Derek

More Plates More Dates

Derek is the creator behind More Plates More Dates (MPMD). His work centers on fitness and endocrine health topics, including natural testosterone optimization, testosterone replacement therapy (TRT), and the evaluation of health supplements. The provided context does not include any academic publications.

97 claims checked on air: 5 context 3 contradicted 5 overstated 73 supported 11 unverified

What they said on air - contradicted

1:15:36contradictedlowHow To Increase Your Testosterone Levels Naturally | Derek f

Tongkat Ali suppresses SHBG and upregulates steroidogenic acute regulatory protein (StAR) to transport cholesterol into mitochondria for testosterone production.

"The main mechanism that people seem to agree on that it does do suppression of SHBG to some extent as well as the upregulation of steroidogenesis intratesticularly, so like locally upregulating I believe it's steroidogenic acute regulatory protein that basically incorporates cholesterol into the mitochondria to actually undergo these enzymatic cleaving sequences that result in the production of testosterone locally." (said at 1:15:36)

The claim asserts that Tongkat Ali (Eurycoma longifolia) suppresses SHBG and upregulates steroidogenic acute regulatory protein (StAR) in Leydig cells to stimulate testosterone production. Randomized controlled trials evaluating Tongkat Ali in healthy young men and aging men found no significant changes in SHBG levels compared to placebo. Furthermore, mechanistic research on Eurycoma longifolia's active quassinoid, eurycomanone, indicates that intratesticular testosterone increases occur primarily via inhibition of aromatase (decreasing the conversion of testosterone to estradiol) and phosphodiesterase, rather than an established primary upregulation of StAR.

1:20:10contradictedmoderateHow To Increase Your Testosterone Levels Naturally | Derek f

Supplements like tribulus, D-aspartic acid, and fenugreek have been disproven as effective testosterone boosters.

"I think a lot of those have been disproven, like tribulus, D-aspartic acid, fenugreek." (said at 1:20:10)

The speaker bundles three supplements into the claim that they have been disproven as testosterone boosters. While the evidence against Tribulus terrestris and D-aspartic acid supports the speaker's statement, the assertion regarding fenugreek is contradicted by published systematic reviews and meta-analyses: 1. Tribulus terrestris: Systematic reviews demonstrate that clinical trials in humans fail to show an increase in testosterone levels (e.g., PMID 24559105, PMID 37697053). 2. D-aspartic acid: Systematic reviews of human randomized trials show inconsistent or absent effects on testosterone concentrations in healthy men (PMID 28280794, PMID 37697053). 3. Fenugreek: In contrast to the claim, systematic reviews and meta-analyses of randomized clinical trials have found that standardized fenugreek seed extract produces statistically significant increases in total and free testosterone concentrations in men (PMID 32048383, PMID 33150931). Because the least accurate component of the bundled claim (fenugreek) is directly contradicted by meta-analytic evidence showing efficacy, the overall claim is graded contradicted.

2:49:00contradictedhighHow To Increase Your Testosterone Levels Naturally | Derek f

Finasteride inhibits two of the three 5-alpha reductase isoenzymes, resulting in approximately 60 to 70% inhibition of systemic DHT.

"versus only 60 to 70% via finasteride, which only inhibits two of the three isoenzymes in the scalp." (said at 2:49:00)

The speaker bundles two assertions: the extent of systemic DHT suppression and the selectivity of finasteride for 5-alpha reductase (5-AR) isoenzymes. While it is true and well-established that finasteride reduces serum DHT by approximately 70%, the claim that finasteride inhibits two of the isoenzymes is incorrect. Finasteride is a selective inhibitor of only the type 2 5-AR isoenzyme at clinical doses (having negligible affinity for type 1), whereas dutasteride is the dual inhibitor that targets both type 1 and type 2 isoenzymes.

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