BrainImmune – Trends in Neuroendocrine Immunology http://www.brainimmune.com BrainImmune features up-to-date and cutting edge information on the brain– and stress–immune interactions and their impact on health and disease. Tue, 09 Apr 2019 19:02:39 +0000 en-US hourly 1 The 20 Most-Read BrainImmune Stories of 2018 http://www.brainimmune.com/most-read-brainimmune-2018/ Fri, 11 Jan 2019 12:31:46 +0000 http://www.brainimmune.com/?p=6905 – The greatest gift is the gift of learning (Native American saying) Over the past couple of years, each month we have posted the list of the top 10 most-viewed articles. You can find this by clicking on the  ‘Most-Read’ tab in the footer area of the BrainImmune Site. New for 2019, as we continue […]

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The greatest gift is the gift of learning (Native American saying)

Over the past couple of years, each month we have posted the list of the top 10 most-viewed articles. You can find this by clicking on the  ‘Most-Read’ tab in the footer area of the BrainImmune Site.

New for 2019, as we continue to evolve and learn, we introduce our first annual countdown for the 20 most-read articles on BrainImmune.

For 2018’s  annual list, the #1 most-read story is Walter Cannon: Homeostasis, the Fight-or-Flight Response, the Sympathoadrenal System, and the Wisdom of the Body. This article is authored by David S. Goldstein, M.D., Ph.D., a Senior Investigator at the National Institutes of Health (NIH), Bethesda, MD, USA. Dr. Goldstein is a recognized worldwide expert in physiology and neuroscience of the human autonomic nervous system, and an author of the Adrenaline and the Inner World: An Introduction to Scientific Integrative Medicine.

Walter CannonWalter Bradford Cannon, one of America’s leading physiologists, and former  Chairman of the Department of Physiology at Harvard Medical School (1906-1942), invented the terms and developed the concepts of ‘homeostasis’ (stability of the inner world);  the ‘Fight or Flight Response’, and The ‘Sympathoadrenal System’. In 1932, Cannon published The Wisdom of the Body, where he popularized the new term of the dynamic equilibrium/steady state of the internal milieu or homeostasis.

We believe that Goldstein’s article about Walter Cannon, in contrast to other sources available online, provides an extensive and comprehensive description and analysis of the nature of these concepts and how these three theories were developed in the first half of the 20th century. Of note, as per David Goldstein, Cannon’s notion of a unitary sympathoadrenal system endures to this day. Many situations, however, entail differential regulation of the sympathetic nervous system and adrenomedullary hormonal system.

Coming in at #2, somewhat surprisingly to us, is The Evolving Link between Social Media Addiction and Depression in Young Adults. At first glance, there is no a direct connection between social media overuse and health risks or neuroendocrine-immune dysfunction. But despite the recent message from the UK Royal College of Pediatrics that there is “no good evidence that time in front of a screen is ‘toxic’ to health, the articleDigital Media, Anxiety, and Depression in Children’ discussed in the above-mentioned social media seems to suggest the opposite. This article was published in Pediatrics, the official journal of The American Academy of Pediatrics.

Major depression is a common but serious mood disorder, where both neuroendocrine and immune dysfunctions play a major role. It is also known that major depression contributes to serious health hazards such as the development of cardiovascular diseases. Thus, the social media overuse, may in fact be linked to health risks and a neuroendocrine-immune dysfunction.

Our 3rd most-read story on the annual 2018 list is The Discovery of Adrenaline. This article is written by Profs. Ashley Grossman and David Jessop, two leading neuroendocrinologists and neuroscientists in the UK. The popularity of this fascinating story may suggest a high readership interest about the history and physiology of adrenaline (also known as epinephrine), a major stress hormone, and major player in regulation of homeostasis and the sympathoadrenal system (see above).

Interestingly, in our top 20 list, 4  articles are related to some historical perspectives of neurosciences and immunology:

Claude Bernard, the Father of Modern Physiology and Experimental Medicine (#5), written by Prof. Vincent Geenen, is in fact very much related to the Walter Cannon’s story mentioned above. In 1865, Bernard published his famous book ‘Introduction to the Study of Experimental Medicine, where he established the general principles of experimentation in physiology and medicine. Alexis Carel said of Bernard: “Before him, medicine was purely empirical. He is responsible for the introduction of the scientific method in the art of healing”. Two of the most famous passages and quotes in the history of physiology belong to Bernard, “The constancy of the internal environment is the condition for free and independent life…All the vital mechanisms, however varied they might be, always have one purpose, that of maintaining the integrity of the conditions of life within the internal environment.” Cannon invented the word homeostasis, but the concept of homeostasis was a direct extension from Bernard’s of the milieu intérieur.

Bartolomeo Eustachius and the Discovery of Adrenal Glands (#13) is directly connected to stress and the peripheral stress system, as the adrenals secrete the two major stress hormones, adrenaline and cortisol.

Hans Selye stressHans Selye and the Birth of the Stress Concept (#9) provides a fascinating story about the investigator who introduced in medicine the widely used and popular term ‘stress’, and how this concept evolved in the 1930s and 1940s. More information about Hans Selye is available at Hans Selye and the 80th Birthday of Stress Research and Stress: From Hans Selye to Paris Hilton.

The Discovery of Interferon, the First Cytokine, by Alick Isaacs and Jean Lindenmann in 1957 (#7).

These last 2 articles are unique – in that the one about the Hans Selye stress concept, and the one about the discovery of interferon, are written by Profs. Istvan Berczi and Derek Burke, two investigators who had the chance to work along Hans Selye and Alick Isaacs, respectively.

Interestingly, the short blog-style post Chronic Urticaria Linked to a Th2/Th17 Shift in Skin Lesions (#15) was our 2nd most unexpected article on the most-read list. This may simply indicate a relatively high readership interest about new evolving immune or neuroendocrine-immune mechanisms contributing to urticaria such as T helper (Th)2 and/or Th17 shift. Or, in addition, mechanisms involving the association between psychological stress and urticaria. This may also indicate a similar mechanism in Graves’ disease as outlined in another BrainImmune article entitled: ‘Stress-Induced Th2 Shift & Thyroid Autoimmunity: Unifying Hypothesis’.

According to the data we’ve compiled from our top 20 list, about  60-70% of our remaining articles pertain to the real, bona fide brain– and stress–immune interactions or neuroendocrine immunology. It appears that there is a continued interest about the role of lymphoid organs innervation, or the effect of different hormones and neuromediators on immune system’s function or homeostasis.

This includes the interactions between thyroid hormones, stress and the immune system leading to a Th1/Th2 imbalance or an increment in Th17/Treg ratio. Or, for example, the role of sex steroids hormones in immunoregulation or autoimmune disease activity, and the Nerve Growth Factor-inflammation interactions.

Importantly, the top 20 list also involves several articles suggesting the evolving links between:

Cross-talk dopamine and innate immunity figure 2‘The dopaminergic system and innate immunity’

‘Inflammation and fatigue’

‘Endogenous catecholamines and immune cells’

‘β2-adrenergic agonists and Parkinson’s disease’

‘The innate immune system and psychological stress’

‘Afferent vagus nerve stimulation and improvement of experimental joint inflammation’

In any case, here are the 20 most popular BrainImmune stories of 2018:

1.       Walter Cannon: Homeostasis, the Fight-or-Flight Response, the Sympathoadrenal System, and the Wisdom of the Body

By David Goldstein

2.       The Evolving Link between Social Media Addiction and Depression in Young Adults

By Ilia Elenkov

3.       The Discovery of Adrenaline

By Ashley Grossman and David Jessop

4.       Thyroid Hormone Modulation of Immune Responses in Physiologic and Stressful Conditions: Implications for Thyroid Diseases

By Graciela Cremaschi and Ana Maria Genaro

5.       Claude Bernard, the Father of Modern Physiology and Experimental Medicine

By Vincent Geenen

6.       Sex Hormones and Immunoregulation

By Marijke Faas, Paul de Vos and Barbro Melgert

7.       The Discovery of Interferon, the First Cytokine, by Alick Isaacs and Jean Lindenmann in 1957

By Derek Burke

Innervation lymphoid organs8.       Innervation of the Human Thymus and Spleen – an Overview

By Valsamo Anagnostou, Ipatia Doussis-Anagnostopoulou, Dina Tiniakos and Christos Kittas

9.       Hans Selye and the Birth of the Stress Concept

By Istvan Berczi

10.   The Cross-talk between the Dopaminergic System and Innate Immunity: An Evolving Concept

By Monica Pinoli

Edith Piaf and arthritis11.   Sex Steroids Hormones and Autoimmune Disease Activity

By Antonio Martocchia, Silvia Raja, Manuela Stefanelli, Anna Cocca and Paolo Falaschi

12.   Understanding the Role of Inflammation in Fatigue Requires Multidimensional Assessments

By Julie Lasselin, Bianka Karshikoff and Tina Sundelin

13.   Bartolomeo Eustachius and the Discovery of Adrenal Glands

By Rita Businaro and Angela Tagliani

14.   Endogenous Catecholamines in Immune Cells: Discovery, Functions And Clinical Potential as Therapeutic Targets

By Marco Cosentino, Natasa Kustrimovic and Franca Marino

15.   Chronic Urticaria Linked to a Th2/Th17 Shift in Skin Lesions

By Ilia Elenkov

16.   β2-Adrenergic Agonists for Parkinson’s Disease: Repurposing Drugs at the Crossroad of the Brain and the Immune System

By Marco Cosentino, Natasa Kustrimovic and Franca Marino

17.   The Innate Immune System Senses Psychological Stress through the ATP/P2X7R-Inflammasome (NLRP3) Cascade

By Javier Caso

18.   Afferent Vagus Nerve Stimulation Activates Brain Locus Coeruleus and Improves Experimental Joint Inflammation

By Gabriel Bassi

NGF19.   Nerve Growth Factor and Inflammation: A Complex Bidirectional Interaction

By Luisa Bracci-Laudiero

20.   The Glucocorticoid Receptor

By Tomoshige Kino

The post The 20 Most-Read BrainImmune Stories of 2018 appeared first on BrainImmune - Trends in Neuroendocrine Immunology.

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Neuroendocrine Immune Implications in Rheumatoid Arthritis and Polymyalgia Rheumatica: Past and Present Unresolved Issues and Optimising Glucocorticoid Treatment http://www.brainimmune.com/neuroendocrine-immune-implications-rheumatoid-arthritis-polymyalgia-rheumatica/ Sat, 08 Dec 2018 16:18:43 +0000 http://www.brainimmune.com/?p=6855 Editorial Introduction and background The dramatic effects of cortisone and pituitary adrenocortical hormone therapy on rheumatoid arthritis (RA) were discovered almost seven decades ago (1) and even longer for the significant disease amelioration during pregnancy as reported by Hench in 1938 (2). However, major questions persist about the underlying adrenocortical and hypothalamic pituitary axis (HPA) […]

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Editorial
Introduction and background

The dramatic effects of cortisone and pituitary adrenocortical hormone therapy on rheumatoid arthritis (RA) were discovered almost seven decades ago (1) and even longer for the significant disease amelioration during pregnancy as reported by Hench in 1938 (2).

However, major questions persist about the underlying adrenocortical and hypothalamic pituitary axis (HPA) predisposition to this disease and the optimal use of glucocorticoids (GCs) (3). A specific ongoing question is if GCs and other neuroendocrine immune (NEI) testing of individual RA patients can guide benefits to harms ratio in glucocorticoid therapy (3). Main considerations have been a constitutional insufficiency of the physiological adrenocortical and NEI system competency or response to stress or inflammation as discriminated from genetic or environmental activators of the immune and inflammatory pathways (3-5). As discussed in this Editorial, relative adrenal insufficiency in RA may contribute to systemic T helper (Th)1 shift and an amplification of the local pro-inflammatory activities in this condition (see Figure 1).

Figure 1 Neuroendocrine Immune Implications Rheumatoid Arthritis Polymyalgia Rheumatica

Figure 1. Adrenal insufficiency driving a T helper (Th)2 to Th1 shift and pro-inflammatory responses in rheumatoid arthritis (RA). In the pathogenesis of RA, a relative adrenal insufficiency could result in less systemic inhibition of the Th1 responses by glucocorticoids (GCs), and less potentiation of Th2 responses by gonadal deficiency, leading to Th1-mediated inflammation. Locally, pro-inflammatory factors including NE, CRH, SP and urocortin participate in persistence of chronic synovitis. Solid lines represent stimulation, while dashed lines inhibition. Abbreviations: APC, Antigen-presenting cell; CRH, Corticotropin-releasing hormone (peripheral); IL, interleukin; NE, norepinephrine; SP, substance P; TNF, tumor necrosis factor; Th, T helper lymphocyte; Th1, a type of effector T helper cell that promotes cell-mediated immune responses. Th2 cells exert mostly anti-inflammatory effects and counteract Th1 influences. Modified from: Calcagni E and I Elenkov, Stress system activity, innate and T helper cytokines, and susceptibility to immune-related diseases, Ann N Y Acad Sci. 2006 Jun; 1069:62-76.

Immunogenetic mechanisms operating within the immune system influence cytokine profiles and may affect disease susceptibility (6). The neuroendocrine and immune pathways complexly interact, and the primary dysfunction is not known, nor are the individual benefits to risks responses to GCs (7). The role of the individual’s neurohormonal background in these processes remains undefined. Hormonal imbalances are documented in immune-related diseases, but it is unclear whether this represents a secondary phenomenon or a primary “defect” related to specific neurohormonal immune phenotype(s) (6). The accumulated data suggest a bi-directional crosstalk between the neuroendocrine, sympathetic nervous system (SNS), and products of the immune system. Greater understanding of the underlying physiology of individual NEI function may guide improved therapy of RA with respect to GCs, related adrenocortical or hormonal therapy, and anti-inflammatory compounds.

Due to the complexity and difficulty of clinical studies on adrenal and HPA physiology (5), a predominant focus on the NEI negative feedback loop emerged (Figures 1, 2). This perspective became a paradigm for studies in selected autoimmune diseases, including RA and polymyalgia rheumatica/giant cell arteritis (PMR/GCA), as reviewed in this Editorial (6, 8-12). In healthy subjects, early studies showed that subcutaneously administered cytokines, like IL-6, induced a dose-dependent increase in the basal metabolism and higher HPA axis activity, with higher cortisol or plasma adrenocorticotropic hormone (ACTH) blood levels (13,14).

Such data suggest hypothalamic mechanisms, including secretion of corticotrophin-releasing hormone (CRH), mediating the influence of inflammatory molecules on the organism’s function. Moreover, IL-6 also provokes growth hormone (GH) and prolactin (PRL) secretion and suppresses thyroid stimulating hormone (TSH) (13,14). The ameliorating effects of pregnancy on rheumatoid arthritis (RA) and its dramatic improvement with pharmacologic doses of cortisone support the role for the HPA axis in RA (1,2).

Other evidences of interrelation between inflammatory processes, cytokine secretion and endocrine functions were studied on a second axis, constituted by the hypothalamus, pituitary gland and gonads (HPG) (15). The role of IL-1α was demonstrated to inhibit reproductive functions through an action on central nervous system and gonads (16, 17). A dysfunctional neuroendocrine-immune interface may play a specific role in the pathogenesis of RA (Figure 2), associated with abnormalities of the ‘systemic anti-inflammatory feedback’ and/or ‘hyperactivity’ of the local pro-inflammatory factors. Better understanding of the neuroendocrine control of inflammation may provide critical insights into mechanisms underlying RA and certain other common human immune-related diseases (18).

Figure 2 Neuroendocrine Immune Implications Rheumatoid Arthritis Polymyalgia Rheumatica

Figure 2. Neuroendocrine-immune feedback loop. Activation of the hypothalamic-pituitary-adrenal (HPA) axis, represented by the green-coded pathway, is a key component of the stress response to various stressors. Adrenal glucocorticoids such as cortisol mediate their negative feed-back, represented by the red-coded pathway. This effect is on the HPA, regulating not only their own adrenal secretion and promoting metabolic effects, but also exerting their immunosuppressive effects in the peripheral tissues. From: Cornelia M Spies, Rainer H Straub, Maurizio Cutolo and Frank Buttgereit, Circadian rhythms in rheumatology – a glucocorticoid perspective, Arthritis Res Ther. 2014 Nov 13;16 Suppl 2:S3 (Open Access).

Hormones and immune system studies in RA

Disparities in sex hormone concentrations seem to contribute to gender differences in autoimmune disorders (19). The anti-inflammatory role of androgens is recognized, but estrogens seem to exercise pro- and anti-inflammatory activities (15). During pregnancy, particularly the 3rd trimester, the increase of estrogens and progesterone may facilitate, or accompanying high cortisol levels, a Th2 shift systemically. In early postpartum, when these hormones return to normal or low normal levels, these changes may induce a rebound of IL-12 and TNF-α production and a Th1 shift. This may explain why Th1-related diseases such as RA and multiple sclerosis (MS) frequently remit during pregnancy, but exacerbate or have their onset in the postpartum period (18).

Physiological concentrations of estrogens boost immune and inflammatory activity, while progesterone (PG) and androgens, like testosterone and dehydroepiandrosterone (DHEA), have selective suppressive activity (20). In vitro, the adrenal androgen-like hormone, DHEA, inhibits IL-6 secretion in cultured human mononuclear cells (21). Serum levels of anti-inflammatory androgens are low in RA. This finding was attributed to a cytokine-induced block of androgen production in adrenal and gonadal glands and an increased conversion of androgens to oestrogens in inflamed tissues (8, 9).

Additionally, melatonin, a hormone secreted during the night by the pineal gland, seems to activate the immune system at normal to slightly elevated levels, and to worsen inflammatory conditions like RA (22, 23). Melatonin secretion is associated with changes in light/darkness periods and consequently it seems to be implicated in the circadian and seasonal rhythms and might contribute to the inflammatory pathways of autoimmune diseases (23, 24).

Rheumatoid arthritis

In RA patients, the hypothesis of a “relative adrenal insufficiency” was formulated, following the observation of reduced cortisol and adrenal androgens secretion (4,5). In particular, the alterations in HPA axis function in RA have been recognized mainly at the adrenal than pituitary or hypothalamic levels (25, 26). Such interpretation is supported by consistent findings of lower levels of adrenal androgens, particularly DHEAS, in premenopausal onset RA patients (27). Although, the findings likely reflect ongoing chronic inflammation, a role of neuroendocrine-related genetic factors such as SULT2A1 and HHEX genes in arthritis have been considered as well. Overall, effects of these DHEAS-related gene variants appear to be relatively small compared to other well-known factors such as age, complex interactions between DHEAS-associated genotypes and adrenal androgen hypofunction phenotype may exist in RA (28).

In support of the role of androgens in RA development, a recent study reported that an RA susceptibility gene polymorphism (rs1790834) encodes for a cofactor for 17, 20-lyase activity, cytochrome b5, on CYB5A gene, governing the decisive step of androgen synthesis (29). An association of RA with other adrenal androgen related genes, including ZKSCAN5 (rs11761528), SULT2A1 (rs2637125), HHEX (rs2497306), and ARPC1A (rs740160) were not confirmed in RA (30). In RA, increased oestrogen concentrations may produce activating effects on synovial cell proliferation, including macrophages and fibroblasts (31).

The cooperative anti-inflammatory coupling of sympathetic nervous system (SNS) and HPA axes functions may be deficient in RA. Low levels of cortisol in relation to SNS neurotransmitters may result in a pro-inflammatory predisposition (32) (Figure 2). In animals, SNS ameliorates collagen-induced arthritis (CIA) in the late phase of the disease, but can have a worsening effect in the pre-symptomatic phase.  One of the early phase effects of sympathetic nervous system activation may be the stimulation of CD4+CD25+ T cells (33,34).

In RA, cholinergic anti-inflammatory nerve fibres from the vagus nerve may have a role in reduction of inflammation. Their stimulation has an influence on disease activity score through inhibition of cytokine production (35,36). The reduced GC secretion, the circadian rhythmicity of symptoms and the release of pro-inflammatory cytokines have been better studied in RA than other diseases (37, 38) (Figure 3). The European League Against Rheumatism (EULAR) and more recently the American College of Rheumatology (ACR) have recommended exogenous glucocorticoid administration from the time of diagnosis, because it could act as a “replacement therapy” (39), which needs further study.

Figure 3 Neuroendocrine Immune Implications Rheumatoid Arthritis Polymyalgia Rheumatica

Figure 3. Relationship between clinical symptoms of RA and hormonal circadian rhythms. In rheumatoid arthritis (RA), clinical symptoms of joint stiffness, pain, and functional disability are commonly most severe in the early morning at around 5-6 am. This clinical worsening of RA in early morning precedes cortisol and testosterone peaks and the melatonin cessation by approximately 2-4 hours. Symptoms subsequently improve in early afternoon hours reflecting effects of immunosuppressive steroids and dip in proinflammatory hormones such as melatonin or prolactin. Modified from: Cutolo M., Glucocorticoids and chronotherapy in rheumatoid arthritis, RMD Open, 2016;2: e000203. doi:10.1136/rmdopen-2015-000203.

The prevention of the circadian up-regulation of the immune-inflammatory mediators has been shown to be more efficient symptomatically, if exogenous glucocorticoids are administered with a night-time-release formulation (40). The concept of chronotherapy in RA is advocated (41). The prevention/treatment of the night up-regulation of the immune/inflammatory reaction has been shown more effective symptomatically in RA and other chronic inflammatory conditions, when exogenous glucocorticoid administration is managed with a night-time-release formulation (42).

The Nobel Prize for Medicine in 2017 was awarded to studies on circadian rhythms, adding a further blueprint for advancement in chronotherapy (43). Circadian rhythms regulate, under action of biological clocks located both at the level of central nervous system and inside peripheral cells. The rhythms control several daily activities, embracing sleep, feeding times, energy metabolism, endocrine and immune functions with related pathological conditions.

Polymyalgia rheumatica/giant cell arteritis

The typical old age incidence of polymyalgia rheumatica/giant cell arteritis (PMR/GCA) is associated with the natural decline of adrenal androgen concentration, like DHEA, DHEAS and androstenedione (ASD), which is also associated with an increase of pro-inflammatory cytokines, including TNF-α and IL-6 (immunosenescence) (44). Low levels of DHEAS were significantly correlated with disease activity (7).

Cortisol levels at time of PMR diagnosis did not significantly differ from healthy controls, but, remained insufficient compared to the inflammatory status (10). The relative clinical insufficiency of endogenous glucocorticoids is supported by the excellent therapeutic response to low-pharmacologic doses of exogenous glucocorticoids (12).  Both the process of aging and the higher TNF-α concentrations were reported to reduce P450 17, 20-lyase activity, with a following decrease of DHEAS production by adrenal glands (10). Regarding IL-6, its concentrations are typically high in PMR/GCA, which stimulates CRH secretion in the hypothalamus and ACTH from the pituitary gland and in the adrenal glands (13). It influences the activity of enzymes involved in steroidogenesis (45).

Some authors hypothesize that, for successful immunosuppression, exogenous glucocorticoid administration could be accompanied by supplementation with DHEA and/or androstendione (ASD) (7). In PMR, the circadian rhythms of pro-inflammatory cytokine release were reported (46). A recent multicentre randomised double-blind study demonstrated a favourable short-term symptomatic efficacy of modified-release versus immediate-release prednisone in early treatment of glucocorticoid naive patients affected by PMR (46).

Conclusions

The altered cortisol and adrenal androgen (i.e. DHEAS and ASD) secretion, observed in the recent decades in RA and more recently in PMR patients (before treatment with glucocorticoids), should be considered as a “relative adrenal insufficiency” in the setting of a sustained inflammatory process, as shown for example by high serum IL-6 levels (47). Future research on the epigenetic mechanisms that mediate glucocorticoid actions and its drug resistance promise to offer biomarkers to optimise individual dose therapy in long term treatment. Chronotherapy with low dose GCs for long term administration seems advantageous (48).

Critically-designed physiologic and prospective controlled studies are needed to determine the effectiveness and safety of individualized GC dosing and other therapies that could modulate the neuroendocrine and immune systems. Such studies promise to clarify optimal GC therapy as well as other endocrine and anti-inflammatory treatments of musculoskeletal and rheumatic diseases (49), and to advance progress in the field.

Authors Affiliations

Maurizio Cutolo – Research Laboratories and Academic Division of Rheumatology, Postgraduate School of Rheumatology, Department of Internal Medicine, University of Genova, IRCCS Polyclinic Hospital San Martino, Genova, Italy; Richard Imrich –  Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovak Republic; Rainer Straub – Laboratory of Experimental Rheumatology and Neuroendocrine Immunology, University Hospital Regensburg, Germany. Ilia Elenkov – Brain Immune Media Ltd, Norwich, Norfolk, UK; Alfonse T. Masi – Division of Rheumatology, University of Illinois College of Medicine at Peoria, Peoria IL, USA.

Corresponding author, Maurizio Cutolo, email: mcutolo@unige.it


List of Non-Standard Abbreviations

ACTH, adrenocorticotropic hormone; CRH, Corticotropin-releasing hormone (peripheral); DHEA, dehydroepiandrosterone; GCs, glucocorticoids; GH, growth hormone; HPA, hypothalamic pituitary axis; IL, interleukin; NEI, neuroendocrine immune; PRL, prolactin (PRL), rheumatoid arthritis; PMR/GCA), rheumatica/giant cell arteritis;TNF, tumor necrosis factor; Th, T helper lymphocyte; TSF, thyroid stimulating hormone.


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  22. Cutolo M, Maestroni GJ. The melatonin-cytokine connection in rheumatoid arthritis. Ann Rheum Dis. 2005;64:1109-11.
  23. Forrest CM,  Mackay GM,  Stoy N,  Stone TW,  Darlington LG.  Inflammatory status and kynurenine metabolism in rheumatoid arthritis treated with melatonin. Br J Clin Pharmacol. 2007;64:517-26.
  24. Straub RH, Paimela L, Peltomaa R, Schölmerich J, Leirisalo-Repo M. Inadequately low serum levels of steroid hormones in relation to interleukin-6 and tumor necrosis factor in untreated patients with early rheumatoid arthritis and reactive arthritis. Arthritis Rheum. 2002;46:654-62.
  25. Imrich R, Rovensky J,  Malis F,  Zlnay M,  Killinger Z,  Kvetnansky R,  Huckova M,  Vigas M,  Macho L,  Koska J. Low levels of dehydroepiandrosterone sulphate in plasma and reduced sympathoadrenal response to hypoglycaemia in premenopausal womn with  rheumatoid arthritis. Ann Rheum Dis. 2005;64:202-6.
  26. Imrich R,  Vlcek M,  Kerlik J,  Vogeser M, Kirchhoff F,  Penesova A,  Radikova Z,  Lukac J,  Rovensky J. Determinants of adrenal androgen hypofunction in premenopausal females with rheumatoid arthritis. Physiol Res. 2014;63:321-9.
  27. Imrich R, Rovenský J. Hypothalamic-pituitary-adrenal axis in rheumatoid arthritis. Rheum Dis Clin North Am. 2010;36:721-7.
  28. Vernerova L, Mravcova M, Paulikova L, Vlcek M, Marko A, Meskova M, Penesova A, Rovensky J, Wendl J, Raslova K, Vohnout B, Jochmanova I, Lazurova I, Killinger Z, Steiner G, Smolen J, Imrich R. Contribution of Genetic Factors to Lower DHEAS in Patients with Rheumatoid Arthritis. Cell Mol Neurobiol. 2018;38:379-83.
  29. Mravcova M, Chovanova L,  Paulikova L, Vlcek M, Rovensky J, Killinger Z, Wendl J, Imrich R. Genetics of neuroendocrine factors in rheumatoid arthritis. Horm Metab Res. 2015;47:411-7.
  30. Stark K, Straub RH, Rovenský J, Blažičková S, Eiselt G, Schmidt M. CYB5A polymorphism increases androgens and reduces risk of rheumatoid arthritis in women. Arthritis Res Ther. 2015;17:56-64.
  31. Cutolo M, Capellino S, Montagna P, Villaggio B, Sulli A, Seriolo B, Straub RH. New roles for estrogens in rheumatoid arthritis. Clin Exp Rheumatol. 2003;21:687-90.
  32. Härle P, Straub RH, Wiest R, Mayer A, Schölmerich J, Atzeni F, Carrabba M, Cutolo M, Sarzi-Puttini PC. Increase of sympathetic outflow measured by neuropeptide Y and decrease of the hypothalamic-pituitary adrenal axis tone in patients with systemic lupus erythematosus and rheumatoid arthritis: another example of uncoupling of response systems. Ann Rheum Dis. 2006;65:51-6.
  33. Härle P, Pongratz G, Albrecht J, Tarner IH, Straub RH.  An early sympathetic nervous system influence exacerbates collagen-induced arthritis via CD4+CD25+ cells. Arthritis Rheum. 2008;58:2347-55.
  34. Capellino S, Cosentino M, Wolff C, Schmidt M, Grifka J, Straub RH. Catecholamine-producing cells in the synovial tissue during arthritis: modulation of sympathetic neurotransmitters as new therapeutic target. Ann Rheum Dis. 2010;69:1853-60.
  35. Levine YA, Koopman FA, Faltys M, Caravaca A, Bendele A,  Zitnik R, Vervoordeldonk MJ, Tak PP. Neurostimulation of the cholinergic antiinflammatory pathway ameliorates disease in rat collagen-induced arthritis. PLoS One. 2014;9:e104530.
  36. Koopman FA1, Chavan SS2, Miljko S3, Grazio S4, Sokolovic S5, Schuurman PR6, Mehta AD7, Levine YA8, Faltys M8, Zitnik R8, Tracey KJ2, Tak PP9. Vagus nerve stimulation inhibits cytokine production and attenuates disease severity in rheumatoid arthritis. Proc Natl Acad Sci U S A. 2016;113:8284-9
  37. Cutolo M. Rheumatoid arthritis: circadian and circannual rhythms in RA. Nat Rev Rheumatol. 2011;7:500-2.
  38. Cutolo M. Glucocorticoids and chronotherapy in rheumatoid arthritis. RMD Open. 2016;2:e000203.
  39. Straub RH, Cutolo M. Glucocorticoids and chronic inflammation. Rheumatology (Oxford). 2016;55(suppl 2):ii6-ii14.
  40. Cutolo M. Chronobiology and the treatment of rheumatoid arthritis.  Curr Opin Rheumatol. 2012;24:312-8.
  41. Paolino S, Cutolo M, Pizzorni C.  Glucocorticoid management in rheumatoid arthritis: morning or night low dose? Reumatologia 2017;55:189-97.
  42. Cutolo M, Sulli A, Pincus T. Circadian use of glucocorticoids in rheumatoid arthritis. Neuroimmunomodulation. 2015;22:33-9.
  43. Guo F, Yu J, Jung HJ, Abruzzi KC, Luo W, Griffith LC, Rosbash M. Circadian neuron feedback controls the Drosophila sleep–activity profile. Nature. 2016;536:292-7.
  44. Straub RH, Konecna L, Hrach S, Rothe G, Kreutz M, Schölmerich J, Falk W, Lang B. Serum dehydroepiandrosterone (DHEA) and DHEA sulfate are negatively correlated with serum interleukin-6 (IL-6), and DHEA inhibits IL6 secretion from mononuclear cells in man in vitro: possible link between endocrinosenescence and immunosenescence. J Clin Endocrinol Metab. 1998;83:2012-7.
  45. Mastorakos G, Chrousos GP, Weber JS Recombinant interleukin-6 activates the hypothalamic-pituitary-adrenal axis in humans. J Clin Endocrinol Metab. 1993;77:1690-4.
  46. Cutolo M, Hopp M, Liebscher S, Dasgupta B, Buttgereit F. Modified-release prednisone for polymyalgia rheumatica: a multicentre, randomised, active-controlled, double-blind, parallel-group study. RMD Open. 2017;3:e000426.
  47. Straub RH, Cutolo M, Zietz B, Schölmerich J. The process of aging changes the interplay of the immune, endocrine and nervous systems. Mech Ageing Dev. 2001;122:1591-611.
  48. Cutolo M. Circadian rhythms and  rheumatoid arthritis. Joint Bone Spine. 2018. Sep 15. pii: S1297-319X(18)30178.
  49. Burmester GR, Bijlsma JWJ, Cutolo M, McInnes IB. Managing rheumatic and musculoskeletal diseases – past, present and future. Nat Rev Rheumatol. 2017;13:443-448.

 

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Biology of Early Life Stress: Understanding Child Maltreatment and Trauma http://www.brainimmune.com/biology-early-life-stress-child-maltreatment-trauma/ Tue, 27 Nov 2018 10:13:37 +0000 http://www.brainimmune.com/?p=6828 The Biology of Early Life Stress: Understanding Child Maltreatment and Trauma is edited by Jennie G. Noll and Idan Shalev, and published by Springer. This innovative collection extends the emerging field of stress biology to examine the effects of a substantial source of early-life stress: child abuse and neglect. Research findings across endocrinology, immunology, neuroscience, […]

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Biology of Early Life StressThe Biology of Early Life Stress: Understanding Child Maltreatment and Trauma is edited by Jennie G. Noll and Idan Shalev, and published by Springer.

This innovative collection extends the emerging field of stress biology to examine the effects of a substantial source of early-life stress: child abuse and neglect. Research findings across endocrinology, immunology, neuroscience, and genomics supply new insights into the psychological variables associated with adversity in children and its outcomes.

These compelling interdisciplinary data add to a promising model of biological mechanisms involved in individual resilience amid chronic maltreatment and other trauma. At the same time, these results also open out distinctive new possibilities for serving vulnerable children and youth, focusing on preventing, intervening in, and potentially even reversing the effects of chronic early trauma.

Included in the coverage:

  • Biological embedding of child maltreatment
  • Toward an adaptation-based approach to resilience
  • Childhood Maltreatment and Pediatric PTSD: Abnormalities in Threat Neural Circuitry
  • Pediatric Posttraumatic Stress
  • Developmental traumatology: brain development and maltreated children with and without PTSD
  • Childhood maltreatment and pediatric PTSD: abnormalities in threat neural circuitry
  • Epigenetics and Early Life Adversity: Current Evidence and Considerations for Epigenetic Studies in the Context of Child Maltreatment
  • An integrative temporal framework for psychological resilience

The Biology of Early Life Stress is important reading for child maltreatment researchers; clinical psychologists; educators in counseling, psychology, trauma, and nursing; physicians; and state- and federal-level policymakers. Advocates, child and youth practitioners, and clinicians in general will find it a compelling resource.

About the Editors/Authors

Jennie G. Noll, Ph.D., is the Ken Young Family Professor for Healthy Children, in the Department of Human Development and Family Studies at Penn State University. She is also the director of the Penn State’s Child Maltreatment Solutions Network and the Principal Investigator of the NICHD P50 Translational Center for Child Maltreatment Studies.  Over the past 25 years, Dr. Noll has been the PI on NIH-funded research grants aimed at (1) the long-term developmental and physical health consequences of childhood sexual abuse, (2) pathways to teen pregnancy and motherhood for maltreated adolescents, (3) the cyber-hygiene and social media behaviors of abused teens, and (4) reversibility of neurocognitive deficits in abused and stress-exposed populations. Results from Dr. Noll’s work have been used to inform public policy recommendations for child abuse prevention and treatment as well as research priorities put forth by the Institute of Medicine and policy statements by the World Health Organization. As its Director, Dr. Noll supports the strategic goals of the Child Maltreatment Solutions Network; to raise the rigor of science, change trajectories for victims, mobilize public investment in prevention and treatment, and train and inspire the next generation of scientists, practitioners, and advocates who will coalesce to solve the complex issue of child maltreatment.

Idan Shalev, Ph.D., is the Mark T. Greenberg Early Career Professor for the Study of Children’s Health and Development and an Assistant Professor in the Department of Biobehavioral Health at Penn State University and a faculty member with the Child Maltreatment Solutions Network at Penn State University. Dr. Shalev’s research entails an interdisciplinary approach to identify mechanisms underpinning the biological embedding of stress across the lifespan. His research combines the disciplines of molecular genetics, endocrinology, neurobiology and psychology. Specifically, his research tests the effects of stress from early life on change in telomere length and other biomarkers of aging across the life course, and the consequences of change in telomere system for physical and mental health problems. Dr. Shalev’s current work explores temporal differences in gene expression and epigenetic changes in response to environmental stressors in the lab, as moderated by early life stress. His research aim to inform new targets for intervention studies to reverse the damaging effects of stress on our body and mind. He is the author of more than 40 scientific articles and chapters and serves on the editorial board of Telomere and Telomerase journal.

Print Length: 162 pages; Publisher: Springer; 1 edition (July 6, 2018).

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The Innate Immune Response to Noninfectious Stressors: Human and Animal Models http://www.brainimmune.com/innate-immune-response-noninfectious-stressors/ Mon, 26 Nov 2018 11:14:07 +0000 http://www.brainimmune.com/?p=6817 The Innate Immune Response to Noninfectious Stressors is edited by Massimo Amadori and published by Academic Press. The Innate Immune Response to Non-infectious Stressors highlights fundamental mechanisms of stress response and important findings on how the immune system is affected, and in turn affects such a response. In addition, this book covers the crucial link […]

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Innate Immune Response Noninfectious StressorsThe Innate Immune Response to Noninfectious Stressors is edited by Massimo Amadori and published by Academic Press.

The Innate Immune Response to Non-infectious Stressors highlights fundamental mechanisms of stress response and important findings on how the immune system is affected, and in turn affects such a response. In addition, this book covers the crucial link between stress response and energy metabolism, prompts a re-appraisal of some crucial issues, and helps to define research priorities in this fascinating, somehow elusive field of investigation.

  • Provides insights into the fundamental homeostatic processes vis-à-vis stressors to help in investigation
  • Illustrates the depicted tenets and how to offset them against established models of response to physical and psychotic stressors in both animals and humans
  • Covers the crucial issue of the immune response to endocrine disruptors
  • Includes immunological parameters as reporter system of environmental adaptation
  • Provides many illustrative examples to foster reader understanding

Some chapters of this book are listed below:

  • An Overview of the Innate Immune Response to Infectious and Noninfectious Stressors
  • Homeostatic Inflammation as Environmental-Adaptation Strategy
  • Metabolic Stress, Heat Shock Proteins, and Innate Immune Response
  • Innate Immune Responses and Cancer Metastasis
  • Modulation of the Interferon Response by Environmental, Noninfectious Stressors

Paperback: 276 pages; Publisher: Academic Press; 1 edition (March 3, 2016).

About the Editor: Professor Massimo Amadori is a Senior Scientist at the Istituto Zooprofilattico Sperimentale della Lombardia e dell’Emilia-Romagna (IZSLER), via A. Bianchi 9, 25124 Brescia, Italy.

Professor Amadori has developed tests of innate immunity in cattle for investigating animal health and welfare, and started and managed the Italian site of the European FMD vaccine Bank. He has been the official responsible for the Italian National Reference Centre for Animal Welfare, and has written 68 articles and chapters in the Journal of Interferon and Cytokine research, amongst others. He has an H index of 62.

Previous books published with the editor’s contribution: 1) “Acute Phase Proteins as Early Non-Specific Biomarkers of Human and Veterinary Diseases,” InTech, Open Access Publisher. 2) “Diagnostic Bacteriology Protocols, 2nd Edition,” Humana Press (Methods in Molecular Biology 345). 3) “New Research on Innate Immunity, Nova Science Publishers.

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The Bi-Directional Effects of Stress on our Immune System http://www.brainimmune.com/bi-directional-effects-stress-immune-system/ Mon, 26 Nov 2018 10:58:23 +0000 http://www.brainimmune.com/?p=6812 The Bi-Directional Effects of Stress on our Immune System is authored by Inna B. Mertsalova and published by FriesenPress. In recent years, we have gained increasing knowledge of the roles stress and stress hormones play in our health. It is amazing how the presentation of a stressor-whether in one event or a series of events-might […]

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Bi-Directional Effects Stress Immune SystemThe Bi-Directional Effects of Stress on our Immune System is authored by Inna B. Mertsalova and published by FriesenPress.

In recent years, we have gained increasing knowledge of the roles stress and stress hormones play in our health. It is amazing how the presentation of a stressor-whether in one event or a series of events-might involve us in appraising the environmental challenge and lead us to the “fight-or-flight” response on a physiological level.

The idea that stress has only harmful effects does not draw a full picture of its role in our health and well-being. It is scientifically proven that stress and stress hormones not only have a negative impact on our bodies, but they also have potentially beneficial properties, aimed at mobilizing our immune system for fighting immunologic confrontations. How does this work?

In The Bidirectional Effects of Stress on Our Immune System, Dr. Inna B. Mertsalova illustrates how our immune system functions under exposure to stress. Understanding these processes can help us cope with stress and stay healthy.

Paperback: 204 pages; Publisher: FriesenPress (May 2, 2017)

About the Author: Inna B. Mertsalova was awarded a PhD in health psychology from Walden University, in addition to already obtained an MSc in psychology and an MA in English and French linguistics. She has performed extensive research in psycho-oncology, focusing on how humans’ vulnerability to stress reactions might influence the physiological state of the body. Believing that knowledge empowers us to understand how we become ill due to stress, she provides the results of health psychology research to the public by writing literature reviews. For more information, visit drinnamertsalova.com.


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Psychosocial Stress and Cardiovascular Disease in Women: Concepts, Findings, Future Perspectives http://www.brainimmune.com/psychosocial-stress-cardiovascular-disease-women/ Sun, 25 Nov 2018 11:51:20 +0000 http://www.brainimmune.com/?p=6806 Psychosocial Stress and Cardiovascular Disease in Women is edited by Kristina Orth-Gomér, Neil Schneiderman, Viola Vaccarino and Hans-Christian Deter, and published by Springer. Not long ago, it was assumed that coronary heart disease mainly–or only–affected men. Now that CHD is recognized as a leading killer of women as well as men, numerous research studies have […]

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Psychosocial Stress Cardiovascular Disease WomenPsychosocial Stress and Cardiovascular Disease in Women is edited by Kristina Orth-Gomér, Neil Schneiderman, Viola Vaccarino and Hans-Christian Deter, and published by Springer.

Not long ago, it was assumed that coronary heart disease mainly–or only–affected men. Now that CHD is recognized as a leading killer of women as well as men, numerous research studies have been made of its diverse presentations in women, causal factors, and possibilities for prevention and treatment.

The expert contributions to Psychosocial Stress and Cardiovascular Disease in Women span the results of this cross-disciplinary awareness. This progressive resource takes a three-dimensional approach to its subject, focusing on epidemiology and risk factors for heart disease in women, the psycho- and neurobiology of stress and coronary disease, and promising clinical interventions. Chapters identify and analyze multiple intersections of social, biological, and psychological factors in affecting women’s heart health, from the social dimensions of depression to genetic/environmental interactions to the demands of balancing work and family. These wide-ranging findings will assist and motivate professionals in choosing and creating interventions, developing appropriate prevention strategies, and reducing gender-based disparities in health care. Among the topics covered:

  • Enhancing women’s heart health: a global perspective.
  • Coronary heart disease in women: evolution of our knowledge.
  • Gender observations on basic physiological stress mechanisms in men and women.
  • Sleep as a means of recovery and restitution in women
  • Life Skills training: benefiting both genders, for different reasons.
  • Gender considerations in psychosocial-behavioral interventions for coronary heart disease.

In particular this book will be helpful for cardiologists and other clinicians who may ask themselves why patients do not seem to make rational choices. “Why do patients not follow the advice they are offered?” is a common complaint. The role of psychosocial stress for patient compliance and adherence can be traced throughout the volume. It is emphasized in the chapters on psychosocial interventions along with other tangible and conceptual suggestions and experiences with psychosocial stress and life style change.

Psychosocial Stress and Cardiovascular Disease in Women offers a deep practical level of understanding of this epidemic to help expand the work of health and clinical psychologists, sociologists, cardiologists, primary care physicians, and epidemiologists.

Some chapters of this book are listed below:

  • Coronary Heart Disease in Women: Evolution of Our Knowledge
  • Psychosocial Risk Factors for Coronary Heart Disease in Women: The Stockholm Studies of Women’s Hearts
  • Depression and Cardiovascular Disease in Women: Behavioral and Biological Mechanisms Involved in this Association
  • On Basic Physiological Stress Mechanisms in Men and Women: Gender Observations on Catecholamines, Cortisol and Blood Pressure Monitored in Daily Life
  • Psychoneuroimmunological Pathways and Sex Differences in Coronary Artery Disease: The Role of Inflammation and Estrogen
  • Neurobiology of Early Life Stress in Women
  • Gender Considerations in Psychosocial–Behavioral Interventions for Coronary Heart Disease
  • How Did the Stress Reduction Program Help Women to Survive? The Patient’s View in the SWITCHD Study

Paperback: 324 pages; Publisher: Springer; Softcover reprint of the original 1st ed. 2015 edition (August 23, 2016).

 

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Takotsubo (Stress) Cardiomyopathy, an Issue of Heart Failure Clinics http://www.brainimmune.com/takotsubo-stress-cardiomyopathy-book/ Sun, 25 Nov 2018 11:40:19 +0000 http://www.brainimmune.com/?p=6802 Takotsubo (Stress) Cardiomyopathy, an Issue of Heart Failure Clinics is authored by Eduardo Bossone and Raimund Erbel, and published by Elsevier. Stress-induced cardiomyopathy, also known as “Takotsubo” cardiomyopathy, broken heart syndrome and apical ballooning syndrome, was first described in Japan, in 1990, by Sato et al. Stress-induced cardiomyopathy represents a transient left ventricle systolic dysfunction […]

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Takotsubo (Stress) CardiomyopathyTakotsubo (Stress) Cardiomyopathy, an Issue of Heart Failure Clinics is authored by Eduardo Bossone and Raimund Erbel, and published by Elsevier.

Stress-induced cardiomyopathy, also known as “Takotsubo” cardiomyopathy, broken heart syndrome and apical ballooning syndrome, was first described in Japan, in 1990, by Sato et al.

Stress-induced cardiomyopathy represents a transient left ventricle systolic dysfunction with electrocardiographic changes that can mimic acute myocardial infarction and minimal release of myocardial enzymes in the absence of obstructive coronary artery disease.

Recent research indicates that myocardial inflammation is an important component of the pathophysiology behind stress-induced cardiomyopathy. Specifically, the stress-induced inflammation, and mostly catecholamine-induced inflammation, might represent the driving force leading to the development of acute symptoms and transiently altered ventricular contractility.

Moreover, a recent PNAS study found that the acute heart injury induced by an experimental PTSD stress model is associated with underlying biological injury processes and alterations of key molecular processes, including an inflammatory response. According to the authors of this study, the finding of acute heart injury in this PTSD animal model suggests common stress-induced heart impairment.

The Takotsubo (Stress) Cardiomyopathy book, in this issue of Heart Failure Clinics, covers stress (takotsubo) cardiomyopathy. Expert authors review the most current information available about imaging modalities, clinical profile, natural history, management, and different types of stress cardiomyopathy. Keep up-to-the-minute with the latest developments in diagnosing and managing this condition.

Series: The Clinics: Internal Medicine (Book 9); Hardcover: 269 pages; Publisher: Elsevier; 1 edition (April 26, 2013).

About the Authors: Eduardo Bossone, Affiliations and Expertise, University of Salerno, Italy; Raimund Erbel, Affiliations and Expertise, University Duisburg-Essen, Essen, Germany.

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Stress and Cardiovascular Disease http://www.brainimmune.com/stress-cardiovascular-disease-book/ Sat, 24 Nov 2018 11:26:00 +0000 http://www.brainimmune.com/?p=6785 Stress and Cardiovascular Disease is edited by Paul Hjemdahl, Annika Rosengren and Andrew Steptoe and published by Springer. An increasing body of evidence indicates that psychological stress and cardiovascular diseases are intertwined more closely than initially suspected about 4-5 decades ago. In fact, many clinical and epidemiological studies have documented the link between psychological stress […]

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Stress and Cardiovascular DiseaseStress and Cardiovascular Disease is edited by Paul Hjemdahl, Annika Rosengren and Andrew Steptoe and published by Springer.

An increasing body of evidence indicates that psychological stress and cardiovascular diseases are intertwined more closely than initially suspected about 4-5 decades ago. In fact, many clinical and epidemiological studies have documented the link between psychological stress and cardiovascular disease.

Stress and Cardiovascular Disease provides an up to date survey of research, highlighting the clinical implications of physiological and population studies of stress.

Each chapter addresses a particular aspect of this exciting field of basic and clinical research.  This multidisciplinary volume will serve as an aid to physicians in their management of stress-related issues in cardiac patients and high-risk individuals.

The main aim of this book is to evaluate the concept of stress and provide tools for physicians to identify patients who might benefit from stress management. This will incorporate a detailed description of the physiological and pathophysiological consequences of acute and chronic stress that might lead to cardiovascular disease.

The book aims to critically evaluate interventional research (behavioral and other therapies) and provides evidence based recommendations on how to manage stress in the cardiovascular patient. The book defines and highlights stress as an etiological factor for cardiovascular disease, and describes an evidence based “tool box” that physicians may use to identify and manage patients in whom stress may be an important contributing factor for their disease and their risk of suffering cardiovascular complications.

Some chapters of this book are listed below:

  • Social Stress and Cardiovascular Disease in Primates
  • Cardiovascular and Autonomic Responses to Stress
  • Sympathetic Neural and Adrenal Medullary Mechanisms in Depression and Panic Disorder
  • Hypothalamic–Pituitary–Adrenal Axis and Cardiovascular Disease
  • Stress, Inflammation, and Coronary Heart Disease
  • Stress Cardiomyopathy
  • The Causal Role of Chronic Mental Stress in the Pathogenesis of Essential Hypertension
  • The Psychological Treatment of Cardiac Patients

Paperback: 404 pages; Publisher: Springer; 2012 edition (23 Nov. 2014).

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Neuro-Endocrine Basis of Immune Modulation: in Response to Stress and Relaxation http://www.brainimmune.com/neuro-endocrine-basis-immune-modulation-book/ Sat, 24 Nov 2018 11:12:25 +0000 http://www.brainimmune.com/?p=6782 The Neuro-Endocrine Basis of Immune Modulation is authored by Nazmul Haque, Mahbub E Sobhani and Asif Ahmed, and published by VDM Verlag Dr. Müller. Traditional medical science has kept the mind separate from the body. In particular, neurosciences and immunology developed independently for many years, and thus, the question of how the brain communicates with […]

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Neuro-Endocrine Basis of Immune ModulationThe Neuro-Endocrine Basis of Immune Modulation is authored by Nazmul Haque, Mahbub E Sobhani and Asif Ahmed, and published by VDM Verlag Dr. Müller.

Traditional medical science has kept the mind separate from the body. In particular, neurosciences and immunology developed independently for many years, and thus, the question of how the brain communicates with the immune system remained enigmatic until fairly recently.

Now people realize that the psyche and the soma are constantly interacting, and recent evidence indicates that the central nervous system receives messages from the immune system and vice versa messages from the brain regulate immune functions.

In this respect, neuroendocrine-immunology or psychoneuroimmunology is the new evolved science that describes such kind of interactions. Many studies show that psychological stress (acute or chronic) has immune modulatory activity.

In this book a typical psycho-neuro-endocrine-immune network has been shown. From this network Corticotrophin Releasing Factor (CRF), Adrenocorticotrophic Hormone (ACTH), glucocorticoids (GC), β-endorphin and Met-enkephalin are found as important endocrine components, and T cells, B cells, monocytes/macrophages, Natural Killer (NK) cells and their cytokines that is Tumor Necrosis Factor-α (TNF-α), interferon gamma (IFN-γ) and interleukins such as IL-1, IL-2, IL-4, IL-6, IL-10, IL-12 etc. are found as important immune components.

Finally, it has been shown that, acute or chronic stress have different immune modulatory activities, which are harmful to one’s homeostasis, and relaxation can help to maintain that homeostasis.

Paperback: 144 pages; Publisher: VDM Verlag Dr. Müller (September 14, 2011).

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Psychological Factors and Cardiovascular Disorders: The Role of Stress and Psychosocial Influences http://www.brainimmune.com/psychological-factors-cardiovascular-disorders-book/ Fri, 23 Nov 2018 11:27:23 +0000 http://www.brainimmune.com/?p=6771 Psychological Factors and Cardiovascular Disorders is edited by Leo Sher, and published by Nova Kroshka Books. Psychological factors significantly affect the cardiovascular system and play an important role in the etiopathogenesis of cardiovascular disorders. In fact, psychological stress in childhood, adulthood or persistent across a person’s life can contribute to high cardiovascular and metabolic risk. […]

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Psychological Factors and Cardiovascular DisordersPsychological Factors and Cardiovascular Disorders is edited by Leo Sher, and published by Nova Kroshka Books.

Psychological factors significantly affect the cardiovascular system and play an important role in the etiopathogenesis of cardiovascular disorders. In fact, psychological stress in childhood, adulthood or persistent across a person’s life can contribute to high cardiovascular and metabolic risk. Also, low stress resilience during youth increase in the risk of developing hypertension in later life.

For the past several decades attention to the psychosocial and behavioral factors in cardiovascular disease has increased significantly. However, the association of proinflammation with stress and cardiovascular disease processes has only recently emerged in the scientific focus.

Multiple lines of evidence suggest that psychosocial factors contribute significantly to coronary heart disease as evidenced by data relating risk to depression, anxiety, personality factors and character traits, social isolation, and chronic life stress.

Furthermore, individuals with PTSD have dysfunctional hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS), the two branches of the peripheral stress system. These individuals also have a higher risk of cardiovascular conditions such as hypertension and stroke, with an increased basal heart rate and blood pressure.

When psychological stresses also tend to cluster together, risk for cardiac events is often substantially elevated, equaling or exceeding that associated with standard biomedical risk factors for coronary disease such as hypertension and hypercholesterolemia.

Understanding the integration of the interactions among multiple psychological and biological factors in the regulation of the cardiovascular system and the development of cardiovascular disorders is an important challenge for future research.

This book will contribute to this goal. The contributors to this book are the leading international experts in the field of the relation between psychological processes and cardiovascular disorders.

This book will be of interest to physicians, psychologists, mental health counselors, other clinicians, medical and psychology students, medical residents, and the general public.

Hardcover: 468 pages; Publisher: Nova Kroshka Books; 1 edition (January 1, 2009).

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