If you live above the 50th parallel, which includes all of Germany, Finland, the Nordics, and most of Northern Europe you have got a huge problem. There's a period of roughly five to six months each year when your skin cannot produce meaningful amounts of vitamin D from sunlight. The sun angle is simply too low for UVB radiation to penetrate the atmosphere in sufficient quantities. [1]
In a way it's a physics problem we northerners try to cure with winter trips to sunny locales from Spain to the Maldives. But that hides the brutal fact that for half the year, your vitamin D status depends entirely on what's in your diet and what's in your supplement stack. But also, critically, whether your body is actually absorbing and activating any of it.
Most people, including yours truly in the past, skip straight to the supplement. After all, buying supplements online is super easy and it gives you a great feeling that you have done something important for your health. We think there is a better way. Even for something as simple as vitamin D supplementation. What we at Aniva believe is that we should be doing first is measuring.
Germany is one of the best-documented cases of widespread vitamin D inadequacy in a wealthy European country. National survey data from the German Health Interview and Examination Survey (DEGS1) found that 30.2% of German adults have deficient vitamin D status (serum 25(OH)D < 30 nmol/L), and only 38.4% have adequate levels. [2] The seasonal swing is dramatic: in summer, 8.3% of adults are deficient. In winter, that number rises to 52%. [2]
That's huge.
Standardized European data from the ODIN project, which applied a unified reference method across 14 population studies and 55,844 individuals, confirmed that mid-latitude countries like Germany, the UK, Ireland, and the Netherlands had higher deficiency prevalence than more northerly countries like Finland and Norway. [3] The reason for this counterintuitive finding has everything to do with policy, and nothing to do with geography.
Finland sits between the 60th and 70th parallels. It has some of the longest winters in Europe. And yet, Finland has one of the best vitamin D statuses on the continent. The reason: a deliberate, national food fortification policy.
In 2003, Finland began mandatory fortification of fluid milk products and fat spreads with vitamin D. When the initial dose proved insufficient, they doubled it in 2010. [4] The results were remarkable. In an 11-year nationally representative follow-up study (Health 2000 and Health 2011 surveys, 10,185 adults), mean serum 25(OH)D rose from 48 nmol/L to 65 nmol/L. The prevalence of levels below 50 nmol/L dropped from 55–57% to just 9% in both men and women. [4] [5]
Among young Finnish men (18–28 years), the impact was even faster: within one year of fortification, mean wintertime serum 25(OH)D increased by 50%, and the prevalence of insufficiency (<40 nmol/L) was cut in half: from 78% to 35%. [6]
Germany has no comparable fortification policy. This means that for German residents, and for most of Europe outside the Nordics, supplement decisions are left entirely to the individual. We as individuals, overwhelmingly, are stuck at guessing.
Vitamin D status is assessed by measuring serum 25-hydroxyvitamin D, written as 25(OH)D. This is the storage form of vitamin D that circulates in your blood and reflects your total input from sun exposure, diet, and supplements over the preceding two to three months. [7] It is not the biologically active form (that's 1,25(OH)₂D, or calcitriol, which is tightly regulated by the kidneys and doesn't reliably reflect your overall vitamin D stores).
If your GP tests "vitamin D," they should be ordering 25(OH)D. Some labs still test 1,25(OH)₂D by default, which can appear normal or even elevated while you're deficient. Creating a dangerously misleading result. Aniva's minerals & nutrients panel measures 25(OH)D, the correct marker.
This is where the controversy lives, and where the biohacking community often oversimplifies.
The Institute of Medicine (IOM) defines sufficiency as 25(OH)D ≥ 50 nmol/L (20 ng/mL). [7] This threshold was set primarily to prevent skeletal disease, including rickets in children or osteomalacia in adults.
The Endocrine Society uses a higher threshold: ≥ 75 nmol/L (30 ng/mL), citing evidence on parathyroid hormone suppression, calcium absorption, and fracture prevention. [7]
Some researchers and functional medicine practitioners argue for even higher targets: 100–150 nmol/L (40–60 ng/mL). They point to observational data linking higher levels with reduced risk of autoimmune disease, respiratory infections, and certain cancers.
What everyone agrees on: below 30 nmol/L (12 ng/mL) is deficiency, and levels between 30–50 nmol/L are inadequate for many biological processes. Beyond that, the "optimal" target depends on your individual risk profile, health goals, and your actual measured level. Which brings us to the central problem.
The supplements alone aren't the answer. The blood test makes for a much better starting point. 52% of German adults are vitamin D deficient in winter, even with supplements readily available. Most of us supplement without testing, andwe have no idea if their dose is working. Aniva's 140+ biomarker panel includes 25(OH)D alongside magnesium, calcium, and every cofactor vitamin D needs to work. The waitlist is free, and a full year of membership is €199.
Here's what the supplement industry doesn't tell you: the same dose of vitamin D produces wildly different blood levels in different people. This isn't a small effect. A randomized controlled trial comparing 4,000 IU/day and 7,000 IU/day found that baseline 25(OH)D concentration alone accounted for a significant portion of variance in outcomes — but even after controlling for baseline, the inter-individual variability was enormous. [8]
Multiple factors determine how much a given dose of vitamin D moves your blood level:
Body composition. Vitamin D is fat-soluble. In individuals with obesity (BMI > 30), vitamin D is sequestered in adipose tissue and less bioavailable. The same dose that brings a lean person to 75 nmol/L may leave someone with higher body fat at 40 nmol/L. [9]
Genetics. Polymorphisms in the vitamin D binding protein (VDBP) gene, the vitamin D receptor (VDR) gene, and the CYP enzymes responsible for hydroxylation all influence how efficiently you absorb, transport, and activate vitamin D. One study found that VDBP genotype significantly affected the 25(OH)D response to identical supplementation doses. [9]
Absorption conditions. Taking vitamin D with the largest meal of the day, ideally one containing fat, improved serum 25(OH)D levels by an average of 50% compared to taking it on an empty stomach, across a wide range of doses. [10]
Cofactor status. This deserves its own section, because it's the piece most people miss entirely.
Vitamin D doesn't work alone. It functions as part of an interconnected system with at least two essential cofactors, magnesium and vitamin K2, and testing vitamin D in isolation is like checking your car's fuel gauge without knowing if the engine is running.
Every enzyme that metabolizes vitamin D in the liver (where vitamin D is converted to 25(OH)D) and in the kidneys (where 25(OH)D is converted to the active form 1,25(OH)₂D), requires magnesium as a cofactor. [11] Without adequate magnesium, vitamin D remains in its inactive form regardless of how much you supplement.
This creates a hidden failure mode that no amount of vitamin D supplementation can overcome. A person can take 4,000 IU of vitamin D3 daily for months, retest, see minimal improvement, double their dose, and still not move the needle, because the bottleneck isn't vitamin D supply. It's magnesium.
This is a direct callback to the problem discussed in our serum vs. RBC testing article: serum magnesium, the standard blood test, reflects less than 1% of your total body magnesium. You can be magnesium-depleted at the tissue level while your serum level looks perfectly normal. Aniva measures both serum and red blood cell magnesium precisely for this reason.
Data from GrassrootsHealth's large-scale observational cohort showed that participants taking both supplemental magnesium and vitamin K2 needed 244% less supplemental vitamin D to achieve a target of 40 ng/mL (100 nmol/L) compared to those taking neither cofactor. [12]
Vitamin D increases intestinal calcium absorption. That's one of its primary roles. But absorption alone is not enough — absorbed calcium needs to go to the right places (bones and teeth) and stay away from the wrong places (arteries, kidneys, soft tissue). This routing function is handled by vitamin K2. [13]
Specifically, vitamin K2 activates two proteins through carboxylation: osteocalcin (which deposits calcium into bone) and matrix Gla protein (which prevents calcium from accumulating in arterial walls). [14] Without adequate K2, high-dose vitamin D supplementation can paradoxically increase the risk of vascular calcification, you're absorbing more calcium, but it's ending up in your arteries instead of your bones. [13]
This is why the clinical recommendation is never to supplement high-dose vitamin D in isolation. The triad of D3 + K2 (as MK-7) + magnesium addresses the coordinated nature of these nutrients and prevents the common clinical error of supplementing vitamin D without the cofactors it needs to function safely and effectively. [14]
If you're supplementing vitamin D without testing — you don't know your starting level, you don't know your body's response, and you don't know whether your magnesium or K2 status is allowing the vitamin D to actually do its job. This isn't minor. It's the difference between a supplement protocol that works and one that's expensive urine.
Vitamin D doesn't work without its cofactors. Neither does testing it in isolation.Your vitamin D level depends on magnesium activation, K2-directed calcium routing, and a dozen individual factors from body composition to genetics. Testing one marker tells you one number. Aniva tests the full picture — vitamin D, magnesium (serum and RBC), calcium, and all the cofactors that determine whether your supplements are actually working.
You wouldn't start a training program without knowing your current max. You shouldn't start a vitamin D protocol without knowing your current 25(OH)D. A baseline measurement tells you whether you need 1,000 IU or 5,000 IU, whether you're mildly insufficient or severely deficient. More importantly, once you retest after 3 months, you get to see whether your dose is actually working for your body.
Vitamin D2 (ergocalciferol) and D3 (cholecalciferol) are not equivalent. While both produce initial increases in 25(OH)D within 72 hours, D3 continues to raise levels for 14 days while D2 does not, making D3 roughly 9.5 times more potent by 28-day area-under-the-curve measurements. [15] Most experts recommend cholecalciferol (D3) exclusively.
The biohacking community sometimes promotes extremely high doses, sometimes 10,000 IU/day or more, without regular blood monitoring. Vitamin D toxicity is real and results in hypercalcemia (dangerously elevated blood calcium), which can cause kidney stones, nausea, cardiac arrhythmias, and calcification of soft tissues. [7] Toxicity is typically associated with 25(OH)D levels above 375 nmol/L (150 ng/mL), which is difficult to reach at standard supplement doses but not impossible with chronic high-dose supplementation, especially in lean individuals with efficient absorption.
Even if you tested once and achieved a good level, your status changes with the seasons. In Northern Europe, levels reliably drop through autumn and hit their nadir in February/March. A level of 80 nmol/L in August might be 45 nmol/L by March without any change in supplementation. This is normal, and it's why Aniva's approach of regular, comprehensive testing is fundamentally different from a one-time snapshot.
A 25(OH)D level of 60 nmol/L means something different in a person with adequate magnesium, K2, and calcium than in a person who is depleted in all three. The number doesn't tell you how much of that vitamin D is being activated, how much calcium is being properly routed, or whether your parathyroid hormone (PTH), which rises when vitamin D is insufficient to maintain calcium homeostasis, is elevated. A comprehensive panel captures these relationships. A single vitamin D test doesn't.
Finland didn't solve its vitamin D problem with supplements alone. It used data. National testing. Evidence-based fortification. A measurable policy that raised mean 25(OH)D from 48 to 65 nmol/L in 11 years. You can apply the same principle to your own body: measure, intervene, remeasure. Aniva makes this practical with 140+ biomarkers per draw, including vitamin D, magnesium, calcium, and inflammation markers. Waitlist is free. Full membership: €199/year.
Vitamin D is not a simple nutrient with a simple fix. In Northern Europe, sun exposure is physically insufficient for nearly half the year. Germany has no national fortification policy, leaving half its adult population deficient in winter. Finland proved that systematic, data-driven intervention works. Raising its national mean 25(OH)D from 48 to 65 nmol/L in a decade through fortification and monitoring. [4]
At the individual level, the same supplement dose produces dramatically different outcomes depending on body composition, genetics, absorption conditions, and cofactor status. Magnesium is required to activate vitamin D. Vitamin K2 is required to safely direct the calcium that vitamin D helps absorb. Without testing, you have no way to know whether your protocol is working — or whether you're spending money on supplements your body can't use.
Aniva's 140+ biomarker panel includes 25(OH)D alongside the cofactors that determine whether vitamin D can do its job: magnesium (serum and RBC), calcium, and the full minerals and nutrients profile. Because the supplement isn't the answer. The blood test is the starting point.
Medical disclaimer: This content is for informational purposes only and is not medical advice. Always discuss results with a qualified healthcare professional.
