wpływ wit D na panel hormonalny.

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Witamina D jest podzielona na dwa rodzaje D 1,25 OH jest to hormon który powinien być w średniej wartości normy jak jest wysoki to zaburza inne hormony LH test, gonadotropowy, jądra, TSH, receptory insulinowe, jest odpowiedzialny za skórę, za kości, włosy może powodować osteoporozę. Wynikiem jego wysokiego poziomu jest obniżenie zawartości wit D 25 OH w organizmie i skutkiem tego wszystkie te powyższe niedomogi.
Sorry za słaby wygląd rysunku ale musiałem go zmniejszyć i tak wyszło

[fallenursus]

Nikt nie zwraca na to uwagi, a nie dobrze. Wit d i jej poziom jest jednym z największych rzeczy na które powinnismy uważać. Od dłuższego czasu suplementuje i różnica jest kolosalna w samopoczuciu jak i uodpornieniu na przeziębienia itd. Gruba wiekszosc osób ma niedobór

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ja tez mam niedobór z badania w 2005r wyszło że witaminy d 025oh mam zaledwie 9 a hormonu d1,25oh wysoko ponad norme ktora jest do 40 a ja miałem 68.

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Science behind vitamin D
A number of studies have suggested that patients with chronic inflammatory diseases are deficient in 25-hydroxyvitamin D ([link widoczny dla zalogowanych Użytkowników]) and that consuming greater quantities of vitamin D, which further elevates 25-D levels, alleviates disease symptoms.
Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress inflammation, which is in line with the reports of short-term symptomatic improvement. The simplistic first-order mass-action model used to guide the early vitamin studies is now giving way to a more complex description of action.
When active, the [link widoczny dla zalogowanych Użytkowników] (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key [link widoczny dla zalogowanych Użytkowników]. Additionally, recent research on the Human Microbiome shows that bacteria are far more pervasive than previously thought, dramatically increasing the possibility that the spectrum of chronic diseases is bacterial in origin.
Emerging molecular evidence suggests that symptomatic improvements among those administered vitamin D is the result of 25-D’s ability to temper bacterial-induced inflammation by slowing VDR activity. While this results in short-term palliation, persistent pathogens that influence disease progression proliferate over the long-term.
Forms and structure of vitamin D
Main article: [link widoczny dla zalogowanych Użytkowników]
All forms of vitamin D are secosteroids, sharing a close structural and functional resemblance to steroids. The full implications of a “vitamin” acting as a steroid has yet to be fully appreciated by many in the research community. The overlap between steroids and secosteroids is key to understanding the [link widoczny dla zalogowanych Użytkowników]. It explains how a “vitamin” can exert short-term palliative effects and long-term harm. Patients on the MP are advised to avoid consuming vitamin D, because of its immunomodulatory effects.
Steps for synthesis of vitamin D
There are a number of vitamin D metabolites in the body. The steps by which one form of vitamin D changes into the next are as follows:

• The body has natural stores of [link widoczny dla zalogowanych Użytkowników], a [link widoczny dla zalogowanych Użytkowników] precursor.
• When exposed to energy, specifically ultraviolet light, 7-dehydrocholesterol becomes pre-vitamin D3.
• Pre-vitamin D3 spontaneously isomerizes to Vitamin D3 via a process called sigmatropic shift.
• In addition to the endogenous production of Vitamin D3, people get D3 from animal meats. Vitamin D2 is found in plants and fungi, and is functionally similar to D3.
• Vitamin D3 and D2 are hydroxylated in the liver, and becomes 25-hydroxyvitamin D (25-D).
• 25-D is further hydroxylated by the enzyme 1α-hydroxylase, into the main biologically active hormone [link widoczny dla zalogowanych Użytkowników] (1,25-D). While this reaction was originally thought to occur only in the kidneys, is now known to take place in tissues throughout the body, including within white blood cells called macrophages.

[IMG]file:///C:\DOCUME~1\RAFA~1\USTAWI~1\Temp\msohtmlclip1\01\c lip_image001.gif[/IMG]
The foundation of the Marshall Pathogenesis is “Figure 1,” a graphic which appeared in Trevor Marshall's 2008 Bioessay.
It's important to understand that the body tightly regulates the different forms as it might a steroid.
Metabolism of vitamin D and the Vitamin D Receptor in chronic disease
Main article: [link widoczny dla zalogowanych Użytkowników]
A number of studies have suggested that patients with chronic inflammatory diseases are deficient in [link widoczny dla zalogowanych Użytkowników] (25-D) and that consuming greater quantities of vitamin D, which elevates 25-D levels, alleviates symptoms of disease. Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress [link widoczny dla zalogowanych Użytkowników], which is in line with the reports of symptomatic improvement. The simplistic first-order mass-action model used to guide the early vitamin studies has given way to a more complex description of action. When active, the [link widoczny dla zalogowanych Użytkowników] (VDR) affects transcription of at least 913 genes and impacts processes ranging from calcium metabolism to expression of key [link widoczny dla zalogowanych Użytkowników].
Located in the nucleus of a variety of cells including immune cells, the VDR is a control system of sorts. When exposed to infection and damage, especially that which is caused by pathogens, the body begins to convert the inactive form 25-D into the active form, [link widoczny dla zalogowanych Użytkowników]. As cellular concentrations of 1,25-D increase, 1,25-D activates the VDR, turning on any number of genes the receptor transcribes.
According to a 2010 analysis, the VDR significantly affects 229 human genes. Many of these genes have long been associated with [link widoczny dla zalogowanych Użytkowników] and [link widoczny dla zalogowanych Użytkowników] including, for example, the genes IRF8 (linked to [link widoczny dla zalogowanych Użytkowników]), and PTPN2 (connected to [link widoczny dla zalogowanych Użytkowników] and [link widoczny dla zalogowanych Użytkowników]).[link widoczny dla zalogowanych Użytkowników] The activation of certain genes also leads to the synthesis of

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antimicrobial peptides. The antimicrobial peptides are the body's “natural antibiotics” and have a potent anti-bacterial effect.
However, bacteria create ligands, which like 25-D, inactivate the VDR and, in turn, the innate immune response. This allows the microbes to proliferate. In response, the body increases production of 1,25-D from 25-D, leading to one of the hallmarks of chronic inflammatory disease: a low 25-D and a high 1,25-D.
This pattern is a result of the disease process rather than a cause. For a variety of reasons, neither increased consumption of vitamin D nor the body's synthesis of additional 1,25-D is ultimately effective at combatting infection.
Supplemental vitamin D tends to be immunosuppressive
Related section: Sunlight can be immunosuppressive
Supplemental vitamin D has been widely lauded for conferring immunosuppressive effects.
Vitamin D affects the immune system at many levels and by a number of mechanisms…. Vitamin D has multiple immunosuppressant properties…. On the whole, vitamin D confers an immunosuppressive effect.
Aronson, Amital, and Shoenfeld 2
Supplemental vitamin D is being touted as having a wide range of benefits in different diseases. A puzzling picture that emerges from the totality of the diseases that they are claimed to affect beneficially, is the belief that supplemental vitamin D will both reduce infections and suppress the immune system at the same time. While it is clear that there exist substances that can be “immunomodulating”, implicating that it can increase production/release of both immunosuppressive and immune activating substances, the important question is what the overall effect is. It is hard to envision that a substance can have strong anti-infectious properties while at the same time having a strong immune suppressive effect.
Supplemental vitamin D show no consistent effects on infection
In studies on acute respiratory tract infection3, tuberculosis4 and overall infections5, the effects of vitamin D have been mixed (and largely unsuccessful) in terms of reducing infectious burden.
A complete evaluation of the above mentioned studies, and the differences between them that can help explain the different results, is not suited for this article. However, on a general basis, one of the reasons for differing effects may be that vitamin D works differently in relatively healthy people as compared to sick people. Thus, vitamin D supplementation may give a marginal benefit in preventing infections in healthy people (see section below), but not in sick people. As of today (Dec 2012) we are not aware of any studies that have shown an actual reduction in infections in sick people (for instance tuberculosis or COPD) by vitamin D supplementation, as measured by culture or genetical detection methods. Furthermore, a general trend seems to be that apparent beneficial effects on infection in healthy people are not seen in individuals who have 25-hydroxyvitamin D levels within the normal range678, adding, as a side point, further weight to the mega dose vitamin D supplementation craze being without merit.
It is however not certain, in spite of some reported benefits in a few studies, that any level of supplementation is beneficial in terms of reducing infection. The studies are still too few to draw firm conclusions, and publication bias, as in any field science, may skew the overall results. Another factor which makes the reported benefits doubtful is that not all studies have reported an actual reduction in infection, but merely symptom based outcomes. Symptom based outcomes are relevant, but in light of the symptom reducing effects therapies that are immune suppressive may have, it is not clear that symptom reduction in the vitamin D supplementation studies are due to an actual reduction in infection. Further, most of the symptoms in upper respiratory tract infections are caused by the body's own immune response, and not the infectious agents9.
In sick people vitamin D supplementation increases infectious burden, and suppresses the immune system:
• monocytes – According to a 2011 interventional study in which patients with multiple sclerosis were given high doses of vitamin , peripheral blood mononuclear cells (monocytes) lose “abnormal reactivity” at 40 ng/mL.10
• Epstein Barr virus – In a 2010 study of pregnancy-associated breast cancer, higher levels of 25-D were positively correlated with serum antibodies to Epstein Barr Virus, suggesting that EBV is able to better proliferate in patients who take vitamin D.11
• toll-like receptors – As discussed elsewhere, the toll-like receptors (TLR) represent an ancient front-line defense system that enables the host organism to sense the presence of microbial components within minutes. As inducers of inflammation, TLRs act as important triggers of distinct entities such as sepsis or autoimmune disease exacerbation.12 For example, found that the TLRs are naturally upregulated in the autoimmune disease, Behcet's disease.13 However, a 2006 study showed that vitamin D3 suppresses the expression of TLR2 and TLR4 protein and mRNA in human monocytes in a time- and dose-dependent fashion.14 Dickie et al. further showed that expression of TLR9 was downregulated in monocytes by vitamin D3 supplementation.15
• reduction in levels of inflammation – A 2011 study showed that in colorectal adenoma patients, the vitamin D supplementation group, TNF-alpha decreased 13%, IL-6 32%, IL-1 beta 50%, and IL-8 15% relative to placebo.16
• short-term symptom resolution – Further evidence for vitamin D’s activity as an immunosuppressant comes in the range of reports of short-term symptom resolution in autoimmune patients taking vitamin D. Online forums are full of such reports.
Role in select diseases and conditions
The following articles discuss the role of vitamin D in select diseases. A more complete list of diseases that have been shown to have low level of 25-D is also available.
Osteoporosis
Main article: Osteoporosis and osteopenia