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Frontal Hairine Loss in a 48 Year old Black Female


I'm a black female 48 years old with what I believe is CCCA. I started loosing my hairline in 2014, however in an 18 month period I lost my entire hairline. For the last 14 months I've been treating my scalp with natural oils/home remedies. The hair loss have stopped. I think my condition could be inactive. If the e disease is in fact inactive, without any medical treatment, can my hair grow back on its own or will I need a hair transplant?


Thanks for the great question. As a physician who sees a lot of women with CCCA, your brief story shouts out to me one main message: this may or may not be CCCA that you have and if it is CCCA, one or more other hair loss conditions might be present too.

Let me begin. Central centrifugal cicatricial alopecia (CCCA) usually starts in the middle of the scalp or in the crown. CCCA does not usually start in the front like you described. However several conditions can affect the frontal hairline just like you described including traction alopecia, cicatricial marginal alopecia and frontal fibrosing alopecia. What’s a bit unexpected from your story is the complete loss of the hairline that you described. That certainly favours a diagnosis of frontal fibrosing alopecia over traction alopecia but of course I would need to see your scalp myself to answer that. An entity called cicatricial marginal alopecia is also on the list.

Your story is not a typical story of CCCA although of course you could have CCCA back in the mid-scalp too. Many black women with hair loss in the frontal hairline also have some degree of CCCA too.

What you really need now is a diagnosis. An expert dermatologist who treats a lot of patients with hair loss might be able to make the diagnosis without a biopsy but if you are thinking of hair transplants down the road a biopsy is going to be helpful to secure the diagnosis and also determine for you (and your doctors) just how active or inactive the disease truly is right now. My advice to anyone with a story like yours would be to consider a sample from the frontal hairline area and also from the crown. Remember that a biopsy always needs to have a hair in it so don’t biopsy any bare area as that is useless.

I’m suspicious about your diagnosis of CCCA but a few things about your story are more definite. First, it’s unlikely you’ll get spontaneous growth if you haven’t had growth since 2014. Depending on the exact and precise diagnosis, you still could get a bit of regrowth with treatment but likely only a bit. Second, you are probably not a candidate for surgery yet. Whether you become a candidate depends somewhat in the diagnosis but also on the activity level of your primary disease. I like to have patients take photos once they feel their disease is quiet... and if there is absolutely no change in hair loss after two years of photography then a hair transplant might be possible. If you feel your scalp has now become quiet, take a picture today and plan to compare that same picture in 2 years. If the two pictures look 100 % identical you might be a candidate for surgery. The longer answer as to whether you are a candidate for surgery actually depends on several factors.

In summary, your story suggests a diagnosis of frontal fibrosing alopecia or traction alopecia much more than it does CCCA. A biopsy could be extremely important for you and your treating physicians right now.

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Hair Loss from Relaxers


Can my scalp be treated after severe damage from a hair relaxer?


Thanks for the great question. This is such an important question and also a very common one. There is a lot to discuss. As you’ll see, the answer to your question is ‘maybe.’ Some patients with hair loss form relaxers will grow back their hair. Some patients do not.

Let’s begin.

When a patient says to me they have hair loss from a relaxer, it’s important to keep in mind that there is not one type of hair loss that they might have. In fact, they might have one or more of many types of hair loss, including hair breakage, inflammatory scarring alopecias, hair loss from chronic inflammation, traction alopecia, telogen effluvium or androgenetic alopecia. Some patients just have one type of hair loss. Others have two or three.

Let’s take a look.

1. Hair breakage (Trichorrhexis nodosa)

Both chemical and heat relaxing of hair can cause breakage of the hair. The hairs simply break off because of the damage to the delicate strand. The heat or chemicals cause “micro tears” in the hair shaft which we call “trichorrhexis nodosa.”

The photo below shows a picture of a hair fibre that has such a tear.

Trichorrhexis nodosa of a hair fiber. This can occur from many agents including heat and chemicals used to relax hair.

Trichorrhexis nodosa of a hair fiber. This can occur from many agents including heat and chemicals used to relax hair.

If trichorhexis nodosa is the only reason for the hair loss, the hair will grow back. The damaged sections may need to be cut off, but the long term prognosis is good. It may take 6-9 months before hair returns back to the way it once was but it will return. Unfortunately, trichorrhexis nodosa as the ONLY and sole reason for a person’s hair loss from relaxers is not common. Ofter there is another reason present as well, and these are discussed below.

2. Telogen Effluvium

Many patients who come to see me with concern about their hair after using a relaxer also have a a diagnosis of telogen effluvium or “TE.” Telogen effluvium is a type of hair loss that occurs when the body feels some type of shock. This can occur from low iron (low ferritin), thyroid problems, anemias, crash diets, weight loss, stress, medications, and illness. Some of these issues such as anemia and low iron levels may make the hair slightly weaker and slightly more susceptible to hair damage. These issues must be addressed fully. For this reason, I always order blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA in all patients who come to see me with concerns about hair loss from a relaxer. Other causes must be fully evaluated.

3. Traction alopecia.

Traction alopecia is a type of hair loss that occurs from the chronic pulling of hair. Patients who use relaxers may be more susceptible to traction alopecia because their hair is subjected to many pulling forces during relaxers and the hair fibers may be weaker. Traction alopecia can occur anywhere on the scalp. The frontal regions near the temple are often a common site of traction.

Treatment for traction alopecia involves stopping the pulling forces that caused the traction in the first place. If traction alopecia is diagnosed and pulling is stopped immediately (within a few months of the new hair care practice), hair might grow back. However, if traction alopecia has been present many months, the hair may not fully return. Long standing traction alopecia is permanent and may even continue to progress once the hair pulling is stopped.

Traction alopecia of the frontal hairline.

Traction alopecia of the frontal hairline.

4. Scarring Alopecia and Chronic Inflammation .

It’s a little known fact but chronic use of relaxers, especially chemical relaxers, can create scalp inflammation. It may not be a type of inflammation that can be seen on the surface but rather a type of inflammation that is occurring deep under the scalp. In some people using relaxers (but certainly not all people), this chronic inflammation triggers the body to also create scar tissue beneath the scalp. The exact mechanism is not clear but micro injury to the skin creates microinflammation and chronic microinflamation may induce scar tissue to form.

This pattern of hair loss from relaxers has been most carefully studied in women with afro-textured hair but likely applies to all hair types. Chronic use of relaxers in women with afro-textured hair may be linked to the development of several types of hair loss including traction alopecia and central centrifugal cicatricial alopecia (CCCA). CCCA often affects the central scalp first. The diagnosis must be caught as early as possible to prevent progress and prevent irreversible loss of hair. Too often women with CCCA are told that their hair loss is simply from a relaxer and it will grow back. CCCA is a cause of permanent hair loss. If there is any doubt, a punch biopsy should be considered to properly evaluate for scarring alopecia. Treatment with agents such as topical steroids, steroid injections, and doxycycline can help stop the disease. Hair growth does not usually occur. A photo of a woman with CCCA is shown below.

Central centrifugal cicatricial alopecia (CCCA) in a woman initially misdiagnosed as having temporary hair loss from a relaxer. The correct diagnosis for this patient was CCCA which causes permanent hair loss.

Central centrifugal cicatricial alopecia (CCCA) in a woman initially misdiagnosed as having temporary hair loss from a relaxer. The correct diagnosis for this patient was CCCA which causes permanent hair loss.

Summary and Conclusion

Thanks again for the great question. Let’s now return to the original question regarding whether or not your scalp can be treated. As we’ve seen above, it really comes down the the exact cause of the hair loss. If the relaxer caused trichorrhexis nodosa, the damaged hair simply needs to be trimmed and hair density will eventually come back. If however, the relaxers have caused traction alopecia, it may or may not come back even if the relaxers are stopped. If the cause is CCCA, the hair is less likely to return and aggressive treatment with various anti-inflammatory medications are needed to stop the inflammation. If there is a telogen effluvium (from low iron for example) that predisposed to some fragility and hair loss, there could be some improvement with iron supplementation and stopping the relaxers as well.

Be sure to see a dermatologists as relaxer related hair loss can be complex sometimes. Blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA might be considered and if any doubt exists, a biopsy might be considered to rule out scarring alopecia.

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What features do you look for in a good biopsy report?




What kind of things do you look for in a biopsy report that tells you it was a good biopsy report?


Thanks for the great question. This is a topic we don’t touch upon all that often and so I’m glad you’ve brought it to attention. Let me begin by saying that biopsies are important for some complex cases of hair loss. They are not needed in every patient. Biopsies can be extremely useful if done properly. They can also be extremely misleading if certain pieces of information are left out. Here are some of the top 10 things I look for when reading a report.



A punch biopsy is deal and should be 4 mm in size. Too often smaller punches (3 or 2 mm) are used in attempt to limit scars for the patient. While this is a good thought, smaller biopsied provided limited information.


Ideally, it’s nice to see that the biopsy goes deep enough into the scalp so that the pathologist has a good chance to see what’s happening at the very bottom of the hair follicles and even into the fat. Conditions like alopecia areata and many autoimmune and inflammatory conditions and scarring alopecias (dissecting cellulitis) go quite deep. A biopsy must be deep enough to capture. this.

Many biopsies are not deep enough. Sometimes, there’s just too much bleeding during the biopsy and a physician is afraid to go deeper. Sometimes the punch technique the physician is using is not adequate and the punch is simply not pushed deep enough when taking the sample.


A biopsy specimen can be cut side to side (horizontal sections) or up and down (vertical sections). Many labs nowadays will do both. It’s nice to have horizontal sections as this gives the pathologist a lot of information on 12-30 hair follicles. Vertical sections give information on 3-7 hair follicles. I prefer to work with a pathologist who reads horizontal sections as it gives a great deal more information. Most labs perform horizontal sections.


If horizontal sections are used to process the sample, it’s important to know exactly what the pathologist sees. In this regard it’s nice to have information about the proportion of terminal hairs, vellus hairs, anagen hairs and telogen hairs in the biopsy.

1) A high proportion of vellus hairs relative to terminal hairs given a clue to possible androgenetic alopecia. Horizontal sections allow the pathologist to comment on the ratio of terminal hairs to vellus hairs - which is a wonderful clue for diagnosing andrognetic alopecia and in some cases also chronic telogen effluvium. A terminal to vellus ratio less than 4:1 means androgneetic alopecia in most cases and a T:V ratio above 8:1 signifies chronic TE.

2) A high proportion of telogen hairs may also offer information about possible underlying telogen effluvium. For example, normally there are less than 12 % telogen hairs in a biopsy. As the percent of telogen hairs rises above 12-15 % one must also wonder if a telogen effluvium is present. The diagnosis of telogen effluvium is more of a clinical diagnosis than a pathology diagnosis. So, even if the percentage of telogen hairs is less than 12 %, it’s still posisble that a patient has a telogen effluvium.


When I read a report, I want to know what’s happening to the sebaceous glands (oil glands). This is often surprising to hear as one would normally imagine one would like to know what’s happening to the hair follicles themselves. I certainly do want to know what’s happening to the hair follicles (see below), but I’d like to know if the sebaceous glands are present, if they appear bigger in the biopsy or if they are reduced. Reduction in the density of sebaceous glands is very much a feature of scarring alopecias. A relative increase in the appearance of sebaceous glands is a feature of many non scarring alopecias such as androgenetic alopecia. This information is sometimes left out of reports and it’s so incredibly helpful to have.


It’s important to know if there is scar tissue present in the skin. Scar tissue is often referred to as fibrosis, and it’s nice to know if there is scarring around the hairs (perifollicular fibrosis) or more widespread in the skin (interfollicular fibrosis).

This is perhaps the most easily confused part of interpreting biopsies since perifolliclar fibrosis can be seen in both non scarring as well as scarring alopecias. It’s easy to over interpret the presence of perifollicular fibrosis as indicating a scarring alopecia.

For example, perifollicular fibrosis is seen in many biopsies from the non scarring hair loss condition known as androgneetic alopecia (male balding). However, the tip off that a biopsy from a patient with male balding is not a scarring alopecia is the fact that the sebaceous glands are still present and there is no lichenoid inflammation (see below). In lichen planopilaris (one of the scarring alopecias), there is perifollicular fibrosis, lichenoid change and reduction in sebaceous glands.


Most biopsies have bits of inflammation here and there (sparse inflammation) and some have more Inflammation. When inflammation is present, it’s nice to know whether the pathologist feels it’s mild, moderate or severe. In addition, it’s important to know where the inflammation is found. Is it up high in the skin… or is it in the middle or is it down low at the level of the bulb. In scarring alopecias and androgenetic alopecia, the inflammation is high up in the level of the so called isthmus (fairly close to the skin level). In alopecia areata, the inflammation is quite deep in the skin around the hair follicle bulb.

I also look for the type of inflammation. Most inflammation in biopsies is comprised of a type of white blood cell called lymphocytes. But the presence of other inflammatory cells like lymphocytes, neutrophils or plasma cells might mean different things in different situations.


If hair follicle cells in the biopsy are dying this is important. There are two mains ways that cells die - apoptosis and necrosis. These is a specific pattern of cell death in scarring alopecias called “lichenoid inflammation” that gives death of hair follicle keratinocytes. The presence of lichenoid inflammation in a biopsy really points towards a diagnosis of certain scarring alopecias such as lichen planopilaris or frontal fibrosing alopecia. . This information on cell death is desperately needed but too often left out of reports.


It’s nice to know the biopsy was looked at carefully. Ideally a report should comment on the presence of inflammation in other parts of the biopsy - not only around the hair follicle. This would include the presence of inflammation around blood vessels (called perivascular inflammation) and the presence of inflammation around other gland structures (like eccrine glands). In addition, some biopsies show that the body has produced and left behind extra material in the skin (like mucin for example). All this information is very helpful to know about.


A variety of special ‘stains’ are available in the world of pathology. These stains are used to help identify specific substances in the skin or specific markers on cells. Special stains are commonly used to identify fungi (PAS stain). Other stains like gram stain may be used for identifying the presence of bacteria. An Alcian blue stain is commonly used to identify a substance in the biopsy known as mucin which may point to come autoimmune processes. Elastic stains are used to identify patterns of scarring.


I don’t usually need a biopsy to make a diagnosis. But if I’m going to do a biopsy, I want the pathology report that comes back to be a good one. I want it to be useful to my patient. I want the report to contain all the features that allows be to be as close to 100 % confident as to what’s going on in the scalp of the patient.

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Hair loss after Breast Cancer Endocrine Therapy



QUESTION: Many of us on breast cancer drugs like Letrazole/Zoladex end up with hair loss.  In my case, it occurred after a few months and was associated with an itchy scalp and diffuse shedding of 200+ hairs a day.  Some have become very fine.

If one stops these drugs, how long does it generally take for them to clear out of the system and stop affecting the hair?


Thanks for the excellent and very important question. These types of questions and their answers are important for both patients and their doctors. These issues continue to be very much overlooked in the present day and so your question has broad relevance.

I’ll review the subject broadly and then return to your question.

Endocrine Therapy for Breast Cancer.

The breast cancer drugs you are referring to are broadly classified as ‘endocrine therapy.’ These drugs include three main categories: 1) the selective estrogen receptor modulators (SERMs), 2) aromatase inhibitors (AI) and 3) GnRH agonists. These drugs have shown benefits in the adjuvant and therapeutic setting for premenopausal or postmenopausal women with early-stage or advanced breast cancer. These drugs may be taken in some cases for 5-10 years to reduce the risk of recurrence.

SERMs. The selective estrogen receptor modulators include tamoxifen, raloxifene, and toremifene. These act as competitive inhibitors of estrogen binding to estrogen receptors. From this group, tamoxifen has been the most widely used for adjuvant endocrine therapy and is still the the gold standard for premenopausal patients at risk of recurrence.

AI. By contrast,aromatase inhibitors, including letrozole, anastrozole, and exemestane. These drugs inhibit the enzyme aromatase and thereby suppress plasma estrogen levels. These drugs are now considered the preferred option for adjuvant endocrine therapy in postmenopausal patients. They all appear to be comparable in efficacy and have similar AE profiles that include hot flashes, mood disorders, osteopenia, and arthralgias.

GnRH agonists. Gonadotropin releasing hormone agonists (GnRH) are used for premenopausal women with hormone receptor–positive breast cancer Drugs like leuprolide are prescribed to suppress estrogen production by the ovary and may be combined with other endocrine therapies or chemotherapies.

Breast cancer endocrine therapy induced alopecia (BC-EIA)

Hair loss is also a potential side effect of the medications used as ‘endocrine therapy’ discussed above including the SERMs, AI, and GnRH agonist. The type of hair loss that can occur in patients using these drugs is broadly referred to as “breast cancer endocrine therapy induced alopecia (BC-EIA)

These changes come about because of the effects of hormone changes on the hair follicle - particularly the reduction in blood levels of estrogen (or estrogen related signals that are sent into cells) that accompanies use of these drugs. The hair follicle has a highly responsive endocrine organ. It produces hormones itself and responses quickly to changes in hormones in the body.

In 2013, the a meta-analysis of 13 415 patients in 35 clinical trials revealed an overall incidence of hair loss of 4.4%. The highest incidence in this study was with with the highest incidence in tamoxifen-treated patients (25%). In 2015, Moscetti and colleagues published data showing that about 8 % of 236 women using aromatase inhibitors stopped treatment on account of their hair loss.

The short answer to your question is that there can be more than one type of hair loss associated with these types of hormone blocking drugs. The main types of hair loss that are associated with these drugs include 1) acute telogen effluvium and 2) androgenetic alopecia.

Possibility 1: The Hair Loss is From a Drug Induced Telogen Effluvium

Telogen effluvium refer to a type of hair loss whereby the affected patient notices increased daily hair shedding. Instead of finding a few hairs in the shower or sink, the individual finds dozens and dozens or even hundreds. The key point here is that the shedding rate is increased over what is normal. Telogen effluvium from a drug typically occurs 2-3 months after the drug was started and can continue in some cases if the drug is continued. if a decision is made to stop the drug, the shedding can last 6-9 months after the drug is stopped.

Telogen effluvium is not common with tamoxifen. In fact, a 2014 study by Kanti et al did not show any changes in telogen hairs in 17 women using tamoxifen who were followed for 28 weeks. Although uncommon, tamoxifen related hair cycle changes are certainly possible and tamoxifen may have a growth inhibitory effects in some situations. Clearly a pure telogen effluvium is not like to be common but it can occur. A 2010 study by Bhatia et al showed that tamoxifen loaded liposomal topical formulation actually arrested hair growth in mice.

The aromatase inhibitors can also trigger a telogen effluvium. For example, Litt’s Drug Eruption Manual lists telogen effluvium from letrozole as occurring in less than 5 % of users.

Leuprolide, the GnRH agonist sometimes used in premenopausal women with breast cancer, may also cause a telogen effluvium. Litt’s Drug Eruption Manual lists telogen effluvium from Leuprolide as occurring in less than 5 % of users.

Possibility 2: The Hair Loss is From Patterned Alopecia (Androgenetic Alopecia)

The most important concept really understand is the development of androgenetic alopecia in women using endocrine therapy for breast cancer.

It’s becoming increasingly recognized that many of the hormone blocking drugs used to treat breast cancer can cause a type of hair loss that very much resembles male and female pattern balding (also called androgenetic alopecia and also called female pattern hair loss, FPHL). This type of hair loss is associated with an actual thinning of the hair strands and generally occurs in specific areas of the scalp. Women with FPHL notice that their hair is thinner and finer and this change typically affects the central scalp and crown area. The sides and the back can be affected as well but these areas are usually less affected than then middle and top of the scalp.

The drugs used as ‘endocrine therapy’ for breast cancer can cause a type of hair loss that very much resembles FPHL. It may be that women with breast cancer with underlying susceptibilities to FPHL (based on their family history or genetics) are more likely to develop this type of hair loss when they are prescribed endocrine therapy.

This type of hair loss is important to identify because it has a different course than the telogen effluvium discussed above. FPHL that develops from endocrine therapy does not improve over time if the drug is continued. Even with stopping of the drug, the hair density may not revert back to the original density. With stopping, however, the rate of hair loss may slow down or even stop.

Let me introduce you to a few important studies.

STUDY 1: Park et al 2014

In 2014, a group in Korea reported five cases of pattern alopecia in female patients who are undergoing anticancer hormonal based therapy (with aromatase inhibitors or selective estrogen receptor modulators) for the prevention of recurrence of breast cancer after surgery. This type of patterned alopecia developed after the full recovery of global hair loss of the entire scalp due to previous cytotoxic chemotherapy. The authors proposed that the androgen-estrogen imbalance caused by the drugs was thought to be the reason for the onset of pattern alopecia in the patients.

STUDY 2: Freites-Martinez A, et al 2018

in 2018, Freitas-Martinez and colleagues performed a retrospective cohort study of 112 patients with BC-ETIA. Alopecia was attributed to aromatase inhibitors in 75 patients (67%) and tamoxifen in 37 (33%). Severity was grade 1 in 96 of 104 patients (92%), and the pattern was similar to androgenetic alopecia.

STUDY 3: Gallicchio L et al. 2013

Gallicchio’s study showed that hair thinning was common with aromatase inhibitors and the chances of developing hair loss was not dependent on the age of the patient nor whether they had received chemotherapy in the past. The study was a survey-based study including a total of 851 female patients with breast cancer receiving aromatase inhibitors. 34% reported hair loss or hair thinning during their last month of therapy, and these hair changes were independent of previous chemotherapy and age.

Possibility 3: The Hair Loss is From A Different Reason Altogether

In patients who have hair loss after breast cancer treatment, one must consider a number of possibilities and keep an open mind. A number of possible reasons for hair loss after breast cancer include:

1) hair loss in the form of a telogen effluvium from the stress associated with illness

2) hair loss in the form of a telogen effluvium from one or more surgeries and the anesthetics involved in those surgeries

3) hair loss from chemotherapy, either a temporary or permanent form

4) hair loss from another issue such as a thyroid disorder, poor diet, cancer associated weight loss, or another medication used as part of treatment.

Treatment of Breast cancer endocrine therapy induced alopecia (BC-EIA)

The ideal treatment protocol for BC-ETIA remains to be determined. Hair loss with these endocrine therapies is known to have a significant effect on quality of life and this makes it imperative to develop strategies to address the hair loss.

Stopping the drug is not always an option as doing so may put the patient and highly increased risk of breast cancer recurrence. Such discussions about stopping require a thorough review by the oncologist and dermatologist.

Minoxidil may be one option for treating BC-ETIA. Freitas-Martinez and colleagues showed in 2018 that after treatment with topical minoxidil, moderate or significant improvement in alopecia was observed in 37 of 46 patients (80%). Low level laser may also be an options but this remains to be fully evaluated. Traditional anti-androgen options for addressing androgenetic alopecia in women such finasteride and spironolactone are usually not recommended for women who have been diagnosed with breat cancer.


Your question is and excellent one and I would encourage you to speak with your doctors about these issues I have raised here. Letrozole is an aromatase inhibitor and Zoladex is a GnRH type analogue. Both of these, as reviewed above, are part of what is termed endocrine therapy. While I can’t comment on whether what you have described truly fits the definition of breast cancer endocrine therapy induced alopecia (BC-EIA), certainly your description would suggest this.

Together with your physicians you can decide whether to continue these treatments or change treatments and whether to now begin specific hair loss treatments such as minoxidil. The data to date would suggest a reasonably good chance of improvement with minoxidil. In some patients minoxidil is combined with low level laser in attempt to further stimulate growth.

We don’t yet know if women with hair loss from one type of endocrine therapy are more or less susceptible to hair loss from another type of therapy. For example, we don’t yet know if women with hair loss from an aromatase inhibitor like Letrozole are less likely to have hair loss if they switch to tamoxifen. It would seem reasonable to conclude that the effects on the hair could be different.

Even with stopping a drug that may have caused BC-EIA hair may or may not improve. Some reduced shedding may occur if a culprit drug was stopped. But the pathways that were triggered often remain triggered to some degree which means the thinning does not revert back to normal in most people. With treatment of course, there can be an improvement.

Thank you again for the question.


Bhatia A, et al. Tamoxifen-loaded liposomal topical formulation arrests hair growth in mice. Br J Dermatol. 2010

Freites-Martinez A, et al. Endocrine Therapy-Induced Alopecia in Patients With Breast Cancer. JAMA Dermatol. 2018 Jun 1;154(6):670-675. doi: 10.1001/jamadermatol.2018.045

Gallicchio L et al. Aromatase inhibitor therapy and hair loss among breast cancer survivors. Breast Cancer Res Treat. 2013;142(2):435-443.

Kanti V, et al. Analysis of quantitative changes in hair growth during treatment with chemotherapy or tamoxifen in patients with breast cancer: a cohort study. Br J Dermatol. 2014.

Moscetti L, et al. Adjuvant aromatase inhibitor therapy in early breast cancer: what factors lead patients to discontinue treatment? Tumori. 2015;101(5):469-473.

Park J, et al. Pattern Alopecia during Hormonal Anticancer Therapy in Patients with Breast Cancer. Ann Dermatol. 2014.

Sagger V et al. Alopecia with endocrine therapies in patients with cancer. Oncologist. 2013;18(10):1126-1134.

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Why isn't my hair loss improving despite improving my iron?


iron levels

I was told that my hair loss was from my low iron levels. However, after working hard for the past 6 months to bring my ferritin levels up from 23 to 55…… I am still not seeing any improvement with my hair at all. Is my hair loss related to iron or not?


Thanks for the question. It’s certainly a possibility that a person’s iron levels are related to their hair loss. It’s just that they are not implicated as often as most people think. For every one patient I meet with whose lower iron levels are truly related to their hair loss, there are 6 or 7 others where the lower iron levels don’t really seem to be playing role. It’s common to hear stories from patients that they were told their low iron is the reason for their hair loss. Many such patients spend months trying to improve their iron only to find that their hair density has not improved even after correcting their iron.

The short answer is that the lower a person’s ferritin is - the more likely it’s related to the hair loss they are experiencing. It’s a scale from “very likely related” when the ferritin is down below 15 to very like unrelated. I often think in terms of the following table:


With a ferritin of 23 you described, there is a good chance it will help. But it’s far from 100 %. In fact, as you’ll see in the studies I discuss below, almost one half of people in the general population with ferritin levels of 23 will have no hair loss problems.

Hypoferritinemia without anemia (HWA): Is it consistently implicated ?

Ferritin is a measure of iron storage levels in body. In order to get a sense of a patient’s iron status, we measure “ferritin” levels rather than iron. Males tend to have higher ferritin levels than females. Premenopausal women tend to have lower ferritin levels than post menopausal women. Extremely low ferritin levels have many potential side effect and may prevent the body from making hemoglobin - a condition which is called ‘anemia’. However, many patients have low ferritin levels without actually having an anemia. This condition is sometimes called hypoferritinemia without anemia or HWA.

Borderline ferritin levels: Evidence for direct role remains poor

The discussion of ferritin levels and hair loss comes down to how low one must go before the low ferritin levels start impacting hair loss. Many females have ferritin levels 20-40 without hair loss. In fact, if you were to measure iron levels (i.e. the ferritin test) in all women between ages 20-40, you'd find many with ferritin 28, 32. 44. You'd find very few with ferritin levels above 50.  You'd find a number with ferritin levels 6, 12, 19.

While it’s often said that one needs to have a ferritin level above 40 (or above 70) for healthy hair growth, this rule is far too simple. We often "aim" for that level in the hair clinic …. but it is completely wrong to say that anytime ferritin is less than 40 there is a problem.


Ferritin levels below 15

Once the iron levels start going low enough, it is true that there is a higher likelihood now that the patient will experience some hair loss an account of those low iron levels. However, it’s now a definite yes or no. It's quite unusual for patient to have normal hair growth with a ferritin of 2 but not completely impossible. However, it’s still within the realm of possibilities for a patient to have normal hair growth with a ferritin of 18.

The biggest challenge is knowing when a patient should be strongly encouraged to increase their iron levels. The simplest rule, as mentioned above, is to recommend to all people with ferritin less than 40. But one must keep in mind that there will be many people with ferritin levels in their 20s and and 30s who are not going to get any benefit from their efforts to increase iron.


As we think about the relationship between low iron and hair loss, there are 4 key studies that everyone should be aware of.


AUTHOR: Sinclair et al. British Journal of Dermatology

TITLE: There is no clear association between low serum ferritin and chronic diffuse telogen hair loss.

DATE: 2002

Sinclair and colleagues set out to evaluate the relationship between low serum ferritin (</=20 micro g L-1) and chronic diffuse telogen hair loss in women. He analyzed nearly 200 women who presented with chronic hair loss. 12 women had ferritin levels less than 20 ug/L. In 5 women with pure chronic telogen effluvium (and no evidence of androgenetic alopecia), iron supplementation was recommended to bring ferritin levels up above 20. None of these women experienced improvements in their hair with iron supplementation.


AUTHOR: Deloche et al European Journal of Dermatology

TITLE: Low iron stores: a risk factor for excessive hair loss in non-menopausal women.

DATE: 2007

Deloche and colleagues assessed the relationship in a very large population of 5110 women aged between 35 and 60 years. Hair loss was evaluated using a standardized questionnaire and iron status was assessed by a serum ferritin assay. patients were categorized into three categories acceding to whether they had an "absence of hair loss" (43%), "moderate hair loss" (48%) or "excessive hair loss" (9%). While it was generally found that women affected by excessive hair loss were more often affected by low iron stores, (59 % vs 48 % in the other two groups), this study reminds us that many patients with no hair loss still have low iron levels.

11.4 % of pre-menopausal women who had concerns about ‘excessive hair loss’ had ferritin levels less than 40 ug/L and 10.2 % had ferritin levels less than 15 ug/L. This compares to just 6.8 % of women with ferritin above 70. This information certainly suggests a link between iron and hair loss. However, one must keep in mind that many patients in the study with low ferritin did not have hair loss. Of all premenopausal women with ferritin levels less than 15 ug/L, about 40 % had no concerns about hair loss at all. This is an important reminder that low ferritin levels are not related to hair loss in all patients.


AUTHOR: Rasheed et al (Skin Pharmacol Physiol.)

TITLE: Serum ferritin and vitamin d in female hair loss: do they play a role?

DATE: 2013

Rasheed and colleagues set out to study the role of several blood tests including iron levels in 80 females (18 to 45 years old) with telogen effluvium (TE) or androgenetic alopecia (FPHL) and compared levels of iron to 40 age-matched females with no hair loss.

Rasheed found that serum ferritin levels were lower in patients with TE (14.7 ± 22.1 μg/l) and FPHL (23.9 ± 38.5 μg/l) compared to the controls (43.5 ± 20.4 μg/l). Interestingly, these levels seemed to decrease with increased disease severity. While these studies suggested a role of low ferritin levels in hair loss the study did not include any investigation as to whether supplementing with iron was a helpful treatment strategy. That was not part of the study.


AUTHOR: Kantor et al, J Invest Dermatol.

TITLE: Decreased serum ferritin is associated with alopecia in women.

DATE: 2003

One of the earlier studies investigating the role of iron was a 2003 study in the Journal of Investigative Dermatology. The authors studied patients with telogen effluvium (n = 30), androgenetic alopecia (n = 52), alopecia areata (n = 17), and alopecia areata totalis/universalis (n = 7). The normal group consisted of 11 subjects without hair loss.

The authors found that the mean ferritin level in patients with androgenetic alopecia (37.3) and alopecia areata (24.9) were statistically significantly lower than in normals without hair loss (59.5). Interestingly, the mean ferritin levels in patients with telogen effluvium (50.1) and alopecia areata totalis/universalis (52.3) were not significantly lower than in normals. This study was a good reminder that low iron may have a role in some types of hair loss but the role in telogen effluvium remained unclear.

Key summary points about iron levels and hair loss

Here's some key 'take home' messages about iron and hair loss

1. Aiming for a ferritin level above 40 is likely good idea for anyone with hair loss.

2. Aiming for a ferritin above 70 is not my recommendation and is very hard to achieve and generally has little benefit for the hair. 

3. If one's ferritin is between 20-40 and they have hair loss, it must always be remembered that the ferritin levels may be just fine for that person. I'd still recommend supplementing with iron tablets, but there is not a lot of good evidence that doing so is going to help their hair

4. Ferritin levels under 15 are often associated with changes in hair cycling.  If ferritin is less than 15, I recommend speaking to one's physician about iron pills

5. If ferritin levels are low and hemoglobin levels are low (something we call iron deficiency anemia), a full workup by a doctor should be booked.  

6. Vitamin C helps iron absorption and taking a vitamin C rich sources with iron pills is often helpful to increase iron.  Limiting the use of caffeine may also help.

7. Many females have ferritin levels 20-40 without hair loss. The ferritin level alone does not mean much without taking everything into perspective. 

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Do you have any suggestions for patients with hair loss deemed a 'mystery'?


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QUESTION: My hair loss seems a mystery to many doctors. Do you have any suggestions on making the right diagnosis?



There’s no doubt that diagnosing hair loss can be challenging. But hair loss is never labelled a mystery until we’ve properly used the tools we have available. These include asking good questions, examining the scalp, blood tests, scalp biopsies and hair collections. 


1.     Asking Questions

There are potentially 500 questions that are relevant to the patient with hair loss. It’s simply not possible to ask every question so one needs to choose the highest yield questions. There are certain questions that must always be asked and certain questions that should be asked if one finds that a certain line of question is uncovering helpful information. 

The proper diagnosis of hair loss must be approached like detective work. One needs to think of the most common scenario and then the least likely ones.  Patients don’t always volunteer information because they don’t know if it’s relevant or not. The clinician must ask. 

A detective would not label a particular case a ‘mystery’ without having asked some good questions. Hair loss should not be labelled a mystery until one has asked some line of questions. 


2.     Examining the Scalp. 

You simply can’t properly diagnose hair loss from sitting across from the patient. One needs to get up, and examine the hair and the scalp. One needs to look at where on the scalp the hair loss is occurring, and what’s happening to the hairs.

If the hair loss is occurring only in certain areas and other areas seem unaffected, the clinician has gained valuable information that he or she is dealing with one of a group of conditions that are part of the so called ‘localized hair loss conditions.’ If the hair loss is occurring all off the scalp in a diffuse manner, the clinician has gained valuable information that he or she is dealing with one of a group of conditions that are part of the so called ‘diffuse hair loss conditions.’ Narrowing it down is helpful. 

Similarly one needs to look at the hair and the scalp. One needs to look if there is redness in the scalp, scaling, pustules, crusting. One needs to determine if the hairs are all the same size of whether some are thinner. The presence of thinner and thinner hair can be an indication of androgenetic alopecia for some. Are there hairs breaking off?  Is their a lot of new regrowth. 

The scalp examination provides key information. Hair loss should not be labelled a mystery until one has carefully examined the scalp.



3.     Blood tests

I’m of the opinion that everyone with hair loss needs blood tests. Some require only a basic blood count, thyroid study and iron level (ferritin test). Others require more detailed testing. But certainly one can’t label any case a mystery without a basic thyroid and iron level. Iron deficiency and thyroid abnormalities are very common and can have a range of different hair loss presentations.

One can’t order all the 150 blood tests that are available. It’s not practical, and it’s not cost effective. Women with irregular periods needs more detailed hormonal testing and so do women with acne and excessive hair growth on the body. Males and females with fatigue, joint pains, chronic headaches and sun sensitive rashes may be worked up for autoimmune disease.  Sexual transmitted diseases need to always be considered in patients with unexplained hair loss.  Zinc levels may be appropriate in patients with poor diet or weight changes. 

Hair loss should not be labelled a mystery until one has at least ordered a blood count, thyroid and iron study and given thought to the relevancy of the other tests we have available.


4. Scalp Biopsy

Scalp biopsies are not needed for most patients with hair loss. In fact, for every 20 patients I see, I might perform a scalp biopsy on only 1 or 2.  But no patient’s hair loss can be considered a mystery if one has not done a biopsy. It’s a tool that can provide helpful information.

The problem with scalp biopsies is they are not the final step in diagnosis and so are frequently incorrectly used. If a biopsy is not taken from the right spot on the scalp and not processed correctly and not interpreted by a pathologist who understands hair loss, it’s better not to do the biopsy at all. There are certainly a good number of inaccurate biopsy results that I see on a weekly basis. 

But a properly conducted and properly interpreted biopsy can give immediate information about whether or not a patient has a scarring alopecia and whether or not there is any component of androgenetic alopecia in the area biopsied. Biopsies are not accurate method for determining telogen effluvium (this is a clinical diagnosis that comes from asking questions and looking at the scalp).

Not everyone needs a scalp biopsy. But certainly hair loss should not be labelled a mystery until one has had a scalp biopsy.


5.     Hair Collections

Hair collections are not used very often but also provide a tool to better understand how much hair a patient is shedding. A five day hair collections requires the patient not to wash the hair for five days and then the hair is collected in a specific way while shampooing. The number of hairs that come out in that wash as well as the length of the hairs give valuable information about shedding patterns and whether genetic hair loss is likely. 


The Role of Physician Experience

Before we leave the topics of history taking, scalp examination, and blood tests, and biopsies one must also respectfully consider that physicians all have different skills in these areas. If one has seen thousands of hair loss conditions, it is more likely that key questions will be asked, subtle or key findings will be picked up on examination of the scalp, key blood tests ordered or biopsies taken from the correct area of the scalp than if a physician has not seen or treated as many hair loss patients. For that reason, one must also consider referral to a physician who specializes in hair loss disorders for any hair loss condition truly deemed a 'mystery.'



Diagnosing hair loss is truly detective work. One needs to come prepared with the right tools. There certainly are a good share of hair loss mysteries in everyday practice but many so called hair loss mysteries are not really mysteries. They are simply patients with hair loss that have not been thoroughly evaluated. 

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