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Hair Loss - Lab Testing & Medication
Answers to common questions about hair loss adapted from recent studies and meta-analyses.
There are two main types of hair loss categories: scarring alopecia and nonscarring alopecia. Scarring alopecia causes permanent hair loss due to damage to the hair follicle. Nonscarring alopecia does not cause permanent damage to the hair follicle, so hair may regrow.
The most common type of hair loss that doctors see is androgenetic alopecia, also known as male-pattern or female-pattern hair loss. This form of hair loss is hereditary, meaning it is passed down through family genes. It affects both men and women, though the pattern and progression of hair loss may differ between the sexes.
In men, androgenetic alopecia typically starts with a receding hairline and thinning at the crown, eventually leading to partial or complete baldness. In women, it usually manifests as diffuse thinning across the entire scalp, with the frontal hairline mostly preserved. The hair loss in androgenetic alopecia is caused by a combination of genetic factors and the hormone dihydrotestosterone (DHT), which affects hair follicles and leads to their miniaturization and eventually hair loss.
The onset of telogen effluvium hair loss after a stressful event can vary from person to person. Typically, hair loss due to telogen effluvium begins around 2 to 3 months after the triggering event, which in this case is the stressful incident. This is because the hair follicles that are affected by the stress move into the telogen (resting) phase prematurely and remain there for a while before the hair starts shedding.
Acute telogen effluvium is a temporary form of hair loss that occurs when a significant number of hair follicles on the scalp enter the telogen (resting) phase prematurely, leading to increased hair shedding and thinning. This hair loss is usually diffuse, affecting the entire scalp rather than specific areas.
Acute telogen effluvium can be triggered by various factors, such as:
- 1.Severe physical or emotional stress
- 2.Illness, surgery, or high fever
- 3.Sudden weight loss or changes in diet
- 4.Hormonal changes (e.g., postpartum hair loss)
- 5.Medications (e.g., certain blood pressure medications, antidepressants, or oral contraceptives)
- 6.Nutritional deficiencies (e.g., iron, vitamin D, or zinc)
The hair loss in acute telogen effluvium usually begins a few weeks to a few months after the triggering event and lasts for several months. In most cases, the hair growth cycle gradually returns to normal, and the hair loss resolves on its own without the need for specific treatment. However, addressing the underlying cause, such as managing stress or correcting nutritional deficiencies, can help promote recovery and prevent future episodes.
Chronic telogen effluvium (CTE) is a type of hair loss that occurs when there is an ongoing disruption in the hair growth cycle, causing an increased number of hairs to enter the telogen (resting) phase. This results in a larger amount of hair shedding and thinning over an extended period of time. Unlike acute telogen effluvium, which is typically temporary and lasts for a few months, chronic telogen effluvium can persist for six months or more.
The exact cause of CTE is not always clear, but it can be associated with various factors, such as hormonal imbalances, nutritional deficiencies, medications, or chronic illnesses. In some cases, the cause remains unknown.
Diagnosis of chronic telogen effluvium often involves a thorough medical history, physical examination of the scalp, and potentially lab tests to rule out other causes of hair loss. Treatment for CTE depends on the underlying cause, if identified, and may include addressing nutritional deficiencies, managing stress, or changing medications. In some cases, hair loss may improve over time without specific treatment.
Acute telogen effluvium primarily affects the scalp, causing diffuse hair shedding and thinning across the entire scalp. However, in some cases, it can also cause hair loss in other areas of the body, such as eyebrows, eyelashes, or body hair. The extent of hair loss varies from person to person and depends on the severity of the triggering event and individual factors.
It is important to note that if you experience widespread hair loss over the entire body, it may be due to another cause, such as a medical condition or certain medications. It is essential to consult a healthcare professional for an accurate diagnosis and appropriate treatment recommendations.
This section includes evidence-based approach to lab testing related to hair loss.
"Evidence-based" is a term used in healthcare to describe a decision-making process that involves using the best available scientific evidence to guide medical treatments and recommendations. When a healthcare professional uses an evidence-based approach, it means they consider well-conducted scientic studies.
An example of a non-evidence-based lab test for hair loss would be a test that lacks scientific validation or is not supported by research in relation to diagnosing or treating hair loss. One such example is hair mineral analysis, which involves testing hair samples for levels of various minerals and toxic elements. This test has not been consistently proven to be reliable or accurate in diagnosing hair loss or determining its underlying causes.
Namkoong S, Hong SP, Kim MH, Park BC. Reliability on intra-laboratory and inter-laboratory data of hair mineral analysis comparing with blood analysis. Ann Dermatol. 2013 Feb;25(1):67-72. doi: 10.5021/ad.2013.25.1.67. Epub 2013 Feb 14. PMID: 23467102; PMCID: PMC3582931.
Vitamin D is a nutrient that is essential for our body. It can be obtained from the food we eat or synthesized in our skin when exposed to sunlight. However, Vitamin D produced by our skin or obtained from our diet is inactive and needs to be activated through a series of processes in our body.
One analysis of 14 studies found that people with AA had lower Vitamin D levels compared to those without AA. Many people with AA also had a Vitamin D deficiency. This led researchers to suggest measuring Vitamin D levels in people with AA and considering Vitamin D supplements for those who are deficient.
One study found significantly lower levels of Vitamin E in patients with AA compared to healthy controls. However, another study did not find any statistical difference in plasma Vitamin E levels between patients with AA and healthy controls.
The association between hair loss and low serum ferritin levels has been debated for many years. There is ongoing discussion about whether low serum ferritin levels should be considered a nutritional deficiency causing hair loss, mainly TE. However, some benefits have been achieved in a few controlled studies.
Selenium is an essential trace element needed for the synthesis of over 35 proteins. It plays a role as a co-factor for glutathione peroxidase, an antioxidant enzyme. Selenium deficiency can happen in low-birth-weight infants, patients requiring total parenteral nutrition (TPN), and people living in areas where the soil lacks selenium.
Selenium deficiency can lead to loss of hair pigmentation and even hair loss. In some cases, patients receiving TPN without selenium experienced hair re-pigmentation after 6-12 months of intravenous selenium therapy. In infants with nutritional support, hair loss and pseudoalbinism improved after starting daily selenium therapy.
A clinical trial found that patients with ovarian cancer undergoing chemotherapy had less hair loss and fewer gastrointestinal symptoms when they received selenium supplementation. This suggests that selenium can be a supportive element in chemotherapy.
Consuming too much selenium (over 400 mcg daily) can cause toxicity. Symptoms include nausea, vomiting, nail brittleness and discolorations, hair loss, fatigue, irritability, and foul breath odor. In some cases, selenium toxicity from a dietary supplement resulted in severe hair loss.
The role of zinc supplementation in hair loss is still debated. Some studies have shown positive results, while others have not found any improvement. It is essential to consult a healthcare professional before starting zinc supplementation for hair loss.
Dehydroepiandrosterone sulfate (DHEAS) and testosterone are both androgens, which are male sex hormones that play a role in hair growth and loss. They can contribute to hair loss, particularly in the case of androgenetic alopecia, which is a common form of hair loss in both men and women. The role of these hormones in hair loss can be explained as follows:
- 1.Testosterone: Testosterone can be converted to a more potent androgen called dihydrotestosterone (DHT) by the enzyme 5-alpha-reductase. DHT is the primary hormone responsible for hair loss in androgenetic alopecia. It binds to androgen receptors in hair follicles, which can lead to miniaturization of the follicle and a shorter hair growth cycle. Over time, this results in thinner, shorter hairs and eventually hair loss.
- 2.DHEAS: Dehydroepiandrosterone sulfate (DHEAS) is a precursor hormone that can be converted to both testosterone and dihydrotestosterone (DHT) in peripheral tissues. While DHEAS itself does not directly cause hair loss, its conversion to DHT can contribute to hair loss in susceptible individuals. However, the role of DHEAS in hair loss is generally considered to be less significant than that of testosterone and DHT.
It is important to note that the extent to which DHEAS and testosterone contribute to hair loss varies among individuals and is influenced by factors such as genetics, hormone levels, and the sensitivity of hair follicles to androgens.
Treatments for androgenetic alopecia often target the hormones responsible for hair loss. For example, finasteride is a medication that inhibits the enzyme 5-alpha-reductase, thereby reducing the conversion of testosterone to DHT and slowing hair loss.
While dehydroepiandrosterone sulfate (DHEAS) and testosterone levels can be relevant in the investigation of hair loss, it may not be necessary for all women to routinely have these tests as part of hair loss investigations. Hair loss in women can result from various causes, including hormonal imbalances, nutritional deficiencies, stress, certain medications, and medical conditions.
When evaluating hair loss in women, healthcare providers typically begin with a thorough medical history and physical examination, considering factors such as the pattern of hair loss, the patient's age, and associated symptoms. Based on these findings, the provider may decide to perform additional tests, such as blood tests, to investigate potential underlying causes.
In cases where hormonal imbalances are suspected, such as polycystic ovary syndrome (PCOS) or other endocrine (hormone) disorders, the healthcare provider may choose to measure DHEAS, testosterone, and other hormones to further investigate the issue. Additionally, hormone testing becomes more important in the context of virilization, which refers to the development of male physical characteristics in females, such as excessive body hair growth, deepening of the voice, increased muscle mass, and difficult-to-treat acne. In particular sudden virilization may indicate an adrenal tumor. If you have noticed these changes, it is important to follow up in-person with a doctor for a thorough examination.
If a woman has with signs of hyperandrogenism (e.g., excessive body hair growth, acne, irregular menstrual cycles) or virilization, testing DHEAS and testosterone levels might be more relevant in order to determine the underlying cause and provide appropriate treatment options.
However, routine testing of DHEAS and testosterone levels in all women experiencing hair loss is not necessary, cost-effective or evidence bxpased. The decision to measure these hormone levels should be based on individual patient factors.
Ordering DHEAS and testosterone tests for all female patients, regardless of their symptoms or clinical presentation, has several downsides, including the possibility of overordering tests that can lead to unnecessary additional testing:
- 1.Unwarranted additional testing: Over-ordering DHEAS and testosterone tests can result in false-positive findings, which may prompt healthcare providers to order additional tests, such as imaging studies of the adrenal glands, to rule out tumors. In virtually all cases, these patients may not have any tumors or clinically significant abnormalities, leading to unnecessary imaging studies.
- 2.Unnecessary costs: The costs associated with additional testing, such as imaging studies, can be substantial for both the individual patient and the healthcare system. An abdominal ultrasound in Ontario costs upwards of $350 in direct costs. These costs may not be justified if the initial hormone tests were not clinically indicated based on the patient's specific symptoms or medical history.
- 3.Anxiety and stress: Undergoing unnecessary additional testing, such as imaging studies to rule out tumors, can cause anxiety and stress for patients, particularly if the results are inconclusive or falsely abnormal. This may lead to even further testing and interventions, creating a cycle of unnecessary investigations and patient distress.
- 4.Radiation exposure: Some imaging tests, like computed tomography (CT) scans, expose patients to ionizing radiation. While the risk of harm from a single imaging test is generally low, unnecessary radiation exposure should be avoided whenever possible. It is estimated that receiving a CT scan causes 0.5-1% of cancers. To interpret that statistic - for every 200 people we send for a CT scan, 1 will develop cancer because they had a CT scan.
- 5.Resource allocation: Healthcare resources, including laboratory capacity, imaging equipment, and personnel, are limited. Over-ordering tests and subsequent additional testing could divert resources from patients with a higher likelihood of benefitting from such testing, potentially delaying diagnosis or treatment for those in greater need.
It is crucial to approach hormone testing based on the individual patient's clinical presentation, symptoms, and medical history. Healthcare providers should use their clinical judgment to determine whether DHEAS and testosterone tests are appropriate for each patient, rather than ordering these tests routinely for all female patients. This approach can help minimize the risk of unnecessary additional testing, costs, and patient anxiety.
There is insufficient evidence to routinely order ANA levels. ANA can be present in low levels in some healthy individuals without any autoimmune disease. This can make it challenging to interpret the results.
ANA tests can also yield false-positive results, especially in low titers. This means that the test may indicate the presence of antinuclear antibodies when there are none, leading to unnecessary anxiety and additional testing.
ANA testing may not be relevant for all types of hair loss, as hair loss can also be caused by non-autoimmune factors such as genetics, hormonal imbalances, or nutritional deficiencies.
An individual might think they have an auto-immune disorder, when in fact they do not. If you believe you require an ANA test, related to hair loss from SLE, we suggest you seek a referral to a rheumatologist to consult whether it is appropriate for you.
There is no strong evidence to suggest that finasteride directly affects weight gain during strength training. Finasteride is a medication primarily used to treat hair loss in men (androgenetic alopecia) and benign prostatic hyperplasia (BPH). It works by inhibiting the enzyme 5-alpha-reductase, which is responsible for converting testosterone to dihydrotestosterone (DHT). By reducing DHT levels, finasteride can help slow hair loss and improve urinary symptoms in men with BPH.
Although finasteride can have an impact on hormone levels, particularly DHT, it is not known to have a significant effect on muscle growth or weight gain during strength training. Factors like diet, exercise routine, sleep, and genetics are more likely to influence weight gain and muscle development.
Propecia, which contains the active ingredient finasteride, is a medication used to treat hair loss, specifically androgenetic alopecia (male-pattern hair loss). It works by inhibiting the enzyme 5-alpha reductase, which converts testosterone to dihydrotestosterone (DHT). DHT is a hormone that contributes to hair follicle miniaturization and hair loss in people with androgenetic alopecia.
While Propecia has been shown to be effective in many individuals experiencing male-pattern hair loss, it is not universally effective for everyone. The effectiveness of the medication can vary depending on individual factors, such as genetics, the severity and progression of hair loss, and the person's response to the medication. Some people may experience significant hair regrowth or a reduction in hair loss, while others may see only minimal improvement or none at all.
It is also important to note that Propecia is primarily used for male-pattern hair loss and is not typically prescribed for women or other types of hair loss. In some cases, finasteride may be prescribed to women under specific circumstances and with careful monitoring by a healthcare professional, but this is not the standard approach.
Information from our FAQ has been adapted from the following resources:
- 1.Almohanna HM, Ahmed AA, Tsatalis JP, Tosti A. The Role of Vitamins and Minerals in Hair Loss: A Review. Dermatol Ther (Heidelb). 2019 Mar;9(1):51-70. doi: 10.1007/s13555-018-0278-6. Epub 2018 Dec 13. PMID: 30547302; PMCID: PMC6380979.
- 2.Cheung EJ, Sink JR, English Iii JC. Vitamin and Mineral Deficiencies in Patients With Telogen Effluvium: A Retrospective Cross-Sectional Study. J Drugs Dermatol. 2016 Oct 1;15(10):1235-1237. PMID: 27741341.
- 3.St Pierre SA, Vercellotti GM, Donovan JC, Hordinsky MK. Iron deficiency and diffuse nonscarring scalp alopecia in women: more pieces to the puzzle. J Am Acad Dermatol. 2010 Dec;63(6):1070-6. doi: 10.1016/j.jaad.2009.05.054. PMID: 20888064.
- 4.Park H, Kim CW, Kim SS, Park CW. The therapeutic effect and the changed serum zinc level after zinc supplementation in alopecia areata patients who had a low serum zinc level. Ann Dermatol. 2009 May;21(2):142-6. doi: 10.5021/ad.2009.21.2.142. Epub 2009 May 31. PMID: 20523772; PMCID: PMC2861201.