Does low testosterone really start with insulin resistance?

What did @drsteveng actually say?

The creator, who lists chiropractic among his hashtags, argues that blood sugar control is "the most overlooked strategy" for testosterone optimization. His core claim: the same factors that drive insulin resistance also "convert your testosterone into estrogen." He then lists five lab markers and gives specific target ranges for each, including a fasting insulin under 6, AST and ALT under 25, triglycerides under 100, fasting glucose between 85 and 92, and hemoglobin A1c between 4.8 and 5.2. These are tighter than most standard clinical reference ranges, which is worth examining carefully.

The framing applies to both men trying to optimize natural testosterone and those already on testosterone replacement therapy. The implication is that metabolic dysfunction is a root cause of low T, not just a correlating factor. That distinction matters a lot clinically.

Does the science back this up?

Partially, and the core connection is real, but it is being simplified in ways that could mislead viewers. The link between insulin resistance and lower testosterone in men is well-established. A 2014 study by Grossmann in the Journal of Clinical Endocrinology and Metabolism confirmed a bidirectional relationship between hypogonadism and metabolic syndrome. Obesity and insulin resistance suppress gonadotropin-releasing hormone, which reduces LH signaling to the testes, which reduces testosterone output. That part checks out.

The aromatase angle, that excess insulin activity and adipose tissue convert testosterone to estrogen, is also supported by evidence. Corona et al. (2010, Journal of Sexual Medicine) found that elevated estradiol in obese hypogonadal men correlated with aromatase activity in fat tissue, not just insulin per se. So the mechanism is real, but insulin resistance and obesity are intertwined, and the video does not distinguish between them clearly. Insulin itself does not directly run the aromatase enzyme. Fat mass does. This is a meaningful nuance the video glosses over.

What did they get wrong (or right)?

The specific lab targets deserve scrutiny. Clinical laboratories use fasting glucose reference ranges of roughly 70 to 99 mg/dL. The creator's recommended range of 85 to 92 is a functional medicine preference, not a standard clinical cutoff. There is no large randomized trial showing that a fasting glucose of 84 is meaningfully worse for testosterone than one of 88. This precision sounds scientific but is not well-validated at that resolution.

The fasting insulin target of under 6 uIU/mL is similarly a functional medicine convention. The American Diabetes Association does not include fasting insulin in its standard diagnostic criteria, partly because insulin assays vary significantly between labs (Greenfield and Russell, 2011, Journal of Clinical Endocrinology and Metabolism). Telling 119,000 viewers their insulin must be under 6 without acknowledging assay variability is a real problem.

On the other hand, recommending triglycerides under 100 and using liver enzymes as metabolic proxies are reasonable clinical approaches. Elevated triglycerides and ALT do track with insulin resistance, and those connections are legitimate.

What should you actually know?

If you have clinically diagnosed low testosterone, metabolic health absolutely belongs in the conversation. A 2016 meta-analysis by Corona et al. in the European Journal of Endocrinology found that weight loss and lifestyle intervention improved testosterone levels in overweight hypogonadal men, sometimes substantially. Treating insulin resistance is not a fringe idea. It is good medicine.

But the framing that blood sugar is the "most overlooked" driver of low T skips over other well-documented causes: primary hypogonadism, pituitary disorders, medication side effects, sleep apnea, and age-related decline. Insulin resistance is one pathway among several. Viewers watching this who have a genuinely broken hypothalamic-pituitary-gonadal axis will not fix their testosterone by optimizing their A1c.

Also worth flagging: the creator does not mention that the relationship between testosterone and insulin resistance is bidirectional. TRT itself can improve insulin sensitivity in hypogonadal men (Kapoor et al., 2006, European Journal of Endocrinology). The video presents it as one direction only, which is an incomplete picture.

• Insulin resistance and low testosterone are genuinely linked, but the mechanism runs mostly through adipose tissue aromatase, not insulin directly.
• The specific lab cutoffs listed are functional medicine conventions, not universally validated clinical thresholds.
• Fasting insulin results vary by lab assay, making a single universal target like "under 6" less reliable than implied.
• Improving metabolic health can raise testosterone in overweight men with secondary hypogonadism, but will not fix primary testicular failure.
• The relationship is bidirectional: low testosterone also worsens insulin resistance, a fact the video omits entirely.

Bottom line

The broad point, that metabolic health matters for testosterone, is legitimate and underemphasized in mainstream care. But the specific numerical targets presented as precise medical standards are not universally validated, the mechanistic explanation oversimplifies the aromatase pathway, and the framing as the single "most overlooked" cause of low T overstates the case. Take the general message seriously. Take the specific numbers back to a board-certified endocrinologist or internist before acting on them.