A vitamin D blood test reports 25-hydroxyvitamin D, the liver’s storage form. It is not the active hormone that the kidney, immune cells and gut lining make from it. Read it as a fuel gauge. The number shifts with the lab method and with high cholesterol. And whether it counts as low depends on which committee drew the line.
She is thirty-eight, and Crohn’s disease has cost her most of her small bowel across two operations. Her vitamin D blood test came back at 47 nmol/L. It was flagged low normal and filed. Nobody asked why a woman who works outdoors and takes a supplement was that low at all.
That report was not wrong, exactly. It answered a different question than the one her body was asking. The video for Chapter 10 of The Angry Gut, by Dr. Gurpreet Singh Padda, MD, MBA, MHP, and Ami Michelle Grimes, argues that vitamin D is a hormone. This article is about the lab slip. It covers what it measures, what moves it, and what a regenerative practice does with it.
What does a vitamin D blood test measure?
The standard test reports 25-hydroxyvitamin D. That is the liver’s storage product, the raw material. The active hormone, 1,25-dihydroxyvitamin D, is made from it in the kidney. It is also made locally inside immune cells and the gut lining.
The two differ hugely in strength. In human cell work, the storage form reached half its gene-steering effect at an average of 322 nM. The hormone did so at 0.48 nM. Below 250 nM, the storage form barely touched gene activity.
Here is the fair objection. Those tests used blood cells, which have very little of the enzyme that activates vitamin D. So they show what the storage form cannot do alone, not what gut tissue does with it. You cannot make the hormone without raw material. But the raw material number is not the tissue’s signal. Treat the report as a fuel gauge, not a speedometer.
Why do vitamin D results differ between labs?
Before you read a level, ask how it was produced. When survey tests were re-standardized, the share of Americans below 50 nmol/L rose from 22% to 31%. A German survey’s share below 30 nmol/L fell from 28% to 13%. The same methods paper found that one person’s level could land anywhere from 20 to 35 ng/mL, depending on the lab method. Its authors called for pausing pooled reviews built on results that were not standardized.
Mass spectrometry is the reference method. In one national survey, the original immunoassay (a common lab test) put 6.5% of people below the deficiency line. Standardizing projected 11.4%. Re-running every stored sample by mass spectrometry confirmed 11.2%.
Can high cholesterol affect a vitamin D blood test?
This detail should change how metabolic patients read their labs. Blood fats throw off the common immunoassay. Compared against mass spectrometry, the immunoassay read low by 5.5 nmol/L overall. In people with lower non-HDL cholesterol, the gap was 4.0 nmol/L. Above the cutoff, it widened to 10.2. Standardizing the test did not remove the error.
Follow that forward. The insulin-resistant patient with high cholesterol gets a falsely low vitamin D. The published link between high cholesterol and low vitamin D partly existed only on that test. The metabolically healthy patient gets reassurance. If your blood fats are high, the method used for your test is not a trivia question.
Who decides what counts as low vitamin D?
A reference range describes a crowd. More than 40 international guidelines exist, and their target levels span 10 to 40 ng/mL. One committee treats 30 nmol/L as the risk line and 50 nmol/L as enough for 97.5% of people. Another starts deficiency at 50 and aims above 75. Around the world, 15.7% of people sit below 30 nmol/L and 76.6% below 75. So it affects one person in seven or three in four, depending on the committee. That is an argument over definitions, not a diagnosis.
The crowd is also not neutral. Across 55,844 Europeans, 17.7% fell below 30 nmol/L in the October-to-March months, against 8.3% in summer. One representative Finnish sample showed big gaps. Below that line were 50.4% of Kurdish immigrants and 28.0% of Somali immigrants. Only 4.5% of Russian-speaking immigrants and 0.4% of native Finnish adults were. Same country, same winter. The intake tables built from these ranges came mostly from light-skinned volunteers living indoor lives. Then they were handed to everyone.
What drains vitamin D from your body?
A damaged bowel lowers the level, not the other way around. Gene-predicted vitamin D cannot be moved by illness. It gave hazard ratios of 0.98 for Crohn’s disease and 1.01 for ulcerative colitis in the Copenhagen and UK Biobank groups. Low vitamin D did not cause her disease.
But deficiency tracks how badly the gut is working. Across inflammatory bowel disease studies, the odds of deficiency were 1.85 with active disease and 1.61 after past surgery. They were 1.78 with biologic drugs and 1.38 for Crohn’s over colitis. Being non-Caucasian carried 3.79, larger than any disease factor. Two drivers add up here. One is a fat-soluble storage form that a shortened or inflamed bowel cannot take in. The other is skin that makes less in weak northern light. Add a third that is social: work, housing and screens that keep people inside.
Treatment evidence in the bowel is thin and short. Across 22 trials and 1,874 patients, one outcome had enough data. Relapse fell, with a risk ratio of 0.57, at low certainty. The 2024 Endocrine Society guideline suggests against routine testing because no trial of a screening plan exists. And it was written for people with no clear reason to test. A missing small bowel is a clear reason.
The gut barrier behind this problem was the subject of the chapter on a gut short of oxygen. The next step, what crosses that barrier and reaches the spine, is in the disc microbiome. It also fits the wider pattern of the gut driving joint pain.
Repairing the deficit without chasing a number
Our position: when someone has a reason to be deficient, we test. We replace daily, not in large one-time doses. We fix the level and stop, instead of pushing it ever higher. No trial has set a vitamin D target for patients who absorb poorly, have had bowel surgery, or have had weight-loss surgery. So the target rests on how the body works and on the harm seen with too much. We apply it to the patient in the room.
The dose is individual. Keeping 97.5% of dark-skinned people at high latitude above 25 nmol/L through winter took about 956 IU a day. The same study warned about intakes high enough to bring everyone to the top target. At those doses, the top 2.5% could reach 158 nmol/L or more.
The repair work sits upstream of the pill. Cool the bowel so it can absorb. Get regular daylight on skin. Skin makes the storage form on a steady schedule the body can control. Cut excess body fat, which holds the molecule out of the blood. This is the same logic behind why metaflammation decides whether treatment works.
When you next see your result, ask three things. Was it immunoassay or mass spectrometry? Are my blood fats high enough to bend it? Which committee’s range is on this report? The full study list, with every number and what each study cannot show, is in the Chapter 10 Deep Dive.
Frequently asked questions
What is a normal vitamin D level?
It depends on which committee you ask. One widely used framework treats 30 nmol/L as the risk line and 50 nmol/L as enough for nearly everyone’s bones. Another calls anything under 50 deficient and aims above 75. Guidelines around the world span 10 to 40 ng/mL. A normal flag tells you where you sit in a crowd, not whether your tissue has enough. We explain how the result matters for repair in vitamin D status and musculoskeletal healing.
Is the vitamin D blood test accurate?
Mass spectrometry is the reference method, and common immunoassays drift from it. In one Canadian survey the immunoassay read 5.5 nmol/L low on average. The gap more than doubled in people with higher non-HDL cholesterol. Re-standardizing has also moved national deficiency rates by several percentage points. Ask which method your lab used. A broader panel for judging whether the body can heal is described in the metabolic audit.
Why is vitamin D called a hormone instead of a vitamin?
Because the body makes it and controls it. Skin makes it from cholesterol in sunlight, and the liver and kidney convert it. It acts through a receptor in the cell’s core, in the same family as the receptors for estrogen, cortisol and thyroid hormone. Parathyroid hormone and fibroblast growth factor 23 then adjust how much becomes active. Its receptor mostly steers immune genes. That links to how the immune system learns what to tolerate.
Should everyone get a vitamin D test?
Not routinely. The 2024 Endocrine Society guideline suggests against testing in the general public because no trial has tested a screening plan. That reasoning does not cover people with a clear reason to run low. Examples are bowel disease, past bowel surgery, darker skin at northern latitudes, or a lot of excess weight. For them the test answers a real question. Inflammation markers deserve the same targeted logic, as in hsCRP and inflammation biomarkers.
Can gut problems cause low vitamin D?
Yes. Vitamin D is fat-soluble. So a bowel that is inflamed, shortened by surgery or absorbing poorly lets less of it in. In inflammatory bowel disease, active disease, past surgery and biologic drugs all raised the odds of deficiency. Gene studies show low vitamin D did not cause the bowel disease itself. The shortfall is a result that renews every day. The barrier at the center of it is covered in the leaky gut wall.
What is vitamin D called on a blood test?
The standard test reports 25-hydroxyvitamin D, the storage form the liver makes. It is the raw material, not the active hormone. The active form, 1,25-dihydroxyvitamin D, is made from it in the kidney and locally inside immune cells and the gut lining. Read the number as a fuel gauge for supply. It does not measure what your tissues are really signaling.
Is it better to take vitamin D daily or in large doses?
When someone has a reason to be deficient, we test. We replace daily, not in large one-time doses. We fix the level and stop, instead of pushing it ever higher. The dose is individual. The repair also sits upstream of the pill. Calm the bowel so it can absorb, get regular daylight on skin, and cut excess body fat, which holds the molecule out of the blood.
What should I ask about my vitamin D test result?
Ask three things. Was the test run by immunoassay or by mass spectrometry, the reference method? Are my blood fats high enough to bend an immunoassay result low? And which committee’s reference range is printed on this report? The answers decide whether a low or normal flag describes your body. It may only describe the lab method and the crowd behind the range.
Read the number in context
A vitamin D result means something only next to your gut, your skin, your cholesterol and the method that produced it. We read it that way, then repair the terrain that set it.
Questions? Call or text us.
Sources
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