Hair Blogs

QUESTION OF HAIR BLOGS


Telogen Effluvium Canis Mortalis: Hair Shedding when a Pet Dies

What do pets mean to humans?

Every now and then, I hear a story of profound sadness in someone’s family with the passing of the family pet. These stories most often centre around the family dog but the passing of other pets certainly carry these emotions. What is remarkable from the perspective of a hair specialist is the evidence that I can see on the scalp that the death of the family pet has triggered hair loss in the owner.

From time to time, I see clear evidence when I examine the scalp of some sort of ‘event’ that happened just a few months prior. Sometimes, it surprises me as it might be something I did not expect to see when I examine a person’s scalp. I might stop and turn to the patient and ask “Was their any type of major stress or illness or new medication or new diet that happened a few months ago?”

The patient might look at me and say “Well, I don’t think so. Everything has been the same. Oh wait - let me think about this - our dog died around that time.”

Hair loss from stress

It’s well known that stress can cause humans to shed hair. Stress, just like low iron levels or thyroid problems, or medications and dieting can cause an increase in the amount of shedding. Instead of losing 50 to 70 hairs per day the patient now loses 100, 200 or 300 hairs per day. There’s a long list of causes of shedding. We instinctively know that stress from loss of the family pet is probably included on these lists, but we just don’t ever see it on the list. I propose that we at least keep it in mind. Most people feel that their concerns will be dismissed as ‘it’s just your dog’ …. and rarely discuss it with health care providers.

Telogen Effluvium Canis Mortalis: Hair Shedding When The Family Dog Dies.

We don’t really have a good word in the medical literature to describe hair shedding that we see when a dog dies. I refer to it as telogen effluvium canis mortalis - and will stick with that until someone offers a better term. I’ve seen many examples over the years. It’s often subtle and one really only picks up on it when they ask about it. The loss of the family pet causes a profound sadness that can affect the body enough to cause hair loss. The shedding usually happens a month or two after the pet dies.

The research surrounding the relationship between pets and humans is truly fascinating. When you look at the research data, it becomes more obvious why delicate hair follicles increasingly fall out of the scalp (in some people) when the family pet dies. Simply put, pets may have an important effect on human function.

In 2017 Swedish researchers investigated whether owning a dog affects how likely people develop heart disease and how likely they are to die after developing some type of heart disease. The authors used a large database of over 3 million people in Sweden (n = 3,432,153) with up to 12 years of follow-up to study the health outcomes of people who own pets. 13 % of people in the study owned dogs. Interestingly, people who owned dogs had less heart disease and a lower risk of death from many causes including heart disease. In 2019, Mubanga and colleagues again looked further into why this might occur. They found the lower risk of heart disease and death was not from pet owners having lower blood pressure or lower cholesterol. Some other factors are involved.

These Swedish studies are sure interesting. In Sweden, people must register their pets in a national database so it’s possible to link a patient’s health to whether they own a pet. Mubanga recently again used the Swedish National Patient Register to look closer at patients aged 40 to 85 presenting to the hospital with heart attacks or strokes. What were the results? Well, dog owners had a lower risk of death after being in the hospital for a heart attack. The same findings was true for those who had strokes. In addition, people who had dogs as pets were less like to have another heart attack (second ‘repeat’ heart attack).

COMMENTS AND CONCLUSION

When it comes to properly evaluating hair loss, everything matters. Yes, it’s a bit daunting sometimes - but everything matters. Physicians must at least consider the family pet as they go about understanding the family structure of the patient and their potential sources of stress when the family pet dies.

It’s clear that having pets affects not only risks for heart disease and stroke, but many aspects of our health. This is an important area of current research around the world. We certainly have a lot to learn but the emphasis here is that pet ownership is tied in to our health. Some studies have shown that pet ownership reduces the risk for some autoimmune diseases like inflammatory bowel disease and ulcerative colitis.

Reference

Cholapranee A et al. Environmental Hygiene and Risk of Inflammatory Bowel Diseases: A Systematic Review and Meta-analysis.Inflamm Bowel Dis. 2016 Sep;22(9):2191-9.

Mubanga et al. Dog ownership and the risk of cardiovascular disease and death - a nationwide cohort study. Sci Rep. 2017 Nov 17;7(1):15821. doi: 10.1038/s41598-017-16118-6.

Mubanga et al. Dog ownership and cardiovascular risk factors: a nationwide prospective register-based cohort study. BMJ Open. 2019 Mar 7;9(3):e023447. doi: 10.1136/bmjopen-2018-023447.

Mubanga et al. Dog Ownership and Survival After a Major Cardiovascular Event: A Register-Based Prospective Study.Circ Cardiovasc Qual Outcomes. 2019 Oct;12(10):e005342.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

The "Dread Shed" - Does it just apply to Rogaine?

The Dread Shed is Both Good and Bad

The term ‘dread shed’ refers to an increased shedding of hair that individuals notice within 1-3 months of starting a new treatment for androgenetic alopecia. Medically, the phenomenon is known to hair specialists by the term "immediate telogen release.” Most famously, the term ‘dread shed’ applies to the increased shedding some people experience with use of minoxidil. However, the term equally applies to other therapies. The 'dread shed' can be frightening when it occurs but is generally mild for most. Understanding why this occurs is important to help individuals decide whether this treatment is right for them to start or not. Let’s take a look first at shedding from minoxidil.

Dread Shed from Minoxidil

Minoxidil lotion and Minoxidil foam are FDA approved for treating androgenetic alopecia (AGA) in men and women. This type of hair loss is also called male pattern balding and female pattern hair loss. A common concern among individuals who are deciding whether or not to use minoxidil is the potential for them to develop an increased amount of daily hair shedding in the first 1-3 months of starting minoxidil. This type of shedding is not to be confused with the shedding that happens when people with androgenetic alopecia incorrectly stop using minoxidil. (One must never stop treatment if they have androgenetic alopecia or else new hair growth will be shed and all benefits will be lost).

Immediate telogen release: Understanding shedding with minoxidil (Rogaine)

The increased shedding that accompanies starting minoxidil needs to occur for most people. It's not something that is really all that abnormal - it just ’looks’ abnormal. When you look closely at the scalps of males and females with androgenetic alopecia (especially early stages of AGA), one will notice that a higher than normal proportion of cells are in the shedding phase of the hair growth cycle (i.e. the so called telogen phase). These hairs are waiting their turn to shed. Hairs generally need to wait in line 2-3 months before they are shed. That's just the rule of the nature. That's what it means to be human.

When minoxidil is applied to the scalp, a signal is sent to all hairs that are waiting in line to be shed. The message that is relayed is that the hairs no longer need to wait 2-2 months in that line. Rather any hair that is waiting in line to be shed is welcome to shed now.  The mandatory 2-3 month waiting period has been temporarily waived. And so what the patient then experiences is an increased amount of hairs coming out on a daily basis once they start minoxidil. What is being shed is hairs that were destined to come out anyways:

Instead of coming out tomorrow, a hair comes out today

Instead of coming out in 2 weeks, a hair comes out in tomorrow

Instead of coming out in 4 weeks, a hair comes out in 1 week

Instead of coming out in 6 weeks, a hair comes out in 2 weeks

This is what the 'dread shed' or 'immediate telogen release is all about.

 

Dread Shed from Spironolactone, Finasteride and Low Level Laser

As we reviewed together in the section above, a dread shed is expected. It’s not that it’s unexpected. It’s expected. If a patient does not get some little bit of increased shedding it’s probably a concern. Now, keep in mind that patients who wash their hair daily may not be able tell they are having increased shedding if the ‘dread shed’ is mild. It’s really only individuals with more marked shedding that will be able to tell they are having a dread shed. As well, people who wash their hair once per week are going to be able to appreciated subtle differences much easier than people who wash their hair daily. (I’m not saying to wash the hair weekly - I’m just say these are the individuals who can appreciate differences the easiest).

Any treatment for androgenetic alopecia that works has the potential to cause a dread shed. I think that’s worth repeating: Any treatment for androgenetic alopecia that works has the potential to cause a dread shed. Minoxidil, spironolactone, PRP, laser, finasteride, dutasteride, flutamide, bicalutamide - they all carry with them the potential to cause a dread shed.

Whenever a patient bring in a product and tells me they have a new wonderful product that does not cause a dread shed - I tell them simply that if the product they have in their hand has a zero percent chance of causing increased shedding then it probably does not help in the treatment of androgenetic alopecia.

Now as we finish our discussion of dread sheds and treatment related shedding in general, it’s important to keep in mind a few points:

  1. Some treatments are more likely to cause marked shedding (i.e. a dread shed) than others. Minoxidil and spironolactone carry with them a greater risk than low level laser therapy.

  2. Some treatments not only cause a dread shed but cause hairs that were not in the telogen phase to also be booted out of the scalp. This is called a drug induced telogen effluvium and can look similar to a dread shed and is challenging to differentiate from a simple dread shed phenomenon. Spironolactone can cause this phenomenon sometimes and so can minoxidil. In this case the shedding does not stop at month 3 -4. Expert advice is needed in these challenging cases.

  3. Not all patients notice increased shedding after they start a treatment - especially patients who wash their hair daily.

  4. The general advice for most patients with androgenetic alopecia who start minoxidil or an antiandrogen or laser therapy and experience increased shedding in the first 1-2 months is to keep going with therapy. Of course, each of these situations should be reviewed with the hair specialist on a case by case basis. But as we have seen above, increased shedding is expected with these therapies.

  5. Not every single person who has shedding with treatment will find that the hair density improves at a time point 6 to 12 months into the future. For some patients with strong genes controlling the androgenetic alopecia, the increased shedding only serves to speed up the miniaturization process. This is not common but always needs to be considered. This is particularly true for those who experience a true drug induced prolonged telogen effluvium from use of these treatments. A small proportion of patients do have shedding when starting treatment and find one year later that the androgenetic alopecia has progressed and the hair density is worse. In some of these cases, the treatment did very little to help and the androgenetic alopecia simply pushed the hair thinning along its course. For others, the therapy accelerated the shedding process which further pushed the hair thinning along its course - ahead of where it would otherwise have been.

The Good and Bad of the Dread Shed

For patients with androgenetic alopecia who start treatment, increased hair shedding is generally viewed as a good thing. It’s something that we expect to occur rather than something are concerned with. The most likely scenario for patients who have shedding is that the shedding will eventfully stop and some amount of stabilization or improvement of the androgenetic alopecia will be seen. However, many variations are possible. In rare cases, shedding does not slow at the 3-4 month mark and hair density does not improve. These situations are rare but must always be considered.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Single Hairs in Lichen Planopilaris: A Reflection of the Destructive Process

Three-Haired and Two-Haired Follicular Units Become Single Haired Units

Lichen planopilaris (“LPP”) is a type of scarring alopecia. It is though to be autoimmune in ethology meaning that the body’s own immune system is triggered to attack and destroy hairs. LPP is a destructive process.

Hairs normally emerge from the scalp in ‘bundles’ of one, two or three hairs (sometimes four). We call these follicular units. Many people expect that hairs emerge from the scalp all by themselves - but that’s not the case. They emerge normally from a single follicular opening or ‘Ostia’ in groups of 1, 2 or three hairs. Most common they come out in bundles of two and three in the middle, crown and back. The temples of humans normally has a lot higher proportion of single haired follicular units (only one hair emerges from the pore).

Single hairs in lichen planopilaris (LPP). Lichen planopilaris is an autoimmune disease whereby the immune system attacks hair follicles. The result is a conversion slowly over time of three and two haired ‘follicular unit' bundles into single haired follicular units. As the disease progresses, the single haired follicular units are also destroy and replaced by scar tissue.

Single hairs in lichen planopilaris (LPP). Lichen planopilaris is an autoimmune disease whereby the immune system attacks hair follicles. The result is a conversion slowly over time of three and two haired ‘follicular unit' bundles into single haired follicular units. As the disease progresses, the single haired follicular units are also destroy and replaced by scar tissue.


LPP is a destructive process and destroys the normal architecture of follicular units.

LPP is a destructive process and destroys the normal architecture of follicular units. Where there were three hairs in a follicular unit before, slowly there becomes two hairs as one hair decides it not survive the immune attack and the changes the hairs incurs on account of the immune attack (loss of oil glands, death of cells in the follicle and permanent scar tissue developing). Where there were two hairs before, slowly there becomes one as one hair decides it not survive the immune attack and the changes the hairs incurs on account of the immune attack (loss of oil glands, death of cells in the follicle and permanent scar tissue developing. Where there was one hair in an area before, slowly there becomes none as the one hair decides it not survive the immune attack and the changes the hairs incurs on account of the immune attack (loss of oil glands, death of cells in the follicle and permanent scar tissue developing. The findings of advanced LPP are scattered single hairs over the scalp.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

On the 'Natural Course' of Hair Loss Conditions

Giving credit where credit is due: A look at the reality of the ‘natural course’ of various hair loss conditions.



Many hair loss patients ask me if doctors give themselves too much credit when a patient has a successful outcome after a treatment. 

“My body might have done this anyways,” is often the comment I hear.

“How do you know that the natural course of my disease would not have been the same?”


Some patients who state that their body would have shut off their hair loss on its own are correct. But some are not. Let’s take a look at 5 common hair loss conditions and how likely it is for the hair to improve on its own.


improvement



EXAMPLE 1: Alopecia areata

Likelihood of improvement without treatment: low to very high



Alopecia areata is an autoimmune disease. About 2 % of the world will be affected by the condition at some point or another. What’s typical of alopecia areata is it’s potential to regrow all on its own - at least in a subset of patients. About 1/3 of patients will regrow their hair “spontaneously” in 6 months and another 1/3 will grow in back “spontaneously” within 12 months. About 1/3 of patients will develop a chronic form of alopecia areata some of whom will develop alopecia totalis and universalis.

Therefore, many patients with alopecia areata can successfully grow back hair even without treatment. Treatment helps it grow back faster and could theoretically reduce the chance of disease flares.

For patients with more advanced forms and patients with disease of longer duration - it’s less and less likely the hair will grow back on its own. If treatment is given in these cases, and the hair does grow back, it’s likely that the treatment (rather than the natural course) that is affecting the regrowth.





EXAMPLE 2: Acute telogen effluvium

Likelihood of improvement without treatment: low to very high



Acute telogen effluvium (or simple “TE”) is a type of hair loss whereby the patient experiences increased shedding. A variety of triggers can cause TE including stress, low iron, thyroid problems, medications and crash diets. In at least 50% of cases, a trigger can not be found in acute telogen effluvium and shedding continues.

In many cases of TE, the hair grows back spontaneously. A patient with a TE that was due to a general anesthetic received in the hospital often just needs time - NOT treatment. With the passage of time, the hair shedding will again slow and the patient will likely regain density (unless another condition is also present such as androgenetic alopecia). 

In this example, the natural course is towards regrowth. In fact, treatment if not needed because the body itself can do it all itself. I would even go further to say that offering treatment is completely inappropriate. To offer therapy of any kind if spontaneous regrowth is suspected is not good practice.




EXAMPLE 3: Chronic telogen effluvium

Likelihood of improvement without treatment: moderate



Chronic telogen effluvium is often mixed up with acute telogen effluvium but is a very different condition. For chronic telogen effluvium (CTE) cessation of shedding and regrowth can also occur. In fact, the classic teaching of CTE is that it is a ‘self-limiting’ condition. But what many people forget is that it can take 5, 10 or 15 or more years in some cases for a CTE to halt. Granted some are faster in their resolution. If a patient with chronic shedding for 2 years comes and sees me and we start treatment and shedding slows down in a matter of months am I to believe it was the therapy I gave or was this natural history of the condition? Odds would favour the treatment being responsible in this case.




EXAMPLE 4: Androgenetic alopecia

Likelihood of improvement without treatment: very low 



Androgenetic alopecia is a common type of hair loss. For men, it is referred to as male pattern hair loss, or male balding. When it occurs in women, it is referred to as female pattern hair loss or simply female thinning.  Without treatment, this type of hair loss is always progressive. It may, however, progress very very slowly for some affected individuals and may even stay relatively stable for some patients for long long stretches of time. It does not, however, improve spontaneously. A patient with androgenetic alopecia who says their hair is actually getting better on its own likely had another issue present as well in the past - such as a telogen effluvium. In that sort of example it’s the telogen effluvium that is getting better - not the androgenetic alopecia.


EXAMPLE 5: Scarring alopecia

Likelihood of improvement without treatment: very low



Scarring alopecias are a group of conditions that are associated with the presence of scar tissue in the scalp.  A variety of scarring alopecias exist including lichen planopilaris, frontal fibrosing alopecia, folliculitis decalvans and central centrifugal cicatricial alopecia. Without treatment all active scarring alopecias by definition will cause further hair loss. For some it can be quite slow (meaning it takes 1 -2 years before any further hair loss occurs). For others, it can be more rapid (meaning it takes just several months before any further hair loss occurs).

I occasionally meet patients with scarring alopecia who believe that there is a high chance their disease will burn out rather quickly. Many of these patients start treatment and experience an improvement in their hair shedding or symptoms and a cessation of further loss. On occasion a patient will ask me something like:


“How do you know my disease would not have just gone quiet anyways?”

or 

“How do you know the natural course would not have been to just go dormant and burn out?”


I’m not sure why it is that some patients feel that these scarring alopecias have such a high chance of spontaneous resolution. This is not accurate. For many patients, the immune response inside the body to destroy hair has been mounting for many, many years - even well ahead of the patient actually experiencing hair loss. It is not likely that that that sort of programmed immune response can simply shut off so quickly. I often say to patients that if it took 2, 5 or 10 years for the immune system to slowly reprogram itself to attack the hair, why would the disease stop in 6 months without treatment? Why would the ‘natural history’ be to stop.

Without treatment, most scarring alopecias grumble along with various levels of activity and slowly destroy hair. It’s true that scarring alopecia can eventually stop - but not for years in the vast majority of patients. Without treatment, some patients with scarring alopecia will find that every few months they are noticing they have less hair and look different. That’s considered fast progression. Other patients will find that it takes about two years for them to sustain enough cumulative hair damage to really appreciate a difference in their hair. That’s slow progression.



Conclusion and Summary

The ‘natural history’ of some hair loss conditions does favour improvement in density. In other words, even without treatment some conditions can improve. This is common for alopecia areata and some forms of acute telogen effluvium. Chronic Telogen effluvium (CTE) can most certainly improve on its own - but it usually takes a number of years. For scarring alopecias, the natural course is not one of rapid cessation of disease activity. A patient with scarring alopecia who sees improvement in the hair after starting treatment should not wonder “perhaps my scalp was going to do that anyways.” That is not the natural course of these diseases. Androgenetic alopecia is slowly progressive without treatment. The natural course (without treatment) is not one of improvement or cessation.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

University of Ottawa 70th Clinical and Scientific Meeting

Division of Dermatology Hosts Meeting on Hair Loss

I was honoured to be invited to the beautiful city of Ottawa this weekend to lecture and participate in the University of Ottawa, Division of Dermatology’s 2 day Clinical and Scientific meeting - devoted entirely to hair loss! Together with my dermatology colleague Professor Lynne Goldberg from Boston University School of Medicine we gave lectures on various topics in hair loss, listened to lectures, met with the residents, and saw patients with a variety of non scarring and scarring hair loss conditions.

Screen Shot 2019-10-06 at 5.49.06 AM.png

Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Chronic Telogen Effluvium (CTE): A Closer Look at the Classic Whiting Study

The 1996 Whiting Study

The field of hair loss has its classic papers. These are papers that stand the test of time and influences the research that comes in the decades that follow. Dr David Whiting did some pioneering work in understanding exactly what chronic telogen effluvium (CTE) is what it is not. Whiting described CTE as a condition which usually affects 30- to 60-year-old women, starts abruptly with or without any sort of “trigger”. Whiting showed that CTE had a long fluctuating course.

CTE-Whiting



Dr. Whiting’s 1996 paper on chronic telogen effluvium effluvium (CTE) is one of these classics. Dr Whiting set out to determine distinctive clinical and pathologic criteria for the diagnosis of CTE. He also wanted to determine how biopsies of CTE differs from biopsies of androgenetic alopecia (AGA). To do so, Whiting studied biopsy findings in 355 patients with CTE. Results were compared to 412 patients with androgenetic alopecia (AGA) and 22 control subjects without hair loss. For patients without hair loss, the average number of hairs in the biopsy was 40, the terminal/velluslike (T:V) hair ratio was 7:1, 93.5% of the terminal hairs were in anagen, and 6.5% were in telogen. For patients with CTE the average number of hairs was 39, the terminal/velluslike (T:V) hair ratio was 9:1, 89% of the terminal hairs were in anagen, and 11% were in telogen. In AGA the average number of hairs was 35, the T:V ratio was 1.9:1, 83.2% of hairs were anagen and 16.8% were telogen phase hairs. Interestingly, significant degrees of inflammation and fibrosis were present in only 10% to 12% of cases of CTE and normal controls, but occurred in 37% of cases of AGA.


Conclusion


This was a classic study and all providers of car to hair loss patients should take the time to understand this study. Evaluation of the T:V ratio in biopsies can help distinguish CTE from AGA. The ratio is 8:1 or higher in CTE and less than 4:1 in AGA. The proportion of hairs in telogen phase was 50% higher in AGA than TE.

Reference

Whiting DA. Chronic telogen effluvium: increased scalp hair shedding in middle-aged women. J Am Acad Dermatol 1996


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Scarring Alopecias: What is the importance of age?

A Closer Look at Scarring Alopecia According to Age

The group of hair loss conditions known as the “scarring alopecias” are less common overall than the non-scarring alopecias. Scarring alopecias include conditions such as lichen planopilaris (LPP), discoid lupus (DLE), frontal fibrosing alopecia (FFA), folliculitis decalvans (FD), central centrifugal cicatricial alopecia (CCCA) and dissecting cellulitis (DSC). This diagram shows the typical age ranges that patients generally first develop these conditions. Dissecting cellulitis and discoid lupus for example for commonly start to affect individuals in their 20s and 30s. In contrast, frontal fibrosing alopecia generally starts affecting individuals in their mid 40s, 50s and 60s. These are “averages” and of course exceptions exist in every aspect of the field of hair loss.

age-scarring-alopecia



Why does age matter?

The implications of this diagram are profound. A 21 year old female who is worried about having FFA probably does not have FFA. Of course she might (as exceptions do exist) but I’d estimate that 2 out of every 1 million women develop FFA at age 21. A 19 year old woman of Afro-Caribbean descent who presents with hair loss is far more likely to have traction alopecia and even scarring forms of traction alopecia than CCCA. Can she have CCCA? Sure. But unlikely. A 90 year old woman developing folliculitis decalvans is unusual. She more likely has infectious causes or causes related to general immune suppression, pustular medication reactions, or erosive pustular dermatosis of the scalp (EPDS)


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Diagnosing Hair Loss: All Steps Must be Considered


The Important Steps in Diagnosis


One can confidently diagnosethe cause of a patient’s hair loss after they have completed a few steps: (1) they have heard the whole story about the hair loss and patient’s past health (2) they have examined the scalp including up close with use of trichoscopy and (3) they have reviewed the patient’s blood tests. (4) Sometimes a fourth step is needed and that is review of the results of a patient’s biopsy. One essentially puts the results of steps 1,2,3 and 4 into the brain and then out pops the diagnosis.


The diagnosis of hair loss is a multistep process. It comes from evaluating the patent’s story of their hair loss, examining the scalp, blood tests and biopsy results if needed.

The diagnosis of hair loss is a multistep process. It comes from evaluating the patent’s story of their hair loss, examining the scalp, blood tests and biopsy results if needed.



We never diagnose hair loss by ordering up blood tests and sitting patiently for the results to come back. Blood tests can be an important part of the story but they are never the entire story. Similarly one never relies 100 % on the results of a biopsy. If one decides to do a biopsy and it comes back showing a non-scarring alopecia but the clinician in really thinking this is a scarring alopecia then one must either ignore the biopsy or take more biopsies from the patient’s scalp or get another pathologist to review the slide.



Many patients eagerly await the results of the biopsy to determine what it is they actually have. This is an error. The diagnosis of hair loss must take into account the  whole story, as well as what the scalp looks like and what the blood tests show.

Many patients eagerly await the results of the biopsy to determine what it is they actually have. This is an error. The diagnosis of hair loss must take into account the whole story, as well as what the scalp looks like and what the blood tests show.


Diagnosing hair loss comes from reviewing information from multiple sources of information.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Rethinking Hair Loss According to Age

Diagram showing the typical age at which patients first receive their diagnosis. There are generalizations rather than rules.

Diagram showing the typical age at which patients first receive their diagnosis. There are generalizations rather than rules.

There are many reasons for women to lose hair. Some conditions are far more likely to occur in certain age groups. This chart shows the average age that patient’s first receive their diagnosis. They are not rule but rather averages. Many exceptions exist

A 72 year olf female does not suddenly start to develop androgenetic alopecia. This typically would have happened much earlier. Alopecia areata can occur at any age but most develop it before age 40. Chronic telogen effluvium and lichen planopilaris affects women mostly starting in the mid 30s and older. Of course, they can occur earlier, but it’s not common. Frontal fibrosing alopecia generally affects women age 45-65 but again there are exceptions. This chart helps organize the clinician’s thinking. Most 23 year old females with concerns about hair loss have female pattern hair loss or telogen effluvium (or both). Most 75 year old women with sudden onset hair loss have telogen effluvium. (CTE=chronic telogen effluvium; LPP=lichen planopilaris; FFA= frontal fibrosing alopecia).


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Anisotrichosis in Androgenetic Alopecia

What is anisotrichosis?

Androgenetic alopecia affects both men and women. There are several features of this condition including increased shedding, hair that does not grow as long as before and a slow and steady reductions in the caliber (diameter) of follicles. The other feature of androgenetic alopecia is that it usually affects some areas of the scalp more than other areas and is therefore said to be a “patterned” type of hair loss.

In 2007, Sewell introduced the term “anisotrichosis” which refers to a variation in diameter of follicles. It’s an important trichoscopic feature of established androgenetic alopecia.

anisotrichosis



In this picture of a female patient with androgenetic hair loss, it can be seen that some hairs are thick and some are much thinner. Two hairs in the photograph are labelled - one being 81 micrometers in diameter and the one right next to it being 32 micrometers in diameter. At one point in the patient’s life, most hairs in the region would have been similar caliber. The process of genetic hair loss has caused some to thin more rapidly than others.

The decrease in caliber is due in part to a decease in the size of the dermal papilla (a part of the hair follicle). Treatments for androgenetic alopecia include topical and oral minoxidil, topical and oral antiandrogens, low level laser, platelet rich plasma and hair transplantation. Scalp micropigmentation provides a method of camouflage for some patients.

Bhamla and collages showed in 2013 that anistrochosis was 75 % sensitive and 61 % specific in the diagnosis of androgenetic alopecia. This means that if one does not see anisotrichosis when evaluating the scalp by trichoscopy, the patient just might not have androgenetic alopecia. However, if anisotrichosis is seen one needs to strongly consider AGA but diagnoses like alopecia areata, traction alopecia (which also cause miniaturization) must also be considered too.

Galliker and Trueb in 2012 proposed that if we see more than 20 % of hairs being of different caliber, then one should strongly consider the diagnosis of androgenetic alopecia.



Reference


Sewell L et al Anisotrichosis: A novel term to describe pattern alopecia. J Am Acad Dermatol 2007; 56: 856.

Bhamla SA et al. Is trichoscopy a reliable tool to diagnose early female pattern hair loss? Int J Trichology. 2013 Jul;5(3):121-5.

Galliker NA, Trüeb RM. Value of trichoscopy versus trichogram for diagnosis of female androgenetic alopecia. Int J Trichology. 2012 Jan;4(1):19-22.






Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Videodermoscopy of Chronic Telogen Effluvium (CTE)

Videodermoscopy of the scalp in a patient with a combination of androgenetic alopecia (AGA) and chronic telogen effluvium (CTE). There is a slight variation in the caliber (diameter) of follicles that can be appreciated but it is subtle. The patient however is troubled by massive amounts of shedding despite the fact that her density is not getting worse over the years. This is typical of CTE.

Chronic telogen effluvium is frustrating for patients because they experience unpredictable shedding. It seems to improve only to worsen again. New products are bought and tried some of which seem to help for a short while only to lose hair again. The reality is that most of these products had no effect and the improvements and worsenings are just what CTE “does.” Many patients with CTE are told they look fine by doctors, friends, spouses, hairstylists but few actually appreciate just how much hair the patient has really lost. Many patients with CTE start out with extremely thick hair and even with a massive reduction in density they still look like they have alot of hair. CTE may slow or eventually stop but it can take a very long time for some to do so (10 + years) and some do not. Most patients with CTE do not have AGA and because of this shedding does not lead to a change in density over time. Most patients are surprised to learn that their density is not worse in subsequent visits to the clinic because of all the shedding they have experienced. Treatments for CTE include minoxidil (topical or oral), laser, biotin, hair and nail supplements, lysine. Rarely other treatments are considered. #chronictelogeneffluvium




Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
1 Comment

Videodermoscopy of Female Androgenetic Alopecia (AGA)


Videodermoscopy of female androgenetic alopecia. “Anisotrichosis” or a variation in the caliber of hairs can be easily seen in this video. Treatments such as minoxidil, antiandrogens, laser, PRP can help slow the condition or in some cases even improve the density. #aga#femalepatternhairloss #hairloss


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Videodermoscopy of Active Lichen planopilaris (LPP)

Videodermoscopy of active lichen planopilaris (LPP). Lichen planopilaris is an immune based scarring hair loss condition that has the potential to lead to permanent destruction of hair follicles. In this video, intense redness can be seen in the scalp. Density of hairs is less than normal due to the progressive destruction. The architecture is altered and many hairs appear as single hairs rather than the bundles of 1.2 and 3 hairs. The scale around some of the hairs is very typical of LPP. The patient is itchy, has burning and is shedding more than normal. Treatment options are many but include topical steroids, steroid injections, topical calcineurin inhibitors, doxycycline, hydroxychloroquine, methotrexate, isotretinoin, mycophenolate, cyclosporine, tofacitinib (topical or oral).






Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Acute telogen effluvium ("TE") vs chronic telogen effluvium ("CTE"): What's the difference anyways?

Acute vs chronic telogen effluvium: What are the key differences?

Acute and chronic telogen effluvium are different conditions and are the source of much confusion.

Acute Telogen Effluvium

Acute telogen effluvium is a form of excessive hair shedding which typically occurs following some type of event that the hair follicle interprets as a “shock.” Stress, low iron, thyroid problems medications, diets, internal disease and scalp inflammatory diseases can all trigger a telogen effluvium. Many cases of telogen effluvium resolve once the original trigger that caused the shedding in the first place is addressed. If the cause was hypothyroidism, then thyroid replacement might be given. If the actual cause was low iron them iron replacement is given. If the cause is a crash diet, only a balanced diet can help  normal hair growth again. Sometimes, we cannot find a cause and the shedding either continues or stops. Acute telogen effluvium can happen at any age. Children frequently develop acute telogen effluvium from fever. Adults develop from medications, stress, dieting surgeries and scalp inflammation.


Chronic Telogen Effluvium

Chronic telogen effluvium is best called chronic idiopathic telogen effluvium. In fact, anything that makes it sound different than acute telogen effluvium is probably a good thing. This is because chronic telogen effluvium is different than acute telogen effluvium. It’s true that some people simply view CTE as any hair shedding that has gone on for more than 6 months. This is not correct interpretation in my opinion. Suppose a patient has a thyroid disorder and is shedding alot of hair. The patient is busy with work and the kids and has not stepped foot into a doctor’s office to get things checked out for over a year since the shedding started. Should we call this CTE? Not at all. This is acute TE that has not yet been diagnosed. See the difference? Chronic idiopathic telogen effluvium is a hair shedding disorder that happens mostly in women 35-65 whereby the patient develops a sudden onset of shedding. Often a trigger can’t be found. These patients often give a story of once having super thick hair - so thick in fact that the hairdresser would joke that they should be charged double. Patients with CTE shed and shed - some days alot and some days only a little. Their blood tests are normal. They look like they have alot of hair when they walk into the office. Examination in the clinic can look fairly normal although some patients do have marked recession in the temples (so called bilateral temporal recession). We don’t know what causes CTE. It’s a complex hair shedding disorder. It can last a very long time but some do experience spontaneous resolution. We don’t yet know how best to treat although minoxidil (topical or oral), low level laser, biotin, hair and nail supplements, lysine, B6 are all part of the treatments. Provided patients with CTE don’t have another hair loss consultation going on as well (like androgenetic alopecia), patients with CTE can be reassured that they won’t develop progressive balding over time. They may or may not easily get back their density but they won’t get worse. Photos are essential to prove to the patient and hair specialist that the hair is not getting worse.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Donovan Medical Honored with Best Medical Hair Loss Clinic 2019 Award

Global Health & Pharma Honors Donovan Medical with Best Hair Loss Clinic 2019

Our clinic was honoured to be the recipient of two awards from Global Health & Pharma in their 2019 awards program including Best Medical Hair Loss Clinic 2019 and Award for Excellence in Patient Education!

GHP 2019 Awards

Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Alopecia Areata: Many Different Forms

Alopecia Areata has Many Different Forms

Alopecia areata is an autoimmune condition which affects the hair and nails. Most individuals with alopecia areata develop circular or oval patches of hair loss. However, these are not the only clinical presentations or “forms” that are experienced. Some patients develop total loss of scalp hair but maintain some hair on the body or eyebrows or lashes. This form is called alopecia areata totalis (or simply alopecia totalis (AT). Some patients lose all hair on the scalp and body and this is called alopecia universalis.


There are many variants of alopecia areata including patchy alopecia areata, alopecia totals, alopecia universalis and ophiasis.

There are many variants of alopecia areata including patchy alopecia areata, alopecia totals, alopecia universalis and ophiasis.


Some patients lose hair just and the back and around the sides. This variant is known as “ophiasis.” When just one patch affects the scalp the term alopecia areata “monolocularis” is sometimes used and when many patches are present the term “multilocularis” is sometimes applied. Localized hair loss of the beard is referred to as alopecia barbae and similar isolated loss can be seen on the eyebrows or lashes. Still other variants and forms of alopecia are recongized including a diffuse form that mimics telogen effluvium (alopecia areata diffusa), alopecia incognito, reticular (interconnecting), perinevoid (around nevi), annular (ring-like).


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Exclamation Mark Hairs in Alopecia Areata Occur at Perimeter of Patch

Where do you find exclamation mark hairs in alopecia areata?

Alopecia areata (AA) is an autoimmune disease that affects 1.7 % of the world’s population. Many patients with AA develop one or more so called “patches” of hair loss which may be circular or oval. Some patients develop a single patch whereas others develop many patches. A characteristic feature of patches of alopecia is that are often devoid of hair and are therefore quite smooth and bare. At the perimeter of the patches, characteristic “exclamation” mark hairs can often be seen. These are short 4 mm hairs which are essentially broken hairs. This photo shows a relatively large patch of alopecia areata.


exclamation hairs


Exclamation mark hairs were clearly noted at the perimeter. Monthly steroid injections with triamcinolone acetonide lead to complete regrowth in a matter of months.



Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Seasonal Shedding of Hair: Five Studies to Know about

Seasonal Hair Shedding: A Late Summer/Fall Shed Really Does Occur

Moulting of hair is common in various animals. Moulting appears to be controlled by a variety of endogenous and exogenous factors. Both changes in air temperature and sunlight exposure likely play a role in how animals shed hair.  Overall, sunlight exposure appears to be far more important than actual changes in temperature.

Seasonal shedding in humans is very much a real issue and peaks in August and September in the northern hemisphere.

Seasonal shedding in humans is very much a real issue and peaks in August and September in the northern hemisphere.

Variation in daylight hours is thought to be very relevant for how mammals shed hair. Many mammals, but not all, grow a winter coat and then shed it to have a lighter coat during summer. Horses for example tend have a winter coat but some donkeys do not show such variations in coat characteristics. Understanding seasonal changes in animal coats has been important in the wool industry as promotion of better wool production has clear benefits. In cashmere goats, reducing the length of sunlight can increase anagen phase and increase cashmere production. The same is true of wool production in sheep.

In humans, seasonality of shedding was not thought to exist in some of the early medical literature. In 1969, Orentreich offered support for a seasonality of hair shedding when he reported three women in New York who experienced maximum hair fall in the month of November. Orentreich also proposed that a second lesser peak occurred in Spring. To date there have been five important studies which support seasonal shedding phenomenon in both men and women. 

 

Seasonal Shedding: 5 Key Studies to know about

 

Study 1: Randall and Ebling, 1991

Randall and Ebling studied the hair growth parameters every 28 days of 14 healthy males. 

 The study was a fascinating one whereby 14 men age 18-39 in Sheffield UK collected beard shavings, shed hair, as well as finger and toe nail clippings every 28 days for 18 months. In addition, every 28 days, hair samples were taken from the study participants from 5 areas of the scalp. The participants were also asked to record the number of hours they had spent outside. 

 Men in the Randall study reported spending more time outdoors in summer than in winter – about 30 hours per week in June and July compared to 11 hours in January and February. 

 The authors found that the proportion of hairs in anagen (by pluck tests) reached peak in March each year and then fell steadily through September. This findings was true for all areas of the scalp studied including the vertex parietal and occipital areas of the scalp. When the authors examined the bags of hair that were collected from participants, they found that shed hair was maximal in August and September and least in March. In fact, the number of hairs lost per day in August was 60 and this was about double the number of hairs loss in March. Interestingly the diameter of growing hairs did not change. 

 Beard growth had a different pattern to that of scalp hair. Beard growth was maximum in July and was lowest in January and February. Finger and toe nails did not show seasonal variations in growth. 

 

Study 2: Courtois et al, 1996

 

The Courtois study from L’Oreal Laboratories in France was a fascinating one which involved studying 10 subjects over a period of 8 to 14 years. Four of these patients did not have other forms of hair loss and 6 did. The authors used phototrichograms to document the percentage of hairs in telogen phase as well as standardized hair collection techniques to determine hair shedding rates. 

 What was remarkable in the detailed study was that the percentage of hairs in telogen varied quite significantly in all patients – but particularly among those with other forms of hair loss.

 In 9 of the 10 subjects, there was a link between sunshine hours and percentage of hairs in telogen. The authors found that late summer and early Autumn (August, September and October) were periods of the highest telogen percentages and December January and February were the periods of minimal shedding. The authors identified a smaller peak of shedding in Feb and March. The authors found that the peak hair shedding from hair collections followed the peak telogen rates by 1-2 months. 

 

 Study 3: Pieard-Franchimont and Pierard, 1999

 The authors performed trichograms of 2857 subjects over 2 consecutive years. They found an increased proportion of telogen effluvium between July and October. The lowest rates were found in January. 

 

Study 4: Kunz et al 2008

A 2008 study from Switzlerand by Kunz, Seifert and Trueb examined shedding patterns in 823 women using trichograms. The authors found that telogen rates were lowest at the beginning of February and highest in July. There was a second peak noted by the authors in April  it was less pronounced than in summer. What was remarkable about the Kunz study was just how many women were studied. Certainly, a study of 823 women is quite large. Second, the authors showed that this seasonal shedding occurred regardless of whether or not the patient had female pattern hair loss and regardless of whether or not they were using minoxidil. 

 

Study 5: Liu et al, 2014

Liu and colleagues studied seasonal changes in hair growth patterns in 41  male and female volunteers from China.  Phototrichograms were used to record the percentage of hairs in anagen and telogen. The authors showed that the highest proportion of telogen hairs were in September and lowest in January. In women, these proportions rose form approximately 8 % in January to 12 % in September. 

 

CONCLUSIONS: Why is seasonal shedding important to know about?

The five elegant studies to date support that notion that hair shedding increases in late Summer and Fall for humans. 

 We don’t really know why humans shed like this although it is proposed that climate factors are very import for humans. We know that mammals moult and patterns of moulting are quite different for different mammals. It has been proposed that delaying shedding until the end of the summer might help protect humans from ultraviolet exposure during summer. 

 These changes in growth may be related to many factors including hormones. It’s interesting that beard growth peaks in the summer in men as it has also been shown that plasma testosterone levels also rise somewhat during the summer and then fall to their lowest levels in January and February.  But a variety of factors likely contribute to these shedding patterns including melatonin, testosterone, thyroid hormones, prolactin.

 These studies are important for patients that come into the office. We need to always take into account the phenomenon of seasonal shedding when evaluating patients. Suppose a patient starts a treatment and is doing really well. In April and May she tells you that she’s so pleased with her hair. Her hairdresser is amazed with her hair. Her friends have noticed a change.  Now in September she contacts you and she is extremely upset. Her hair is shedding terribly. She has lost ground.  Of course, you need to consider all the factors. Is she using the right medications?  Is their actually another diagnosis present? But seasonal shedding needs to be considered. 

A 2017 study in the British Journal of Dermatology  also supports that people are more concerned about hair loss in the Summer and Fall than in the Winter and Spring. Specifically, a study by Hsiang and colleagues looked at the Google Trends for the search term “hair loss” in Summer, Fall, Winter and Spring.  Compared to the Spring, searches were 5.74 times more frequent in Summer and 5.05 times more frequent in Fall compared to the Spring.  Searches about hair loss in Winter were 2.63 times more frequent in Winter than Spring. Spring was a time of least entries related to hair loss.

 

 

Reference

Reinberg A et al. Circadian and circannual rhythms in plasma hormones and other variables in five healthy young males. Acta Endocrinology 1978; 88: 417-27

 Smals AGH et al. Circannual cycle in plasma testosterone levesl in man. J Clin Endocrin Metab 1976; 42: 979-82.

Orentreich N. Scalp hair replacement in man. In: Advances in Biology of Skin. Vol IX: Hair Growth. (Montagna W, Dobson RI, eds). Oxford: Pergamon. 1969. 99-108.

Courtois et al.Periodicity in the growth and shedding of hair. Br J Dermatol, 1996 Jan;134(1):47-54.

 Hsiang EY et al. Seasonality of hair loss: a time series analysis of Google Trends data 2004-2016. Br J Dermatol2018; 178(4):978-79   

Maurel D et al. Effects of photoperiod, melatonin implants and castration on molting and on plasma thyroxine, testosterone and prolactin levels in the European badger (Meles meles). Comp Biochem Phyiol A Comp Physiol. 1989;93(4):791-7.

Zhang et al. Comparative study on seasonal hair follicle cycling by analysis of the transcriptomes from cashmere and milk goats. Genomics 2019 Feb 16 

Liu et al. A Microarray-Based Analysis Reveals that a Short Photoperiod Promotes Hair Growth in the Arbas Cashmere Goat, PLoS One. 2016 Jan 27;11(1):e0147124.  

Pearson AJ et al. Inhibitory effect of increased photoperiod on wool follicle growth. J Endocrinol 1996 Jan;148(1):157-66.

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Methotrexate for Treatment of Alopecia Areata: How long until results are seen?


How long does it take individuals with alopecia areata to see results with methotrexate?


Studies have shown that hair growth can take 2.5-3 months before changes are seen. 2014 studies by Hammerschmidt et al showed that patients who were going to respond often showed responses by the end of the 3rd month (after approximately 180 mg of the drug, taken as 20 mg weekly). This information is important so that patients with alopecia areata don’t stop treatment with MTX too early without giving it the appropriate trial. We don’t see results in a matter of weeks.



Reference

Hammerschmidt et al. Efficacy and safety of methotrexate in alopecia areata. An Bras Dermatol 2014; 89; 729-734.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
2 Comments

The Diagnostic Algorithm: How do we diagnose hair loss?

A Stepwise Approach to Diagnosing Hair Loss


Diagnosing hair loss can be challenging in some cases. Even when it seems one has figured out the diagnosis, there are many instances where one questions the diagnosis.

In this commentary, I review a formal approach to the diagnosis of hair loss. It is what I term the Diagnostic Algorithm.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
Share This
No Comments

Blogs by Topic





Share This
-->