The Bloodwork I Read in an Integrative Oncology Consultation
This article is educational and reflects how I approach laboratory interpretation in clinical practice. It is not medical advice, it does not diagnose any condition, and it is not a substitute for the care of your own physician or oncology team. Please don't change your treatment, diet, or supplements based on this article without first speaking to your doctor.
Most oncology panels stop at a CBC and a complete metabolic panel, the minimum, not the full picture. In twenty years of practice, I have rarely, if ever, seen insulin or hs-CRP ordered as part of a standard oncology workup. Vitamin D is different, rare years ago, but I'm seeing it tested more and more now. Even then, it's usually the patient who has to ask for it, and the request is often met with skepticism, despite research linking higher vitamin D levels to better cancer outcomes. Most people assume time in the sun is enough. What I see tested rarely confirms that, and even supplementing doesn't guarantee adequate levels, a clinical trial I co-authored found the delivery form of the supplement affected whether people reached sufficiency at all, even at an identical labeled dose. Neither insulin nor vitamin D status is standard in conventional oncology, but naturopathic oncology has been reviewing this information for decades.
A reference range on a lab report describes the statistical spread of a testing population, not a picture of health. Those ranges are built from whoever got tested, and as more of that population carries excess weight, insulin resistance, and chronic inflammation, the range shifts along with them. Look around at the people you know. Most aren't thriving. A result that falls inside a range built from a population that isn't healthy doesn't tell you much about what your own body is capable of. What I'm interested in is optimal, not the average of a population that keeps getting sicker.
When I sit with someone's labs, I'm not searching for the one number that explains why cancer developed. Cancer doesn't work that way, and no single value carries that kind of answer. Instead I read for patterns, weighing each marker against an optimal target rather than the wide band a lab is willing to call normal. How is this body handling sugar and insulin, where is inflammation sitting and how loudly, and what does the metabolic environment look like that treatment is now happening inside of?
None of these markers diagnose cancer. None of them predict recurrence. What they offer is context. They show me where a body may need support while you move through treatment and into the years that follow. Below are some of the markers I return to most, along with the ranges I'm working toward.
Fasting Insulin
Fasting insulin is the one marker on this panel almost nobody's ever had checked, even though it usually tells me more than glucose, which is the one test everybody's already had.
Insulin does more than move sugar out of the blood. It's a growth signal, speaking to pathways involved in metabolism, inflammation, and how readily cells divide, and it runs in the same circuitry as IGF-1, another growth factor I watch closely and one that deserves its own discussion. Conventional labs often flag fasting insulin only when it climbs into the high teens or low twenties. The target I'm working toward is far tighter. A fasting insulin around 2 to 3 microIU/mL is where I consider metabolic signaling calm and well regulated.
This is why a normal glucose can be so misleading. When insulin runs high while glucose still reads normal, that combination tells me the body is working overtime to keep the glucose number looking reassuring. The effort is real even when the result on paper looks fine. Higher circulating insulin has been linked with poorer outcomes in several cancers, breast, colorectal, and pancreatic among them, so this is one of the first places I look. I go deeper into the blood sugar and cancer connection elsewhere on the site.
IGF-1
Fasting insulin isn't the only marker missing from a standard panel. IGF-1 runs on a related, separate track. Where insulin comes from the pancreas in direct response to glucose, IGF-1 is produced mainly by the liver in response to growth hormone, and the two axes only partially overlap.
IGF-1 is a growth signal. It binds the IGF-1 receptor, which many tumors, breast, colorectal, and prostate cancer among them, carry directly on their cell surface, along with a hybrid receptor that binds both insulin and IGF-1. When IGF-1 binds either receptor, it activates the same downstream pathway insulin does, PI3K, AKT, and mTOR, pushing the cell to keep dividing and to resist the signals that would normally tell it to stop or die. A tumor carrying these receptors sitting in a body with elevated IGF-1 has more fuel feeding that signal directly, which is why I track it alongside insulin rather than treat it as a side note.
Unlike fasting insulin or glucose, IGF-1 doesn't have one clean number I'm working toward across every patient. It shifts with age, sex, and how much muscle mass and resistance training someone is doing, all independent of metabolic health. A younger, athletic person can run a higher IGF-1 than a sedentary person with identical insulin sensitivity, and that difference reflects a normal growth and repair signal rather than dysfunction.
Diet plays a role too. Circulating IGF-1 rises with dietary protein intake, dairy protein especially, largely independent of what insulin is doing. Someone with excellent insulin sensitivity and a fasting insulin sitting right at target can still be running a higher IGF-1 purely from how much animal protein and dairy they're eating.
This is where insulin and IGF-1 connect at the mechanism level. Insulin plays a permissive role in how responsive the liver is to growth hormone, meaning adequate portal insulin is part of what allows the liver to convert a GH signal into IGF-1 in the first place. This is part of why prolonged fasting tends to lower insulin and IGF-1 together, rather than IGF-1 rising to compensate for falling insulin. When insulin drops far enough, the liver's ability to respond to growth hormone drops with it.
I don't read IGF-1 in isolation, and I'd be cautious of any source handing you a single universal target for it. What I look for is the pattern alongside insulin, glucose, and HOMA-IR, and whether an elevated IGF-1 traces back to something adjustable, like protein intake, or reflects a training and muscle mass pattern that's serving the body well.
Fasting Glucose
I still check glucose, especially read next to insulin. A result under 100 mg/dL gets called normal, and 100 to 125 gets called pre-diabetic. The range I'm working toward is lower and narrower, roughly 70 to 85 mg/dL, where glucose sits steady without the pancreas or adrenal glands having to work overtime to keep it there.
On its own, glucose can look perfectly steady while insulin is already climbing, which is the trap of reading it in isolation. What I'm usually watching is the trend as much as the single value. Is it holding steady, or drifting upward across successive panels? Is it improving as someone does the work? The direction of travel tells me as much as where the number lands on one particular morning.
HOMA-IR
Insulin and glucose become more revealing read together than apart, and there's a simple way to combine them called HOMA-IR. You multiply fasting glucose in mg/dL by fasting insulin in microIU/mL and divide by 405. A value below 1.0 is where I consider insulin sensitivity intact. As that number climbs, it tells me the body is spending more and more insulin to keep glucose in range, often long before glucose itself looks abnormal on any standard report. If you want one calculation that captures metabolic health in a single figure, this is the one I'd reach for first. I go further into this insulin-mitochondria relationship in The Metabolic Roots of Chronic Disease.
Hemoglobin A1c
Where a fasting glucose is a single snapshot, A1c is the three-month average. It reflects how blood sugar has behaved over roughly the prior ninety days, which makes it far harder to flatter with one disciplined morning before the draw.
The conventional cutoffs put 5.7% at the entry to pre-diabetes and 6.5% at diabetes. 5.7% marks disease, not health, and it's not what I'm aiming for. The level I consider optimal is 5.0% or below. Glucose that stays elevated over time feeds oxidative stress, low-grade inflammation, and damage to blood vessels, and it can reveal metabolic strain that's been building quietly for years. When A1c comes back high, it opens a longer conversation about food, movement, sleep, stress, and how sensitive the body still is to its own insulin.
High-Sensitivity C-Reactive Protein
Inflammation runs underneath nearly every chronic disease, cancer included. Hs-CRP is a protein the liver releases when inflammatory signaling picks up. It won't tell me where the inflammation is coming from, only that the process is switched on somewhere in the body.
The widely used cutoffs read under 1.0 mg/L as low risk, 1 to 3 as moderate, and above 3 as high. The target I want in this setting is under 1.0 mg/L, and the closer to the floor, the better. Plenty of things can push it up: visceral fat around the organs, insulin resistance, a smoldering infection, an autoimmune condition, broken sleep, chronic stress that never fully resolves. So when hs-CRP is elevated, my first question is why. What's feeding the signal, and which of those inputs can we change together? Reductions in inflammation come from addressing the drivers underneath, rather than from chasing the value on the page. Immune function and inflammation intersect directly with treatment response too, which I cover in What Determines Whether Your Immunotherapy Works.
Vitamin D
Vitamin D does far more than look after bone. Its receptors show up throughout the body, including on immune cells, and adequate status plays into immune regulation, how cells mature and differentiate, and the balance of inflammation.
Most labs call anything above 30 ng/mL sufficient. The level I'm working toward is a good deal higher, in the range of 70 to 80 ng/mL, where the immune and regulatory roles of vitamin D have the most room to operate. Low vitamin D is common in the general population and more common still among people facing cancer. It isn't a cancer treatment, and I'm careful never to frame it as one. What adequate levels can do is support immune function and resilience during treatment and afterward. I check it early in nearly every workup, partly because deficiency is so frequent and partly because it's one of the more straightforward things to correct once we see it. I've written more on vitamin D's role in immune regulation here.
Ferritin
Ferritin is a marker I'm cautious about pinning to one universal number, because the right target depends on the person in front of me, but broadly, I like to see it around 70 ng/mL. It gets used as a simple iron-storage value, and it's rarely that simple. Low ferritin can mean depleted iron stores, and that shows up as fatigue, low stamina, and slow recovery. High ferritin can mean excess iron, or it can climb purely because inflammation is present, since ferritin doubles as an acute-phase reactant.
Broadly, I want enough stored iron to stay clear of deficiency while avoiding the accumulation and the inflammatory elevation that push ferritin upward, which for most people means a moderate range rather than either extreme. That double meaning is why I never read it alone. I want it alongside iron saturation, total iron binding capacity, a complete blood count, and the inflammatory markers. When ferritin runs high, the question is whether that reflects true iron loading or simply active inflammation, and those companion tests are what let me tell the two apart. A prospective cohort of 455 breast cancer patients found that a pre-treatment ferritin above roughly 163 µg/L was an independent predictor of severe acute skin reactions during radiotherapy, nearly tripling the risk compared to lower levels. That's a number I want visibility on well before treatment starts, not after a reaction has already begun.
Reading the Whole Panel, Not One Number
Lab work earns its value when I read it as a system, and when I read it against optimal rather than merely normal, since those normal ranges keep drifting as the population they're drawn from gets sicker. Someone with insulin above target, an hs-CRP over 1, vitamin D sitting at 32, and an A1c creeping toward 5.7 is showing me something quite different from someone with a single lone result out of range. Each of those might be called normal on its own report. Together, they form a pattern that a single result never shows, and that pattern points me toward the parts of physiology where nutrition, lifestyle, metabolic support, and targeted therapies can help. Healing the Terrain goes deeper into this whole systems approach.
Bloodwork has limits, and one of the biggest is that it's a snapshot, not a fixed reading. A panel drawn three months ago can look completely different from one drawn today, and the same person can get different numbers depending on whether they slept well the night before or came in running on three restless nights and stress. It doesn't stand in for pathology or imaging, and it doesn't replace the oncology care you're already receiving. What it offers is a window into the internal environment where recovery and long-term health are taking place, and when I can see that environment clearly, held to a standard of optimal rather than average, I can help you support it with intention rather than guesswork.
If you've been told your labs are normal and still sense that something is off, that instinct deserves attention. The functional patterns I've described often live quietly inside a normal report, shaping how a body handles treatment and what its terrain looks like once treatment ends. Bringing that level of attention to your own physiology is exactly the kind of work I do with patients who want to look past the surface of a result.
Common Questions
What is the difference between a normal lab result and an optimal one?
A normal result means a value falls inside the range a lab uses to flag statistical outliers, drawn from a general testing population. An optimal result reflects what supports health and resilience, which is often a tighter and more demanding target. Many results sit inside normal while sitting well outside optimal.
What is an optimal fasting insulin level?
I work toward a fasting insulin around 2 to 3 microIU/mL. Many labs won't flag insulin until it reaches the high teens or beyond, so a result can look normal while insulin is doing far more work than it should.
Do these blood markers diagnose cancer or predict recurrence?
No. They don't diagnose cancer and they don't predict recurrence. I use them to understand inflammation, metabolic health, immune function, and nutritional status, the environment in which treatment and recovery are taking place.
Are these tests a replacement for my oncologist's bloodwork?
No. They sit alongside conventional oncology care, never in place of it. Pathology, imaging, and your oncology team remain central, and this work adds a functional, metabolic layer to the picture.
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If you want a clinician who reads your bloodwork against optimal rather than average and builds a plan around the whole picture, you can work with me here.
References
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