Most direct-to-consumer men's health companies use a template. A patient picks a goal, fills out a survey, gets routed to one of three or four standard protocols. The clinician's job is to rubber-stamp the routing.
That is not how Vane works. The protocol gets written after a clinician has read the panel and the intake, with the patient's specific physiology in mind, by a human who is accountable for the result. This piece walks through what that looks like.
The patient in the example is composite. The details are real, recombined to protect anyone's identifying information.
The intake
"Mark" is 43. He lifted seriously in his twenties, fell off in his thirties when his second child was born, and is now 22 pounds heavier than his college weight. He sleeps about six hours a night, drinks two or three nights a week, and rates his sex drive at "noticeably lower than five years ago." He had a physical eight months ago and his primary-care doctor told him his labs were normal.
He fills out the Vane intake, uploads the eight-month-old labs, and books the Baseline draw. The labs come back on a Wednesday.
The first read
A Vane clinician opens the panel and starts with the cardiovascular block. Mark's lipid numbers look approximately normal. LDL of 122, HDL of 41, triglycerides of 168. His ApoB, which the prior physical did not include, is 108 mg/dL. His Lp(a) is 78 mg/dL, which is elevated.
The reading at this stage is not "Mark has high cholesterol." The reading is: Mark has more atherogenic particles than the LDL alone suggests, and a meaningfully elevated genetic risk on top of that. The cardiovascular protocol will be more aggressive than the LDL number alone would predict.
The metabolic block: fasting glucose 96, fasting insulin 14, HbA1c 5.6. The A1c is borderline. The fasting insulin is clearly elevated. The combination is early insulin resistance with a normal-appearing A1c. The same picture covered in the OGTT versus HbA1c piece.
The hormonal block: total testosterone 412 ng/dL, free testosterone 8.4 pg/mL, SHBG 41 nmol/L. The total T is at the low end of "normal." The free T is below optimal. The SHBG is mid-range and not driving the picture. Mark's symptoms (low libido, fatigue, body composition drift) line up with the numbers.
Inflammation: hsCRP 3.4 mg/L. Elevated. Worth investigating.
Micronutrients: vitamin D 22 ng/mL. Low. B12 380 pg/mL. Functionally low.
The pattern
The clinician now has the picture. Mark is not "one thing." He is the common mid-forties pattern: early insulin resistance, suboptimal androgen status, elevated atherogenic particle count compounded by genetic risk, low-grade inflammation, and easily fixable micronutrient gaps. None of these are emergencies. All of them are trending wrong.
A template would either pick one (probably testosterone, because that is what generates revenue) and ignore the rest, or stack four medications and hope. Neither is good medicine.
The protocol decision
The Vane workflow is to identify the dominant driver and write the protocol around it. For Mark, the dominant driver is metabolic. The insulin resistance is upstream of the testosterone picture and the inflammation. Fixing the metabolic state will move several markers at once.
The protocol the clinician writes:
- Lifestyle first, with structure. Resistance training three times a week with a written program. Protein target of 1.6 g/kg. Sleep target of seven hours minimum. No alcohol Sunday through Thursday. Specific, measurable, time-limited.
- A low-dose GLP-1. Semaglutide at 0.25 mg/week, microdosed, with explicit instructions that the goal is metabolic signal and visceral fat, not maximum weight loss. The dosing logic is the same as in the GLP-1 microdose piece.
- Atorvastatin 10 mg. Started for the ApoB elevation, with the Lp(a) reading driving the decision to start now rather than in five years. Target ApoB under 70 mg/dL.
- Vitamin D 5,000 IU daily and methylcobalamin B12 1,000 mcg sublingual to correct the micronutrient gaps.
- Testosterone, deferred. The clinician explicitly does not start TRT yet. The metabolic intervention will move SHBG and free testosterone over 12 weeks. If free T is still suboptimal after the metabolic block has moved, TRT is on the table. Starting TRT first would mask the metabolic problem and bake in a lifetime medication for a fixable upstream issue.
The protocol is written, reviewed, and signed by the clinician. Mark reads it in plain English, gets a 15-minute video walkthrough, and starts.
What happens over twelve weeks
Mark trains. He eats more protein. He sleeps better, mostly. He hits the GLP-1 dose without nausea because the dose is small. The atorvastatin is unremarkable. The vitamin D and B12 are correctively boring.
At week twelve, he comes back for a follow-up panel.
The numbers:
- ApoB: 71 mg/dL (down from 108)
- Fasting insulin: 8.4 microIU/mL (down from 14)
- HbA1c: 5.3 (down from 5.6)
- hsCRP: 1.8 mg/L (down from 3.4)
- Total testosterone: 528 ng/dL (up from 412)
- Free testosterone: 12.1 pg/mL (up from 8.4)
- SHBG: 38 nmol/L (essentially unchanged)
- Vitamin D: 41 ng/mL (up from 22)
- Weight: down 11 pounds, DEXA shows muscle mass unchanged
The TRT conversation never has to happen. The metabolic protocol moved free testosterone into a clearly adequate range by removing the insulin resistance that was suppressing it.
Why the same protocol is not written twice
A different patient with similar headline numbers would get a different protocol. If Mark's SHBG had been 65 instead of 41, the testosterone picture would have read differently and the clinician would have looked harder at obesity, alcohol, and inflammation as upstream drivers. If his Lp(a) had been 18 instead of 78, the statin decision would have been less urgent. If his hsCRP had been 0.8 instead of 3.4, the inflammation work would have moved off the protocol.
The marker combinations are nearly infinite. The templates are a few. That mismatch is where most direct-to-consumer men's health gets the medicine wrong.
What we ask of a Vane clinician
The hiring bar is internal medicine training, primary-care experience, and a willingness to write the protocol that fits the patient rather than the protocol that fits the inventory. Every protocol is co-signed. Every panel is reread before the next decision. The clinician who started with the patient is the clinician who stays with the patient.
This is slower than the rest of the industry. It is also the reason the numbers move.
The bottom line
A good protocol comes out of a real read of a real panel by a clinician who is accountable for the result. There is no shortcut to that, and there is no template that produces it. Mark's labs, twelve weeks later, are the artifact of the workflow doing its job.
If you want a panel read this way, that is what we built.
