Can you take dhea with prednisone. Complementary and Alternative Medicine
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Can you take dhea with prednisone
Rapid response to:. It is my hypothesis that dehydroepiandrosterone DHEA was selected by evolution because it optimizes replication and transcription of DNA. Therefore, all tissues may be affected by levels of DHEA. Some molecules are more universal and some are more specific.
That is, some molecules stimulate growth in many tissues, such as growth hormone, while others are specific, such as nerve growth factor, among many. Growth and addiction may be controlled by the same mechanism. Prednisolone may act in this manner.
Since I think all tissues are affected by levels of DHEA, this includes the immune and nervous systems. The term, HIV, did not exist at the time. Subsequently, I decided that low DHEA may result in vulnerability to other infectious agents; this has been supported in many areas. This is supported. The symptoms of leprosy may also be due to loss of DHEA in a manner characteristic of the infectious agent dissimilar to that caused by the HIV. I suggest this is the basis of the effects of glucocorticoids in infants whose lungs are poorly developed and positively stimulated by glucocorticoids.
However, it is known that some infants of this type are not helped by this treatment. They may represent infants who developed poorly because of low DHEA in utero and who cannot respond to glucocorticoids at birth because they cannot produce sufficient DHEA upon glucocorticoid stimulation. In the case of Smith, et al. Low DHEA in these individuals may result in the both the infection and nerve damage, among other symptoms. In those who cannot maintain DHEA levels, the nerve damage continues.
Evidentally, nerve damage may indicate when DHEA is too low to respond to prednisolone. The mechanism involves prolactin, which has been shown to specifically and positively affect DHEA production. It is my hypothesis that melatonin and DHEA reciprocate to produce our circadian rhythms.
When melatonin is high, sleep occurs. When DHEA is high, consciousness occurs. Melatonin induces sleep by reducing levels of DHEA. This small recruitment of DHEA during sleep maintains brainstem function during sleep.
It is known that the first slow wave sleep is the deepest with each subsequent cycle lessening in depth of SW sleep. This is due to the recruitment. Melatonin induces sleep, or DHEA reduction, by inhibiting prolactin production.
Just before morning consciousness, there is a large production of prolactin. Prednisolone is used to inhibit prolactin production.
Drugs of abuse affect prolactin production. If prolactin production is inhibited by prolonged, excessive use of glucocorticoids, many tissues are adversely affected. I suggest this occurs because of excessive, prolonged reductions in DHEA. Competing interests: None declared Competing interests: No competing interests. Skip to main content. Research Steroid prophylaxis Article Related content Article metrics Rapid responses Response. Competing interests: None declared. Competing interests: No competing interests.
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Replacement therapy with DHEA plus corticosteroids in patients with chronic inflammatory diseases — substitutes of adrenal and sex hormones. Z Rheumatol 59 Suppl 2 , — Download citation. Published : 26 April Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.
Skip to main content. These studies clearly indicate that chronic inflammation alters, particularly, the adrenal response. However, at this point, the reason for the specific alteration of adrenal function in relation to pituitary function remains to be determined.
Since one of the down-regulated adrenal hormones, DHEA, is an inhibitor of cytokines due to an inhibition of nuclear factor-kappa B NF-kappa B activation, low levels of this hormone may be deleterious in chronic inflammatory diseases. However, scientific studies in humans are needed before DHEA can be used for this purpose in people.
Barbiturates -- Animal studies suggest that DHEA may increase the effects of barbiturates, a class of medications often used to treat sleep disorders. These medicines include butabarbital, mephobarbital, pentobarbital, and phenobarbital. However, clinical studies in humans are needed before it is known whether this same effect occurs in people and whether it is safe for DHEA and barbiturates to be used together.
Steroids -- Laboratory studies suggest that DHEA may increase the effects of prednisolone, a steroid medication used to treat inflammation and other disorders. Additional research is needed to determine if this effect applies to people. For this reason, some women on estrogen replacement therapy may need to adjust their dosage.
Some molecules are more universal and some are more specific. That is, some molecules stimulate growth in many tissues, such as growth hormone, while others are specific, such as nerve growth factor, among many.
Growth and addiction may be controlled by the same mechanism. Prednisolone may act in this manner. Since I think all tissues are affected by levels of DHEA, this includes the immune and nervous systems.
The term, HIV, did not exist at the time. Subsequently, I decided that low DHEA may result in vulnerability to other infectious agents; this has been supported in many areas.
This is supported. The symptoms of leprosy may also be due to loss of DHEA in a manner characteristic of the infectious agent dissimilar to that caused by the HIV.
A dysfunction of the hypothalamic-pituitary-adrenal HPA axis was found in animal models of chronic inflammatory diseases, and the defect was located in more central portions of the HPA axis. This defect of neuroendocrine regulatory mechanisms contributes to the onset of the model disease.
Since these first observations in animal models were made, evidence has accumulated that the possible defect in the HPA axis in humans is more distal to the hypothalamus or pituitary gland: In chronic inflammatory diseases, such as rheumatoid arthritis, an alteration of the HPA stress response results in inappropriately low cortisol secretion in relation to adrenocorticotropic hormone ACTH secretion.
Furthermore, it has recently been shown that the serum levels of another adrenal hormone, dehydroepiandrosterone DHEAwere significantly lower after ACTH stimulation in patients with rheumatoid arthritis without prior corticosteroids than in healthy controls.
These studies clearly indicate that chronic inflammation alters, particularly, the adrenal response. However, at this point, the reason for the specific alteration of adrenal function in relation to pituitary function remains to be determined. Since one of the down-regulated adrenal hormones, DHEA, is an inhibitor of cytokines due to an inhibition of nuclear factor-kappa B NF-kappa B activation, low levels of this hormone may be deleterious in chronic inflammatory diseases.
Since IL-6 is an important factor for B lymphocyte differentiation, the missing down-regulation of this cytokine, and others such as TNF, may be a significant risk factor in rheumatic diseases. Since in these patients, administration of prednisolone or the chronic inflammatory process itself alters adrenal function, endogenous adrenal hormones in relation to proinflammatory cytokines change. Furthermore, these mechanisms may also lead to shifts in steroidogenesis which have been demonstrated in chronic inflammatory diseases.
Since DHEAS is the pool for peripheral sex steroids, such as testosterone and 17 beta-estradiol, lack of this hormone leads to a significant sex hormone deficiency in the periphery. As a consequence, we suggest a combined therapy with corticosteroids plus DHEA in chronic inflammatory diseases.
Abstract A dysfunction of the hypothalamic-pituitary-adrenal HPA axis was found in animal models of chronic inflammatory diseases, and the defect was located in more central portions of the HPA axis.
Publication types Review.
The importance of DHEAS deficiency will be demonstrated with respect to osteoporosis. As a consequence, we suggest a combined therapy with corticosteroids. We found no evidence for greater suppression of adrenal androgens or lesser suppression of cortisol with alternate day prednisone treatment. Basal serum DHEA. If you are under 40, you shouldn't take DHEA without your doctor's Laboratory studies suggest that DHEA may increase the effects of prednisolone. Do not take DHEA if you are taking anastrozole (Arimidex). Medications for inflammation (Corticosteroids)Interaction Rating: Minor Be. Smanjena aktivnost DHEAS sulfataze i sni`enje koncentracije cirkuli{u}e DHEAS pra}eno je padom Th 1 aktivnosti i dovodi do stanja koje je. The Basics.Des weiteren kann DHEA in peripheren Zellen wie beispielsweise Makrophagen zu antiinflammatorisch wirksamen Geschlechtshormonen wie Testosteron umgewandelt werden. A dysfunction of the hypothalamic — pituitary — adrenal HPA axis was found in animal models of chronic inflammatory diseases, and the defect was located in more central portions of the HPA axis.
This defect of neuroendocrine regulatory mechanisms contributes to the onset of the odel disease. Since these first observations in animal models were made, evidence has accumulate that the possible defect in the HPA axis in humans is more distal to the hypothalamus or pituitary gland: In chronic inflammatory diseases, such as rheumatoid arthritis, an alteration of the HPA stress response results in inappropriately low cortisol secretion in relation to adrenocorticotropic hormone ACTH secretion.
Furthermore, it has recently been shown that the serum levels of another adrenal hormone, dehydroepiandrosterone DHEA , were significantly lower after ACTH stimulation in patients with rheumatoid arthritis without prior corticosteroids than in healthy controls.
These studies clearly indicate that chronic inflammation alters, particularly, the adrenal response. However, at this point, the reason for the specific alteration of adrenal function in relation to pituitary function remains to be determined.
Since IL-6 is an important factor for B lymphocyte differentiation, the missing down-regulation of this cytokine, and others such as TNF, may be a significant risk factor in rheumatic diseases. Since in these patients, administration of prednisolone or the chronic inflammatory process itself alters adrenal function, endogenous adrenal hormones in relation to proinflammatory cytokines change.
Furthermore, these mechanisms may also lead to shifts in steroidogenesis which have been demonstrated in chronic inflammatory diseases. As a consequence, we suggest a combined therapy with corticosteroids plus DHEA in chronic inflammatory diseases.
This is a preview of subscription content, access via your institution. Rent this article via DeepDyve. Straub klinik. You can also search for this author in PubMed Google Scholar. Reprints and Permissions. Straub, R. Replacement therapy with DHEA plus corticosteroids in patients with chronic inflammatory diseases — substitutes of adrenal and sex hormones.
Z Rheumatol 59 Suppl 2 , — Download citation. Published : 26 April Issue Date : October Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search SpringerLink Search. Summary A dysfunction of the hypothalamic — pituitary — adrenal HPA axis was found in animal models of chronic inflammatory diseases, and the defect was located in more central portions of the HPA axis.
Straub, J. Zietz Authors R. Straub View author publications. View author publications. Rights and permissions Reprints and Permissions. About this article. Cite this article Straub, R. Copy to clipboard.
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