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SHBG and 'free testosterone': what the science says about lowering it

Dr. Michele Oller, PharmD

TikTok creator

3.9K viewsWatch on TikTok→

Quick answer

SHBG is a hepatically-produced glycoprotein that binds testosterone and estradiol, reducing their bioavailability. Elevated SHBG in the context of normal total testosterone can produce symptomatic androgen deficiency, and the clinical drivers, including insulin resistance, thyroid dysfunction, and oral estrogen use, each require distinct management approaches rather than direct SHBG-targeting strategies. Free testosterone measurement and interpretation should be contextualized against the laboratory method used, as calculated free testosterone has meaningful accuracy limitations.

Our take · Written by FormBlends editorial team · Reviewed by FormBlends Medical Team· This is not a transcript. It is our independent review of the video above.

What did @michelehormonehealth actually say?

The creator argues you can't lower SHBG directly, you have to fix what's causing it to be elevated in the first place. She points to low insulin signaling, undereating, thyroid dysfunction, estrogen, and oral medications affecting liver metabolism as the common culprits. She mentions supplements like boron, magnesium glycinate or taurate, and vitamin D as having "decent data" but frames them as supporting players, not the main event. She closes with the practical point that if your testosterone reads normal on paper but you feel lousy, elevated SHBG could be binding enough free testosterone to explain the gap.

To her credit, she doesn't promise a fix. She's describing a clinical framework, not a protocol. That's a meaningful distinction in a space full of people selling you the answer before they know the question.

Does the science back this up?

Mostly, yes. The core claim, that SHBG is a downstream marker rather than a primary target, is well-supported. Research consistently shows SHBG rises in response to upstream signals, and treating the number without addressing the cause is a dead end.

On insulin signaling: this is one of the more solid connections in SHBG research. Studies, including work by Goodman-Gruen and Barrett-Connor (1997, Journal of Clinical Endocrinology and Metabolism), showed inverse relationships between insulin resistance markers and SHBG. More recent work by Wallace et al. (2013, JCEM) confirmed that insulin suppresses hepatic SHBG production directly. The thyroid connection is also legitimate. Hyperthyroidism raises SHBG; hypothyroidism tends to lower it. Plymate et al. (1985, JCEM) documented this relationship clearly.

On oral estrogens affecting liver SHBG production: this is accurate. First-pass hepatic metabolism from oral estradiol raises SHBG significantly more than transdermal routes. That's a clinically relevant distinction, particularly for perimenopausal patients on hormone therapy.

On supplements: boron has some data (Naghii and Samman, 1997, Environmental Health Perspectives showed modest effects on sex hormone levels), but the effect sizes are not large. Magnesium has indirect mechanistic plausibility through insulin sensitivity, but direct SHBG-lowering evidence is thin. Vitamin D research here is mixed. She appropriately hedges with "decent data" rather than overclaiming.

What did they get wrong (or right)?

She gets the framework right. The critique that people try to lower SHBG directly is a fair observation about how patients often approach this online, and her redirection toward root causes is clinically sound.

Where the video is thin: she mentions "estrogen, rut like oral and liver metabolism" in a way that's clearly garbled in the transcript, likely a recording artifact, but it points to a real gap. The nuance that oral estrogen raises SHBG while transdermal estrogen does not to the same degree is important clinical information that doesn't fully land here. Patients on oral estradiol or oral contraceptives dealing with SHBG issues need to know the route of administration matters, not just the hormone class.

She also lumps magnesium glycinate and taurate together as roughly equivalent options without distinguishing them. These are different forms with different absorption profiles. The "glycerate" mentioned appears to be a verbal slip for glycinate. It's a small error, but in a medical context, form matters.

No dangerous claims are made. No dosing is prescribed. The supplement recommendations are hedged appropriately. For a TikTok video under two minutes, this is more responsible than most in this category.

What should you actually know?

SHBG is produced in the liver, and almost everything that raises or lowers it does so by changing liver signaling. That's why oral medications, metabolic status, thyroid function, and nutritional state all matter. If your free testosterone is low because SHBG is high, the question is always: why is SHBG elevated in the first place?

The free testosterone calculation itself deserves scrutiny. Most labs report calculated free testosterone, not directly measured free testosterone. The Vermeulen calculation, which is commonly used, has known accuracy limitations depending on the albumin value used. If you're making clinical decisions based on this number, it's worth knowing how your lab derived it.

Boron supplementation has legitimate but modest supporting evidence. Do not expect dramatic SHBG reductions from supplements alone if you have significant metabolic dysfunction, thyroid disease, or are on oral hormones driving the elevation. Fixing the driver matters more than any single supplement. Talk to a clinician who will actually measure your full hormone panel, not just total testosterone.

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SHBG is a hepatically-produced glycoprotein that binds testosterone and estradiol, reducing their bioavailability.

FormBlends verdict

SHBG is a hepatically-produced glycoprotein that binds testosterone and estradiol, reducing their bioavailability. Elevated SHBG in the context of normal total testosterone can produce symptomatic androgen deficiency, and the clinical drivers, including insulin resistance, thyroid dysfunction, and oral estrogen use, each require distinct management approaches rather than direct SHBG-targeting strategies. Free testosterone measurement and interpretation should be contextualized against the laboratory method used, as calculated free testosterone has meaningful accuracy limitations.

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What it helps with

  • SHBG is a hepatically-produced glycoprotein that binds testosterone and estradiol, reducing their bioavailability. Elevated SHBG in the context of normal total testosterone can produce symptomatic androgen deficiency, and the clinical drivers, including insulin resistance, thyroid dysfunction, and oral estrogen use, each require distinct management approaches rather than direct SHBG-targeting strategies. Free testosterone measurement and interpretation should be contextualized against the laboratory method used, as calculated free testosterone has meaningful accuracy limitations.
  • SHBG is produced in the liver and regulated primarily by insulin signaling and thyroid hormones, not by testosterone levels themselves.
  • Wallace et al. (2013, JCEM) confirmed insulin directly suppresses hepatic SHBG production, making metabolic health a first-line target in elevated SHBG cases.

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  • It may not cover eligibility, contraindications, medication interactions, lab history, or dose escalation.
  • Compound access, legal status, and product quality still need a separate safety check.
  • Social video captions rarely show the full evidence base behind a claim.

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What You'll Learn

  • SHBG is produced in the liver and regulated primarily by insulin signaling and thyroid hormones, not by testosterone levels themselves.
  • Wallace et al. (2013, JCEM) confirmed insulin directly suppresses hepatic SHBG production, making metabolic health a first-line target in elevated SHBG cases.
  • Oral estrogen raises SHBG substantially more than transdermal estradiol due to first-pass liver metabolism, a clinically important distinction for patients on hormone therapy.
  • Calculated free testosterone, the number most labs report, is a mathematical estimate with known accuracy limitations depending on the albumin assumption used.
  • Boron supplementation showed modest sex hormone effects in small studies, but effect sizes are not large enough to substitute for addressing metabolic or thyroid drivers of high SHBG.
  • Thyroid dysfunction is a documented SHBG driver in both directions: hyperthyroidism raises it, hypothyroidism lowers it, per Plymate et al. (1985, JCEM).
  • Symptomatic androgen deficiency with 'normal' total testosterone is a real clinical pattern, and free testosterone with SHBG measurement should be part of any evaluation of hormone-related symptoms.

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About the Creator

Dr. Michele Oller, PharmD · TikTok creator

3.9K views on this video

How to lower SHBG (sex hormone binding globulin) Most people try to lower it directly — but that’s not actually how this works. If your testosterone looks “normal”… but you don’t feel it — SHBG might be why. What I look at first: • Undereating / low insulin signaling • Thyroid patterns • Oral estrogen route • Liver metabolism Support can help — but it’s not the main driver. Boron has the most direct data for lowering SHBG. Magnesium helps more indirectly (binding + overall physiology). I b

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Educational use only. This fact-check is editorial content for general information. Nothing here is medical advice. Talk to a licensed provider about your specific situation before starting, stopping, or changing any supplement, peptide, or medication regimen.

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Not medical advice. This video was made by Dr. Michele Oller, PharmD, not by FormBlends. Our write-up above is an editorial review, not a medical recommendation. Talk to your doctor before making any decisions about medications or treatments.