
4. Kamp E, Nielsen-Scott A, DeGiovanni C. The impact of menopause on eczema. British Journal of Dermatology. 2024.
5. Kamp E, Ashraf M, Musbahi E, DeGiovanni C. Menopause, skin and common dermatoses. Part 2: skin disorders. Clinical and Experimental Dermatology. 2022.