What Causes Bumpy Arm Skin (or Keratosis Pilaris)?

Run your hand up and down the outer side of your arm. Is the skin smooth and soft? Or is it bumpy? Maybe you get little whiteheads, or have dry, rough patches.

This is called Keratosis pilaris (colloquially referred to as Chicken Skin). It usually appears on the upper arms, thighs, cheeks or buttocks. The bumps generally don’t hurt or itch, but they aren’t the most attractive – especially if you have the tendency to pick.

Let’s look at WHY you could have this, and how to treat it!

Hypothyroidism and keratosis pilaris

Why does skin do this?

The skin is our largest organ, and one big job it does is help to excrete toxins and byproducts of biochemical processes.


Our lymphatic system sits just under the skin, and this is the drainage system of our body. When our lymphatic system is dirty, then our skin will try to help out by excreting some of the gunk causing Chicken Skin.


Another reason our skin can show signs of distress is related directly to our GUT. Researchers as far back as 1930 suspected a link between gut and skin health. Inflammation in the digestive tract, which can be caused by food intolerances, medications (ibuprofen), surgeries, radiation treatment, all contributes to Intestinal permeability (a.k.a. “leaky gut”) which causes both systemic and local inflammation, which in turn contributes to skin conditions, and in this case Keratosis Pilaris.


When our liver is congested, fatty, or not working optimally due to a suboptimal thyroid, or methylation issues, one symptom is very obvious through the skin. Skin will get dry, dull, and sallow. When coupled with sluggish lymph, you can get Keratosis pilaris.

Thyroid link

We often find that people with a thyroid issue – whether that is known about, or undiagnosed sub-optimal levels – experience Chicken Skin. They often have an itchy back as well, due to slower circulation, dry skin, and sluggish liver.


Taking gluten out of the diet usually makes this issue go away.


Gluten is a small wedge-shaped protein that lodges into the interstitial spaces on the gut barrier – sort of like a splinter. This causes inflammation. Inflammation builds to leaky gut.

Keratosis Pilaris Treatment

The body is an amazingly complex organism, and trying to treat one symptom without ever understanding or addressing the underlying cause is like taking Panadol to manage the pain of a stone in your shoe. When you understand the root cause, it is easy and common sense to treat!

However, understanding the root cause is not standard medical care. This is where functional medicine comes in because it is all about discovering the root cause to treat the body holistically. In other words, we aim to take the stone out of the shoe, rather than mask the symptom with a drug.

DIY tips
  • Drink the right amount of water for your body’s needs.
  • Limit unnecessary medications, drugs, alcohol, tobacco etc.
  • Dry skin brush every day before your shower.
  • Don’t eat junk – eat a clean diet full of vegetables and adequate protein.


You can put up with minor complaints like skin pimples, or treat them with a medicated cream. But it doesn’t fix the root problem. And left unaddressed, with time, and the natural aging process, these seemingly minor issues will build into a more serious health concern. We can help either way, but getting in early resolves issues quickly. Whereas chronic concerns take longer to balance, and degenerated health situations will need medication as well as natural health support to give you the best quality of life possible.

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Either way, we are here to help you feel better!

Book a free 15-minute consultation if you want expert guidance to feel great, lose weight, and balance your body.

— Update: 16-02-2023 — cohaitungchi.com found an additional article Thyroid Autoimmunity in Patients with Skin Disorders from the website www.intechopen.com for the keyword hypothyroidism and keratosis pilaris.

1. Introduction

Thyroid disorders are known to involve all the organ systems of the body and the skin is no exception. Some dermatological skin findings and diseases may be the first symptoms of thyroid disease [1]. Available data suggest that thyroid hormone plays a pivotal role in embryonic development of mammalian skin as well as in maintenance of normal cutaneous function an adult skin. Thyroid hormone stimulates epidermal oxygen consumption, protein synthesis, mitosis, and determination of epidermal thickness [2]. Thyroid hormone is an important regulator of epidermal homeostasis. In tissue culture studies using surrogates for DNA expression, T 3 has been shown to stimulate growth of both epidermal keratinocytes and dermal fibroblastes [3, 4]. In addition, thyroid hormone appears to be necessary for both the initiation and maintenance of hair growth and normal secretion of sebum.

Both hypothyroidism and hyperthyroidism are known to cause skin change. Hypothyroidism may result from either inadequate circulating levels of thyroid hormone or target cell resistance to hormonal action. Primary hypothyroidism is as a result of glandular failure is the most common cause and most frequently result from autoimmune disease [5]. In hypothyroidism, the skin is cold, xerotic and pale. The coldness is due to reduced core temperature and cutaneous vasoconstriction. The decreased skin perfusion has been documented with nail fold capillaroscopy [6]. It has been suggested that the diminished skin perfusion is reflex vasoconstriction compensatory to diminished core temperature. The diminished core temperature itself may be secondary to reduced thermogenesis [7]. Occasionally, purpura may be noted in hypothyroid patients as a result of diminished levels of clothing factors and the loss of vascular support secondary to the dermal mucin [8]. The dryness of hypothyroid skin results from decreased eccrine gland secretion. The mechanism for decreased sweating is not clear although the hypothyroid glands are atrophic on histologic examination [9]. Hypohidrosis, possibly accompanied by diminished epidermal sterol biosynthesis, may lead to acquired palmoplantar keratoderma. Xerosis is due to a change in skin texture and poor hydratation of the stratum corneum. The skin is rough and covered with fine scales. Palms and soles may be quite dry. The epidermis is thin and hyperkeratotic, and there is follicular plugging. Because the changes are generalized, they can be differentiated from similar alterations in the skin of atopic individuals and keratosis pilaris, where the findings are more prominent on the extremities [10]. Hypothyroidism also may affect the development of the lamellar granules (Odland bodies), which are vital in the establishment of a normal stratum corneum [11]. In hypothyroidism, the skin tends to be pale both because of the dermal mucopolysaccharides and dermal water content which alter the refraction of light. The name myxedema refers to the associated skin condition caused by increased glycosaminoglycan deposition in the skin. Generalized myxedema is still the classic cutaneous sign of hypothyroidism. The mucopolysaccharides that accumulate in the dermis are hyaluronic acid and chondriotin sulfate. They appear first in the papillary dermis and are most prominent around hair follicles and vassels. They separate the collagen bundles and there may be some secondary degeneration of collagen [10]. Generally, myxedema is diffuse, but focal mucinous papules have been describes. Skin may appear swollen, dry, pale, waxy, and firm to the touch. In addition, increased dermal carotene may appear as a prominent yellowish discoloration on the palms, soles and nasolabial folds. Hypothyroid patients may sometimes suffer Candida folliculitis. It has been theorized that because the sebaceous glands of hypothyroid patients secrete decreased sebum relative to those of euthyroid persons, the hair follicles may develop a flora with lipophilic organisms, which are replaced by Candida albicans [12]. The hypothyroid skin heals slowly, and this tendency is proportional to the degree of hormone deficiency. In hypothyroidism, hair can be dry, coarse, brittle and slow growing. There is both patchy and diffuse loss of scalp hair, a very characteristic loss of the outer third of the eyebrow (madarosis), and diminished body hair. Pubic and axillary hair may be sparse. The alopecia connected to hypothyroidism may be mediated by hormone effects on the initiation as well as the duration of hair growth. Massive telogen effluvium may occur when there is abrupt onset of hypothyroidism, and the percentage of scalp hairs in telogen is generally increased in hypothyroid states [10]. Using DNA flow cytometry, Schell et al. observed that cell proliferation indices were reduced in hair bulbs of hypothyroid subjects and increased in hyperthyroidism compared with normal values [13]. Hypothyroid patients, especially children, frequently develop long, lanugo-type hair on the back, shoulders, and extremities [10]. Diminished sebum secretion contributes to the coarse appearance of the hair. Sometimes, hair loss is the only apparent symptom of hypothyroidism and the dermatologist is the first to diagnose and treat the condition. Nails grow slowly and tend to be thickened, striated and brittle. Onycholysis is also associated with hypothyroidism [1].

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The specific pathophysiology linking hyperthyroidism to classic cutaneous findings remains to be well explained (5). In hyperthyroidism, the skin is warm, soft, moist and smooth. The epidermis is thin but not atrophic, and the stratum corneum is well hydrated. While the smooth skin is an epidermal finding, the warmth is caused by increased cutaneous blood flow and the moisture is a reflection of the underlying metabolic state [10]. The warmth is often accompanied by a persistent flush of the face, redness of the elbows, and palmar erythema. Hyperhydrosis, especially on palms and soles may be observed. Scalp hair may be fine and soft, and may be accompanied by a diffuse nonscarring alopecia. In vitro studies suggest increased hair growth rate in thyrotoxicosis. L-Triiodothyronine was shown to stimulate proliferation of outer root sheath keratinocytes and dermal papilla cells [14]. Hypertrichosis is can be observed in cases of thyroid dermatopathy and may be related to alterations in the proteoglycans associated with dermal papilla [15]. Sometimes an early symptom of hyperthyroidism is loss of pigment and early gray hair development. Nail changes may also occur, characterized by a concave contour accompanied by distal onycholysis (Plummer’s nails). Hyperpigmentation has been described in thyrotoxic patients in both localized and generalized distribution. There is speculation that the hyperpigmentation is due to increased release of pituitary adrenocorticotropic hormone compensating for accelerated cortisol degradation [16]. Hyperthyroidism may also induce pruritus with or without urticaria [17]. Patients with autoimmune mediated thyrotoxicosis may also have distinct cutaneous manifestations such as pretibial myxedema and acropachy. Pretibial myxedema is the localized thickening of the pretibial skin due to accumulation of acid mukopolysaccharides. It usually present with firm nodules and plaques varying in colour from pink to purple-brown, and sometimes accompanied by woody induration on extensor surfaces. A diffuse brawny edema may be present without nodules. Localized hyperhydrosis has been reported in cases of pretibial myxedema. Less common is an elephantiasis nostras variant in which the extremity becomes enlarged and covered with verrucous nodules [10]. Thickening of the skin of the extensor surface of the forearm (preradial myxedema) has been reported [18]. Excessive amounts of hyaluronic acid and chondriotin are present in lesions as well as in clinically normal skin [19]. The precise pathogenesis of pretibial myxedema remains to be defined. One leading theory is that pretibial fibroblasts are the target for antithyroid antibodies. After stimulation by thyroid autoantibodies, fibroblasts may produce excess glukosaminglycans [5]. Other theories have implicated T cells as the primary effector of dermopathy. T-cells may interact with an autoantigen that is either identical or cross-reactive with a thyroid autoantigen in the dermis. In turn, this may induce secretion of cytokines such as glycosaminoglycan-stimulatory lymphokine, interleukin1, tumor necrosis factor, and gamma interferon, which activate fibroblasts to secrete hyaluronic acid and chondriotin sulfate [20]. Thyroid acropachy consist of the triad of digital clubbing, soft-tissue swelling of the hands and feet, and characteristic periostal reactions. The vast majority of cases are associated with Graves’ disease, although it has been reported to occur in Hashimoto’s thyroiditis. Scleromyxedema has been reported in the setting of hyperthyroidism. This rare entity is comprised of numerous firm, white, yellow, or pink papules scattered on the face, trunk, and extremitates. Cutaneous lesions are the result of accumulation of acid mucopolysaccharides, mostly hyaluronic acid, in the dermis, accompanied by large fibrocytes [5].

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Skin manifestations of thyroid dysfunction may be divided into two main categories: (I) direct action of thyroid hormone on skin tissues, and (II) autoimmune skin disease associated with thyroid dysfunction of autoimmune etiology. Direct thyroid hormone action on skin is mediated through thyroid hormone receptor (TR). All three widely recognized thyroid hormone binding isoforms of TR have been identified in skin tissues [14, 21]. TRs have been detected in epidermal keratinocytes, skin fibroblasts, hair arrector pili muscle cells, sebaceous gland cells, vascular endothelial cells, and a number of cells types that make up the hair follicle [9]. The demonstration of TR expression in hair follicle cells indicates that thyroid hormone can affect hair growth directly, rather than through an intermediate mechanism such as a general metabolic status [22]. In addition, several thyroid hormone responsive genes have been identified in skin.

When thyroid disease is of autoimmune etiology, additional skin findings may be evident which reflect associated autoimmune disease [9]. Patients with autoimmune thyroid disease are at increased risk for other autoimmune diseases, both tissue-specific and generalized. In autoimmune disease such as Graves’ disease and Hashimoto’s thyroiditis the skin manifestations may be related to either thyroid hormone levels themselves or to associated T and/or B cell abnormalities [23]. A list of autoimmune conditions apparent when examining the skin includes alopecia areata, vitiligo, chronic urticaria, bullous disorders, connective tissue diseases and palmoplantar pustulosis.

There is convincing evidence of a significant association between thyroid autoimmunity and skin disorders. Most commonly reported cutaneous disorder related with thyroid diseases is alopecia areata, which have especially autoimmune etiology.


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