Rapid weight loss can sometimes lead to hair loss- which is not exactly the duo most people expect while on their health journey. If you’ve noticed both a smaller waistline and thinning hair, it’s good to understand what’s going on. While obesity itself does not directly cause hair loss, heart disease, and circulatory issues can trigger or accelerate hair thinning and loss.
The Link Between Weight Fluctuations and Hair Loss
Changes to your general health and wellness can lead to a number of different symptoms and problems throughout the body. Fluctuations in your weight can trigger hair loss or hair thinning. If the weight loss is related to a major systemic illness, for instance, it's not uncommon for your hair to thin as your body's response to the sudden changes in your body. Basic weight loss that's normal may trigger hair loss. Should psychological issues or mental health issues occur along with weight loss, this may exacerbate or trigger the loss of hair.
Rapid Weight Loss and Nutrient Deficiencies
Hair loss caused by weight loss is usually seen in people who have a nutritional deficiency. Extreme/rapid weight loss may result in nutritional deficiencies that lead to hair loss, anemia, weak bones, or increased risk of infection. Since you’re eating fewer calories, it’s more important than ever to make sure the food you eat is filled with nutrients. Slow, gradual weight loss doesn’t cause any problems with hair growth. However, suddenly losing lots of weight can cause hair loss. In addition, crash dieting often causes hair loss, especially if you’re losing lots of weight and quickly regaining it. Make small, gradual changes to your diet over time instead of trying to completely change your lifestyle all at once.
Growing hair is a big task for your body; it needs the correct fuel - such as protein, iron, and a star-studded cast of vitamins and minerals (A, B, C, and D, for example).
- Protein: Hair is primarily made up of protein, so adequate protein intake is essential for hair growth. Daily Value (DV) for protein is 50 grams per day.
- Iron: The most common nutritional deficiency worldwide is iron deficiency.
- Vitamin D: This vitamin stimulates the growth of new hair follicles, so being deficient can cause hair loss or thinning.
Telogen Effluvium
Hair loss caused by weight loss can also be seen in people who shed significant weight in a short amount of time. If you’ve already noticed a difference in hair quantity - more on your brush and pillow and less on your head - after losing some weight, don’t worry. The vast majority of telogen effluvium simply resolves itself. If your hair loss persists and it seems it’s more than just temporary, hair loss treatments can help get your hair back on track.
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Obesity and Hair Loss: An Indirect Relationship
Research has shown that people who are overweight are at higher risk of androgenetic alopecia, also known as male or female pattern baldness. Obesity is directly linked to some of the leading causes of preventable, premature death, such as heart disease, stroke, type 2 diabetes, and certain types of cancer.
Fortunately, obesity is not a direct cause of hair loss. However, some habits and lifestyle choices associated with obesity affect your hair growth. Being overweight or obese does not directly contribute to thinning hair or hair loss. Still, many of the medical conditions associated with and caused by obesity have the potential also to cause hair loss.
Sedentary Lifestyle
Many people in today’s modern world lead a sedentary lifestyle. The pressures of demanding jobs and increased computer use makes it hard to fit in enough exercise. But even a little exercise makes a big difference for your hair. Don’t worry if you don’t have time to spend hours at the gym each day. Simple, gradual changes over time lead to significant improvements in your health and hair growth. Choose an easy exercise that you can commit to every day, whether it’s parking at the back of the grocery store parking lot or walking to the end of the street and back after work.
Stress
A growing body of evidence links obesity to stress. Chronic high stress levels lead to challenges for your whole body, and hair loss might be the first physical sign of chronic stress. Having a high-stress job doesn’t mean you don’t have any options. Try incorporating a little physical activity or carving out some time to relax.
Hormone Imbalances
Obesity causes other hormone imbalances that lead to hair loss. Taking small steps to manage your body weight helps regulate your hormones. In addition to improved hair growth, weight management brings your hormones into balance. Hormone fluctuations result in thinning hair by interrupting the hair growth cycle. Being overweight causes an increase in fat and estrogen levels.
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Cardiovascular Health and Circulation
This illness adversely affects your circulatory system, which contributes to improper blood flow. This disruption also interrupts your hair growth cycle because your follicles depend on efficient blood flow to deliver nutrients. Fortunately, it’s possible to reverse the symptoms once it’s identified via a routine blood test. According to one scientific study, bald men have a higher chance of developing heart disease. It’s also a comorbid condition of obesity. Medical practitioners also consider hair loss as a visual sign of heart problems. A conclusive diagnosis of heart disease involves reviewing your patient history and performing a physical exam. You also need imaging and blood tests.
Having a healthy scalp and hair is directly related to a healthy cardiovascular system, and hair loss is recognized as being a visual cue for heart disease. Poor circulation and disrupted blood flow, or a weak heart can reduce blood flow to the hair follicle and limit its ability to grow healthy hair.
Type 2 Diabetes
Being overweight or obese significantly increases the risk of a person developing type 2 diabetes, also known as insulin-resistant or adult-onset diabetes. Type 2 diabetes is a condition where the body produces sufficient insulin, but cells become resistant to absorbing it, creating a situation where your blood glucose level is persistently high. Consistently high blood glucose levels can damage blood vessels as well as the nerves that control your heart. Diabetes is a contributing factor for other ailments such as heart disease and stroke, and can also interrupt the hair growth cycle, causing thinning hair and hair loss.
Co-occurring Conditions Linking Weight and Hair Loss
The two are also intertwined through co-occurring conditions, conditions that often accompany hair loss.
- Autoimmune disease: Many can cause hair loss, including lupus and even psoriasis.
- Thyroid dysfunction: Thyroid hormones are essential for the health of hair follicles. Thyroid problems may cause unexplained weight gain, hair loss, and fatigue to occur together. Hyperthyroidism and hypothyroidism may be present for months before diagnosis.
- Hormone imbalance: Many hormones influence weight, and many also contribute to hair growth, cycle, and density.
When you experience multiple symptoms such as weight gain, hair loss, and fatigue at the same time, you may feel confused and anxious. You may wonder if it’s a mere coincidence or a genuine health concern. Weight gain, hair loss, and fatigue are often linked to stress, diet, and lifestyle changes. Medical conditions, such as thyroid dysfunction and iron deficiency anemia, can sometimes also be the cause.
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Thyroid Dysfunction
Hypothyroidism, also called “underactive thyroid,” occurs when your thyroid gland doesn’t produce enough thyroid hormone. The thyroid hormone has multiple roles that regulate:
- metabolism
- growth
- contraction of skeletal muscles
- heart rate
Some symptoms of hypothyroidism, such as brittle hair, weight gain, and fatigue, develop gradually. Some people may notice them after several years. Your hair follicles have thyroid hormone receptors that play a role in the hair growth cycle. Impaired thyroid function may affect the frequency of your hair’s active growth phase. Low thyroid hormone levels can increase your cholesterol levels, reduce fat breakdown, and slow down your metabolism. According to the American Thyroid Association, hypothyroidism-related weight gain is usually due to a buildup of salt and water in your body. Most people gain about 5 to 10 pounds. Your thyroid also helps to regulate your body’s energy demands, so reduced thyroid function can lead to fatigue.
Other symptoms include:
- sensitivity to cold
- brittle nails
- dry and scaly skin
- irregular periods
- loss of sexual desire
- muscle aches and general weakness
Hyperthyroidism is the opposite of hypothyroidism. People with this condition have higher than typical thyroid levels. Also called “overactive thyroid,” this condition is more common in women ages 20 to 40. Hyperthyroidism ramps up your metabolism. Increased metabolism can disrupt sleep and affect your energy levels and mood, leading to fatigue. This condition can also cause hair thinning. Weight gain isn’t a common symptom of hyperthyroidism, but some people may experience it due to an increased appetite.
Hyperthyroidism can also cause:
- anxiety
- muscle weakness
- pounding of the heart
- irregular heart rate
- trembling of the hands and fingers
- changes in bowel patterns, particularly more frequent bowel movements
- unusual sweating
- weight loss
Iron Deficiency Anemia
Iron deficiency anemia occurs due to low amounts of iron in your blood. Your blood needs iron to produce hemoglobin, a protein that allows red blood cells to carry oxygen to different parts of your body. When your cells lack oxygen, you can get tired and short of breath. Low energy and reduced metabolism can make it harder to exercise or burn calories, which may increase the chance of weight gain. Iron deficiency can also affect cells that repair and stimulate hair growth, causing hair loss.
Other symptoms of iron deficiency include:
- skin that looks paler than usual
- brittle nails
- chest pain
Vitamin B12 Deficiency
Vitamin B12, or cobalamin, is a natural vitamin found in foods, predominantly animal sources. This vitamin plays a vital role in:
- brain function
- nerve cell health
- DNA production
- red blood cell production
How much vitamin B12 you need varies by age. Pregnant and breastfeeding people need higher amounts of B12. A condition called megaloblastic anemia, the hallmark of vitamin B12 deficiency, can cause fatigue and weakness. Megaloblastic anemia can also cause hair changes, including hair loss that may be due to an impairment in DNA synthesis. Research on how vitamin B12 deficiency affects weight is mixed. The National Institutes of Health (NIH) notes that vitamin B12 deficiency tends to cause weight loss more than weight gain, but a 2020 review of studies suggests that low vitamin B12 levels may contribute to obesity in children and pregnant people.
Diabetes
Diabetes is a chronic condition that causes high levels of glucose in your blood. Since diabetes affects the way your body converts food to energy, it may likely affect your weight. Diabetes weight gain may be due to increased calorie consumption and insulin therapy, a common diabetes treatment approach. Diabetes can also cause fatigue and lethargy. The cells that need glucose for energy barely get enough. Untreated diabetes can also damage your blood vessels, which makes it difficult for your blood to carry oxygen and nutrients to your cells, including your hair cells. This can lead to hair loss.
Other symptoms include:
- frequent urinating
- numbness or tingling sensation in the hands or feet
- blurry vision
- feeling thirsty
- constant feeling of hunger
Stress and Hair Loss
Stress is also known to play a role in at least three types of hair loss. They include alopecia areata, telogen effluvium, and trichotillomania. Research is still ongoing regarding whether obesity causes depression or vice versa.
The Aging Factor
As you grow older, your body’s metabolism slows down. It’s easy to gain weight if you don’t take deliberate steps to follow a healthy lifestyle.
Maintaining a Healthy Weight and Lifestyle
Identifying the cause of hair loss is an important step toward hair restoration. Although our clients experience hair loss from various causes, maintaining a healthy weight might reduce the risk and severity of hair loss.
Adopting a healthy diet is the most effective way of achieving a suitable BMI range. It might also reverse hair loss by improving blood circulation and treating some conditions associated with obesity. A hair-healthy diet contains a variety of nutrients. They include Omega-3 fatty acids, Vitamin C, iron, biotin, zinc, and lean protein. You can also tackle obesity through physical fitness.
When to Seek Medical Advice
It’s best not to overlook symptoms such as unexplained changes in weight, hair loss, and fatigue. Consider speaking with a doctor if you experience these symptoms, especially when they occur with other unusual symptoms. These changes aren’t always the result of a medical condition. Still, it’s often best to seek medical attention, especially when these symptoms persist, to be sure your bodily functions aren’t impaired. On the surface, weight gain, hair loss, and fatigue seem unrelated. If they occur at the same time, it may be due to an underlying medical condition. Consider speaking with a doctor about your symptoms. A doctor may perform an examination and run some tests.
Some conditions such as hormone imbalance require a medical solution. We recommend seeing a qualified physician who can pinpoint the exact cause of your weight gain.
Scientific Studies on Obesity and Hair Loss
Published in final edited form as: Nature. 2021 Jun 23;595(7866):266-271. Obesity, a worldwide epidemic, predisposes to many ageing-associated diseases, yet its exact impact on organ dysfunction is largely unknown1. Hair follicles, mini-epithelial organs that grow hair, miniaturize by ageing to cause hair loss through the depletion of hair follicle stem cells (HFSCs)2. Here, we report that obesity-induced stress such as by high-fat diet (HFD) feeding primarily targets HFSCs to accelerate hair thinning. Chronological gene expression analysis revealed that HFD feeding for four consecutive days directs activated HFSCs toward epidermal keratinization by generating excessive reactive oxygen species yet retains HFSC pools in young mice. Integrative analysis with stem cell fate tracing, epigenetic analysis and reverse genetics revealed that further feeding of HFD subsequently induces lipid droplets and NF-κB activation within HFSCs via autocrine/paracrine IL-1R signaling. Those integrated factors converge on the profound inhibition of Sonic hedgehog (Shh) signal transduction in HFSCs, thereby further depleting lipid-laden HFSCs through their aberrant differentiation and inducing hair follicle miniaturization and eventual hair loss. Conversely, Shh activation by transgenes or compounds rescues HFD-induced hair loss. Obesity predisposes to many ageing-associated diseases and is tightly associated with the human lifespan3-5. While many organs functionally and structurally decline with obesity and/or ageing, whether obesity and/or a high fat diet (HFD) directly impact organ function and regeneration, which cell populations are targeted and how it happens are still largely unknown in most organs6,7.
Tissue stem cells underlie organ homeostasis and ageing8-10. Hair follicle stem cells (HFSCs) in the bulge region self-renew and produce differentiated progenies at the onset of the proliferating phase (anagen) for cyclical regeneration of hair shafts. An age-associated deficiency of COL17A1, a hemidesmosome component that anchors HFSCs to the basement membrane, causes the depletion of HFSCs through their epidermal differentiation, resulting in stem cell-centric “hair follicle ageing” that causes hair follicle miniaturization and hair thinning2,11. First, to determine whether a western diet, such as a HFD, accelerates hair loss/thinning, elderly male littermates of C57BL/6N (wild-type, wt) mice that had not shown obvious hair thinning were fed a HFD or a normal diet (ND) for a month. Those HFD-fed aged mice showed diffuse type hair thinning (Fig. 1a). Next, to examine the effects of obesity in hair follicles, wt male mice were fed a HFD or a ND from two months old to twelve months old. The HFD-fed mice also showed decreased numbers of hairs with shaggy appearance and that was more obvious after hair cycle induction by hair depilation (Fig. 1b). Furthermore, a few rounds of hair cycle induction in HFD-fed mice but not in ND-fed mice induced severe and irreversible hair loss (Fig. 1c, Extended Data Fig. 1a, Supplementary Fig. 2), indicating that cyclic hair regeneration is targeted by HFD-induced stress and accelerates hair thinning.
We next analyzed genetically obese mice, chemically diabetic mice, wt mice fed a high sucrose diet, HFD-fed female mice, and HFD-fed male C57BL/6J mice. Genetic models of obesity (db/db, Ay/+ and ob/ob) mice and HFD-fed C57BL/6J mice also showed severe hair loss at 6 months (Extended Data Fig. 1b-f) following four rounds of hair regeneration, while HFD-fed female mice showed hair loss at 8 months (Extended Data Fig. 1g). In contrast, streptozotocin (STZ)-treated diabetic mice or mice fed a high sucrose diet did not show hair loss (Extended Data Fig. 1h-k).
To examine the overall structures of hair follicles in HFD-fed mice, we conducted whole mount staining analysis of COL17A1 and K14 to identify HFSCs in the bulge and basal cells, respectively. The results showed that hair follicle bulges have disappeared in some hair follicles of HFD-fed mice with or without retention of relatively large sebaceous glands (Fig. 1d, Extended Data Fig. 1l). Genetically obese ob/ob mice and HFD-fed female mice also followed the same processes of HFSC depletion (Extended Data Fig. 1m-o). Importantly, the degree of hair loss was correlated with body weight in HFD-fed mice (Extended Data Fig. 1p). Zigzag hairs became thinner and shorter in HFD-fed mice than awl hairs (Extended Data Fig. 2a,b), indicating that the small type of hair follicles with lower numbers of HFSCs are affected more severely. Eventually, the dermis also became atrophic whereas the dermal adipose layer expanded in HFD-fed mice13 (Extended Data Fig. 2c), similarly to aged skin14. The epidermal thickness was comparable in HFD-fed mice, suggesting that HFSCs are more sensitive to a HFD than epidermal stem cells (Extended Data Fig. 2c). Further, entry into anagen (growing phase) was precociously induced in HFD-fed mice. Strikingly, precocious entry into telogen (resting phase) with a shorter hair cycle duration was also found in those mice (Extended Data Fig. 2d-f), probably because of the altered surrounding microenvironment including expanded dermal adipocytes that control the hair cycle15,16. No obvious inflammatory cell infiltrations were histologically detectable (Extended Data Fig. 2e) and no conspicuous reduction of the capillary network or innervation was found around hair follicles in the skin of HFD-fed mice (Extended Data Fig. 2g,h).
Next, to investigate the stem cell dynamics in HFD-induced hair loss, we tracked the fate of GFP+ HFSCs after HFD feeding in K15CrePR; Rosa-H2B-EGFP mice. In ND-fed mice, GFP+ HFSCs remained in the bulge providing their progeny to the cycling portion of hair follicles to grow a hair shaft through their downward contiguous localization17. In contrast, after three months of HFD feeding, GFP+ HFSCs were reduced in the bulge and became contiguously localized in the upper portion including sebaceous glands and the junctional zone, and also in the epidermis (Fig. 1e,f). The HFSC progeny in the epidermis can be distinguished from the small number of GFP+ resident basal cells (2.3%) that were labelled upon treatment with RU486 even without HFD-feeding (Extended Data Fig. 3a). Those data collectively indicate that HFD-fed metabolic stress induced the fate change of HFSCs into the lineages of the upper portion of hair follicles including sebaceous glands and epidermal keratinocytes which are also found in aged skin2. Importantly, the stem cell fate dynamics were specifically found at anagen when HFSCs are activated. The aberrant localization of those epidermally-committed HFSC progeny was detectable as the ectopic appearance of K1+ differentiating cells above the bulge area even during the natural hair cycle as well as following depilation or chemical hair removal that does not induce any significant apoptosis in the skin (Extended Data Fig. 3b-h).
To identify the pathway(s) responsible for HFD-induced fate switching of HFSCs, we performed microarray, RNA-seq and Assay for Transposase Accessible Chromatin with high-throughput Sequencing (ATAC-Seq) analysis of FACS-sorted HFSCs from HFD-fed or ND-fed mice and HFSCs from young and from aged mice. Microarray analysis showed that the mRNA expression level of Col17a1, a key gene regulating HFSC self-renewal and ageing, was reduced in HFSCs of aged mice but not in HFD-fed mice (Extended Data Fig. 4a), suggesting the existence of distinct mechanisms that cause HFD-induced hair loss. A motif analysis of ATAC-Seq peaks revealed that chromatin accessibility of NFATc1 and MED-1, which have crucial roles in maintaining the quiescent state of HFSCs18, was reduced in HFD-fed mice (Extended Data Fig. 4b). These data may epigenetically explain the premature anagen induction by the HFD. Microarray data showed that several different changes including profound reductions of the MAPK and Sonic Hedgehog (Shh) pathways were found in anagen HFSCs of HFD-fed mice (Fig. 2a). The reduced MAPK signaling elicited by the HFD might represent the dysfunction of a niche-derived FGF signal19 that represses HFSC quiescence. To further explore responsible pathways, we performed RNA-seq analysis for anagen HFSCs from ND- or HFD-fed mice. Again, Shh pathways were found to be reduced in HFSCs by HFD-feeding (Extended Data Fig. 4c-e). qPCR analysis also demonstrated that the Shh pathway is inhibited in anagen HFSCs in HFD-fed mice (Fig. 2b), in ob/ob and in db/db mice (Extended Data Fig. 4f) but was not found in different types of alopecia such as in the alopecia areata model20.
To examine whether the inhibition of Shh signaling by HFD feeding causes the fate change and the depletion of HFSCs, we analyzed K15CrePR; Rosa-rtTA; TetO-Gli2ΔC transgenic mice24, where the Shh pathway is specifically and transiently inhibited by expression of the dominant negative form of GLI2 in HFSCs (Fig. 2c). Inhibition of Shh signaling for 1 week with the concomitant induction of the hair cycle caused a depletion of HFSCs, the miniaturization/loss of hair follicles and hair loss after one month (Fig. 2d,e, Extended Data Fig. 5a,b). Lineage tracing showed that GFP+ cells became localized in the junctional zone, sebaceous glands and in the epidermal layer, similar to their localization in HFD-fed mice (Fig. 2f,g, Extended Data Fig. 5c,d). To characterize the mechanism involved in the specific inhibition of Shh signaling we further searched for responsible changes in gene expression profiles. Firstly, we found that multiple inflammatory cytokine signaling pathways, including the IL-1R pathway, that naturally converge on NFκB activation are activated within HFSCs in HFD-fed mice (Fig. 3a, Extended Data Fig. 6a,b). qPCR results showed that Il-1β expression was increased in total epidermis of HFD-fed mice (Fig. 3b). Consistently, immunostaining of skin sections revealed that NFκB became localized within the nuclei of HFSCs in HFD-fed mice (Extended Data Fig. 6c). Increased expression of Il-1β was also found in ob/ob and in db/db mice (Extended Data Fig. 6d). Secondly, 8-oxoguanine, a marker of oxidative damage, was also increased in the HFSCs of HFD-fed mice (Fig. 3c, Extended Data Fig. 6e), which is consistent with the fact that reactive oxygen species (ROS) are generated during free fatty acid metabolism and are augmented by inflammatory cytokine signaling with obesity25. Thirdly, lipid droplets accumulate within HFSCs in mice with long-term exposure to a HFD but not in mice with short-term exposure (Fig. 3d,e, Extended Data Fig. 6f-h), which suggests that lipotoxicity occurs in HFSCs due to dyslipidemia. Those lipid-laden GFP+ cells divide and differentiate into corneocytes (squames) or into sebocytes that excrete sebum lipids through the follicular opening (Extended Data Fig. 6g,h). To determine the responsible factor(s) that inhibit Shh signaling, we treated keratinocytes from neonatal epidermis that contains growing hair germs26 with a lipid mixture (LM), with inflammatory cytokines (IL-1β27, IL6 and TNFα), or with H2O2. The results showed that treatment with IL-1β, IL6, LM or H2O2 inhibited the expression of Shh signal targets, including Gli1, Gli2 and Ptch1, while treatment with TNFα did not (Fig. 3f, Extended Data Fig. 6i), which suggests that those inflammatory signaling factors and oxidative stress collectively repress the Shh signaling pathway in HFSCs. Local administration of IL-1β inhibited Shh signaling in anagen HFSCs of 7-week-old, 17-month-old and 22-month-old mice (Fig. 3g, Extended Data Fig. 6j). In contrast to old mice, Cox2 expression was not increased by local administration of IL-1β in young mice, suggesting that there is a homeostatic mechanism that resists acute inflammatory signals in young animals. Furthermore, IL-IRa KO mice, in which the IL-1R pathway is constitutively activated28, displayed partial hair thinning with some reduction of bulge number (p value = 0.0883) (Extended Data Fig. 6k-m and Supplementary Fig. 4).