Stress & The Effects on the Skin

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stress

It has been established in recent years that the skin is a direct target of psychological stress via a cascade of hormones, neuropeptides, and neurogenic signals (causing nerve hypersensitivity and inflammation). The skin has been shown to be capable of launching its own local response to stress as well by producing many of the same substances that the brain produces, further enhancing the local effect at the skin level when someone is under acute or prolonged stress. It is no surprise that the skin can perceive and respond to stress similar to the brain and nervous system, since the two systems have evolved from the same germ layer during embryonic development.

The main skin cells (keratinocytes), mast cells (involved in allergy type reactions and inflammation), immune cells, and peripheral nerve endings all will have an effect on various cell behaviour and processes within the skin under stress that can lead to skin disruption, premature ageing and disease development.

The skin is rich in nerve endings, so when an individual is stressed the peripheral nerve endings secrete numerous substances such as Substance P and Nerve growth factor that contribute to hypersensitivity, inflammation, and allergic reactions.

Due to the impact of stress related hormones and peptides, and growth factors on the skin, stress can play a role in the development and exacerbation of skin disorders such as Eczema, Acne, Psoriasis, and Rosacea.

Psychological stress activates the autonomic nervous system to trigger release of catecholamines [e.g. epinephrine and norepinephrine] from the adrenal glands, and in situations of chronic stress corticotrophin releasing hormone [CRH] and ACTH (adrenocorticotropic hormone), mediate a release of glucocorticoids (Cortisol) from the adrenal cortex.

Here is a brief outline of some key stress mediators and the effect that they have on the skin:

Glucocorticoids:

Excess levels can cause atrophy and impaired wound healing by interfering with keratinocyte and fibroblast function. Keratinocytes are the primary skin cells that form the epidermis of the skin, and fibroblasts are responsible for collagen and elastin formation.

This manifests as atrophy and thinning of the skin, increased trans-epidermal water loss related to disruption to the skin permeability barrier, and easy bruising with impaired wound healing.

The skin barrier is also negatively impacted by excess cortisol as this effects the lamellar bodies in the skin cells which are responsible for lipid synthesis; the lack of essential lipids weakens the barrier resulting in dry skin, allergies and sensitivity, delayed healing and infections.

Insulin:

Excess glucocorticoids stimulate Insulin production and lead to insulin excess and Insulin resistance. Elevated Insulin stimulates IGF2 (Insulin growth factor) which increases growth of keratinocytes, and stimulates abnormal keratinocyte growth, (exacerbates Psoriasis and Acne) and increases androgens and testosterone release.

Substance P:

This is neuropeptide released in times of stress. Substance P stimulates sebaceous germinative cells and proliferation of sebaceous glands which results in excess oil production and blockage of the oil ducts and the development of acne. Substance P also activates mast cells, increasing histamine release and itch sensation. Substance P induces vascular permeability and inflammation, which aggravates conditions like Eczema and Rosacea.

Corticotropin Releasing Hormone (CRH):

CRH stimulates release of MSH (melanocyte stimulating hormone) causing hyperpigmentation and blotchy skin.

Catecholamines (Adrenaline, Noradrenaline)

Decrease blood perfusion to skin reducing availability of oxygen and nutrients resulting in poor texture and sallow / pallor. Catecholamines have also been shown to cause immune suppression, interfere with DNA repair and contribute to ageing.

Managing stress

While the effects of stress on the skin are only briefly outlined above, it illustrates the significant impact this can have on individuals predisposed to skin conditions. It is therefore imperative to minimise stress where possible in order to avoid any exacerbation of skin disorders.

There are some straight forward tips to reduce stress such as getting a good night’s sleep, exercising and following some simple dietary guidelines (listed below).

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Reduce salt intake

Avoid alcohol

Avoid caffeine

Avoid skipping meals

Avoid refined, processed foods.

Avoid high fat foods

Do eat high fibre, low glycaemic index diet

In the following blogs we will present some relaxation techniques that are easy to implement and will have a direct effect in reducing the side effects of stress.

 

References

  1. Dunn, Jeffrey HKoo, John; Psychological Stress and skin aging: A review of possible mechanisms and potential therapies; Dermatology Online Journal 19 (6): 1 University of Colorado, School of
  2. Medicine, 2 University of California, San Francisco, Department of Dermatology 2013 Permalink: http://escholarship.org/uc/item/3j0766hs
  3. Jessica M. F. Hall, desAnges Cruser, Alan Podawiltz, Diana I. Mummert, Harlan Jones, Mark E. Mummert; Psychological Stress and the Cutaneous Immune Response: Roles of the HPA Axis and the Sympathetic Nervous System in Atopic Dermatitis and Psoriasis; Dermatology Research and Practice Volume 2012, Article ID 403908, doi:10.1155/2012/403908
  4. Ying Chen, John Lyga; Brain – Skin Connection: Stress, Inflammation and Skin Aging; Inflammation & Allergy – Drug Targets, 2014, 13, 177-190
  5. Theoharis C. Theoharides, Jill M. Donelan, Nikoletta Papadopoulou, Jing Cao, Duraisamy Kempuraj, Pio Conti; Mast cells as targets of corticotropin releasing factor and related peptides; TRENDS in Pharmacological Sciences Vol.25 No.11 November 2004

Atopic Dermatitis (Eczema) and BACTERIAL CUTANEOUS (SKIN) INFECTIONS

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Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory disorder that causes significant morbidity and has a wide range of allergic and non-allergic comorbid disorders.

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease. The patient with AD has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with AD.

   Cutaneous (skin) infections including:-

   Bacterial – Staphylococcal   / Impetigo contagiosum 

    1, 2, 3, 4, 5, 6, 7

Patients with AD are highly susceptible to certain bacterial, fungal and viral infections.

They have also been noted to have an increased incidence of warts caused by the human papillomavirus (HPV), and fungal infections caused by Trichophyton rubrum and also have a higher incidence of the fungal infections:- tinea pedis, tinea unguium, tinea manuum, tinea cruris, and tinea corporis, as well tinea barbae.7

AD Patients are also susceptible to severe infections caused by herpes simplex type 1 virus (eczema herpeticum or Kaposi’s varicelliform), vaccinia virus (eczema vaccinatum) coxsackie A virus and molluscum contagiosum virus. These viral infections can cause serious complications in AD patient and if not treated promptly have the potential to be life threatening.7

Signs of Secondary Infection include:

  • Sudden flaring (worsening) of eczema all over the body.
  • Weeping crusted areas – crusts are often a golden colour
  • Clusters of pustules (yellow/white pimples).
  • Fever, Shivering and extremely painful skin.
  • Chicken pox-like blisters and sores – this can be caused by the cold sore virus and may require urgent medical attention (Kaposi’s varicelliform)

BACTERIA and ATOPIC DERMATITIS (AD)

The skin is colonized by various different species of bacteria, fungi, and viruses that together are known as the skin microbiome, mainly Corynebacterium spp., Propionibacterium acnes and Staphylococcus epidermidis.

Each person will carry a different combination of these depending upon health and environment. The colonization of bacteria on specific regions on the body depends upon the local skin environment including moisture levels, pH, and keratinocyte cell surface adhesion proteins (Skin Barrier). For instance, Staphylococcus and Corynebacterium species thrive in specific environments on the skin such as the sole of the foot and the back of the knee. Dry environments such as the inside forearm and palm of hand are more prone to harbour a mixed population of bacteria including Propionibacterium acnes. 7

Babies are born microbe free until exposure to the external environment allows for immediate colonization of their skin, this first colonization usually starts as they pass through the vagina. As the child grows and they are exposed to different environments and in physical contact with different people their microbiome will change.7

Environmental factors such as diet, age, and gender also play a role in the makeup of the skin microbial flora.7

Staphylococcus aureus (S. aureus) and Staphylococcus epidermidis (S. epidermidis) are the two most common clinical isolates of the microbiota that is normally found in the nasal passages and on the skin of healthy people. They are Gram-positive cocci found in clusters. S. epidermidis comprises greater than 90% of the aerobic resident flora found on the skin and is considered a normal inhabitant of the skin surface. Some strains of S. epidermidis produce bacteriocins that are toxic to other bacterial species such as Staphylococcus aureus. S. epidermidis can also target S. aureus can prevent S. aureus biofilm formation and growth thus promoting a stronger skin barrier and immune response.7

In AD patients, when the patient suffers skin barrier breakdown and lowered immunity both S. aureus readily colonizes the affected skin lesions. Studies have shown that between 80% and 100% of patients with AD present nasal and skin colonization by with S. Aureus, as opposed to the prevalence of only between 5 to 30% in individuals without AD. To further break down the colonization statistics S. aureus has been isolated from 55–75% of unaffected AD skin, 85–91% of chronic lichenified (thickened/ scratched) lesions and 80–100% of acute exudative (weepy) skin lesions.7, 8

Impetigo contagiosum (contagiosa)

Impetigo is a skin infection caused by Staphylococcus aureus and Streptococcus pyogenes. In Europe and colder climate regions, Staphylococcus aureus is the most common cause. Impetigo can affect any one but is more common in children aged 2yrs. – 6 yrs. of age. It is highly contagious and is spread by direct contact. Children and those affected need to be kept home from day care, kindergarten, school and work.9

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Impetigo is commonly found in people who have skin conditions that cause impaired skin barrier e.g. eczema, scabies, fungal infections or via skin trauma e.g. insect bites. It is also common in crowded environments e.g. schools, day care centres etc. It can be spread through contact sports e.g. wrestling. Impetigo caused by Streptococcus pyogenes is common in hot humid regions.

There are two types of impetigo. The most common is called crusted or non-bullous impetigo. It starts as small blisters, which quickly burst and crust over. The other type, called bullous impetigo, causes large blisters that break easily. It is less common, and mainly affects babies.

Non Bullous Impetigo normally presents as:

  • Small vesicles that rupture, dries and forms golden- coloured, brown or even brownish black crusts/scabs.
  • Lesions can be up to 2cm in diameter.
  • Usually found on the face – around the mouth and nose, but they can also be found on the limbs.
  • In mild cases there is normally no systemic symptoms, but if it is an extensive eruption, it may be accompanied by fever and swelling.

Bullous Impetigo presents as:

  • Large fluid filled blisters > 2cm, which rupture easily.
  • May be golden in colour, brown or even brownish black.
  • The limbs and torso are more likely to be affected.
  • It is normally accompanied by fever and swelling.

Bullous impetigo is only caused by S aureus.

Atopic_6 Atopic_7

Impetigo has been commonly called “school sores”. It is important, due to the contagious nature of the condition, that hands are washed regularly and especially after having touched or scratched the impetigo lesions. Anything that has been in contact with the sores e.g. clothing or anything that has been on the sores can spread the infection to other family members, friends and colleagues. In order to prevent the spread of the condition it is very important that clothes, towels, pillows and bed linen, nail scissors, razors or toothbrushes etc. are not shared. Clothing, towels and bedding etc. should be washed separately using hot water, washing powder and a disinfectant or eucalyptus/tea tree oil added to the wash.

REFERENCES

  • Simpson EL.; Comorbidity in Atopic Dermatitis; Curr Dermatol Rep. 2012 March 1; 1(1): 29–38. doi:10.1007/s13671-011-0003-5
  • Augustin M. et al.; Epidemiology and Comorbidity in Children with Psoriasis and Atopic Eczema; Dermatology 2015;231:35–40 DOI: 10.1159/000381913
  • Deckert S. et al.; Nonallergic comorbidities of atopic eczema: an overview of systematic reviews; Allergy 69 (2014) 37–45 © 2013
  • Ellis CN. et al.; Validation of Expert Opinion in Identifying Comorbidities Associated with Atopic Dermatitis/Eczema; Pharmacoeconomics 2003; 21 (12)
  • Silverberg J.I. and Silverberg N.B.; Atopic Dermatitis: Update on Pathogenesis and Comorbidities
  • Cogen A.L. et al.; Skin microbiota: a source of disease or defence?; Br J Dermatol. 2008 March ; 158(3): 442–455. doi:10.1111/j.1365-2133.2008.08437.x
  • Williams M. R. et al.; The Role of the Skin Microbiome in Atopic Dermatitis; Curr Allergy Asthma Rep (2015) 15: 65 DOI 10.1007/s11882-015-0567-4
  • Baviera G. et al.; Staphylococcus Aureus And Atopic Dermatitis: Which Came First, The Chicken Or The Egg?; EMJ Dermatol. 2015;3[1]:92-97.
  • Petry V. et al.; Bacterial skin colonization and infections in patients with atopic dermatitis; An Bras Dermatol. 2012;87(5):729-34.
  • Leung DYM.; The role of Staphylococcus aureus in atopic eczema; Acta Derm Venereol 2008; Suppl 216: 21–27
  • Baker S.; The role of microorganisms in atopic dermatitis; 2006 British Society for Immunology, Clinical and Experimental Immunology, 144: 1–9

Atopic Dermatitis (Eczema) and Psychological Disorders

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Psychological Disorders: –

Depression

Anxiety

Attention Deficit/Hyperactivity Disorder (ADHD)

Autistic Spectrum Disorder (ASD)

Atopic Dermatitis (AD) is a multifactorial, immune mediated, chronic and relapsing skin disease, with significant emotional distress, sleep disturbance and Quality of Life (QoL) difficulties. 1,2,3

Most cases of AD begin in childhood or adolescence, with more than 80% of pediatric patients having persistent symptoms of itch and dry skin in adulthood. The early age of onset and disease chronicity, plus impaired quality of life weighs heavily on a child’s psychological and behavioural development. This often leads to delayed social development throughout life and very high rates of psychological and behavioural disorders.5, The impairment of quality of life caused by childhood AD has been shown to be greater than or equal to other common childhood diseases such as asthma and diabetes, emphasising the importance of AD as a major chronic childhood disease.1,2,3

AD patients have been described with lower self-competence and self-efficacy, when compared with healthy individuals and there is also a clear relationship between the prevalence of a mental health disorder and the reported severity of the skin disease. 1,2,3

Psychological stress and AD symptoms seem to form a vicious cycle. However, the exact mechanism as to how stress affects AD is as yet largely unknown. Evidence suggests that stress stimulates the hypothalamic-pituitary-adrenal (HPA) axis releasing neuropeptides and neurotrophins, which influence the development and course of AD, inducing epidermal barrier dysfunction, and lowering the itch threshold.4

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The current incidence of psychiatric disorders among dermatological patients is estimated at about 30-40% and the association between anxiety and depression, and AD is well documented in scientific and medical journals.1,2,3 AD and clinical depression interact closely, and causal relationships between the two conditions have frequently been observed; e.g. the onset or exacerbation of AD often follows stressful life events such as severe disease in a family member, divorce, or parental separation.5

This may reflect the psychological distress produced by both the stigma associated with visible AD skin lesions and the unpredictability of disease flares, and may be manifested by the high proportion of patients (approx. 60%) who reported being embarrassed by or self-conscious of their skin condition in various studies. The psychological burden can further negatively impact mood and QoL. Thoughts of suicide have been reported in 15% of patients in an AD population in Europe and up to 20% of individuals with severe disease.3

In Dermatology Life Quality Index (DQLI) questionnaires, approximately 46% AD patients report severe pruritus (itch) with almost 15% rating it as unbearable, 86% experience itching every day and approx. 42% state that they itch up to 18 hours per day. Nearly all patients also reported the frequent occurrence of bleeding, oozing, cracking, flaking, or drying of their skin. AD and itching has a significant impact on patient-reported sleep with approx. 68% of patients reporting that itch delayed falling asleep and occasionally or frequently woke them up at night, with up to 36% reporting that their sleep was disturbed every night. Loss of sleep may contribute to daytime sleepiness and fatigue, further reducing functional activities and adversely affecting mood and QoL due to the fact that sleep likely has a reciprocal relationship with mental health.3

Children with AD face a slightly different set of challenges and often have negative self-esteem (subjective perception of self-worth) and poor self-image (subjective perception of abilities, appearance). They experience frustration, fussiness, irritability, unhappiness, loneliness, self-consciousness and emotional sensitivity. Parents have reported that their AD children often cry, and are nervous and insecure. Researchers observed perfectionism, rigid and obsessive thought patterns, anxiety and depression, obsessive and compulsive traits in paediatric AD patients. Children with AD also have difficulties in social interaction and impaired social competence.6

Atopic_2

Sixty percent of children with AD experience sleep disturbance caused by their disease, with 83% reporting sleep disturbance during exacerbations. The sleep of children with eczema was characterized by problems with settling and maintaining sleep while their daytime functioning was characterized by excessive daytime sleepiness and higher ADHD and Oppositional Behaviour scores as well as poor performance in daytime activities, specifically school performance.6 Problematic behavioural patterns that include hyperactivity, impaired attention, scratching to get attention; stubbornness, aggressiveness, disruptive and oppositional behaviour have been documented. A significant association was found between Attention Deficit Hyperactivity Disorder (ADHD) and AD. It is suggested that these behavioural difficulties are possibly mediated by disturbed sleeping patterns, difficulty in coping with the discomfort of AD and its treatment, disfigurement, stigmatisation and disciplinary challenges.7

Various studies have consistently indicated an association between AD and Autism Spectrum Disorder (ASD) and ADHD which is independent of environmental exposures and other comorbidities. Particularly infant AD appears to be associated with later development of ADHD symptoms. Children with previous or prevalent AD have an approximately 43 % increased risk to be diagnosed with ADHD or to display clinical ADHD symptoms.8, 9

It has been speculated that ADHD/ASD symptoms, AD, food hypersensitivity and sleep disruption may be linked by shared pathophysiological factors and that these impairments are characterized by a relevant developmental interplay, especially in early infancy and childhood. Disturbed sleep is a characteristic feature of ASD/ADHD and eczema and may be one mediating factor in the observed associations. However, other mechanisms may also be involved such as genetic or neuro-immunomodulatory mechanisms. It has been suggested that the non-allergic activation of TH1 and TH17 cells, which mediate the inflammatory processes, may be of relevance in the association between AD and ADHD. Also excessive cytokine release may impact on the central nervous system as they are able to pass the blood–brain barrier, thus possibly affecting both neurotransmission and brain circuits which are known to be involved in ADHD and/or affecting the sleep–wake rhythm.8, 9

Recent studies have also linked sleep disturbance to obesity and hypertension (blood pressure PB) in children.  The long-term effect of increased BP are unknown in children, but it is possible that cumulative increases of BP are associated with cardiovascular disease later in life, similar to that observed in psoriasis. The mechanism of association between obesity and AD remains unknown. Previous studies have suggested that adipose (fat) tissue may directly influence the risk of AD. 10  The association between AD and in particular, central obesity – where excessive fat is stored around the stomach and abdomen, in particular, is of major concern. Central obesity has previously been reported to have particularly harmful effects on a variety of medical disorders, including asthma, dyslipidemia, diabetes, coronary artery disease, and myocardial infarction.

 

Also read our BLOGS – Stress, Anxiety, Depression – Atopic Eczema (AE)/Atopic Dermatitis (AD) and associated Itch

Stressed About Your Skin Condition – Identify Your Stressors and Your Stress Responses 

REFERENCES

  • Lewis-Jones S. (2006), Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema. International Journal of Clinical Practice, 60: 984–992. doi:10.1111/j.1742-1241.2006.01047.x
  • Mina, Shaily et al. “Gender Differences in Depression and Anxiety Among Atopic Dermatitis Patients.”Indian Journal of Dermatology 2 (2015): 211.PMC. Web. 20 Oct. 2016.
  • Simpson M.I. et al.; Patient burden of moderate to severe atopic dermatitis (AD): Insights from a phase 2b clinical trial of dupilumab in adults; J AM ACAD DERMATOL MARCH 2016
  • Sang Ho Oh et al.; Association of Stress with Symptoms of Atopic Dermatitis; Acta Derm Venereol 2010 Preview
  • Sewon Kim er al.; The Association between Atopic Dermatitis and Depressive Symptoms in Korean Adults: The Fifth Korea National Health and Nutrition Examination Survey, 2007–2012; Korean J Fam Med 2015;36:261-265
  • Gouws A.; The Impact Of Atopic Dermatitis On The Psycho-Social Wellbeing Of Children And Their Families; Current Allergy & Clinical Immunology, March 2016, Vol 29, No 1
  • Camfferman D et al.; Eczema, Sleep, and Behavior in Children; Journal of Clinical Sleep Medicine, Vol. 6, No. 6, 2010
  • Schmitt J. et. Al.; Association of atopic eczema and attention-deficit/hyperactivity disorder – meta-analysis of epidemiologic studies; Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie (2015), 41, pp. 35-44. DOI: 10.1024/1422-4917/a000208
  • Tzu-Chu Liao et al.; Comorbidity of Atopic Disorders with Autism Spectrum Disorder and Attention Deficit/Hyperactivity Disorder; The Journal of pediatrics · February 2016 DOI: 10.1016/j.jpeds.2015.12.063
  • Silverberg J. I. et al.; Central Obesity and High Blood Pressure in Pediatric Patients With Atopic Dermatitis; JAMA Dermatology February 2015 Volume 151, Number 2

ATOPIC DERMATITIS (ECZEMA) AND COMORBIDITIES

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Atopic dermatitis (AD), also known as atopic eczema, is a chronic inflammatory disorder that causes significant morbidity and has a wide range of allergic and non-allergic comorbid disorders.

Comorbidity is a concurrence of multiple diseases or disorders in association with a given disease. The patient with AD has an increased risk of developing one or more of a number of other diseases/conditions that share many immunological features with AD.

 CHART 1: Comorbidities Associated with AD

Cutaneous (skin) infections including:-

Bacterial – Staphylococcal   / Impetigo contagiosum

Viral – eczema herpeticum

Fungal

 

Other Skin Conditions:

Vitiligo

Psychological and Psychiatric Disorders – Depression

Anxiety

Attention Deficit/Hyperactivity Disorder (ADHD)

Autistic spectrum disorder (ASD)

Food Allergies/Intolerances Cardiovascular Disease – Arterial hypertension/ Atherosclerosis

Stroke

Prediabetes

Diabetes

Obesity

Fatty Liver

Dyslipidemia (Raised cholesterol)

Allergic conjunctivitis

Cataracts 

Atopic keratoconjunctivitis (AKC) 

Allergic rhinitis

Hayfever

Asthma

Acute upper respiratory infection

Acute pharyngitis

Fatigue, insomnia  

1, 2, 3, 4, 5, 6, 7

Most cases of AD begin in childhood or adolescence, with more than 80% of pediatric patients having persistent symptoms of itch and dry skin in adulthood. The early age of onset and disease chronicity, plus impaired quality of life, secondary to AD weigh heavily on a child’s psychological and behavioural development, with delayed social development throughout life and very high rates of psychological and behavioural disorders and quality-of-life impairment.6 Various studies have consistently indicated an association between AD and ADHD which is independent of environmental exposures and other comorbidities. Particularly infant AD appears to be associated with later development of ADHD symptoms. Sleeping problems due to AD are suggested as playing an important role for the observed association between AD and ADHD. Children with previous or prevalent AD have an approximately 43 % increased risk to be diagnosed with ADHD or to display clinical ADHD symptoms.8

Researchers have found that adults with AD have higher rates of cigarette smoking, consumption of alcoholic, lower rates of exercise, and higher classification of obesity with category II / III consistently indicated in children and adults, hypertension, prediabetes, diabetes, and high cholesterol.6, 7

staph-infection

Bacterial superinfection by staphylococcal aureus is the most common complication in atopic dermatitis and is almost always present in AD flares.  S. aureus is an important human pathogen that causes a variety of  infections ranging from localised skin and soft-tissue infections (SSTIs) to severe necrotising fasciitis and life-threatening infections.7 , 8  S. aureus can be isolatedfrom 55–75% of unaffected AE skin, 85–91% of chronic lichenified lesions and 80–100% of acute exudative skin lesions.9 The correlation between AD severity and colonization with S. aureus has already been well documented, and it is generally known that this colonization is an important mechanism involved in the continued aggravation of the disease in patients.

S. aureus has shown a capacity to develop resistance to antimicrobials that were originally active against the species. In 1961, there were reports of strains that were methicillin resistant, and they were called methicillin-resistant Staphylococcus aureus (MRSA). By 1980, MRSA strains became an endemic problem in hospitals in several countries. Reports on MRSA infections in AD patients have been published since 2005. Some authors suggest that MRSA should be considered when patients with AD present with more intense and generalized erythemas (redness of the skin), and with the predominant location of infection in these patients being the face, and a fetid (fishy) odour present. Studies worldwide suggest that the prevalence of MRSA in the population with AD varies from 0 to 30.8% depending upon the country of research.10

Colonization by streptococcus generally precedes the development of impetignized lesions (by about 10 days). Group A streptococci often colonize the pharynx of asymptomatic people, especially school-age children. In cases of infected atopic dermatitis lesions, a high prevalence of co-infection by staphylococci and streptococci was reported, and these bacteria were present in about 70 to 85% of patients. B-hemolytic streptococci are the main cause of impetigo and are more commonly isolated on the skin of people with AD than on the skin of healthy individuals or of those with other skin diseases.11

Eczema herpeticum (EH) is caused by Herpes simplex virus-1 (HSV-1), Herpes simplex virus-2 (HSV-2), Herpes zoster virus, Coxsackie virus, etc. Also, EH may occur in children who have AD after smallpox vaccination. If corticosteroid therapy is used in these patients because of misdiagnosis, the lesions may worsen. Therefore, if skin lesions or another pre-existing dermatitis is aggravated after varicella (smallpox) infection then EH must be considered and antiviral therapy must be started immediately.11

AD, is an immunoglobulin E (IgE)-mediated disease with a complex etiology (cause) that is accompanied by superficial inflammation and itchy rashes. An association with asthma and Allergic rhinitis (Hayfever) is well documented. Fifty percent of all those with AD develop other allergic symptoms within their first year of life. In the International Study of Asthma and Allergies in Childhood (ISAAC), among the 56 countries, the prevalence of AD in children varied significantly from 0.3% to 20.5% but shows consistent trends in increasing disease prevalence over time. The main risk factors for progression and persistence of asthma are early onset, IgE sensitization, and severity of AD. Approximate 70% of patients with severe AD develop asthma compared with 20-30% of patients with mild AD and approximately 8% in the general population. Epidemiologic studies have consistently demonstrated strong associations between rhinitis and asthma. Recent clinical and basic science evidence indicated that the two diseases share anatomical, physiological, immuno-pathological, and therapeutical factors. Allergic rhinitis is an inflammatory condition affecting nasal mucosal membranes. In sensitized individuals, allergens such as pollens, moulds, and animal dander provoke this allergic response.12, 13

The relationship between food allergy and AD is complex and the presence of food sensitization and allergy earlier in life predicts a prognosis of severe AD. Around 50–70% of children with an early onset of AD are sensitized to one or more allergens. These are mainly food allergens (cow’s milk, hen’s egg and peanuts being the foods most frequently involved). Food allergy is actually much more common in children with AD with studies reporting ranges from 20 to 80% of children being affected.12,13

Allergic conjunctivitis (AC), either seasonal and/or perennial, is one of the most common types of ocular inflammation which causes redness and swelling of the eyes. Estimates vary, but these types of allergy are said to affect at least 15–20% of the population and higher incidences in those with AD. Its pathophysiology also involves a type I IgE-mediated immune reaction triggered by allergens contacting surface of the eye.2 Atopic keratoconjunctivitis (AKC) is a bilateral chronic inflammatory disease of the ocular surface and eyelid. Its pathomechanism involves both a chronic degranulation of the mast cell mediated by IgE, and immune mechanisms mediated by Th1- and Th2-lymphocyte derived cytokines. It is considered the ocular counterpart of AD. Eczematous lesions may be found on the eyelids, or any place on the body. Skin lesions are red and elevated. They often occur in the antecubital (inner elbow) or popliteal (behind the knees) regions. Typically, eczematous lesions are itchy, and scratching them makes them itchier. Ocular findings vary. The eyelid skin may be chemotic (inflamed eyelid) with a fine sandpaper-like texture. There may be mild, or severe, red and swollen eyes.14

If you have any questions please do not hesitate to contact our clinic by either emailing us at info@goodskincare.com.au or message us on our Facebook page https://www.facebook.com/PsoriasisEczemaClinic/

 

 REFERENCES

  • Simpson EL.; Comorbidity in Atopic Dermatitis; Curr Dermatol Rep. 2012 March 1; 1(1): 29–38. doi:10.1007/s13671-011-0003-5
  • Augustin M. et al.; Epidemiology and Comorbidity in Children with Psoriasis and Atopic Eczema; Dermatology 2015;231:35–40 DOI: 10.1159/000381913
  • Deckert S. et al.; Nonallergic comorbidities of atopic eczema: an overview of systematic reviews; Allergy 69 (2014) 37–45 © 2013
  • Ellis CN. et al.; Validation of Expert Opinion in Identifying Comorbidities Associated with Atopic Dermatitis/Eczema; Pharmacoeconomics 2003; 21 (12)
  • Gradman J. et al.; Allergic conjunctivitis in children with asthma, rhinitis and eczema in a secondary outpatient clinic.
  • Silverberg J.I.; Eczema and cardiovascular risk factors in 2 US adult population studies; J Allergy Clin Immunol 2015;135:721-8.
  • Silverberg J.I. and Silverberg N.B.; Atopic Dermatitis: Update on Pathogenesis and Comorbidities
  • Baviera G. et al.; Staphylococcus Aureus And Atopic Dermatitis: Which Came First, The Chicken Or The Egg?; EMJ Dermatol. 2015;3[1]:92-97.
  • Leung DYM.; The role of Staphylococcus aureus in atopic eczema; Acta Derm Venereol 2008; Suppl 216: 21–27
  • Petry V. et al.; Bacterial skin colonization and infections in patients with atopic dermatitis; An Bras Dermatol. 2012;87(5):729-34.
  • Celtik C. et al.; A Life-Threatening Condition In A Child With Chicken Pox: Eczema Herpeticum; Open Journal of Pediatrics 1 (2011) 1-3
  • Tao Zheng et al.; The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma; Allergy Asthma Immunol Res. 2011 April;3(2):67-73. doi: 10.4168/aair.2011.3.2.67
  • Nutten S.; Atopic Dermatitis: Global Epidemiology and Risk Factors; Ann Nutr Metab 2015;66(suppl 1):8–16
  • La Rosa M. et al.; Allergic conjunctivitis: a comprehensive review of the literature; Italian Journal of Pediatrics 2013, 39:18 http://www.ijponline.net/content/39/1/18

Itch (Pruritus) & Eczema

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Scratching is the natural response to itch (Pruritus) and, by definition, inseparable from it. The act of scratching not only diminishes itch, but it has been found to be rewarding and addictive. The itch-scratch cycle is a complex phenomenon involving sensory, motor and emotional components. The urge to scratch can be remarkably intense because the reward provided by scratching brings such intense relief and may also be associated feelings of pleasure and enjoyment. Recent studies have shown that rating scratching as a pleasurable experience is correlated with the intensity of the underlying itch, both in patients with chronic itch and healthy individuals.1 Various functional brain imaging studies have discovered that the itch-scratch cycle in humans can be tracked to specific regions of the brain, including areas related to reward, pain sensation, and addiction.1,2

The Itch-Scratch-Rash cycle is commonly used to describe this ongoing, never ceasing, always constant itch that makes eczema very different from many other skin condition. Eczema has often been called the “Itch that Rashes” rather than the “Rash that Itches”.3 

Itch_1

The itchier a patient feels, the more scratching of the skin that occurs and which ultimately lead to skin damage and the appearance of a red rash. Often, in chronic presentations it becomes a completely unconscious habit and patients are often not even aware that they are scratching. When a patient scratches, the skin becomes inflamed, this inflammation then causes the skin to itch even more, thus making it even harder for the patient to resist the urge to scratch. This vicious circle can become so severe that it causes sleeplessness, irritability, anxiety and stress. In extreme cases it can lead to significant excoriations (open, bloody and deep scratch wounds) on the skin or even severe lichenification (thickening of the skin) and pain. 

The Practitioner and Patient need to recognize and address various aspects of itch, including:

(1) Identification and elimination of trigger factors;

(2) Maintaining the skin barrier through emollients – Oil based and Water Based;

(3) Targeting inflammation through topical medications and systemic (oral) medications

(4) Addressing psychological and behavioural components; and

(5) Education – understanding the condition.

The sensation of pruritus can be triggered by endogenous (internal) and exogenous (external) stimuli, which activate specific peripheral nerve endings in the epidermis and dermis layers of the skin.3

Trigger Factors3

Allergies                                   House dust mites, food allergens, air-born contact dermatitis (pollen, etc.), animals (e.g. cat                                                        dander), jewellery, certain cosmetic ingredients.

Infections                                 Staphylococcus aureus, viral infections (herpes, molluscum), yeasts (eg, Trichophyton,                                                                malassezia).

Exogenous                               Soaps, solvents, wool, sweat, chemicals, toxins, cigarette smoke, smog.

Physical stimuli                       Temperature: humidity, cold dry air, clothes rubbing on the skin.

Emotional                                Anxiety/Stress /Anger/ Depression.

How to rate your Itch4

Based on the Eppendorf  Itch Questionnaire.

Rate each of the following from 0 to 4

The following describes your Itch………

 01234
  Painful     
  Pulsating     
  Throbbing     
  Prickling     
  Hurting     
  Tickling     
  Stinging     
  Worse when Cold     
  Less when Cold     
  Worse when Hot     
  Less when Hot     
  Dull     
  Sharp     
  Burning     
  Feels like ants     
  Comes in waves     
  Unbearable     
  Annoying     
  Physical urge to scratch     
  Numbing     
  Relentless     
  Cruel     
  Tormenting     
  Tiring     
  Numbing     
  Severe     
  Uncontrollable     
  I only can think of the Itch     

When do you feel the need to Itch?

 01234
  In the Morning     
  In the Evening     
  At night     
  At rest     
  Worse in Bed     
  After a hot shower     
  After exercise     
  After being outside     
  After being in the Sun     
  After gardening     
  After Dusting, Sweeping/Vacuuming/ Changing beds     
  After eating certain foods

  Specify

     

How would you describe the need to Scratch?

 01234
  I find it enjoyable     
  It is a physical urge     
  It is compulsive     
  I forget when I do it     
  I always want to scratch     
  I find it satisfying     
  I find it pleasurable     
  It hurts but I cannot stop     
  Other –     

What action do you take when you feel the urge to scratch?

 01234
  I rub     
  I scratch with my nails     
  I scratch with my fingertips     
  I scratch with my knuckles     
  I use a pencil/pen/ruler/stick     
  I rub     
  I pinch     
  I use a cold pack     
  I use a heat pack     
  I take a cold shower     
  I take a warm shower     
  I take a hot shower     
  I put the air conditioner on     
  I turn down the ducted heating     
  I dig my fingernails in     
  I bite my lip     
  I scratch until I bleed     
  I apply pressure     
  Other –     

Which areas of the body do you scratch the most?

                              Front                                                           Back

What distracts you from the urge to scratch?

 01234
  Company distracts me     
  Watching Television     
  Reading a Book     
  Using a Computer/IPhone/IPad     
  Listening to music     
  Applying heat pack     
  Applying ice pack     
  Exercising     
  Doing something with my hands   (hobby)     
  Other –     

When you understand your itch, when you itch, what you do when you scratch and what distract you from scratching, you may be able to plan your approach to your itch more methodically and with more control. You may decide that you need to start a meditation or behavioural therapy class to help you control the need to scratch. You may find that you will learn the best times to apply your creams so that you circumvent the urge to scratch e.g. applying creams before gardening or mowing the lawn or doing housework etc.

What can a Patient do to avoid or control the urge to itch?

Scratching is difficult to resist because it gives the mental impression of easing the itch – but this is only for the short-term. Eventually the sensation to itch comes back – even worse that before you scratched. 

Basic tips to control the urge to itch:- 

  • Keep nails short to avoid tearing the skin when scratching. 
  • Keep cool. Over-heating can trigger the itch. Try to keep your body temperature as constant as you can, wear light layers of cotton clothes.
  • Avoid overheated rooms, keep ducted heating to a minimum, and at night keep the bedrooms cold.
  • Avoid heavy blankets and doonas – use cotton blankets if possible. 
  • Gently rub with the back of the fingers, place pressure or gently pinch the area instead of scratching. 
  • Use a cold compress 

Parents of children often ask “How can I stop my child from scratching?” And as scratching is an instinctive reaction to itching which can become a compulsive/unconscious habit, that question is not an easy one to answer. Parents can help by keeping their child’s nails short and, especially at night, by covering their hands with cotton mittens. 

With older children, it is important that you explain to them how scratching will actually make them feel worse, not better. And that their skin will become redder, more cracked and feel itchier and sorer. 

Become aware of any habits of scratching that your or your child may be developing and take especial note as whether it is at a particular time of day, or during a particular activity, such as playing sport or just watching television. If you or the parents of a child become aware of these types of habits then it is important to try to break the habit.

Nonpharmacological Treatments for the Management of Atopic Dermatitis Itch

 Cognitive-behavioural methods3,5,6

Cognitive-behavioural methods alter dysfunctional habits by interrupting and altering dysfunctional thought patterns (cognitions) or actions (behaviours) that damage the skin or interfere with dermatologic therapy. e.g. Itch-coping Training Programme or Habit Reversal Training, cognitive-behavioural methods for the reduction of itch and scratching behaviour, including self-monitoring, guidance in skin care and coping skills to manage itch- and scratch-triggering factors, stress-management methods with relaxation techniques and habit reversal. The habit reversal technique teaches patients to recognize the habit of scratching, identify situations that provoke scratching, and train them to develop a competing response practice, for example, a child who unconsciously scratches can be taught to recognize the early signs of the sensation of itch and instead of scratching be taught to clench his/her fists or place his/her hands underneath his/her legs as soon as they feel the sensation of itch.

Biofeedback5,7

Biofeedback can enhance the patient’s awareness of tension and help them to relax; improving skin disorders that flare with stress or that have an autonomic nervous system aspect. Biofeedback is a mind-body therapy that uses electronic instruments to assist patients to gain awareness and control over psychophysiological processes. The patient is connected to a machine that measures muscle activity, skin temperature, electrodermal activity, respiration, heart rate, heart rate variability, blood pressure, brain electrical activity, and brain blood flow and visually gives the patient feedback as they go through various “game” like tasks. Chronic itch, which may be somatic, emotional and cognitive, may be treated with therapies that can modulate the autonomic nervous system stress response. Behavioural biofeedback techniques that reduce stress and anxiety have been used to treat chronic pain and itch and could potentially alter the sympathetic over-activity noted in patients with AD.

Hypnosis / Meditation8

With proper training, an individual can intensify this trance state in himself or herself and use this heightened focus to induce mind-body interactions that help alleviate suffering or promote healing. The state of altered consciousness known as a “trance state” may be induced using guided imagery, relaxation, deep breathing, meditation techniques, self-hypnosis or by a trained medical practitioner. Researchers have used relaxation, stress management, direct suggestion for non-scratching behaviour, direct suggestion for skin comfort and coolness, ego strengthening, posthypnotic suggestions, and instruction in self-hypnosis. Their results were statistically significant for reduction in itch, scratching, sleep disturbance, and tension. Reported topical corticosteroid use decreased by 40% at 4 weeks, 50% at 8 weeks, and 60% at 16 weeks. For milder cases of atopic dermatitis, hypnosis along with moisturization can suffice as a primary alternative treatment. For more extensive or resistant atopic dermatitis, hypnosis can be a useful complementary therapy that reduces the amounts required of other conventional treatments.

Read also our Blogs for Psoriasis …. The same techniques can be used for Eczema

Simple Mental/Mind Relaxation Techniques Part 1 – For Psoriasis Patients

Simple Mental/Mind Relaxation Techniques Part 2 – For Psoriasis Patients

Itch_4 Itch_5 Itch_6

References

 

  • Papoiu A. D. P. et al.; Brain’s Reward Circuits Mediate Itch Relief. A Functional MRI Study of Active Scratching; PLOS ONE, www.plosone.org 1 December 2013, Volume 8, Issue 12, e82389
  • Mochizuki H. et al.; Chapter 23Brain Processing of Itch and Scratching; http://www.ncbi.nlm.nih.gov/books/NBK200933/?report=printable
  • Hong J. et al.; Management of Itch in Atopic Dermatitis; Seminars in Cutaneous Medicine and Surgery; Elsivier; doi:10.1016/j.sder.2011.05.002; Pg 71-88
  • Darsow U. et al.; New Aspects of Itch Pathophysiology: Component Analysis of Atopic Itch Using the ‘Eppendorf Itch Questionnaire’; Int Arch Allergy Immunol 2001;124:326–331
  • Shenefelt PD.; Psychological interventions in the management of common skin conditions; Psychology Research and Behavior Management 2010:3 51–63
  • Evers Et al.; Effectiveness of a Multidisciplinary Itch-coping Training Programme in Adults with Atopic Dermatitis; Acta Derm Venereol 2009; 89: 57–63
  • Tran BW. Et al.; Effect of Itch, Scratching and Mental Stress on Autonomic Nervous System Function in Atopic Dermatitis; Acta Derm Venereol 2010; 90: 354–361
  • Shenefelt PD. ;Hypnosis in Dermatology; Arch Dermatol / VOL 136, MAR 2000

 

Stress, Anxiety, Depression – Atopic Eczema (AE)/Atopic Dermatitis (AD) and associated Itch

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Atopic dermatitis may be caused by genetic predisposition and environmental conditions, including hereditary factors, allergens, and neurogenous (arising from the nervous system, or from some lesion of the nervous system) and immunological factors. However, the major contributing cause remains unknown. AD may cause psychosocial problems such as anxiety, depression, sleep disorders, emotional excitability, stigmatization, social isolation, and discrimination and on the other hand, all of these factors may also contribute to and exacerbate the symptoms of AD. Of the many factors related to atopic dermatitis, psychological stress is considered to be among the most important.1

 The psychological, physical and social impact of AD is complex and varies among different ages. The relationship of stress, anxiety, depression, not to mention feelings of stigma, shame, embarrassment, and low self-esteem all impact upon a person who is suffering from a skin condition such as AD. Research has confirmed that adults with AD exhibit high levels of anxiety, depression, and emotional excitability. Children with AD also have higher levels of emotional distress and more behavioral problems than healthy children or children with minor skin problems. Psychosocial factors contributed in the form of exacerbating factors in as high as 94% of AD hospitalized patients. Clinically, it has long been appreciated that both acute stress (stressful life events) and chronic psycho-emotional stress can trigger or enhance pruritus.2, 3, 4,5

Pruritus, or itching, is a main symptom of AD and is often one of the first presenting symptoms.

Itching leads to scratching, which leads to and exacerbates the skin lesions.

  • AD has been referred to as the “itch that rashes.”
  • The cycle of itching and scratching is considered an important factor in the maintenance of AD symptoms and is believed to be one of the first symptoms of an impending AD flare.
  • Scratching tends to cause further itching, leading to the so-called “itch-scratch cycle.” 6

Results of one study found that in patients with AD the itching intensity played an important role in determining the patient psychosocial well-being and that a relationship between pruritus and depression was also found.6

 Scratching often begins automatically in association with stress and emotions, and becomes habitual, being performed many times every day. In addition to the psychological factors, such as anger, irritation, impatience, relief, anxiety, etc., many patients say that they somehow find themselves scratching even when they do not feel itchy. Research has identified that habitual scratching is involved in the formation of the lesions of AD. The scratching is patterned, with the rash exhibiting a bilaterally symmetrical distribution over the back and normal skin remaining in the middle where the hands cannot reach, producing a “butterfly” sign. The prominent red face can also be explained by this scratching behavior.4

 This vicious cycle can cause sleeplessness in over 65% of AD sufferers leading to sleep deprivation which leads to tiredness, mood changes and impaired psychosocial functioning of the sufferer and their family, particularly at school and work. Embarrassment, comments, teasing and bullying frequently cause social isolation and may lead to depression or school/work avoidance. The sufferer’s lifestyle is often limited, particularly in respect to clothing, holidays, staying with friends, owning pets, swimming or the ability to play or do sports. For parents caring for a child with eczema, restriction of normal family life, difficulties with complicated treatment regimens causing an increased work load together with disturbed sleep can lead to parental exhaustion and feelings of hopelessness, guilt, anger and depression. And so the whole family is impacted by the condition.5,6,7

Research has suggested that some AD patients might benefit from certain psychological interventions: patients showing psychological characteristics that comprises high depression, low agreeableness and high public self-consciousness would probably benefit from psychological interventions, such as cognitive restructuring, anger management and self-assertiveness training, because these interventions might be able to modulate the extent of the personality characteristics that are associated with induced itch.8

Recent emerging research indicates that mindfulness meditation training may have beneficial effects across a spectrum of health conditions, but the mechanisms linking mindfulness meditation training with health are unknown. One striking feature of the mindfulness training literature to-date is that mindfulness training effects on disease outcomes have been observed in diseases where stress is known to trigger the onset or exacerbation of disease symptoms and pathogenesis (e.g., HIV, psoriasis, depression, pain, chronic inflammation).9   Research has indicated that relaxation techniques appear to be helpful in the treatment of patients suffering from chronic itch in patients that are open to it. And it is becoming a standard recommendation by many Practitioners and hospitals that relaxation training be considered clinically in patients who report that their itch increases during periods of heightened stress.10

The challenge for sufferers of AD is, with the aim of improving their quality of life, to help themselves to find, together with their practitioner, the best personal treatment plan and then sticking to it. The main challenges in the effective management of AD, comes down to patient adherence to the treatment plan and their emotional resilience.

 

References

  • Kwon1 J.A. et al.; Does Stress Increase the Risk of Atopic Dermatitis in Adolescents? Results of the Korea Youth Risk Behavior Web-Based Survey (KYRBWS-VI); PLOS ONE, www.plosone.org; August 2013, Volume 8, Issue 8, e67890
  • Han-Ting Wei et al.; Risk of developing major depression and bipolar disorder among adolescents with atopic diseases: A nationwide longitudinal study in Taiwan; Journal of Affective Disorders 203 (2016) 221–226
  • Buske KIrschbaum Hellhammer et al.,; Endocrine and immune responses to stress in chronic inflammatory skin disorders; 992. 231-240 (2003)
  • Sang Ho Oh et al.; Association of Stress with Symptoms of Atopic Dermatitis; Acta Derm Venereol 2010; 90: 582–588. The Journal of Clinical Investigation; http://www.jci.org; Volume 116, Number 5, May 2006
  • Kamide R.; Atopic Dermatitis: Psychological Care; Journal of the Japan Medical Association (Vol. 126, No. 1, 2001, pages 59–62).
  • Brown T.M. et al.; Assessing Pruritus Among Patients With Atopic Dermatitis: Targeted Literature and Instrument Review; https://www.rtihs.org/sites/default/files/Brown_isporposter_May2012.pdf
  • Lewis-Jones S. Quality of life and childhood atopic dermatitis: the misery of living with childhood eczema. Int J Clin Pract. 2006;60(8):984-992.
  • Schut C. et al.; Personality Traits, Depression and Itch in Patients with Atopic Dermatitis in an Experimental Setting: A Regression Analysis; Acta Derm Venereol 2014; 94: 20–25
  • Creswell J.D. et al.; Brief mindfulness meditation training alters psychological and neuroendocrine responses to social evaluative stress; Psychoneuroendocrinology (2014) 44, 1—12
  • Schut C. et al.; Psychological Interventions in the Treatment of Chronic Itch; Acta Derm Venereol 2015 Preview

HEALTHY SKIN and WATER INTAKE – PART 1

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Water is an essential element for our existence as it performs a number of vital functions in the body.  It is a key component of the fluid that forms the basis of saliva that helps us to swallow, of synovial fluids that cushion the joints and of the fluids that fill our eyeballs and lubricates our eyes. It provides the medium for by which most of the chemical reactions in the body occurs, it acts as a cushion for the nervous system (cerebrospinal fluid), allows us to get rid of waste products principally via the kidneys and urine production, and helps to regulate body temperature by the process of sweating. 1,2,3

Healthy_1

The body tightly controls its water volume and, under normal conditions, the volume fluctuates by less than 1% per day. Dehydration can be defined as a 1% or greater loss of body mass due to fluid loss e.g. urine, eye lubrication, sweating, breathing etc. 1,2,3

Research experiments using fluid restriction to induce dehydration, has shown that loss of body mass of about 1% can be seen after 13 hours, about 2% after 24 hours and nearly 3% after 37 hours when no fluids and only relatively dry foods are consumed. It was noted, however, that the subjects undergoing fluid restriction had a strong desire to drink and would have been unlikely to become dehydrated to such an extent accidentally. These experiments do show how quickly body fluid loss can occur and the importance of continued rehydration by the consumption of water. 1,2,3

 If water losses are not sufficiently replaced, dehydration will occur and extreme dehydration is very serious and can be fatal. More mild dehydration (about 2% loss of body weight) has been shown to result in headaches, fatigue, increased stress/anxiety, reduced physical performance and cognitive function. Some studies have refined the level of dehydration, where detectable symptoms and changes occurred, to the following: in males, dehydration of 1·59 % body weight loss and in females   1·39 % body weight loss. Such modest loss in body weight can occur in everyday activities, demonstrating the importance of maintaining optimal hydration. Taking into consideration various changes attributable to factors such as ambient temperature, physical activity, state of health, the European Food Safety Authority has recommended that the appropriate water intake should be approximately 2 litres per day for women and 3 litres per day for men. Higher water intake requirements will, of course, be higher for athletes and those that are physically active in hotter climates.4,5,6  

The Stratum Corneum (SC) of the skin consists of the essential barrier between the internal and external environment. Although most of the skin is between 2-3mm (0.10 inch)  thick, the SC plays a vital role in forming a protective barrier and helps to prevent percutaneous entry of harmful pathogens (e.g. germs) into the body. In addition to serving as a physical barrier, the SC has other important functions, including the regulation of body heat (thermoregulation), respiration and maintenance of the body’s water content – transepidermal water loss (TEWL)   Stratum Corneum properties and its protective function can be modified by various internal and external/environmental factors.7

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So what happens to human skin when the body becomes dehydrated?

Any change in the structure of the stratum corneum (SC) is potentially associated with alterations of both its barrier function and water holding capacity. Decreased hydration with reduced elasticity of the stratum corneum is responsible for cracks and fissures in the skin. The rate of TEWL is higher in dry skin than in normal skin where the integrity of the barrier function is not disturbed. The impaired barrier in skin conditions such as psoriasis and atopic eczema makes the SC less efficient in excluding substances that come in contact with the surface and patients with skin conditions e.g. atopic dermatitis are believed to be more prone to contact dermatitis than a normal population and those with psoriasis more susceptible to flare ups after exposure to chemicals.8 

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How can you tell if you are dehydrated?

One simple test is to gently pinch the skin on your hand …. hold for a few seconds and then release the skin. If the skin springs back you are not dehydrated, if the skin remains tented (turgor) then it is a sure sign that you are dehydrated and need to drink at least two glasses of water immediately. Another way of checking is the simple observation of the colour of your urine when you go to the toilet. Some charts have numerous colour options but the simple chart that the NSW Government Health Department has on their website “Beat the Heat” is probably the best and easiest to use:-

REMEMBER IF YOUR URINE IS DARKER THAN THAT INDICATED THEN YOU ARE SERIOUSLY DEHYDRATED AND SHOULD ATTEND YOUR NEAREST HOPSITAL EMERGENCY DEPARTMENT

URINE COLOUR CHART

This urine colour chart will give you an idea of whether you are drinking enough water or you are dehydrated (lost too much water from the body)

 Very Dehydrated ……. DRINK 1 litre of water 
 Dehydrated …….. DRINK 2 -3 glasses of water 
 Somewhat Dehydrated ……. Drink 1 glass of water 
 Hydrated, You are drinking enough, continue drinking as normal

http://www.health.nsw.gov.au/environment/beattheheat/Pages/urine-colour-chart.aspx

 

Also read our blog “HEALTHY SKIN and WATER INTAKE – PART 2

 

REFERENCES

  • Popkin B. M. et al.; Water, Hydration and Health; Nutr Rev. 2010 August ; 68(8): 439–458. doi:10.1111/j.1753-4887.2010.00304.x.
  • Benelam B. and Wyness L.; Hydration and health: a review; Journal compilation © 2010 British Nutrition Foundation Nutrition Bulletin, 35, 3–25
  • Je´quier E. and Constant ; Water as an essential nutrient: the physiological basis of hydration; European Journal of Clinical Nutrition (2010) 64, 115–123
  • Ganio M. S. et al.; Mild dehydration impairs cognitive performance and mood of men; British Journal of Nutrition (2011), 106, 1535–1543 doi:10.1017/S0007114511002005
  • Armstrong L. E. et al.; Mild Dehydration Affects Mood in Healthy Young Women; The Journal of Nutrition Ingestive Behavior and Neurosciences; First published online December 21, 2011; doi:10.3945/jn.111.142000
  • EFSA (2008). Draft dietary reference values for water. Scientific Opinion of the Panel on Dietetic Products, Nutrition and Allergies, (agreed on 11 April 2008 for release for public consultation). (http://www.efsa. europa.eu/it/scdocs/doc/1459.pdf

PSORIASIS and CHEMICAL EXPOSURE to POLLUTION

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Human beings are continuously exposed to environmental pollutants. Because of its critical location, the skin is a major interface between the body and the environment and provides a biological barrier against an array of chemical and physical environmental pollutants. The skin can be defined as our first defense against the environment because of its constant exposure to oxidants, including ultraviolet (UV) radiation and other environmental pollutants such as diesel fuel exhaust, cigarette smoke (CS), halogenated hydrocarbons, heavy metals, and ozone (O3). The exposure to environmental pro-oxidant agents leads to the formation of reactive oxygen species (ROS) and the generation of bioactive molecules that can damage skin cells.1

 The skin is a potential target for oxidative injury, as it is continuously exposed to UV radiation and other environmental stresses generating reactive oxygen species (ROS). ROS mediated oxidative damage involves a vast number of biological molecules since it causes lipid peroxidation, DNA modification, and secretion of inflammatory cytokines.2 ROS induced oxidation of polyunsaturated fatty acids results in the metabolization of the lipid peroxidation into malondialdehyde (MDA). Lipids are structural components of cell membranes, critical in the formation of the permeability barrier of cells, whilst MDA is used as a biomarker of lipid peroxidation.2,3

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Alterations that disturb the skin barrier function in either stratum corneum lipid metabolism or protein components of the corneocytes are involved in the development of various mild or severe skin diseases, including erythema, oedema, hyperplasia, “sunburn cell” formation, skin aging, contact dermatitis, atopic dermatitis, psoriasis, and skin cancers.1

The mechanism by which environmental insults exert a detrimental effect the skin barrier function is through the generation of oxidative stress, which overwhelms the skin’s defenses by quickly depleting the enzymatic (glutathione peroxidase, glutathione reductase, superoxide dismutase, catalase) and nonenzymatic (vitamin E, vitamin C, and glutathione) antioxidant capacity, thus leading to deleterious effects.1 The enzymes, including glutathione peroxidase, superoxide dismutase (SOD) and catalase (CAT) decrease the concentration of the most harmful oxidants, hence an inadequate antioxidant protection or excess ROS production generates oxidative stress and contributes to the development of cutaneous diseases and disorders.

Increased capacity for chemotaxis (the directional movement of cells in response to chemical stimuli), adhesion (the interaction of a cell with a neighbouring cell or with the underlying extracellular matrix, via specialized multi-protein adhesive structures) and increased ROS production in neutrophils, keratinocytes and fibroblasts of the skin matrix, have been reported in patients with psoriasis. Research results have shown that increased oxidative stress in these patients, as demonstrated by the high plasma malondialdehyde (MDA) levels and compromised levels of the antioxidant defense enzymes, have been observed even at the time of diagnosis itself. Other reports have suggested that, fibroblasts in the lesion-free skin of psoriasis patients have shown signs of increased oxidative damage even before the formation of the characteristic psoriatic plaque/lesions which may indicate the involvement of abnormal immune reactions leading to the onset of the disease.2

Sun UV rays, Ozone (O3 – the primary constituent of smog), cigarette smoke (CS) exposure, and pollutants, in addition to the natural process of aging, contribute to the generation of free radicals and reactive oxygen species (ROS) that interact with lipid-rich plasma membrane and initiate the so-called lipid peroxidation reaction cascade. The progressive depletion of antioxidant content in the stratum corneum leads to the cascade of effects which result in an active cellular response in the deepest layers of the skin. ROS is known to stimulate the release of pro-inflammatory mediators from a variety of skin cells. Skin inflammation, in turn, leads to skin infiltration by activated neutrophils and other phagocytic cells that generate further free radicals (both reactive oxygen and nitrogen species), thus establishing a vicious circle.1

 There is no doubt that the skin is continuously and simultaneously exposed to several oxidative stressors, and these can have additive, if not synergistic, effects. Whilst UV ray therapy has been proven to be an effective treatment for psoriasis and there is certainly anecdotal information that indicates sun exposure also improves psoriatic lesions, there has been little or no research on the effects of combined UV and O3 on the inducement and or exacerbation of psoriasis.  While environmental UV radiation penetrates into the epidermis (UV-B) or into the dermis (UV-A) and is known to induce the release of tissue-degrading enzymes, O3 oxidizes biological systems only at the surface. Therefore, because O3 and UV cooperatively damage subcutaneous (SC) components they exert an additive effect in cutaneous tissues. Research results have suggested that UV irradiation has been shown to compromise the skin barrier and simultaneous exposure to O3 may enhance this phenomenon by perturbing SC lipid constituents that are known to be critical determinants of the barrier function. It has been proposed that the by-products of O3-induced lipid oxidation penetrate the outer skin barrier and cause effects on constituents of the deeper epidermis that can lead to activation of transcription factors, such as Nuclear factor kappa B (NF-?B), which regulates a variety of proinflammatory cytokines. NF-?B is a protein transcription factor that orchestrates inflammation and other complex biological processes. It is a key regulatory element in a variety of immune and inflammatory pathways, in cellular proliferation and differentiation and in apoptosis. Therefore NF-?B is a crucial mediator involved in the pathogenesis of psoriasis.1,3,4,6

It has been theorized that responses to air pollutants may be age related, and several recent studies have shown that skin responses to pollutants are modulated by age. The free radical theory of aging is supported by finding that oxidative damage to biomolecules accumulates and increases with age. In aging skin, the process oxidative damage involves not only proteins, lipids and DNA but also is linked with alteration of the collagenous extracellular matrix in the dermis. The extensive research in the aging process of human skin found that levels of MMP-1 increased with age and contributed to fragmentation and disorganization of collagen fibers in the dermis. Researchers have also found that both a contact of fibroblasts with collagen fibers and collagen cross-links of collagen fibers are strongly reduced in aged skin (80% and 75%, respectively). Despite a large body of knowledge a detailed molecular mechanism of the skin aging is not fully recognized.1,5

Further research is required to determine exactly how air pollutants can induce and/or exacerbate psoriasis and other skin conditions. However one theory proposed for the most likely cause is thought to be due to skin injury caused by exposure to the chemical pollutant and the subsequent initiation of the Koebner effect.

See our blog “Koebner Phenomenon”, “Psoriasis and Chemical Exposure” and “Psoriasis and Smoking”

References

  • Valacchi et al.; Cancer Cutaneous responses to environmental stressors ; Annals Of The New York Academy Of Sciences;  Issue: Nutrition and Physical Activity in Aging, Obesity, and Cancer; Ann. N.Y. Acad. Sci. ISSN 0077-8923; https://www.semanticscholar.org/paper/Cutaneous-responses-to-environmental-stressors-Acad-Sci/09cdc1c7eda0a59cce84c65631d380a180cc4f1b/pdf
  • Ayala A. et al.; Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal; Oxidative Medicine and Cellular Longevity Volume 2014, Article ID 360438, 31 pages; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/360438.pdf
  • Kadam P. et al.; Role of Oxidative Stress in Various Stages of Psoriasis; Ind J Clin Biochem (Oct-Dec 2010) 25(4):388–392; file:///C:/Documents%20and%20Settings/marg/My%20Documents/Downloads/12291_2010_Article_43.pdf
  • Goldminz AM. Et al.; NF-?B: an essential transcription factor in psoriasis.; J Dermatol Sci.2013 Feb;69(2):89-94. doi: 10.1016/j.jdermsci.2012.11.002. Epub 2012 Nov 14.
  • Kruk J., Duchnik E.; Oxidative Stress and Skin Diseases: Possible Role of Physical Activity; Asian Pacific Journal of Cancer Prevention, Vol 15, 2014
  • Burke KE,Wei H.; Synergistic damage by UVA radiation and pollutants.; Toxicol Ind Health May/June 2009 25: (4-5): 219-224

Simple Mental/Mind Relaxation Techniques Part 2

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Are you having trouble controlling your thoughts and finding it difficult to let yourself float in the Full Body Scan Meditation or the Releasing Troubles and Worries Exercise?

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WELL DON’T WORRY!!!!!!!

Here is a “Thought-Stopping” Exercise that can be used during either the Full Body Scan Meditation or the Releasing Troubles and Worries Exercise or when trying to get to sleep.

In thought-stopping, you would do this exercise FIRST. So lie on a yoga bed for the exercises or in bed to get to sleep.

Think about something that you know is worrying you and will keep you awake …… something troubling you that you will know your mind will churn over and make it difficult to relax or go to sleep.  Force your mind to concentrate on that issue or person e.g. the project at work is in trouble and you know your boss is going to get angry at you and the team. Turn this over in your mind again and again and then suddenly in your mind “Shout Out” STOP!!!!!!. Breath easily and try to relax …… if you feel the issue creeping back into your mind ….. repeat the STOP exercise again and again until your mind releases the thought.

This STOP exercise basically is forcing your brain to recognize when to stop thinking about something …. It abruptly interrupts the thought process and makes the brain shift its focus … this is where the relaxation technique, that you have chosen should now be used.

A number of sites on the internet offer some wonderful guided meditations, and alternative Relaxation Techniques. Below we have listed some of the techniques and their links:-

SAFE HAVEN” – VISUALIZATION – Page 19 http://www.mirecc.va.gov/visn16/docs/Franklin_Relaxation_Therapist_Manual.pdf

QUICK RELAXATION STRATEGIES

https://www.k-state.edu/paccats/Contents/Stress/Quick%20Relaxation%20

Strategies.pdf

 

ABC GUIDED AUDIO MEDITATIONS

http://www.abc.net.au/radionational/programs/lifematters/features/meditation-toolkit/audio-practice/4326674

 

Also read our blog “Stress, Anxiety, Depression and Psoriasis, Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses, Simple Physical Relaxation Techniques for Psoriasis Patients, Simple Mental/Mind Relaxation Techniques Part 1 – For Psoriasis Patients, Simple Mental/Mind Relaxation

 

REFERENCES

  1. National Center for Health Promotion and Disease Prevention (NCP); Manage Stress Workbook; http://www.prevention.va.gov/mpt/2013/docs/managestressworkbook_dec2013.pdf
  2. Relaxation Techniques for Health: What You Need To Know; National Institutes of Health; U.S. Department of Health and Human Services; https://nccih.nih.gov/sites/nccam.nih.gov/files/Get_The_Facts_Relaxation_Techniques_02-06-2015.pdf
  3. Progressive Muscle Relaxation; http://www.cci.health.wa.gov.au/docs/ACF3944.pdf
  4. Manzoni G.M. et al.; Relaxation training for anxiety: a ten-years systematic review with meta-analysis ; BMC Psychiatry 2008, 8:41 doi:10.1186/1471-244X-8-41
  5. Franklin C.L. et al.: Relaxation Enhancement Therapist Manual; http://www.mirecc.va.gov/visn16/docs/Franklin_Relaxation_Therapist_Manual.pdf

Simple Mental/Mind Relaxation Techniques Part 1

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As we indicated in the Simple Physical Relaxation Techniques blog, it is important that you take control and find some relaxation techniques that best assist you to relax and to control your stress levels and increase your emotional resilience. Once you have mastered the 4 exercises that you found or will find in our Physical Relaxation Techniques blog it is time to combine any one of these with some simple Mental/Mind Relaxation Exercises and find the one that works for you:-

RELEASING YOUR TROUBLES AND WORRIES

 Create a Picture in Your Mind

Think of a view or a place or an object that you find simple, quiet and inspiring or use one of the following.

simple_mental_part1_2simple_mental_part1_1simple_mental_part1_3simple_mental_part1_4

Study every minute detail in your mind.

If you are sitting on the sand on the beach, feel the aetting sun warming your face, feel the breeze on your skin, smell the ocean air, taste the salty tang on the breeze, hear the waves washing right up to you and as you hear each and every wave, release all of your stress and throw it onto the waves to wash out into the ocean …… take a bad feeling and do the same with this feeling and just release it to the waves, repeat with a troubled thought, or a person who riles you or who has upset you … do it with everything that has angered, troubled, annoyed, worried or upset you until you are totally relaxed and free from all troubles and worries.

When using the sunset …. Do the same as you imaging the colour changing and fading until you are free from all troubles and worries and looking at a beautiful starry night.

When using the rainbow … do the same as you climb higher onto the rainbow ……. with each step leave another thing behind you. Climb right to the top of the rainbow and view the world free from all troubles and worries and as you begin to make your way down the rainbow know that you remain free from all of you troubles and worries as you step into a field of beautiful flowers and lush grass.

When using the garden …. Smell the flowers, hear the bees, watch the sun glint on dragon fly wings, and as you go through the gate leave all of your troubles behind you and imagine yourself walking along a golden path into beautiful warm, fern forest. Wind the path back to the garden but notice that when you walk back into the garden your troubles and worries have all gone and you a free to enjoy the garden with a feeling of peace and serenity.

RELEASING PAIN AND DISCOMFORT

Body Scan Meditation

To practice the Body Scan Meditation, get into a comfortable position, by lying on a yoga mat on the floor or on a bed. You can use a pillow under your head. You can also sit in a chair on in the Yoga position. Use the Controlled Breathing or the Progressive Relaxation exercise from our Simple Physical Relaxation Technique blog and gently bring your awareness to the present.

1. Concentrate on a specific body part, e.g. your right arm. As you breathe deeply, scan that part of your body for sensations – heat, pain or burning. Notice the sensations but try not to get lost in thought and feel the heat, pain or burning. Repeat in your mind – “ALL HEAT, PAIN, or BURNING IS GONE”…………. Repeat three times

Gradually let your focus move to different body parts—each leg, your hips, stomach, chest, hands, arms, and head. And do the same.

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2. Practice the Body Scan Meditation and do not worry if you become aware of your mind’s tendency to drift to other thoughts. When you notice this happening, just let the thought go and gently bring your attention back to your body. If you have any pain or discomfort, just notice it, accept it, and release it using the mantra and continue scanning

The more you do this exercise the greater control you will achieve over your pain or discomfort.

Also read our blog “Stress, Anxiety, Depression and Psoriasis, Stressed about Psoriasis – Identify Your Stressors and Yours Stress Responses, Simple Physical Relaxation Techniques for Psoriasis Patients, Simple Mental/Mind Relaxation Techniques Part 2 – For Psoriasis Patients, Simple Mental/Mind Relaxation

 

 

REFERENCES

  •  National Center for Health Promotion and Disease Prevention (NCP); Manage Stress Workbook; http://www.prevention.va.gov/mpt/2013/docs/managestressworkbook_dec2013.pdf
  • Relaxation Techniques for Health: What You Need To Know; National Institutes of Health; U.S. Department of Health and Human Services; https://nccih.nih.gov/sites/nccam.nih.gov/files/Get_The_Facts_Relaxation_Techniques_02-06-2015.pdf
  • Progressive Muscle Relaxation; http://www.cci.health.wa.gov.au/docs/ACF3944.pdf
  • Manzoni G.M. et al.; Relaxation training for anxiety: a ten-years systematic review with meta-analysis ; BMC Psychiatry 2008, 8:41 doi:10.1186/1471-244X-8-41
  • Franklin C.L. et al.: Relaxation Enhancement Therapist Manual; http://www.mirecc.va.gov/visn16/docs/Franklin_Relaxation_Therapist_Manual.pdf