What did @thetestosteroneconsultant actually say?
The creator claims to have reviewed bloodwork from over 1,000 men and identified five common factors suppressing testosterone. Three are deficiencies: vitamin D3 (called "by far and away the biggest one"), copper, and B12. Two are elevations: prolactin, which he says will "kill everything," and cortisol, described as acting "like a ceiling on testosterone." He also flags zinc imbalance as connected to the copper issue, noting that excess zinc can throw off copper-to-zinc ratios. This is a practical, bloodwork-oriented framing rather than a supplement sales pitch, which is worth noting upfront. The claims vary considerably in how well they hold up to scrutiny.
Does the science back this up?
Partially, yes. The vitamin D and prolactin claims are the strongest. The copper and B12 claims are weaker and more conditional. The cortisol mechanism he describes is partly accurate but oversimplified in a way that could mislead viewers.
Vitamin D deficiency is associated with lower testosterone in observational data. A 2011 randomized controlled trial by Pilz et al. in Hormone and Metabolic Research found that vitamin D supplementation significantly increased testosterone in deficient men compared to placebo. That said, the effect size in replete men is modest, and correlation in population studies does not mean every low-T man is D3-deficient.
Prolactin suppressing testosterone is well-established endocrinology. Elevated prolactin inhibits gonadotropin-releasing hormone (GnRH) pulsatility, which reduces LH and FSH signaling to the testes. This is not controversial.
Cortisol's relationship with testosterone is real but nuanced. Chronic HPA axis activation does suppress the HPG axis, but saying blood vessels "close up" is not a recognized physiological mechanism. That framing is inaccurate.
Copper and B12 are the thinnest claims. Evidence linking isolated copper deficiency to low testosterone in otherwise healthy men is sparse. B12 deficiency affects neurological function and red blood cell production, but a direct causal link to testosterone suppression in humans is not well-established in clinical literature.
What did they get wrong (or right)?
Credit where it's due: flagging vitamin D and prolactin is legitimate clinical practice. Endocrinologists routinely check both when evaluating hypogonadism. The zinc-copper ratio point is real, though often overstated in wellness circles. High-dose zinc supplementation does compete with copper absorption, and some practitioners do monitor this.
Where he goes wrong: the cortisol explanation. Saying "your blood vessels close up" when cortisol is high is not how cortisol suppresses testosterone. The actual mechanism involves cortisol inhibiting GnRH release at the hypothalamus and potentially increasing SHBG, which binds free testosterone. The vascular framing sounds intuitive but is not supported by endocrinology literature.
The B12 claim is the weakest of the five. B12 deficiency causes serious problems, but calling it a common driver of low testosterone without citing a mechanism or evidence is a stretch. It may appear on bloodwork panels simply because comprehensive panels include it, not because it reliably predicts testosterone status.
The copper claim sits in murky territory. Animal studies show copper is involved in testosterone synthesis, but human data on isolated copper deficiency causing low testosterone in otherwise healthy adult men is thin. Burak et al. (2015, Biological Trace Element Research) found correlations between serum copper and testosterone, but correlation in a cross-sectional study is not causation.
What should you actually know?
If your testosterone is low, getting bloodwork is the right first step. A responsible workup typically includes total and free testosterone, LH, FSH, prolactin, SHBG, a comprehensive metabolic panel, and vitamin D. Prolactin and cortisol are worth checking if there are clinical reasons to suspect elevation.
What this video gets right directionally is that bloodwork context matters. Low testosterone does not exist in a vacuum, and identifying reversible causes like vitamin D deficiency or hyperprolactinemia before jumping to TRT is sound medicine. A 2020 review by Bhasin et al. in the Journal of Clinical Endocrinology and Metabolism outlines exactly this kind of stepwise diagnostic approach.
What this video gets wrong is presenting copper and B12 deficiency as common testosterone drivers with the same confidence as vitamin D and prolactin. The evidence base is not equivalent. Viewers who go out and buy copper supplements based on this video are acting on weak evidence.
- Vitamin D deficiency is a legitimate, well-studied factor in testosterone levels in deficient men.
- Elevated prolactin is a real clinical cause of low testosterone and is routinely tested.
- The cortisol-testosterone relationship is real, but the vascular explanation given here is not the actual mechanism.
- Copper and B12 claims lack strong human clinical evidence as primary testosterone drivers.
- Any findings on bloodwork should be interpreted by a licensed clinician, not acted on with self-directed supplementation.