Is high DHT a good or bad thing and why?
- Thread starter OMI100
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There is a study out that claims that elevated DHT is associated with a higher risk of ischemic stroke and CVD, I don't know how solid their data is:
Cardiovascular risks and elevation of serum DHT vary by route of testosterone administration: a systematic review and meta-analysis
specifically see this figure:
http://www.ncbi.nlm.nih.gov/pmc/arti...4/figure/Fig4/
Cardiovascular risks and elevation of serum DHT vary by route of testosterone administration: a systematic review and meta-analysis
specifically see this figure:
http://www.ncbi.nlm.nih.gov/pmc/arti...4/figure/Fig4/
Nelson Vergel
Founder, ExcelMale.com
HarryCat
Good find!
I like studies that are clear about their limitations:
Limitations
Reporting of AEs may be open to interpretation and so may vary somewhat among trials. Using the most serious CV events (stroke, myocardial infarction, and CV-related death) might be more unambiguous. Because of very long follow-up periods, such events are common enough to assess in observational studies [16,22,23]. However, due to shorter study duration, serious CV events are not common enough to study in clinical trials of TRT. As a result, our analyses are based on all CV events, serious or not.
The data on oral TRT must be interpreted with caution, since only four studies met the inclusion criteria. Of those, two had very low rates of CV events in both the treated and placebo groups [61,64] and one study had very high post-treatment serum T concentrations [32], possibly due to the presence of liver disease in the study subjects. The latter study was not included in the analysis of TRT-induced elevations of T/DHT because DHT was not measured. However, among the four studies analyzed for T/DHT, there was considerable variation in serum concentrations. Variation may result from the fact that serum T concentrations are not sustained following oral TRT and the time of blood acquisition is therefore critical.
Two studies included in the analysis of CV risk were stopped early. One study of oral TRT was stopped because of lack of evidence for efficacy unrelated to CV [32] and one study of gel TRT was stopped early for excess CV events in the group receiving testosterone [7]. The first study, whose stopping was uninfluenced by CV has no bias associated with early stopping. The second, may actually be associated with a slight bias estimate away from the null, actually strengthening the null conclusion. There is no way to adjust for this without serial patient level data and the exact stopping rules used.
Interpretation of the data on TRT-induced elevations of T and DHT may be limited by the fact that DHT was assayed by several methods in the included studies. The latter include mass spectroscopy (MS) based methods and various radioimmunoassays (RIAs). MS-based assays provide highly accurate measurements of DHT. RIAs are specific for DHT [90] but the values are somewhat higher than those obtained with MS-based assays [91]. The enzyme-linked immunosorbant assay (EIA) for DHT is not valid as we have recently shown [24] and studies using this method were excluded. The current analysis is based on clinical trials that have a high rate of compliance. An additional limitation in extending our findings to a clinical setting is that compliance may be lower. Schoenfeld et al. have shown that TRT gel adherence is only 37.4% at six months [92]. Similarly, Donatucci et al. [93] reported that at three months, adherence to transdermal TRT was 52% and adherence to injected TRT was 32%.
Good find!
I like studies that are clear about their limitations:
Limitations
Reporting of AEs may be open to interpretation and so may vary somewhat among trials. Using the most serious CV events (stroke, myocardial infarction, and CV-related death) might be more unambiguous. Because of very long follow-up periods, such events are common enough to assess in observational studies [16,22,23]. However, due to shorter study duration, serious CV events are not common enough to study in clinical trials of TRT. As a result, our analyses are based on all CV events, serious or not.
The data on oral TRT must be interpreted with caution, since only four studies met the inclusion criteria. Of those, two had very low rates of CV events in both the treated and placebo groups [61,64] and one study had very high post-treatment serum T concentrations [32], possibly due to the presence of liver disease in the study subjects. The latter study was not included in the analysis of TRT-induced elevations of T/DHT because DHT was not measured. However, among the four studies analyzed for T/DHT, there was considerable variation in serum concentrations. Variation may result from the fact that serum T concentrations are not sustained following oral TRT and the time of blood acquisition is therefore critical.
Two studies included in the analysis of CV risk were stopped early. One study of oral TRT was stopped because of lack of evidence for efficacy unrelated to CV [32] and one study of gel TRT was stopped early for excess CV events in the group receiving testosterone [7]. The first study, whose stopping was uninfluenced by CV has no bias associated with early stopping. The second, may actually be associated with a slight bias estimate away from the null, actually strengthening the null conclusion. There is no way to adjust for this without serial patient level data and the exact stopping rules used.
Interpretation of the data on TRT-induced elevations of T and DHT may be limited by the fact that DHT was assayed by several methods in the included studies. The latter include mass spectroscopy (MS) based methods and various radioimmunoassays (RIAs). MS-based assays provide highly accurate measurements of DHT. RIAs are specific for DHT [90] but the values are somewhat higher than those obtained with MS-based assays [91]. The enzyme-linked immunosorbant assay (EIA) for DHT is not valid as we have recently shown [24] and studies using this method were excluded. The current analysis is based on clinical trials that have a high rate of compliance. An additional limitation in extending our findings to a clinical setting is that compliance may be lower. Schoenfeld et al. have shown that TRT gel adherence is only 37.4% at six months [92]. Similarly, Donatucci et al. [93] reported that at three months, adherence to transdermal TRT was 52% and adherence to injected TRT was 32%.
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