Androstenedione, 4-androstenediol, 5-androstenediol, 19-norandrostenediol and 19-norandrostenedione are commonly referred to as "Andro" prohormones. Over the last few years, supplementation using these prohormones has been aggressively marketed to the general public. Supplement manufacturers often claim that Andro use improves serum testosterone concentrations, increases muscular strength and muscle mass, helps to reduce body fatness, enhances mood, and improves sexual performance. However, to date, most studies contradict these claims. In contrast, several studies using oral Andro related prohormones show that Andro use can abnormally elevate estrogen related hormones as well as alterations in hormonal markers (i.e., abnormal elevations in serum estrogen) thought to increase a person's risk for developing prostate or pancreatic cancers. In addition, most studies also indicate that significant declines in high-density lipoproteins occur leading to an increased cardiovascular disease risk. Thus, to date, the current research base suggests that Andro prohormone use does not support manufacturer claims. But it does suggest there should be strong concerns regarding long-term oral Andro prohormone use, especially regarding its effects on blood lipids and estrogen hormone profiles.

Much of our current understanding regarding trauma, mechanisms of healing, and treatment strategies have evolved as a result of injuries suffered during armed conflict. While our understanding of these processes has advanced during and since these conflicts, treatment methods of traumatic wound healing have failed to progress significantly in the last forty years. The overall objective of this research was to test the hypothesis that the immune regulating hormone Androstenediol (AED) modulates the host’s immune system to promote wound healing under conditions where it has been inhibited by stress and infection. In an effort to characterize the effects of Androstenediol on healing following trauma, this research focused on strategies to evaluate which levels of trauma, immunosuppressive agents, and Androstenediol are required to reverse inhibition of healing. Sprague-Dawley rats were assessed for their response to trauma and intervention through assessment of white blood cell levels, cytokine and chemokine expression, and quantification of wound closure. While these studies did provide some trends reflecting modulation of cell counts and protein expression following AED treatment in immune-suppressed animals, measurement of wound closure failed to reveal a significant response.

"Prostate cancer (Pca) is the number one cancer in U.S. men and a leading cause of cancer-related deaths. The disease is initially dependent upon active male androgens for survival, such as testosterone or dihydrotestosterone. However, relatively inactive androgens like 5-androstenediol (5Adiol) have been considered to play larger roles in disease progression than previously considered. 5Adiol is synthesized in the prostate, is not affected by current anti-androgen therapies, and activates the androgen receptor in human prostate cancer cell lines more effectively than active male androgens. The causal relationship between androgens and prostate cancer progression has significantly risen due to anabolic steroid abuse in competitive sports and recreational athletes. The evidence surrounding an association between androgen abuse and prostate cancer, as well as various other carcinomas, is of great concern within this demographic because of its preventability. Despite their prohibited use, anabolic products continue to be marketed and available for purchase as nutritional supplements. Surveys on current steroid user trends have documented high dosing regimens, extended periods of use, multiple self-diagnosed side effects, and unsafe injection practices. Because few studies have investigated the effects of advertised 5Adiol products on prostate cancer progression, the goal of this study was to investigate whether Value Nutrition’s 5Adiol product possesses comparable mitogenic stimulant activity to testosterone in the androgen-dependent cell line, LNCaP. It should be noted that while this compound is banned by the U.S. Drug Enforcement Administration and is no longer sold through this company, alternative steroids continue to be marketed to consumers. Additional goals included determining whether this product would affect the proliferation of liver cells using the HepG2 cell line, if HepG2 metabolism of the product would play a role in the proliferation of LNCaP cells, and whether the LNCaP cells are capable of converting the 5Adiol product into testosterone. Multiple assays determined that the LNCaP cells were androgen responsive to the 5Adiol product, HepG2 proliferation was stimulated, and HepG2 metabolism of the 5Adiol product increased LNCaP mitogenicity, although significant differences were unattainable primarily due to the LNCaP cells reduced adhesion properties. Because reverse-phase HPLC was unable to detect compounds within 5Adiol even at high concentrations, the mitogenicity observed in both cell lines is unable to be correlated with a particular component in this product. While it is possible that 5Adiol is present at extremely low levels, contamination with other factors, hazardous or not, cannot be ruled out. In conclusion, these results suggest that the use of nutraceuticals have inherent risks for men at risk of developing prostate cancer. The mitogenic effects observed from small levels of unknown compounds in the tested 5Adiol product raise serious questions as to the legitimacy of allowing companies to market and self-regulate their own products."

DHEA has been determined to have medically significant activity and is the parent compound to the more active metabolites; 17α-AED, 17β-AED and 17β-AET, which exhibit strong biological activity that has been attributed to androgenic, estrogenic or anti-glucocorticoid activity in vivo and in vitro. This study compared DHEA, 17α-AED, 17β-AED and 17β-AET for their ability to activate the human AR, ER and GR receptors and determine the relative androgenicity, estrogenicity and glucocorticoid activity. The results show that, at the receptor level, these androstene hormones are weak AR and even weaker ER activators. Direct androstene hormone activation of the human AR, ERα, and ERβ may not be essential for their biological function. Similarly, these hormones indirectly activated the human GR receptor; only in the presence of high dexamethasone concentrations. These results underscore the major difference between androstene hormone interactions with these nuclear receptors. 17β-AED and 17α-AED, androstene epimers that produce either survival or death, were utilized to treat T98G Glioblastoma cells. We identified 26 genes oppositely regulated by 17β-AED and 17α-AED to directly affect the cellular life or death decision. Network analysis demonstrated that these 26 genes are essential to regulating three critical Glioblastoma pathways. This report, for the first time, demonstrates that naturally occurring, chemically identical adrenal hormones (17β-AED or 17α-AED) direct a cellular life or death decision through contrasting modulation of identical signaling pathways and core regulators. Chronic pressure ulcers represent a significant health problem and are characterized by hypoxia, bacterial infection, repetitive ischemia/reperfusion and altered cellular and systemic stress responses. Whole genome microarray analysis was utilized in conjunction with IPA® premiere networking software to analyze chronic wound edge tissue. IPA® network analysis identified Ubiquitin C (UBC) as the most significant network. Sixteen (16) ubiquitin C associated genes were identified to be different in the chronic pressure ulcer and normal skin control. Targeted network analysis associated core regulators to 8 UBC associated genes that are unique to chronic pressure ulcers. The identification of these genes will allow the establishment of more effective treatments for Spinal Cord Injury (SCI) patients with chronic pressure ulcers.

No description available.

No description available.