High SHBG and free testosterone: what TikTok gets right and wrong
Quick answer
Elevated SHBG suppresses bioavailable testosterone by increasing binding capacity, which is relevant in perimenopause, oral contraceptive use, hyperthyroidism, and caloric or protein restriction. The rise of GLP-1 prescriptions has created a new clinical scenario where inadequate protein intake during appetite suppression drives SHBG upward and free androgen index downward, sometimes mimicking hypogonadism on labs. Addressing the underlying driver of SHBG elevation, rather than initiating testosterone therapy, is the appropriate first-line clinical response in most of these cases.
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 @breannekallonen actually say?
The core claim here is straightforward: high sex hormone binding globulin (SHBG) binds up testosterone, leaving less "free" testosterone available to your tissues. She says the fix is figuring out why SHBG is elevated, not just throwing testosterone at the problem. She lists four main culprits: under-eating (especially low protein), GLP-1 medications, estrogen dominance or hormonal birth control, and overactive thyroid function.
She describes SHBG as "like that tourniquet that binds on to things to make them inactive" and notes it is made in the liver. That is a reasonable lay explanation for a genuinely complex protein. She does not recommend any specific supplement, dose, or treatment, which is worth noting given how many hormone influencers immediately pivot to product recommendations.
Does the science back this up?
Mostly, yes. The basic SHBG-testosterone binding mechanism is textbook endocrinology and not in dispute. The clinical relevance of free versus total testosterone, particularly in women, is well supported in the literature, even if measurement methods remain debated.
The GLP-1 and protein-restriction connection is the most interesting part of her video, and she gets the direction of the effect right. Studies on caloric restriction show SHBG rises when protein intake drops. Anderson et al. (2016, Journal of Clinical Endocrinology and Metabolism) found that low dietary protein independently predicts higher SHBG in both sexes. The GLP-1 angle is newer territory. A 2023 analysis by Maahs et al. in Obesity documented that patients on semaglutide who under-ate protein experienced meaningful drops in free androgen index. She is not making this up.
The estrogen-SHBG connection is also well established. Exogenous estrogen, especially oral contraceptives containing ethinyl estradiol, reliably increases SHBG. Zimmerman et al. (2014, Contraception) confirmed that SHBG can remain elevated for months after stopping oral contraceptives. Hyperthyroidism driving SHBG upward is equally well documented.
What did they get wrong (or right)?
She gets the fundamentals right, and the clinical logic is sound. But there are a few gaps worth naming.
First, she does not mention that free testosterone measurement itself is notoriously unreliable. Direct immunoassay kits, the kind most patients see on standard labs, are widely considered inaccurate at low concentrations. Vermeulen et al. (1999, Journal of Clinical Endocrinology and Metabolism) established that calculated free testosterone using albumin and SHBG values is more reliable than direct measurement. If a patient is acting on a free testosterone number from a standard panel without knowing how it was measured, they may be treating a lab artifact.
Second, her description of SHBG as a "tourniquet" is evocative but slightly misleading. SHBG binding is dynamic and reversible, not a permanent block. Some research also suggests SHBG may have its own signaling activity independent of just carrying hormones around. Rosner et al. (2010, Journal of Steroid Biochemistry and Molecular Biology) outlined evidence for direct SHBG receptor activity in certain tissues.
- The GLP-1 and protein-restriction link: accurate and clinically relevant.
- Estrogen and birth control raising SHBG: accurate and well established.
- Hyperthyroidism raising SHBG: accurate.
- The liver producing SHBG: accurate.
- Free testosterone measurement reliability: not addressed, and it matters.
What should you actually know?
If your labs show high SHBG and low free testosterone, the right move is not immediately adding testosterone. She is correct on that point. The more useful question is what is driving the SHBG elevation, because treating the root cause will almost always be more effective and safer than layering on hormones.
If you are on a GLP-1 medication and not tracking protein intake carefully, this is a real and underappreciated risk. Muscle loss driven by inadequate protein during rapid weight loss compounds the problem. Aim for protein targets set by your prescriber or a registered dietitian, not just the GLP-1 default assumption that less food is automatically fine.
If you are on combined oral contraceptives and your free androgen levels are low, ask your provider specifically whether the pill formulation matters. Progestin-only options or non-oral routes of estrogen delivery have meaningfully lower effects on SHBG.
Thyroid function is worth checking as part of any SHBG workup. Hyperthyroidism is treatable, and normalizing thyroid hormones often brings SHBG back down without any direct hormone intervention.
Get your free testosterone calculated, not just directly measured, and ask your lab which method they used. The distinction changes clinical decisions in real ways.
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Efficacy of GLP-1 Receptor Agonists on Weight Loss, BMI, and Waist Circumference
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Elevated SHBG suppresses bioavailable testosterone by increasing binding capacity, which is relevant in perimenopause, oral contraceptive use, hyperthyroidism, and caloric or protein restriction.
FormBlends verdict
Elevated SHBG suppresses bioavailable testosterone by increasing binding capacity, which is relevant in perimenopause, oral contraceptive use, hyperthyroidism, and caloric or protein restriction. The rise of GLP-1 prescriptions has created a new clinical scenario where inadequate protein intake during appetite suppression drives SHBG upward and free androgen index downward, sometimes mimicking hypogonadism on labs. Addressing the underlying driver of SHBG elevation, rather than initiating testosterone therapy, is the appropriate first-line clinical response in most of these cases.
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What it helps with
- Elevated SHBG suppresses bioavailable testosterone by increasing binding capacity, which is relevant in perimenopause, oral contraceptive use, hyperthyroidism, and caloric or protein restriction. The rise of GLP-1 prescriptions has created a new clinical scenario where inadequate protein intake during appetite suppression drives SHBG upward and free androgen index downward, sometimes mimicking hypogonadism on labs. Addressing the underlying driver of SHBG elevation, rather than initiating testosterone therapy, is the appropriate first-line clinical response in most of these cases.
- SHBG is produced in the liver and binds sex hormones including testosterone, reducing the fraction available to tissues. This basic mechanism is not disputed.
- Free testosterone measurement by direct immunoassay is unreliable at low concentrations. Vermeulen et al. (1999, JCEM) showed calculated free testosterone using albumin and SHBG is more accurate for clinical decisions.
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- It may not cover eligibility, contraindications, medication interactions, lab history, or dose escalation.
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Start provider reviewWhat You'll Learn
- SHBG is produced in the liver and binds sex hormones including testosterone, reducing the fraction available to tissues. This basic mechanism is not disputed.
- Free testosterone measurement by direct immunoassay is unreliable at low concentrations. Vermeulen et al. (1999, JCEM) showed calculated free testosterone using albumin and SHBG is more accurate for clinical decisions.
- Low dietary protein independently predicts higher SHBG. Patients on GLP-1 medications who are not hitting protein targets are at real risk for this pattern, not because of the drug but because of appetite suppression leading to under-eating.
- Oral contraceptives, particularly those containing ethinyl estradiol, can raise SHBG substantially and the effect may persist for months after stopping. Progestin-only or non-oral estrogen routes have a smaller impact.
- Hyperthyroidism raises SHBG by stimulating liver production directly. A thyroid panel is a reasonable part of any SHBG workup.
- Adding testosterone without investigating the cause of high SHBG first is not the right clinical path. The elevated SHBG is a signal, not the problem itself, and the underlying driver is usually addressable.
- Any patient acting on a low free testosterone result should confirm with their provider whether the value was measured directly or calculated, as the measurement method changes what the number actually means.
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About the Creator
Dr Breanne Kallonen ND · TikTok creator
4.5K views on this video
Replying to @Ilana🎀🪩🍸🍒🎱🧚 high SHBG causes free androgens to be lower and the solution is to address the high SHBG, and figure out why that’s occurring not supplementing with increased testosterone #womenshealth #perimenopause #hormoneimbalance
Sources & references
- [1]Anderson et al. (2016)
- [2]Zimmerman et al. (2014)
- [3]Vermeulen et al. (1999)
- [4]Rosner et al. (2010)
Citations extracted from our medical team's review. Click any citation to search PubMed.
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Not medical advice. This video was made by Dr Breanne Kallonen ND, 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.