What Blood Work Should You Actually Be Running? | Weekly Q&A

Most doctors run two things when you ask for blood work, a basic metabolic panel and a CBC, and that tells you if your kidneys are failing and whether you are anemic. It tells you almost nothing about whether you are building plaque in your arteries, whether your thyroid is converting hormone properly, or whether your pancreas is quietly working overtime to keep your blood sugar flat.

So before getting into which markers matter, understand the shape of the problem. Your body runs on a handful of signaling systems that talk to each other constantly, and standard panels sample one or two points in those systems and call it a checkup.

Cardiovascular is the place to begin, and a full lipid panel gives you total cholesterol, LDL, HDL and triglycerides, which is a reasonable floor to work from. On top of that I want APOB and HSCRP.

What APOB does is count particles rather than cholesterol content. Every atherogenic lipoprotein in your blood carries exactly one APOB molecule, so measuring APOB is measuring how many cholesterol-carrying particles are circulating rather than how much cholesterol is riding inside them. A 2024 analysis in the European Heart Journal found APOB discordant with non-HDL cholesterol and triglycerides often enough that the three markers meaningfully disagree about who is actually at risk.

HSCRP is a measure of systemic inflammation, and it catches something lipids cannot. Bassuk, Rifai and Ridker reviewed high-sensitivity CRP and found it added to risk prediction across the range of LDL values, including in people whose LDL looked fine.

And so these two paired together, APOB, which is, again, the quality of your cholesterol and then HSCRP, which measures your inflammation, give you a wider read than the lipid panel alone. I cannot point you to a study that tested that exact pairing head to head against LDL. What I can tell you is what I see with clients. Most of the time, just HSCRP is a much better predictor of a cardiovascular event than any other marker. And nine times out of 10, if there was a heart attack event that occurred, LDL actually did a worse job of predicting an HSCRP. OK? HSCRP is also going to help us to understand what's going on in terms of other hormonal function, including testosterone, growth hormone production, function of the thyroid, gut health.

There is supporting work on inflammation as a combined signal. Cui and colleagues, in a 2024 national cohort study, found that pairing HSCRP with the triglyceride-glucose index predicted cardiovascular disease better than either marker on its own.

OK, especially if you're on TRT, keto, some type of modified diet where you have high fat, right? There's a lot of things or even worse, you're doing things like Mastron or other gear that's also going to influence your lipid profile. Your standard panel will flag the LDL and miss the particle count entirely.

Thyroid is where the gap between a standard panel and a useful one gets widest, because most clinics order TSH alone and treat that single number as the whole system.

OK? So the way that your thyroid system works is your hypothalamus is going to send a signal to your pituitary gland, which is going to trigger the release of TSH thyroid stimulating hormone. TSH travels to the thyroid and tells it to produce.

About 70 percent of the hormone produced at the thyroid is T4 and the other 30 or so percent is T3. T4 sits there dormant, doing nothing for your metabolism until something downstream converts it.

And we'll get into this a little bit later, but there are different places in your body that will convert T4 to T3 for different reasons. Your liver, your kidneys, your brain, your muscle tissue all run their own conversion.

Basically, the idea here is the thyroid is basically intended to give your body the inactive form of thyroid hormone that it needs so that it can fine tune and optimize your energy requirements on the fly by converting more T3 and adjusting or modifying your metabolic rate at any given time.

Think of T4 as fuel in the tank and T3 as fuel in the injector. The tank can be full while the engine starves.

OK, so we have T3, which is the thyroid that's actually doing the heavy lifting in terms of influencing your metabolic rate. Which means a normal TSH and a normal T4 can sit alongside symptoms that look exactly like hypothyroidism, because the conversion step is where it broke.

Then there is reverse T3, which is the thyroid's equivalent of SHBG for testosterone. So it's an inactive form of T3 that binds up the receptor to prevent the actual active form of T3 from binding and doing its job. Under stress, dieting or illness, your body shunts more T4 down the reverse T3 path and your metabolic rate drops with every marker still reading normal.

Maybe you're short on selenium or you have some type of vitamin deficiency that's preventing you from actually producing the hormone. Selenium is a cofactor for the enzymes that strip an iodine off T4 to make T3, so a deficiency there breaks conversion without touching TSH.

So not having all of these markers, TSH, free T4, free T3, reverse T3, is basically giving you just a small picture of what's actually happening inside of your body.

And a lot of times what ends up happening when they do that is they either misdiagnosed with something like Hashimoto's, which is probably the most commonly diagnosed thyroid condition in existence, in which case they're going to prescribe like T4 levothyroxine, or they're completely missing other problems that could be happening. Handing T4 to someone who cannot convert T4 just raises the number on the paper.

In addition to these four, we're also doing TPO antibodies, which is making sure that we don't have autoimmune conditions related to the thyroid, such as Hashimoto's. And then we're also running a thyroglobulin panel as well, which is going to give us an idea of what your thyroid tissue health is.

Testosterone works through the same split between total supply and usable supply that governs thyroid hormone. Total testosterone is what sits in the tank, free testosterone is what your receptors can actually use, and SHBG is the thing deciding the split.

If all of your testosterone is bound up by SHBG, you could have a testosterone level of five, six, seven, eight hundred and still feel like crap because your SHBG is to the ceiling. Which is why the full panel runs total T, free T, SHBG, sensitive LCMS estradiol, progesterone, LH, FSH, DHEA and prolactin, plus PSA for men.

OK, anti-malarion hormone is specifically important for women, especially going through perimenopause or feel like they've already reached menopause is because when this has been depleted, that's how we know you've reached menopause. And this is important because it determines whether or not it's appropriate for us to prescribe estradiol with your HRT therapy.

And one thing that's really interesting is not only do women experience a significant drop in testosterone levels like during the menopausal years, but it's actually consistently lowering year after year after the age of 20. So a woman in her mid thirties can be genuinely low without being anywhere near perimenopause, and nobody checks because she is the wrong age for the diagnosis.

On the metabolic side, HbA1C gives you a three month average blood sugar, which is useful and slow. Fasting insulin is the one that moves first, because insulin resistance means your cells stop responding and your pancreas compensates by producing more, and that compensation can run for years before glucose budges.

And then the other one that you're going to want to pull that we also have on ours is your fructosamine, which is a two to three week blood sugar window, which can be used in correlation with your HbA1C to see if you're moving in the right direction.

Add uric acid for metabolic health and gout risk, AST and ALT for liver enzymes, and GGT for true liver health, meaning the actual alcohol and toxin stress on the organ. Hard training raises AST and ALT on its own, and so does retatrutide, so context matters before anyone panics.

Creatinine elevated from creatine supplementation is not kidney damage. It is the breakdown product of the thing you are taking.

For micronutrients, run vitamin D, B12, folate, a ferritin panel for iron, and intracellular magnesium rather than serum, because serum magnesium only shows a very small picture of what you actually have in your body.

Most of what I know about this came out of conversations in the free community, so if you want the rest of it and somewhere to ask, the men's group is here: https://www.skool.com/jh-iron-forge-brotherhood/about

Research: Sniderman et al., European Heart Journal 2024; Bassuk, Rifai & Ridker, Current Problems in Cardiology 2004; Cui et al., Cardiovascular Diabetology 2024.

References

Sniderman AD, Dufresne L, Pencina KM et al.. Discordance among apoB, non-high-density lipoprotein cholesterol, and triglycerides: implications for cardiovascular prevention. Eur Heart J. 2024. https://pubmed.ncbi.nlm.nih.gov/38700053/

Bassuk SS, Rifai N, Ridker PM. High-sensitivity C-reactive protein: clinical importance. Curr Probl Cardiol. 2004. https://pubmed.ncbi.nlm.nih.gov/15258556/

Cui C, Liu L, Qi Y et al.. Joint association of TyG index and high sensitivity C-reactive protein with cardiovascular disease: a national cohort study. Cardiovasc Diabetol. 2024. https://pubmed.ncbi.nlm.nih.gov/38715129/