- Symptom orientation!
- Autism!
- Cancer!
- Fibromyalgia!
- Psoriasis
- Multiple Sclerosis!
- Osteomalacia!
- More about VitaminD!
1. Symptom orientation!
General view on distraction from solutions by declaring the symptoms of the diseases to be their reasons.
https://geoarchitektur.blogspot.com/p/symptom-orientation-autism-cancer.html
Chapters of this article have been put into separate pages, but the content list and numbering of the chapters ist kept as original.
2. Autism!
Symptom orientation: Autism - A collection of scientific studies!
https://geoarchitektur.blogspot.com/p/symptom-orientation-autism-collection.html
3. Cancer
Symptom orientation: Cancer - A collection of scientific studies!
4. Fibromyalgia
Symptom orientation: Fibromyalgia - A collection of scientific studies!
5. Psoriasis
Psoriasis
Cold Spring Harb Perspect Med. 2014 Aug; 4(8): a015354.
doi: 10.1101/cshperspect.a015354 PMCID: PMC4109580
Paola Di Meglio,1,4 Federica Villanova,2,3,4 and Frank O. Nestle2,3
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4109580/
"Psoriasis is a common chronic inflammatory skin disease with a spectrum of clinical phenotypes and results from the interplay of genetic, environmental, and immunological factors. Four decades of clinical and basic research on psoriasis have elucidated many of the pathogenic mechanisms underlying disease and paved the way to effective targeted therapies. Here, we review this progress and identify future directions of study that are supported by a more integrative research approach and aim at further improving the patients' life."
"Psoriasis affects 2%–4% of the population in Western countries, with prevalence rates influenced by age, geographic location, and genetic background (Chandran and Raychaudhuri 2010)."
"Prevalence is higher in adults (from 0.91% to 8.5%) as compared with children (from 0% to 2.1%) with a dual peak of incidence: ∼30–39 years and ∼60 years of age. Disease prevalence is different across countries, with a geographical pattern suggesting less prevalence in those closer to the equator as compared with the more distant ones, in line with the beneficial effects of UV radiation exposure and clinical amelioration of psoriasis (Hart et al. 2011). Prevalence in Europe varies from 0.73% to 2.9%, similar to the Unites States (0.7%–2.6%) and higher than Latin America, Africa, and Asia ..."
"Plaque-Type Psoriasis
Plaque-type psoriasis, occurring in 85%–90% of affected patients, is the most common form of psoriasis and is characterized by oval or irregularly shaped, red, sharply demarcated, raised plaques covered by silvery scales (Fig. 1A–C) (van de Kerkhof and Nestle 2012)."
"Guttate Psoriasis
Guttate psoriasis, from the Latin “gutta” for tear drop, is characterized by multiple small scaly plaques usually occurring around the trunk and upper arms and thighs. The rash has often sudden onset, usually within 2–4 wk after a bacterial infection of the upper ways, notably streptococcal pharyngitis in children and young adults, and is therefore associated with type I psoriasis (Griffiths et al. 2007)."
"Generalized Pustular Psoriasis
GPP, also known as von Zumbush psoriasis, is a rare but potentially life-threatening disease characterized by episodic, widespread skin and systemic inflammation."
"Erythrodermic Psoriasis
Erythrodermic psoriasis, one of the rarest forms of psoriasis (1%–2.25% of patients with psoriasis), represents the most severe phenotype; it carries substantial morbidity and can be potentially life threatening (Boyd and Menter 1989)."
"PSORIATIC ARTHRITIS
About 20%–30% of psoriasis patients develop a seronegative, chronic inflammatory muscoskeletal disorder named psoriatic arthritis (PsA), which occurs, in most cases, about a decade after the appearance of psoriasis (Gladman et al. 2005)."
"PsA can affect different tissues (synovium, cartilage, bone, entheses, tendons); it presents common involvement of distal joints, asymmetric articular distribution, erythema over-affected joints, spinal involvement, and enthesitis (Gladman et al. 2005) and eventually leads to erosion and loss of function of the affected areas."
"Because ∼80% of the patients develop PsA following psoriasis (Ellinghaus et al. 2012b), PsA is sometime considered as a disease within a disease (Eder et al. 2011)."
"Nevertheless, PsA shares several key cellular and molecular mediators with psoriasis, such as lymphocytes infiltrating the inflamed skin or joint (Pitzalis et al. 1996; Shen et al. 2006) and critical cytokines such as tumor necrosis factor (TNF), IL-23, and IL-17 (Gullick et al. 2010). Genetic association with class I HLA molecules and clinical evidence supports an important role of CD8 T cells in PsA, with the presence of oligoclonally expanded CD8 T cells in the joint fluids of individuals with active PsA (Costello et al. 2001). TNF is a critical disease player as it is in psoriasis and ∼70% of patients successfully respond to anti-TNF therapy in terms of signs and symptoms improvement, and, in some cases, also by radiographic progression (Anandarajah and Ritchlin 2009)."
"The systemic manifestation of the disease results in comorbidities including, but not limited to, metabolic syndrome, cardiovascular disease (CVD), diabetes, depression, and cancer (Griffiths and Barker 2007)."
"Finally, psoriasis carries a severe psychosocial burden with anxiety, depression, and perceived stress appearing at a higher rate in psoriasis patients (O’Leary et al. 2004)."
"ENVIRONMENTAL TRIGGERS
In contrast to the fast-growing list of psoriasis susceptibility genes, the environmental factors concurring in initiating the disease are still ill-defined. Among known environmental triggers of psoriasis, there are drugs, infections, physical trauma, smoking, alcohol, and stress."
"Disease Initiation
One of the best-characterized initiation mechanisms, leading to dysregulated skin immune responses, involves KCs releasing the cationic antimicrobial peptide (AMP) LL-37 following physical trauma (Koebner phenomenon) or infection. LL-37 binds to self-DNA/RNA fragments (Lande et al. 2007; Ganguly et al. 2009) also released by damaged skin cells (Ganguly et al. 2009; Lin et al. 2011), forming LL-37/self-DNA/RNA complexes found in psoriasis lesions."
"THERAPY
In common with other immune-mediated complex diseases, there is no definitive cure for psoriasis, and available treatment is only to decrease disease activity and improve symptoms."
"Therapies are administered according to disease severity and assessed by the Psoriasis Area and Severity Index (PASI, ranging from 0 to 72), which takes into account appearance and extension of the lesions."
Why only vitamin D "analogs", not real vitamin D?
Why not UVA/UFB phototherapy from the beginning?
"Classic therapies span from topical treatments (emollients, topical corticosteroids, vitamin D analogs) used in mild-to-moderate psoriasis, to UVA/UVB phototherapy or systemic therapies reserved to moderate-to-severe cases.
Among systemic therapies, which include retinoids, methotrexate, and cyclosporine, the folic acid antagonist methotrexate, which has immunosuppressive, cytostatic, and anti-inflammatory activity and is rather inexpensive, is often used as first line of treatment. However, classic therapy has not completely met patients’ needs, especially in the most severe cases.
In the past decade, a better understanding of disease immunopathogenesis has been successfully translated into new drugs, known as “biologics,” targeting key inflammatory mediators and currently representing an effective third-line therapy in moderate-to-severe psoriasis patients, unresponsive to nonbiologic systemic agents."
"Anti-T-Cell Therapies
The first biologic to be approved was Alefacept in 2003, a lymphocyte function-associated antigen (LFA)-3/IgG1 fusion protein binding CD2 on T cells and, thus, selectively inducing apoptosis of CD2+ human memory-effector T cells in vivo (da Silva et al. 2002), although further studies suggested a broader immunomodulatory effect (Chamian et al. 2005; Haider et al. 2007). Clinical efficacy was shown in phase III studies with 40% of patients achieving a PASI75 response (75% reduction of the PASI) (Krueger et al. 2002) and more that 50% achieving PASI 50 (50% reduction of the PASI) (Lebwohl et al. 2003a)."
"A second anti-T-cell strategy was approved in 2003 and consisted of a humanized antibody (Efalizumab) binding and blocking CD11a, a key molecule for T-cell activation and migration through the circulation into the skin (Jullien et al. 2004)."
"Despite a good efficacy profile, efalizumab (Gordon et al. 2003; Lebwohl et al. 2003b;Leonardi et al. 2005, 2008a; Menter et al. 2005; Gottlieb et al. 2006; Papp et al. 2006) has been withdrawn from the market in 2009 because of three cases of progressive multifocal leukoencephalopathy (Tan and Koralnik 2010), highlighting the importance of carefully monitoring the long-term safety of immunomodulatory therapies."
"Anticytokine Therapies
An alternative strategy to anti-T-cell targeting aims at interfering with the psoriasis cytokine network (Nickoloff 1991) by using anticytokine biologic drugs.
TNF blockade, using etanercept, a human p75 TNF receptor fusion protein (approved in 2004), infliximab, a humanized chimeric anti-TNF monoclonal antibody (approved in 2006), or adalimumab, a fully human monoclonal antibody (approved in 2008) is another effective therapeutic strategy.
[Adaalimumab is sold as HUMIRA:
https://www.humira.com/]
[Etanercept is sold as ENBREL:
https://www.enbrel.com/]
Etanercept efficacy have been shown in three phase III trials with about 50% of patients achieving PASI75 at week 12 in the high-dose group (Leonardi et al. 2003;Papp et al. 2005, 2011d; Tyring et al. 2006). TNF neutralization causes early down-modulation of myeloid cell-related genes, with decrease of Th17 cell products and downstream molecules in just 2 wk after commencing therapy (Gottlieb et al. 2005; Zaba et al. 2007; Johansen et al. 2010). Interestingly, only patients who downregulate the expression of Th17 pathway genes successfully respond to etanercept treatment (Zaba et al. 2007; Zaba et al. 2009c)."
[Ustekinmab is sold as STELARA:
http://www.janssen-med.de/stelara]
"The latest biologic to be approved for psoriasis in 2009, ustekinumab, is a monoclonal antibody simultaneously blocking the heterodimeric proteins IL-12 and IL- 23 via its biding to the shared subunit p40. Its efficacy is quite high, with 67% of patients achieving PASI75 at 12 wk of treatment (Leonardi et al. 2008b; Papp et al. 2008)."
"Some serious adverse events, such as opportunistic infections and reactivation of latent tubercolosis, have been reported for these monoclonal antibodies (Sivamani et al. 2013). Long-term safety data (up to 4 and 5 yr treatment) are now available for etanercept and ustekinumab (Leonardi et al. 2003; Papp et al. 2005, 2012d, 2013a; Tyring et al. 2006), suggesting a safe use of these drugs."
"A number of other biologic drugs is currently (mid-2013) being investigated in clinical trials. In line with the prominent role of IL-23/IL-17 axis in psoriasis, two antibodies (guselkumab [formerly CNTO1959] and MK-3222) targeting the specific IL-23p19 subunit are in phase II and III, respectively (Janssen 2013; Merck 2013a,b)."
"Monoclonal antibodies blocking either IL-17A (ixekizumab and secukinumab) (Leonardi et al. 2012; Papp et al. 2013b; Rich et al. 2013) or IL-17R brodalumab (Papp et al. 2012b) have shown striking efficacy in phase II clinical trials with >70% of patients achieving PASI75 and more than half receiving a remarkable PASI90. Although phase III clinical trials are currently ongoing (Amgen 2013a,b,c; Eli Lilly 2013a,c,d,e,f; Novartis 2013b), initial molecular data showed that the effect of IL-17 blockade on expression of genes synergistically regulated by IL-17 and TNF-α is greater than in previous studies with anti-TNF therapy (Krueger et al. 2012)."
"Notwithstanding the efficacy of the biologic drug currently available in the clinic, at least one third of patients do not respond to biologic therapy (Gudjonsson et al. 2012) or lose initial responsiveness because of the development of antidrug antibodies (ADA), which causes decreased drug efficacy and/or induction of adverse events (Sathish et al. 2013; Vincent et al. 2013). Moreover, biologic drugs pose a considerable economical burden because of their costs (Poulin et al. 2009; Liu et al. 2012). Finally, a sizable number of patients with mild-to-moderate psoriasis still rely on traditional topical treatments."
Influence of Vitamin D Status and Vitamin D3 Supplementation on Genome Wide Expression of White Blood Cells: A Randomized Double-Blind Clinical Trial
PLoS One. 2013; 8(3): e58725.
Published online 2013 Mar 20. doi: 10.1371/journal.pone.0058725 PMCID: PMC3604145
Arash Hossein-nezhad,1 Avrum Spira,2 and Michael F. Holick1,* Moray Campbell, Editor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3604145/
"Conclusion/Significance
Our data suggest that any improvement in vitamin D status will significantly affect expression of genes that have a wide variety of biologic functions of more than 160 pathways linked to cancer, autoimmune disorders and cardiovascular disease with have been associated with vitamin D deficiency. This study reveals for the first time molecular finger prints that help explain the nonskeletal health benefits of vitamin D."
"These results suggest that to maximize vitamin D's effect on gene expression may require even higher doses than 2000 IUs of vitamin D3 daily."
"Vitamin D supplementation has proven skeletal health benefits [3],[4], particularly in individuals at risk for vitamin D deficiency. "
Vitamin D and its role in psoriasis: An overview of the dermatologist and nutritionist
Rev Endocr Metab Disord. 2017; 18(2): 195–205.
Published online 2017 Feb 7. doi: 10.1007/s11154-017-9411-6 PMCID: PMC5486909
Luigi Barrea,1 Maria Cristina Savanelli,1 Carolina Di Somma,2 Maddalena Napolitano,3 Matteo Megna,4Annamaria Colao,5 and Silvia Savastano
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5486909/
"The dermatologist’s point of view
Patients suffering from psoriasis present a broad range of clinical phenotypes. Psoriatic lesions are classified into plaque, guttate, pustular, and erythrodermic types according to clinical features, especially regarding lesions size and distribution [1]. Disease onset may occur at any age, including childhood, with two peak age ranges, 16 to 22 and 57 to 60 years [2, 3]. Psoriasis lesions are characterized by hyper-proliferation with incomplete differentiation of epidermal keratinocytes and decreased keratinocyte apoptosis, associated with inflammatory cellular infiltrate in both dermis and epidermis [12]. Psoriasis Area and Severity Index (PASI) score is currently the preferred method for the assessment of the disease severity and extent [13]."
"Effects of vitamin D on skin biology
The role of vitamin D as main regulator of skin physiology is very complex (Table (Table1).1).
The epidermis is composed of four layers:
- basal layer (stratum basale),
- spinous layer (stratum spinosum),
- stratum granulosum and stratum corneum.
The process of epidermal differentiation is complex, sequential, and tightly controlled [11].
The precursor of vitamin D, 7-dehydrocholesterol, is located in the membranes of keratonocytes of the basal and spinous layer of epidermis [10].
By the action of UVB (wavelength between 290 and 315 nm), via a photochemical reaction, the B ring of 7-dehydrocholesterol is broken to form pre-vitamin D3 or cholecalciferol, which is subsequently converted first to 25-hydroxyvitamin D (25OHD) by the enzymes CYP27A1 and CYP2R1 and then to 1,25-hydroxyvitamin D (1,25(OH)D or calcitriol) the active form of vitamin D, by CYP27B1 [15].
Physiologically, the active form of vitamin D and its receptor regulate the differentiation and proliferation of keratinocytes, the balance of the cutaneous immune system and the process of apoptosis.
The 1,25(OH)D has been shown to exert anti-proliferative effects on keratinocytes [16]. Numerous in vitro and in vivo studies have demonstrated dose-dependent effects of vitamin D on proliferation and differentiation of keratinocytes. Of interest, low concentration of vitamin D promotes keratinocyte proliferation in vitro, while at higher pharmacological doses a clear inhibitory effect became apparent [14, 17].
Moreover, 1,25(OH)D and analogs reduce S100A7 levels, generally up-regulated in psoriatic skin, in the reconstituted human epidermis stimulated by IL-22 [18], in interleukin (IL)-17-stimulated keratinocytes and in skin of patients with psoriasis [19].
Indeed, 1,25(OH)D regulates the cell proliferation in the stratum basale and increases the synthesis of keratins (K1 and K10), involucrin, transglutaminase, loricrin, and filaggrin, in the stratum spinosum [11, 14, 15].
Furthermore, vitamin D helps to regulate the synthesis of glycosylceramides needful for the barrier integrity and permeability in the stratum corneum [11, 14, 17]. These actions are due to the capacity of vitamin D to regulate intracellular calcium level, through induction of the calcium receptor, and the phospholipase C enzymes [19, 20].
A decrease or deficiency in 1,25(OH)D or a loss-of-function of its receptor has been shown to disrupt the differentiation of the epidermis, with reduced levels of involucrin and loricrin and loss of keratohyalin granules, resulting in hyperproliferation of the basal layer [11, 21–23]."
"Vitamin D regulation of apoptosis in keratinocytes
Calcitriol stimulates the synthesis of ceramide by inducing the neutral Mg2+-dependent sphingomyelinase (thereby increasing the conversion of sphingomyelin to ceramide) and in return, ceramide enhances the pro-differentiating effect of calcitriol on keratinocytes in a feedback loop [10, 24]. It has been demonstrated that physiological concentrations of calcitriol do not initiate apoptosis in cultured keratinocytes but, in contrast, pharmacological concentrations of calcitriol exert a pro-apoptotic effect on keratinocytes [25]."
"Effects of vitamin D on the cutaneous immune system
Psoriasis pathogenesis implicates the innate and adaptive segments of the immune system. In particular, it is centrally controlled by T cells, in which an important role is played by T-helper (Th)1, Th17 and Th22, interplaying with numerous cell types via different cytokines, including tumour-necrosis factor-α (TNF-α), IL-6 and IL-17 [26]. The activity of these cells is modulated by specific T lymphocytes, named regulatory T cells (Treg) [9]. Regulatory T cells (Tregs) are able to inhibit the immunological response and to preserve the cutaneous immunological homeostasis, preventing autoimmune response against self-antigens [27]."
"Vitamin D and psoriasis linkage
In psoriasis, vitamin D is involved in the maintenance of cutaneous barrier homeostasis. Several studies identified an association between polymorphisms of vitamin D receptor (VDR) and psoriasis susceptibility [9]. Richetta et al., have found that the A-1012G promoter polymorphism of the VDR gene is associated with psoriasis risk through a lower expression of VDR mRNA, favoring conditions that may alter cutaneous barrier and the development of psoriatic lesions [31]. In addition, in psoriatic skin a decreased expression of VDR and reduced tight-junction proteins is associated [32]. Tight junctions are fundamental to regulate adhesion and permeability of keratinocytes, and to polarize cutaneous cell differentiation, to regulate extracellular calcium gradient, interacting with nuclear and cytoplasmic proteins and influencing the regulation of specific genes involved in keratinocytes differentiation and proliferation [32, 33]. Different studies have focused on the possible role of low vitamin D status in the pathogenesis of psoriasis [34–36]."
"Indeed, several studies reported that vitamin D is a key modulator of inflammation function [37, 38]. The active metabolite of vitamin D exert an anti-inflammatory effect on the inflammatory profile of human monocytes/macrophage [39–42], down-regulating the expression and production of several pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, and IL-8 [43]. Moreover, dendritic cells differentiation, maturation, chemotaxis and antigen presentation seem to be dampened, and hydrogen peroxide secretion in human monocytes is also activated by 1,25(OH)D resulting in an increased oxidative burst potential [9, 44]. These anti-inflammatory effects support a role a low vitamin D status in the pathogenesis of psoriasis. Recent studies have shown that 1,25(OH)D values are significantly lower in psoriatic patients than in control subjects, even after adjusting for confounding factors in a multivariate analysis [11, 35]. In another study, vitamin D levels were lower in women with psoriasis in comparison with men, a difference not observed among controls [45]. Therefore, low levels of vitamin D are negatively associated with markers of inflammatory activation (C-reactive protein, CRP) and obesity [35]. Moreover, other studies showed that serum vitamin D levels were also reduced in patients with psoriatic arthritis and being inversely linked to disease activity [46, 47]."
"Topical vitamin D in psoriasis treatment
The beneficial effects of vitamin D induced by exposure to sunlight in the treatment of psoriasis have been known for decades. The effectiveness on psoriasis of vitamin D and its derivatives (calcitriol, calcipotriol, tacalcitol, hexafluoro-1,25(OH)D and maxacalcitol) have been known since 1985, being confirmed in numerous trials [45, 48]. The therapy with vitamin D, is one of the most popularly prescribed topical medications for this disease as the first-line, singly or in combination with topical corticosteroids, and numerous studies documented the efficacy and safety of using topical calcipotriol in the treatment of cases of localized plaque psoriasis [49–54]. Vitamin D analogs are particularly helpful for hard-to-treat areas such as the face or inguinal regions that are sensitive to steroid-induced atrophy [55]. Vitamin D analogs do not exhibit tachyphylaxis, as seen with corticosteroids, and topical treatment can be continued indefinitely without serious adverse side effects [9, 55]. Additionally, they are effective in the treatment of psoriatic skin lesions in children and elderly population [56–58]. A recent meta-analysis on the effectiveness of topical vitamin D therapies evidenced not only comparable efficacies to corticosteroids when used as monotherapy, but also superior effects when vitamin D used in combination with a potent topical steroid. According to these results, as topical vitamin D derivatives demonstrated a favorable safety profile, with “steroid-sparing” effects, and should be considered an indispensable component of the current physician’s arsenal in the treatment of psoriasis [11].
The therapeutic effects of topical vitamin D occur via a VDR mediated genomic mechanism resulting in inhibition of keratinocyte proliferation and mediated non-genomic mechanisms inducing keratinocyte differentiation by increasing intracellular calcium levels [59]. The anti-inflammatory effects may also result from inhibition of production of IL-2, IL-6, and interferon-gamma (IFN-γ). Further, topical calcipotriol inhibits human beta defensin and proinflammatory cytokines which are found in increased levels in psoriatic lesions [60]. Allelic variations in individual VDR genes may determine a different response to treatment: the isoform A of VDR is associated with a greater therapeutic response in psoriatic patients [61]."
"The nutritionist’s point of view
Severe psoriasis has been associated with nutritional deficiencies because of an accelerated loss of nutrients, in particular of vitamin D, from the hyperproliferation and desquamation of the epidermal layer of skin [62–64]. Vitamin D supplementation is of particular interest to Nutritionists for two important reasons. First, besides its topical use, oral vitamin D supplementation represents an important adjunctive treatment option for psoriatic patients [9]; second, vitamin D supplementation might be very important for the prevention of psoriasis-related comorbidity [65], hypertension [66] and metabolic syndrome [67]."
"Food and vitamin D
There are two ways to meet vitamin D requirements in mammals: via nutrition and via synthesis in skin by from the sun or other UVB source [8]. Several recommendations were published regarding the dietary intake of vitamin D [68–70]. In particular, these recommendations they refer to dietary reference intakes for calcium and vitamin D updated by the Institute of Medicine (IOM) in 2010 [71]. To date, as the evidence for extra-skelatal effects of vitamin D are inconsistent and insufficient, the intake recommendations were based on beneficial effects of vitamin D only on skeletal health. The Recommended Dietary Allowances (RDAs) covering requirements of ≥97.5% of the population are shown in Table Table2.2. Other organizations recommended different RDAs: the Endocrine Society suggested that adults aged 19–50 years require at least 600 international unit (IU) of vitamin D daily to maintain bone and muscular function [72]. However, the task force further annotated that 1500–2000 IU per day are necessary to consistently raise the serum level of 25(OH)D above 30 ng/mL. Finally, for older adults aged 60 and above, the International Osteoporosis Foundation (IOF) recommended a RDA of 800–1000 IU in order to reach a serum 25(OH)D level of 30 ng/mL [73]."
"The diet is an important determinant of vitamin D status [71, 74]. Some studies have calculated that the amount of vitamin D intake that would ensure that the majority of the population (97.5%) maintains plasma 25(OH)D concentrations >25 nmol/l throughout the year is 8.7 mg/d [75]. Only few foods contain naturally vitamin D, and these foodstuffs are mainly of animal origin. The vitamin D status is the sum from the combination of synthesis in the skin after sun exposure and intake of the two main dietary forms of vitamin D: ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3) [76]."
"The fish (especially fatty fish and fish liver) have the highest natural content of vitamin D [80] Also egg yolk has a high vitamin D3 content [80], which strongly correlates with the content of vitamin D3 of the hen’s feed [77]. Depending on the hen’s diet [81] and UVB exposure [82], the vitamin D3 and 25(OH)D3 were transferred from the hen to the egg yolk. Regarding of meat products, the content of vitamin D depends on the contents of vitamin D in the fodder, the fat content of the meat product, and latitude where the animals have grazed [83]. Finally, the vitamin D3 is also available through dietary supplements, and is the form present in vitamin D-fortified foods such as milk, orange juice, and cereals. The fortification of food with vitamin D has been considered to be the most promising strategy with the broadest reach and impact [84–86]. In fact, in countries where this strategy was adopted proved to have a significant influence on the daily vitamin D intake in the average adult [87]. The food sources of vitamin D are listed in Table Table33 [88]."
"Bioavailability and influence of processing and cooking
The vitamin D, like other fat-soluble vitamins (A, E, K), is absorbed incorporated in mixed micelles from the intestine into the enterocytes by non-saturable passive diffusion. Subsequently, the vitamin D is transported in the chylomicrons via lymph to the circulation [89]. The more polar metabolite 25(OH)D is absorbed better and faster than vitamin D because it is also taken up directly from the proximal jejunum into the portal vein [79]. There are few data on its availability from natural sources. The absorption of vitamin D from supplements may differ depending on the used vehicle substance, such as oils, powders, ethanol [90]. For example, it has been reported that the bioavailability of vitamin D from fortified hard cheese is equivalent to supplements [91] and that vitamin D bioavailability is not influenced by the fat content of the fortified milk [92]."
"The cooking does not much influence the vitamin D content of animal foods. Mattila et al. [93] found that, in eggs boiled for 10 min, the vitamin D3 concentration was 1–6% lower and 25(OH)-D-3 content was 6–11% lower compared with raw eggs. In addition, also in fish, the cooking effect was moderate: baking various kinds of fish (e.g., perch, rainbow trout, Baltic herring) in the oven at 172 °C or 200 °C for 20 min induced a vitamin D3 loss of 93]. The stability of vitamin D3 and 25(OH)D and vitamin D2 in foodstuffs during cooking has been shown to vary widely with heating process and foodstuffs, with reported retentions in eggs, margarine and bread after boiling, frying and baking of between 40% and 88% [94]."
"The nutritionist and vitamin D supplementations
Supplements are the most important determinant of variation in vitamin D intake [85, 86, 95] A number of studies showed that the daily intake of vitamin D was higher in adults using vitamin D supplements than in those without vitamin D supplementations (348 IU vs 84 IU of vitamin D) [86]. Most nutritionists recommend the use of vitamin D3 to treat and prevent vitamin D deficiency, because several studies indicating a higher efficacy for vitamin D3 in raising serum 25(OH)D concentrations when compared to vitamin D2 [96]. Although a significant inter-individual variation exists, due to different variables including body weight, sunlight exposure and calcium intake, it has been calculated that supplementation of 1000 IU of vitamin D3 daily leads to an approximate increase in 25(OH)D levels by 10–20 ng/mL (25–50 mmol/L), [97–99]. Findings from randomised placebo-controlled trials conducted during the winter have shown that each 1 mg of supplemental vitamin D is associated with an increase in serum 25(OH)D of between 0.7 nmol/L [100] and 2 nmol/L [75]."
"Several studies have observed the safety concerns regarding the dosage of vitamin D supplementation. However, oral vitamin D intakes of up to 10,000 IU daily were not associated with any harmful effects [101], since this dose is comparable to the maximum cutaneous vitamin D production, and reports of vitamin D intoxication from cutaneous synthesis alone do not exist [101]. In this context, the IOM and the European Food and Safety Authority (EFSA) recommend a safe tolerable upper intake level of 4000 IU vitamin D perday for all adults, including pregnant and lactating women [102], although, to date, very few studies have investigated the long-term effects of a vitamin D intake above the suggested threshold of 4000 IU per day [103, 104]. To reach a steady state, after two to three consecutive months of treatment with vitamin D supplementation, it’s necessary a re-measurement of 25(OH)D serum levels [98]."
"Thus, the Nutritionists should consider a general vitamin D supplementation in populations at high risk for vitamin D deficiency, such as psoriatic patients [105]. The compounds of vitamin D commonly used in clinical trials varied from 1,25(OH)D, the physiologically active form of vitamin D, to 1αOHD, alfa-calcidol, requiring only liver metabolism to be converted to the active form to vitamin D or cholecalciferol, requiring both liver and kidney metabolism to become active. Perez et al. observed an overall 88% of clinical improvement of psoriasis with oral vitamin D with a decrease in mean PASI scores [61]. The results were confirmed in different studies on limited number of patients, reporting moderate or greater improvement in psoriasis in 25–50% of subjects [106–109]. It has also been proposed the therapeutic use of systemic alpha-calcidol in patients with psoriatic arthritis [61]. Another study demonstrated that a combination of acitretin and oral calcitriol resulted in a faster reduction of PASI in patients of chronic plaque psoriasis [110]. A study on a large population sample including 70,437 US females over a period of 14 years, examined the vitamin D intake levels and the incidence of psoriasis in the population. After adjusting for confounding variables, the study found that there was no significant association between vitamin D intake (dietary, supplementary, and total vitamin D) and the risk of incident psoriasis. Thus, the authors proposed that there was no role of dietary or supplemental vitamin D intake to prevent the development of psoriasis [111]. However, current recommendations for dietary intake of vitamin D are based only on its effect on skeletal health, while no information is present as regards psoriasis. In addition, a discrepancy between recommended RDAs and actual daily vitamin D intake exists. Therefore, solutions like food fortification and personalized diet or vitamin D supplementation in psoriatic patients need to be developed. In addition, taking into account the common association among psoriasis, obesity and Mets of which will be discussed in the next chapter, the advantage of the potential use of oral vitamin D supplementations to treat psoriasis and metabolic syndrome concurrently through its anti-inflammatory effects was strongly supported by a comprehensive meta-analysis including the results of clinical trials using vitamin D supplementation in psoriasis [106]."
"Conclusions
Due to its role in proliferation and maturation of keratinocytes, vitamin D has become an important local therapeutic option in the treatment of psoriasis. Indeed, significant associations between low vitamin D status and psoriasis have been systematically observed. Although the exact role of vitamin D in the pathogenesis of psoriasis is unclear, understanding the possible bi-directional relationships between low vitamin D status and psoriasis is also important for delineating the risk profile for co-morbidities that may result from psoriasis, such as obesity, type 2 diabetes, and MetS. To date, the successful treatment based on adequate dietary intake of vitamin D or oral vitamin D supplementation in psoriasis represent an unmet clinical need and the evidence of its beneficial effects remains still controversial. Nevertheless, the Nutritionists should consider a general vitamin D supplementation in populations at high risk for vitamin D deficiency, such as psoriatic patients. This information is important either for Dermatologists and Nutritionists to increase the knowledge on the potential usefulness of vitamin D in psoriasis with the aim to reduce not only its clinical severity, but also cardiac risk factors and psoriasis co-morbidities. Future well-designed dietary intervention trials with vitamin D supplementations on large population samples are needed to define the specific dose of vitamin D supplementations for psoriasis.
1,25(OH)D, 1,25-hydroxyvitamin D or calcitriol; 25OHD, 25-hydroxyvitamin D; BMI, body mass index; CRP, C -reactive protein; IL, interleukin; MetS, metabolic disease; PASI, psoriasis area and severity index; RDAs, recommended dietary allowances; TNF, tumor necrosis factor;VDR, vitamin D receptor."
Vitamin D and its role in psoriasis: An overview of the dermatologist and nutritionist
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5486909/
How might vitamin D help with psoriasis?
https://www.medicalnewstoday.com/articles/314549.php
Psoriasis and vitamin D deficiency
https://www.health.harvard.edu/diseases-and-conditions/psoriasis-and-vitamin-d-deficiency
How might vitamin D help with psoriasis?
https://www.medicalnewstoday.com/articles/314549.php
6. Multiple Sclerosis
7. Osteamalacia
Symptom orientation: Multiple Sclerosis - A collection of scientific studies!
https://geoarchitektur.blogspot.com/p/symptom-orientation-multiple-sclerosis.html
8. More about VitaminD
Symptom orientation: More about VitaminD - A collection of scientific sources!https://geoarchitektur.blogspot.com/p/symptom-orientation-more-about-vitamind.html
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