Today I want to highlight one of the most underrated but powerful factors for healthy aging and longevity: vitamin D. Optimizing your vitamin D status is simple, affordable, and can have a profound impact on your overall health. While most people think of vitamin D mainly for bone health, research shows its influence reaches far beyond that. And that is immunity, energy, mood, metabolism, and even lifespan.

In this post, we’ll explore why vitamin D deficiency is so common, the science-backed links between low vitamin D and accelerated aging, and the optimal blood levels to aim for. You’ll also learn exactly how much to supplement, how to monitor your status, and key safety considerations so you can feel confident in getting it right.

Let’s dive into the evidence and break down step-by-step how you can use vitamin D to support your health and longevity.

Table of Contents

• Introduction: Why I care so much about vitamin D
• What vitamin D does: beyond bones
• Why vitamin D deficiency is so widespread
• The biological evidence: vitamin D and aging
• Human evidence connects low vitamin D to worse outcomes
• Randomized controlled evidence and biomarkers of aging
• What do blood tests mean: deficiency, insufficiency, and the sweet spot
• How much vitamin D raises blood levels: dosing math
• My practical vitamin D protocol: step-by-step
• Why monitoring matters: genetic variability and responsiveness
• Special populations and considerations
• Safety: toxicity, monitoring, and co-factors
• Choosing a supplement: form, timing, and brand considerations
• Real-world dosing examples
• Why I personally target 40–60 ng/mL
• Monitoring timeline and what to do if numbers don’t move
• What about getting vitamin D from sun exposure and diet?
• Key takeaways and my recommendations
• Where to go from here
• Frequently asked questions (FAQ)

Vitamin D is often described as a vitamin, but that is a misnomer that understates how important it is. Vitamin D3 (cholecalciferol) is converted in the body into a steroid hormone that travels into the nucleus of cells and binds to the vitamin D receptor. That receptor acts like a switchboard in our DNA, turning genes on and off by recognizing specific sequences called vitamin D response elements.

To give you a sense of scale: more than 5 percent of the protein-encoding human genome is regulated directly by vitamin D, as detailed in a genomic analysis of vitamin D receptor binding sites across human tissues (MDPI Genes). That is a huge proportion of our genome being influenced by a single hormone-like molecule. If that regulation is off, it affects a broad range of physiological processes — from immune function to cellular repair to metabolism — all of which influence how we age.

Most people associate vitamin D with bone health, and that’s only part of the story. When active, vitamin D binds to the vitamin D receptor (VDR) and either activates or represses target genes. This genomic action affects immune function, inflammation, cell proliferation and differentiation, and many other processes that determine tissue health and resilience.

Because vitamin D acts at the level of gene regulation, deficiency isn’t a minor biochemical hiccup. It changes how genes are expressed across multiple tissues, and those small changes, when widespread and chronic, compound over years and decades.

Across the US population, roughly 70 percent of people have inadequate vitamin D levels — most commonly defined as serum 25-hydroxyvitamin D below 30 ng/mL — with the highest rates among African Americans, women, and during winter months (Frontiers in Nutrition) There are multiple, often compounding reasons for this:

• Synthesis requires UVB radiation. The skin makes vitamin D3 when exposed to UVB wavelengths. Anything that reduces UVB exposure reduces vitamin D synthesis.
• Sunscreen. Modern sunscreen blocks UVB and therefore reduces cutaneous vitamin D production.
• Skin pigmentation. Melanin is an effective natural sunscreen. People with darker skin must spend significantly more time in the sun to produce the same amount of vitamin D as lighter skinned individuals.
• Latitude and season. At higher latitudes the sun’s angle prevents UVB wavelengths from reaching the surface for months of the year. In those months, cutaneous synthesis is negligible.
• Age. As we age, our skin becomes less efficient at making vitamin D. A 70-year-old produces much less vitamin D3 from the same sun exposure than a 20-year-old.
• Modern indoor lifestyle. We work indoors under artificial light, commute in cars, and generally spend far less time outdoors than previous generations.

To give you a concrete example from the research: studies have shown that African Americans may need to spend six to ten times longer in the sun than fair-skinned Caucasians to produce the same amount of vitamin D3. Combine darker skin pigmentation with living at a northern latitude, and the effect multiplies.

When we look across species and models, vitamin D signaling clearly affects aging-related processes. In 2009, researchers created mice that lacked the vitamin D receptor. Those animals developed a range of accelerated aging phenotypes compared with wild-type controls. Organs and tissues showed signs of premature decline. That visual study is stark because it directly ties the receptor for vitamin D to systemic aging pathways.

Of course mice are not humans. There are limitations to translation because mice are nocturnal and live very different lives. Still, those models provide useful mechanistic clues: interrupt vitamin D signaling, and you disrupt the orchestration of a large set of genes that maintain tissue function over time.

In humans, the epidemiology is consistent. Large observational studies find that low 25-hydroxyvitamin D levels are associated with increased all-cause mortality, higher cancer mortality, and higher mortality from respiratory illnesses. However, observational data can’t prove causation because of confounding factors — people with higher vitamin D levels might simply be healthier on average, more active, or have other advantages.

That’s where genetic methods such as Mendelian randomization help. We all carry genetic variants that affect how we metabolize vitamin D into its circulating form, 25-hydroxyvitamin D. Some variants reduce conversion efficiency and therefore produce chronically lower circulating levels. Mendelian randomization treats these genetic variants as natural randomization; it examines whether people who are genetically predisposed to lower vitamin D have different health outcomes independent of lifestyle.

Multiple Mendelian randomization studies — which use genetic variants as natural experiments — have linked chronically lower vitamin D levels to higher risks of all-cause, cancer-related, and respiratory disease mortality, strengthening the case for a causal role (Epidemiology Review, Springer).

Long-term mortality randomized controlled trials specifically designed to test vitamin D for decades are unrealistic. But we can test intermediary endpoints related to aging biology. One of these is epigenetic age, which uses DNA methylation patterns as a biomarker of biological aging. In a randomized clinical trial of overweight African Americans with low baseline vitamin D, supplementation with 4,000 IU per day slowed biological aging markers, reducing epigenetic age by nearly two years compared with controls (Journal of Gerontology).

That finding is powerful because it looks at a mechanistic aging biomarker and shows a measurable reversal of epigenetic age with vitamin D repletion in people who started deficient.

When we talk about vitamin D status we are referring to serum 25-hydroxyvitamin D, abbreviated 25(OH)D. Different organizations define cut points slightly differently, but a practical framework is:

• Deficiency: less than 20 ng/mL
• Insufficiency: less than 30 ng/mL (a common clinical threshold)
• Sufficiency: typically greater than 30 ng/mL

However, when researchers look at all-cause mortality across many studies, the lowest mortality tends to cluster when 25(OH)D is in the 40 to 60 ng/mL range. That is the sweet spot I personally target for otherwise healthy adults aiming for longevity outcomes.

Practical dosing is the most actionable part of this conversation. Two important points:

• Vitamin D3 (cholecalciferol) is the preferred supplemental form. It raises serum 25(OH)D more reliably than vitamin D2.
• On average, 1,000 IU per day of vitamin D3 raises serum 25(OH)D by about 5 ng/mL. Use this as a rule of thumb for dose calculations, but remember individual response varies.

I use this simple math to calculate approximate starting doses. For example, if your baseline 25(OH)D is 15 ng/mL and you want to reach 50 ng/mL, you need an increase of 35 ng/mL. Using the rule of thumb (1,000 IU raises ~5 ng/mL), 35 ng/mL increase would require about 7,000 IU per day in total. In practice I often start with 6,000 to 8,000 IU per day for several weeks and then recheck blood levels to refine the dose.

Important safety note: the generally accepted tolerable upper intake level for adults is 4,000 IU per day. That value is conservative and is set to minimize risk of toxicity in the general population without lab monitoring. Many clinicians use short term doses higher than 4,000 IU to replete severe deficiency, but that should be done with appropriate follow up and often under medical supervision.

Because people differ genetically and metabolically, some individuals require far higher doses to reach the same 25(OH)D level. Genetic polymorphisms in enzymes that convert vitamin D3 to 25(OH)D can significantly change responsiveness. You can uncover these variations through our personalized DNA insights, which help explain why two people on the same dose may end up with very different blood levels. The only reliable way to know is by testing.

Below is the exact step-by-step protocol I recommend. It is intentionally simple so you can implement it immediately. Adapt it for special clinical conditions, pregnancy, or if you have complex medical issues and always coordinate with your clinician when making big changes.

1. Baseline test: Order a serum 25-hydroxyvitamin D test. I also recommend getting a basic metabolic panel that includes serum calcium and creatinine if you have risk factors for kidney disease or hypercalcemia.
2. Interpret the result:
   • <20 ng/mL: deficient
   • 20–29 ng/mL: insufficient
   • 30–39 ng/mL: low-normal
   • 40–60 ng/mL: target sweet spot
   • >80 ng/mL: potentially excessive and warrants evaluation
3. Choose initial supplement dose based on baseline (rule-of-thumb math using 1,000 IU ≈ +5 ng/mL):
   • Baseline <10 ng/mL: repletion dose such as 6,000–8,000 IU per day for 8–12 weeks, then recheck. Some providers use a single higher bolus dose followed by maintenance, but daily dosing is often better tolerated and predictable.
   • Baseline 10–19 ng/mL: consider 4,000–6,000 IU per day until levels reach the target.
   • Baseline 20–29 ng/mL: 2,000–4,000 IU per day to reach 40–60 ng/mL depending on how far above 20 you are.
   • Baseline 30–40 ng/mL: 1,000–2,000 IU per day may be enough to reach and maintain 40–60 ng/mL.
   • Once in target range, consider maintenance dose that keeps you at ~40–60 ng/mL—often 1,000–4,000 IU daily.
4. How to take supplements:
   • Use vitamin D3 (cholecalciferol), not D2.
   • Take with a meal containing fat for optimal absorption.
   • Once daily dosing is simple and consistent, but weekly dosing (for example, 20,000–50,000 IU weekly) can be used under guidance.
5. Re-check labs: Re-test serum 25(OH)D 8–12 weeks after starting or changing dose. If you increased a large amount, checking earlier at 6–8 weeks is reasonable. Also check serum calcium if you are taking high doses or have risk factors.
6. Adjust dose: Use your follow up level to adjust the dose to maintain 40–60 ng/mL. If your 25(OH)D is still low despite dosing, consider genetic variability, malabsorption, or drug interactions and work with a clinician to investigate.

You can also explore how we build this into broader lifestyle and supplementation strategies in BetterLife Integrate.

Not everyone responds the same to the same dose. Genetic differences in the enzymes that convert vitamin D into circulating 25(OH)D affect how much supplementation is necessary. Some people carry single nucleotide polymorphisms that blunt conversion efficiency; others have differences in vitamin D binding proteins that alter serum levels. That means two people taking 2,000 IU per day can end up with different serum 25(OH)D concentrations.

That is why I emphasize testing. Guessing is inefficient and may leave you under-repleted or, rarely, over-repleted. You cannot manage what you do not measure.

Here are some groups who commonly need higher doses or special attention:

• People with dark skin pigmentation — require more sun exposure or higher supplementation to reach the same serum level.
• Older adults — produce far less vitamin D in skin; supplementation is often necessary.
• Obese individuals — vitamin D is fat soluble and can be sequestered in adipose tissue, reducing circulating levels. Obese people often need larger doses to achieve the same serum concentrations.
• People living at high latitudes or with low sun exposure — winter months often require year-round supplementation.
• People on certain medications — some drugs affect vitamin D metabolism (for example, anticonvulsants, glucocorticoids, and some HIV medications) and may necessitate higher dosing or closer monitoring.
• People with malabsorption syndromes — conditions like celiac disease, Crohn’s disease, gastric bypass, or chronic pancreatitis may impair absorption of oral vitamin D and require different strategies such as higher oral doses or monitored intramuscular injections.

Vitamin D toxicity is rare but can occur with very high, prolonged doses and is mediated by hypercalcemia. Symptoms of vitamin D toxicity include nausea, vomiting, weakness, frequent urination, dehydration, and in severe cases, kidney damage. Toxicity is far more likely if serum 25(OH)D is extremely high (>150 ng/mL) and is typically accompanied by elevated serum calcium.

To stay safe:

• Don’t routinely exceed 4,000 IU per day without monitoring, unless under clinician supervision for repletion.
• Check serum 25(OH)D after 8–12 weeks when changing doses.
• Check serum calcium if you are using high doses, have symptoms, or have conditions that predispose to hypercalcemia.
• Consider co-factors: magnesium is required for several enzymes in vitamin D metabolism and many people are magnesium deficient. Vitamin K2 helps direct calcium into bone rather than arteries and soft tissues. I often recommend ensuring adequate magnesium status and considering a food-based or K2 supplement if you are taking higher dose vitamin D, but coordinate with your clinician for personalized recommendations.

When selecting a vitamin D supplement:

• Prefer vitamin D3 (cholecalciferol). It is more effective at raising 25(OH)D than D2. You can browse the BetterLife product collection for vetted options we trust and personally recommend.
• Pick a dose appropriate to your goal and baseline level. Many over-the-counter vitamin D3 tablets come in 1,000 IU, 2,000 IU, or 5,000 IU sizes. Liquid drops allow for precise dosing when needed.
• Take with a meal that contains dietary fat to enhance absorption.
• Store appropriately and follow package instructions.

A note about weekly dosing: some people use large weekly doses (for example, 50,000 IU weekly) to improve adherence. That approach can work for maintenance and is commonly prescribed for repletion in clinical practice, but daily dosing is more physiologic and avoids wide peak-trough fluctuations. Either approach can be used, provided you re-check serum levels and monitor clinically.

Below are simple example plans to translate the math into real life. These are examples only. Test and adjust based on your labs and clinical situation.

• Example A — Mild insufficiency: Baseline 25(OH)D 25 ng/mL. Goal 50 ng/mL. Required increase 25 ng/mL. Using 1,000 IU ≈ +5 ng/mL, estimated dose increase ≈ 5,000 IU per day. Recommended starting dose: 4,000 IU per day for 8–12 weeks, then retest.
• Example B — Moderate deficiency: Baseline 12 ng/mL. Goal 50 ng/mL. Required increase 38 ng/mL. Estimated dose increase ≈ 7,600 IU per day. Recommended starting dose: 6,000–8,000 IU per day for 8–12 weeks, then retest and reduce to a maintenance dose once you reach target.
• Example C — Maintenance: Baseline 45 ng/mL. Goal 45–55 ng/mL. Recommended maintenance: 1,000–2,000 IU per day, or 5,000 IU every 3 days depending on response. Retest every 3–6 months.

Two reasons drive my target. First, observational meta-analyses consistently show the lowest all-cause mortality in cohorts with 25(OH)D values in the 40–60 ng/mL range. Second, studies that use mechanistic aging biomarkers, like the epigenetic clock, show measurable improvements when deficient individuals are repleted toward that range. The combination of population-level mortality data and mechanistic biomarkers informs a conservative yet effective target for optimization.

After you start supplementation, I recommend re-checking serum 25(OH)D at 8–12 weeks. If levels have risen as expected, you can reduce to a maintenance dose designed to hold you in the 40–60 ng/mL range. If levels have not increased as predicted, consider the following steps:

• Verify adherence to the supplement regimen.
• Confirm you are taking vitamin D3, not D2.
• Take the supplement with a fat-containing meal to improve absorption.
• Consider other causes of malabsorption or drug interactions.
• Consider that obesity can sequester vitamin D in adipose tissue; higher doses may be required.
• Consult with a clinician about possibility of genetic polymorphisms that affect vitamin D metabolism and consider adjusted dosing strategies or targeted testing.

Sun exposure is the most natural source. However, the amount of sun needed varies by latitude, season, skin pigmentation, age, and sunscreen use. For many people, especially at higher latitudes or during winter months, sun exposure alone is insufficient to maintain 25(OH)D in the optimal range.

Few foods contain significant amounts of vitamin D. Oily fish, cod liver oil, mushrooms exposed to UV light, and fortified dairy or plant milks can contribute, but it is often challenging to reach the 40–60 ng/mL range through diet alone without substantial supplementation or frequent deliberate sun exposure.

• Vitamin D is a hormone-like regulator that controls expression of a large fraction of the protein-coding genome and influences processes central to aging and disease risk.
• Roughly 70 percent of people in the US have suboptimal vitamin D levels. Causes include sunscreen use, indoor lifestyles, skin pigmentation, latitude, age, and genetic differences.
• Aim for a serum 25-hydroxyvitamin D concentration in the 40–60 ng/mL range for longevity and lowest observed all-cause mortality.
• Use vitamin D3 supplements; a practical rule-of-thumb is that 1,000 IU daily raises serum 25(OH)D by about 5 ng/mL, but individual responses vary substantially.
• Start with a baseline test, dose to reach the target based on the math above, recheck 8–12 weeks after starting, and adjust as needed. Monitor serum calcium when using high doses or in at-risk individuals.
• Co-factors like magnesium and vitamin K2 matter for metabolism and calcium balance; ensure adequate intake and discuss supplements with your clinician.

If you want a simple action plan to implement right now:

1. Order a serum 25-hydroxyvitamin D test and a basic metabolic panel if you have risk factors.
2. Start a vitamin D3 supplement at a dose appropriate to your baseline (see dosing examples above).
3. Retest at 8–12 weeks and adjust the dose to achieve and maintain 40–60 ng/mL.
4. Consider optimizing co-factors like magnesium and vitamin K2 as part of an overall strategy for bone, cardiovascular, and metabolic health.

If you want an evidence-backed, convenient resource to help walk through testing and dosing, I post protocols and tools at Betterlifeprotocols.com. My goal is to make these simple, high-value strategies accessible so you can get the measurable benefits for aging and longevity.

Vitamin D optimization is among the highest value, lowest cost interventions I recommend for longevity and overall health. It is cheap, safe when monitored, and has strong mechanistic, genetic, and clinical signals linking adequate status with lower mortality and improved markers of biological aging.

Start with a baseline serum 25-hydroxyvitamin D test, calculate a pragmatic dose based on the guidance above, re-check after 8–12 weeks, and aim for the 40–60 ng/mL range. If you need help translating your lab values into a dosing plan, visit Betterlifeprotocols.com for resources and simple calculators that make the math straightforward.

Optimizing vitamin D is not a silver bullet, but it is one of the most effective, measurable steps you can take today to improve long-term health and resilience. You don’t need to guess. Test, dose, and measure — and you will know whether your cells are getting the hormonal signaling they need.

Q: Do I need to take vitamin K2 with vitamin D?

A: Vitamin K2 is not strictly required to take with vitamin D, but it is a sensible co-factor for people taking higher dose vitamin D long term. Vitamin K2 helps regulate calcium deposition, favoring bone and teeth where it belongs and discouraging deposition in soft tissues and arteries. If you’re looking for a simple, evidence-based option, we include a high-quality Vitamin D3 + K2 supplement in our BetterLife Protocols VIP bundle (featuring CanPrev Vitamin D3 + K2)

Q: Is a single large bolus dose of vitamin D safe and effective?

A: High bolus dosing (for example, 50,000 IU weekly) is commonly used clinically and can be effective for repletion. However, daily dosing is more physiological and avoids very high peaks and low troughs. Some studies have suggested high single bolus doses may have paradoxical short-term adverse effects on immunity. If you use bolus dosing, do so under guidance and monitor levels.

Q: How often should I test my vitamin D?

A: Test 8–12 weeks after initiating or changing a dose to allow levels to stabilize. Once you are in your target range and on a stable maintenance dose, testing every 6–12 months is reasonable, or sooner if you change dose, lose weight, start medications that interfere with vitamin D metabolism, or have symptoms of hypercalcemia.

Q: Can vitamin D supplementation reduce cancer risk?

A: Observational and Mendelian randomization studies link low vitamin D to higher cancer mortality. Some randomized trials and meta-analyses suggest vitamin D supplementation may modestly reduce cancer mortality though results vary. The best evidence suggests vitamin D deficiency is harmful; correcting deficiency is prudent. More definitive randomized trials are ongoing. Aim to maintain adequate vitamin D as part of a broader cancer prevention and health optimization strategy.

Q: What dose is safe during pregnancy?

A: Pregnancy is a special situation. Many obstetricians recommend routine vitamin D supplementation during pregnancy because vitamin D deficiency is common and associated with adverse outcomes. Typical prenatal vitamin D content varies. Doses up to 4,000 IU per day have been used safely in pregnancy in clinical studies, but always work with your obstetrician to determine the right dose and testing schedule during pregnancy.

Q: If I spend time in the sun, do I still need supplements?

A: It depends on your skin type, where you live, and how much direct sun exposure you get without sunscreen. For many people, especially those with darker skin, older adults, or people living at higher latitudes, sun exposure alone is not sufficient year-round. The pragmatic approach: test serum 25(OH)D and supplement as needed to reach the target range.

Q: Are liquid or capsule formulations better?

A: Both liquid and capsule formulations work. Liquids offer flexible dosing for precise titration. Capsules and tablets are convenient and easy. For those with fat malabsorption, a formulation that is emulsified or taken with a fatty meal may improve absorption. Choose a reputable brand and ensure the product lists cholecalciferol (vitamin D3).

Q: Can I take too much vitamin D?

A: Yes. Chronic very high intakes can cause toxicity, usually through hypercalcemia. Toxicity is rare but possible when serum 25(OH)D exceeds very high levels. Don’t exceed 4,000 IU per day without monitoring unless you are under clinical supervision and being monitored with serum tests.

Q: Should I measure 25-hydroxyvitamin D or 1,25-dihydroxyvitamin D?

A: Measure serum 25-hydroxyvitamin D. It is the best indicator of vitamin D stores and intake. The active form, 1,25-dihydroxyvitamin D, is tightly regulated and often remains normal until severe deficiency or kidney disease develops. 1,25-dihydroxyvitamin D is typically measured in specific clinical scenarios but is not the routine test for assessing vitamin D sufficiency.