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Every August, tens of thousands of football players — from Pop Warner fields to NFL training camps — report for two-a-days under the same summer sun that their great-grandfathers trained under. But something has changed since then: most of these athletes, and most of the rest of us, now spend the other twenty hours of the day indoors, under artificial light, often slathered in sunscreen the moment we step outside. The result is a population — elite athletes and average gym-goers alike — that is, in surprisingly large numbers, deficient in a hormone that happens to regulate the very tissue that both a linebacker and a weekend runner depend on: skeletal muscle.

This isn’t a fringe concern, and it isn’t only a pro-sports story. When researchers at the University of Pittsburgh Medical Center measured serum 25-hydroxyvitamin D [25(OH)D] in 80 professional football players, the average level was 27.4 ng/mL — below the 30 ng/mL threshold most endocrinologists consider adequate — and Black players averaged just 25.6 ng/mL versus 37.4 ng/mL for white players, a highly significant racial disparity driven by differences in skin pigmentation and dermal vitamin D synthesis (Maroon et al., 2015). A separate study of 214 athletes at the NFL Combine found that 59% had inadequate vitamin D status, including 10% who were frankly deficient, and that players with a history of lower-extremity muscle strains or core muscle injuries were significantly more likely to be among them (Rebolledo et al., 2018). But zoom out from the training room to the general population and the picture is, if anything, worse: national survey data show that roughly 70% of U.S. adults fall below the 30 ng/mL sufficiency threshold, with 28.9% frankly deficient (Amrein et al., 2020), and a more recent analysis of over 71,000 Americans found that only about 34.5% of adults reach full sufficiency (Cui et al., 2022). The muscle biology described in this article, in other words, doesn’t stop applying at the stadium gates. It’s operating identically in the cells of a middle linebacker, a high school running back, the person doing squats at the gym after work, and grandpa walking around the block — because it’s the same receptor, in the same tissue, responding to the same hormone.

The old evidence nobody remembers, and the new evidence nobody’s applying

The idea that sunlight-derived vitamin D drives muscle performance isn’t new; it’s just been forgotten by nearly everyone except serious researchers. German sport scientists documented seasonal swings in muscular “trainability” tied to sun exposure back in the mid-twentieth century (Hettinger & Müller, as cited in Cannell et al., 2009), and a formal review in the flagship journal of the American College of Sports Medicine concluded that vitamin D “may improve athletic performance in vitamin D–deficient” individuals, particularly through its effects on fast-twitch muscle (Cannell, Hollis, Sorenson, Taft, & Anderson, 2009). As described in The Sunlight Solution (2026) then came a real-world case study that put the hypothesis on the map: after Chicago Blackhawks team physicians began screening and treating players for vitamin D deficiency — putting most of the roster on 5,000 IU/day — the team went from near the bottom of the NHL standings in 2009 to a Stanley Cup championship in 2010, a turnaround later referenced in the peer-reviewed sports-nutrition literature as an illustrative case (Grant, Lahore, & Rockwell, 2020). One team’s championship run obviously proves nothing on its own — correlation is not causation, and dozens of other variables changed that season too — but it’s a memorable illustration of a mechanism that deserves to be taken seriously on its own biological merits.

Importantly, the same biology has been documented well outside the world of elite sport. A landmark study of over 4,000 U.S. adults aged 60 and older found that higher serum 25(OH)D was associated with meaningfully better lower-extremity function — in both physically active and physically inactive people (Bischoff-Ferrari, Dietrich, Orav, Hu, Zhang, Karlson, & Dawson-Hughes, 2004). In other words, this isn’t a performance-enhancement story exclusive to athletes chasing a competitive edge. It’s a baseline-function story that applies to anyone who wants their muscles to work the way they’re designed to.

Fast-twitch fibers: the receptor is sitting right there — in everyone’s muscle

Here’s the part of the story that rarely makes it into training-room conversations, let alone the average person’s understanding of their own body: skeletal muscle is a direct target organ for vitamin D, and it is not uniform in how it responds. Muscle biopsies from vitamin D–deficient adults — not just athletes, but adults in general — consistently show selective atrophy of Type II — fast-twitch — muscle fibers, the fibers responsible for explosive force, sprinting, jumping, and, just as importantly, catching yourself before a fall, while enlarged interfibrillar spaces and fatty infiltration accumulate around them (Girgis, Clifton-Bligh, Hamrick, Holick, & Gunton, 2013). This isn’t just an association; a randomized controlled trial in elderly stroke survivors found that just 1,000 IU/day of vitamin D2 significantly increased both the diameter and the relative proportion of Type II fibers over two years, with a direct correlation between serum 25(OH)D and fiber diameter (as reviewed in Girgis et al., 2013). Imagine what 5000 IUs per day would do…see. Blackhawks story above. Also, read in The Sunlight Solution my role in the Blackhawks success.

The mechanistic reason fast-twitch fibers are so vitamin D–sensitive traces back to the vitamin D receptor (VDR) itself, which is present in muscle regardless of whether that muscle belongs to a professional athlete or someone who has never set foot in a weight room. VDR knockout mice — animals genetically incapable of responding to vitamin D — develop significantly weaker grip strength than normal mice, along with smaller, structurally abnormal muscle fibers, and this weakness worsens with age (Girgis, Cha, Houweling, Rao, Mokbel, Lin, Clifton-Bligh, & Gunton, 2015). This same study found that vitamin D–deficient mice — not just receptor-knockout mice — independently developed the identical phenotype, confirming that it is the deficiency itself, not some unrelated genetic quirk, driving the weakness (Girgis et al., 2015). For an athlete whose sport is decided in fractions of a second, the fiber type most affected by vitamin D status is exactly the fiber type that decides the outcome — a defensive lineman’s first step off the snap. For an average adult, that same fiber type is what determines whether a stumble on the stairs becomes a quick recovery or a fall. Different stakes, identical biology.

Satellite cells: vitamin D as a switch for muscle repair and growth, at any level of training

Every rep in the weight room — whether it’s an NFL strength coach’s program or a first-time gym-goer’s beginner routine — creates microscopic muscle damage that has to be repaired and rebuilt. That repair job belongs to satellite cells, the resident stem cells of skeletal muscle. When activated, satellite cells proliferate, differentiate into new muscle fibers, and fuse with existing fibers to drive both recovery and hypertrophy.

Satellite cells express the vitamin D receptor directly (Braga, Simmons, Norris, Ferrini, & Artaza, 2017), and treating isolated satellite cells with active vitamin D [1,25(OH)2D3] increases expression of the core myogenic regulatory factors that drive muscle formation — MyoD and myogenin — along with troponin, IGF-1 and IGF-2, and other pro-growth signaling molecules, while promoting the fusion of myoblasts into mature myotubes (Braga et al., 2017). A systematic review of thirteen in vivo studies concluded that vitamin D increases satellite cell proliferation during rapid-growth periods and that, in acute muscle injury, vitamin D deficiency measurably impairs satellite cell differentiation and slows regeneration (Alfaqih, Tarawan, Sylviana, Goenawan, Lesmana, & Susianti, 2022). This is the same repair system whether the injury in question is a torn hamstring on a practice field or the ordinary micro-damage from a Tuesday-night workout — the muscle doesn’t know or care whether the person attached to it has a jersey number.

Myostatin: the brake pedal everyone’s muscle has, and vitamin D helps release

If satellite cells and fast-twitch fibers are the accelerator, myostatin is the brake. Myostatin is a member of the TGF-β superfamily whose entire biological job is to limit skeletal muscle growth; animals and humans with loss-of-function myostatin mutations develop dramatic, well-documented muscle hypertrophy. The less myostatin signaling present, all else being equal, the more permission the body has to build muscle — and this brake pedal exists in identical form in a professional athlete’s quadriceps and in anyone else’s.

This is where the vitamin D connection becomes genuinely compelling. Treating muscle cells and primary satellite cells with active vitamin D consistently decreases myostatin gene and protein expression while simultaneously increasing follistatin, myostatin’s natural inhibitor (Braga et al., 2017; as reviewed in Girgis et al., 2013). VDR-knockout mice and diet-induced vitamin D–deficient mice both show significantly increased myostatin expression in quadriceps muscle alongside smaller fiber size and reduced grip strength — the first study to establish an in vivo link between vitamin D status, myostatin, and functional muscle strength (Girgis et al., 2015). A 2024 mouse study reported that normal and high-dose dietary vitamin D lowered circulating myostatin relative to a deficient diet, redirecting surplus calories toward muscle rather than fat (Long et al., 2024).

Taken together, this is a coherent mechanistic story built on solid in vitro work and one well-replicated in vivo knockout/deficiency model. Human trial data directly testing myostatin as an outcome is essentially absent both in elite athletes and in the general population, which is why this whole connection — while mechanistically well-grounded in animal and cell models — should be labeled supportive-maturing rather than established in humans. But the mechanism itself doesn’t discriminate: whoever is trying to build or preserve muscle, from a training-camp roster to someone fighting age-related muscle loss, is working with the same brake pedal and the same hormone that helps ease off it.

As an aside, my son has been on high dose vitamin D (StarPower) since he was 9 or 10. In 2015, when the Chicago Cubs drafted him he was the first player taken out of high school in Vermont since 2003. The Colorado Rockies drafted him again in 2018 out of Wake Forest as a pitcher. He is currently making a comeback in the independent professional leagues throwing in the high 90s hoping to be picked up by an MLB-affiliated team soon.

One biological system, two very different audiences

To be clear about the boundaries here: none of this evidence justifies treating vitamin D as a shortcut around training, nutrition, or sleep, for a professional athlete or anyone else. The strongest, most consistent finding across this entire literature is that vitamin D’s effects on muscle show up in people who are deficient or insufficient to begin with — correcting a real deficiency removes a biological constraint (as reviewed in Owens, Allison, & Close, 2018). But the exciting part again is the unknown, do high doses of vitamin D, over long periods, create an optimal biochemical environment for elite athletic performance? Of course they do. We can either await longitudinal studies to tell us what we already know, or we can act now. Time is a wastin’.

Given that the majority of both football players tested across multiple independent cohorts (Maroon et al., 2015; Rebolledo et al., 2018) and ordinary American adults (Amrein et al., 2020; Cui et al., 2022) have been found insufficient or deficient, the practical implication cuts across every level of athletic ambition: this is a cheap, safe, and easily measurable variable that almost nobody — not NFL training staffs, and certainly not the average person managing their own fitness — is systematically tracking. A single blood draw for 25(OH)D, paired with a repletion protocol for anyone found low, is a low-cost intervention aimed squarely at the biological machinery — fast-twitch fiber integrity, satellite cell function, and myostatin regulation — that determines whether anyone’s training, at any level, translates into the strength, resilience, and explosiveness their body is capable of.

References

Alfaqih, M. S., Tarawan, V. M., Sylviana, N., Goenawan, H., Lesmana, R., & Susianti, S. (2022). Effects of vitamin D on satellite cells: A systematic review of in vivo studies. Nutrients, 14(21), 4558. https://doi.org/10.3390/nu14214558

Amrein, K., Scherkl, M., Hoffmann, M., Neuwersch-Sommeregger, S., Köstenberger, M., Tmava Berisha, A., Martucci, G., Pilz, S., & Malle, O. (2020). Vitamin D deficiency 2.0: An update on the current status worldwide. European Journal of Clinical Nutrition, 74(11), 1498–1513. https://doi.org/10.1038/s41430-020-0558-y

Bischoff-Ferrari, H. A., Dietrich, T., Orav, E. J., Hu, F. B., Zhang, Y., Karlson, E. W., & Dawson-Hughes, B. (2004). Higher 25-hydroxyvitamin D concentrations are associated with better lower-extremity function in both active and inactive persons aged ≥60 y. American Journal of Clinical Nutrition, 80(3), 752–758. https://doi.org/10.1093/ajcn/80.3.752

Braga, M., Simmons, Z., Norris, K. C., Ferrini, M. G., & Artaza, J. N. (2017). Vitamin D induces myogenic differentiation in skeletal muscle derived stem cells. Endocrine Connections, 6(3), 139–150. https://doi.org/10.1530/EC-17-0008

Cannell, J. J., Hollis, B. W., Sorenson, M. B., Taft, T. N., & Anderson, J. J. B. (2009). Athletic performance and vitamin D. Medicine & Science in Sports & Exercise, 41(5), 1102–1110. https://doi.org/10.1249/MSS.0b013e3181930c2b

Cui, A., Xiao, P., Ma, Y., Fan, Z., Zhou, F., Zheng, J., & Zhang, L. (2022). Prevalence, trend, and predictor analyses of vitamin D deficiency in the US population, 2001–2018. Frontiers in Nutrition, 9, 965376. https://doi.org/10.3389/fnut.2022.965376

Girgis, C. M., Clifton-Bligh, R. J., Hamrick, M. W., Holick, M. F., & Gunton, J. E. (2013). The roles of vitamin D in skeletal muscle: Form, function, and metabolism. Endocrine Reviews, 34(1), 33–83. https://doi.org/10.1210/er.2012-1012

Girgis, C. M., Cha, K. M., Houweling, P. J., Rao, R., Mokbel, N., Lin, M., Clifton-Bligh, R. J., & Gunton, J. E. (2015). Vitamin D receptor ablation and vitamin D deficiency result in reduced grip strength, altered muscle fibers, and increased myostatin in mice. Calcified Tissue International, 97(6), 602–610. https://doi.org/10.1007/s00223-015-0054-x

Grant, W. B., Lahore, H., & Rockwell, M. S. (2020). The benefits of vitamin D supplementation for athletes: Better performance and reduced risk of COVID-19. Nutrients, 12(12), 3741. https://doi.org/10.3390/nu12123741

Long, C., Casella, A., Nguyen, M., Danahy, L., Seiler, C., Lei, M., Mark, J., & Roizen, J. (2024). High dose dietary vitamin D allocates surplus calories to muscle and growth instead of fat via modulation of myostatin and leptin signaling [Preprint]. Research Square. https://doi.org/10.21203/rs.3.rs-4202165/v1 (Note: not yet peer-reviewed at time of writing; findings are in mouse models.)

Maroon, J. C., Mathyssek, C. M., Bost, J. W., Amos, A., Winkelman, R., Yates, A. P., Duca, M. A., & Norwig, J. A. (2015). Vitamin D profile in National Football League players. American Journal of Sports Medicine, 43(5), 1241–1245. https://doi.org/10.1177/0363546514567297

Owens, D. J., Allison, R., & Close, G. L. (2018). Vitamin D and the athlete: Current perspectives and new challenges. Sports Medicine, 48(Suppl 1), 3–16. https://doi.org/10.1007/s40279-017-0841-9

Rebolledo, B. J., Bernard, J. A., Werner, B. C., Finlay, A. K., Nwachukwu, B. U., Dare, D. M., Warren, R. F., & Rodeo, S. A. (2018). The association of vitamin D status in lower extremity muscle strains and core muscle injuries at the National Football League combine. Arthroscopy, 34(5), 1280–1285. https://doi.org/10.1016/j.arthro.2017.10.005

Thanks for reading StarPower: All Things Vitamin D! Subscribe to receive new posts and support my work. Founding Member subscriptions include the hardcopy version of my new book, The Sunlight Solution, and a years supply of our proprietary StarPower vitamin D (~$150 value).

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The Sunlight Solution was published June 23, 2026 by Skyhorse.

It is essential reading to fully understand and appreciate these articles on how sunlight and vitamin D work to keep you disease-free and thriving. Link on Amazon https://a.co/d/0eH8MzBY

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General Recommendations for Vitamin D for Healthy Adults

The U.S. Institute of Medicine (IOM), now the National Academy of Medicine, recommends a dietary reference intake of 600 IU (International Units) per day for adults up to age 70, and 800 IU for those over 70, to maintain bone health (Institute of Medicine, 2011). However, this amount is orders of magnitude too low considering that the human body “uses” at least 4000 IU vitamin D per day.

However, there is a vast literature on the extraskeletal functions of vitamin D for maintaining optimal functioning of the immune system, muscular system and ideal aging that indicates that optimal levels of serum vitamin D are much, much higher (e.g., Grant et al. 2020).

Based on Blood Levels

A blood test provides a clear picture of vitamin D status. Levels are typically categorized as follows (Holick et al., 2011; Wang et al., 2017):

Link to StarPowerLifeSciences.org for more information

DISCLAIMER: This publication is educational and informational in nature. Nothing published here — including articles, case reports, reader comments, or author responses — constitutes medical advice, a diagnosis, or a treatment recommendation. Dosing figures and administration methods discussed here reflect information from published scientific literature or the personal experiences of individual readers; they are not prescriptions and are not tailored to any individual’s health situation. Always consult a qualified physician or licensed health professional before making any change to your medical care or beginning any self-treatment. The case reports presented reflect the personal experiences of individual contributors and may not be representative of others. We make no claim that any outcome described here is typical or predictable. Statements have not been evaluated by the Food and Drug Administration. Do your own research.

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A sobering number, right on cue for kickoff

Football season is here, and so, right on schedule, is the latest reminder of the sport’s darkest cost. A study published this week in The BMJ by Daneshvar et al., (2026) at Mass General Brigham, drawing on the UNITE Brain Bank at Boston University, found that at least 25% of former NFL players who died between 2016 and 2021 had chronic traumatic encephalopathy (CTE) at the time of death — a floor estimate the study’s lead author, Dr. Daniel Daneshvar, called the “low end,” with the true figure plausibly much higher. Among brains donated specifically for CTE research, the prevalence was far higher still — 93% — though that figure is skewed by the fact that families who donate a brain often do so because they already suspected something was wrong. At the extreme, if every undiagnosed former player were assumed positive, the ceiling estimate reached 97%. The study also found that severe, Stage IV CTE correlated strongly with dementia diagnosed in life, while milder or CTE-negative cases showed a murkier relationship — underscoring how much is still unknown about how repetitive head trauma actually produces long-term brain disease.

This is important, rigorous epidemiology, and it deserves the attention it’s getting. But it also leaves the most actionable question sitting untouched on the table: why do two players who take similar hits over similar careers end up with such different outcomes? The BMJ study, like most CTE research, is built around counting cases and diagnosing after death — it is not designed to explain why some brains withstand repetitive trauma better than others. That’s a biological question, not just an epidemiological one. And Chapter 23 of my book, The Sunlight Solution, argues that a significant, underappreciated piece of the answer is sitting in blood test panels that almost no team is running: serum vitamin D status.

Reframing the hit: it’s not just about force

The conventional way we talk about concussion treats it almost entirely as a biomechanics problem — how hard was the hit, what angle, what helmet. Rule changes, guardian caps, and equipment innovation all attack this side of the equation, and rightly so. But biomechanics only tells you about the input. It says nothing about how a given brain processes that input once the hit lands. Two players can absorb comparable forces and come away with wildly different outcomes — one shaking it off, another sidelined for weeks with an outsized inflammatory response. The overlooked variable in that gap is the biochemical readiness of the brain before the injury ever occurs.

That reframing matters because it turns concussion from a purely mechanical event into what it actually is at the cellular level: an immune and inflammatory response to trauma. And immune responses can be primed to be either controlled and self-limiting, or chaotic and self-destructive — depending in significant part on whether the brain has adequate vitamin D on board.

What actually happens inside the skull after a hit

The modern neuroscience of traumatic brain injury (TBI) describes a cascade, not a single event:

• The stretch. The real damage isn’t the brain bouncing against the skull — it’s rotational and acceleration/deceleration forces shearing and stretching axons, the long fibers that wire neurons together.

• The energy crisis. That stretching forces open ion channels, triggering a chaotic influx of calcium into neurons. The cell’s energy pumps go into overdrive trying to restore balance, burning through ATP just as blood flow to the brain is often reduced. The result is a mismatch between skyrocketing energy demand and a collapsing energy supply — which is what produces the classic fog, fatigue, and slowed thinking of a concussion.

• The inflammatory aftermath. Damaged mitochondria and calcium overload activate the brain’s resident immune cells — microglia and astrocytes. In a well-regulated response, these cells clean up debris and support healing. In an unregulated one, they flood the tissue with pro-inflammatory chemicals, damage the blood-brain barrier, and let more inflammatory agents pour in from the bloodstream. This runaway neuroinflammation is increasingly viewed as the actual driver of long-term damage — including the pathology that defines CTE.

Where Vitamin D fits into that cascade

Vitamin D is not a bystander in this process — it’s a steroid hormone with receptors expressed throughout neurons and glial cells, and the brain’s own enzymatic machinery to activate it locally. When levels are adequate, vitamin D helps regulate calcium channel activity and mitochondrial function, meaning a vitamin D–replete neuron is better positioned to survive the initial energy crisis with less damage. More critically, vitamin D acts directly on microglia and astrocytes to suppress pro-inflammatory cytokines like TNF-α and IL-6 while promoting anti-inflammatory signaling. In a deficient brain, that braking mechanism is gone — glial cells activated by trauma become hyper-inflammatory, and the resulting damage to healthy neighboring tissue and to the blood-brain barrier is more severe and more prolonged.

There’s a second, less-discussed mechanism worth flagging here: aquaporin-4 (AQP4), the water channel on astrocytes responsible for regulating brain swelling after injury. Post-TBI, AQP4 channels become dysfunctional, contributing to the cytotoxic edema that raises intracranial pressure and drives secondary injury. Research out of Dr. Donald Stein’s TBI lab at Emory University has linked vitamin D status to proper AQP4 expression and function — meaning a replete brain is mechanically better equipped to manage swelling after a hit, while a deficient one is more vulnerable to this dangerous complication.

The population most at risk is also the most deficient

If vitamin D is genuinely neuroprotective, the population most exposed to head trauma should show high rates of deficiency — and that is exactly what the data show. A 2015 study of NFL players found that 86% had insufficient or deficient vitamin D levels (Maroon et al., 2015). A separate study presented to the American Academy of Orthopaedic Surgeons found that vitamin D–deficient NFL players were significantly more likely to sustain muscle injuries generally, pointing to a broader pattern of biochemical vulnerability rather than an isolated finding. Black players are especially Vitamin D deficient therefore at most risk.

This is not confined to the pros — low vitamin D status is common across collegiate and youth-level contact sports as well. The players absorbing the most repetitive trauma are, on average, the least biochemically prepared to manage the immune response that trauma triggers.

Does correcting it actually change outcomes?

The direct clinical trial evidence connecting vitamin D repletion to concussion outcomes in athletes is still thin — this is a hypothesis under active development, not an established treatment protocol. But the early signals are worth taking seriously rather than dismissing. One anecdotal but striking case: a New York high school football team that suffered fifteen concussions across two seasons implemented a vitamin D testing and optimization program; over the following two seasons, with players maintained at sufficient levels, the team recorded a single mild concussion. That is a single, uncontrolled, real-world data point — not a trial — and I want to be explicit that it should be read that way. But it’s directionally consistent with the mechanisms above, and it’s the kind of finding that should be motivating a properly controlled prospective trial in athletic populations, not sitting as a forgotten anecdote.

More rigorous evidence comes from outside sports: a 2024 randomized clinical trial in patients with moderate to severe TBI found that high-dose vitamin D3 administration measurably reduced inflammatory biomarkers compared to standard care (Masbough et al., 2024). That’s a clinical signal in the right direction, in the right population, even if it doesn’t yet answer the specific question of whether pre-injury repletion changes concussion severity or CTE risk in athletes over a career.

The timing detail that changes everything

Here is the finding I think deserves the most attention, and it connects directly to the broader argument I’ve made elsewhere about vitamin D as an uncontrolled variable in drug research. Dr. Stein’s group has extensively studied progesterone as a neuroprotective post-TBI treatment, and found a powerful synergy with vitamin D — but only under a specific condition. Vitamin D enhanced progesterone’s protective effect only when the brain was already in a state of chronic vitamin D sufficiency before the injury occurred. Administering vitamin D after the fact, alongside progesterone treatment, did not replicate the benefit. Chronic pre-injury repletion, not reactive post-injury dosing, was the prerequisite for the therapy to work at all.

That single finding reframes the entire conversation. It means a locker room vitamin D protocol isn’t something you reach for after a player goes down — it has to already be in place, quietly, all season, as baseline physiological infrastructure. It also raises a question I think the pharmaceutical and TBI-treatment research community should be asking more directly: how many other neuroprotective interventions are being tested in trial populations whose vitamin D status was never measured, controlled, or brought to sufficiency before treatment began?

A proactive plan, not a reactive one

None of this is a claim that vitamin D prevents CTE or concussion, or should replace helmets, rule changes, or medical evaluation after a head injury — it does not, and CTE itself can currently only be diagnosed after death, which is precisely why prevention-oriented thinking matters so much here. What the evidence does support is a low-cost, low-risk standard-of-care addition for any organization fielding athletes in contact sports:

1. Baseline testing. Every athlete should have serum 25(OH)D measured at the start of preseason.

2. Set the target above the deficiency floor. The goal isn’t merely avoiding deficiency (<20 ng/mL) — for neuro-immune function specifically, a target range of 80–100 ng/mL is a more meaningful benchmark (Masbough et al., 2024).

3. Personalize the dose. Achieving that range typically requires 5,000–8,000 IU/day of vitamin D3, guided by a healthcare professional and adjusted to the individual’s baseline and body size.

4. Maintain it year-round. Levels drop in winter months even for athletes who train outdoors in summer; annual retesting keeps the target range in place continuously — which, per the timing finding above, is the only way this protective effect actually works.

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Impacts to the head are inevitable in many sports; it really is part of the game. Concussions are not going away, and they shouldn’t be minimized or explained away by any single variable — this is genuinely a multifactorial problem involving equipment, rules, coaching technique, and individual injury history. But a brain that meets a hit already biochemically prepared to mount a controlled, self-limiting immune response is playing a fundamentally different game than a brain meeting that same hit while running on immunological empty. As this football season’s inevitable string of head-injury headlines rolls in, the question worth asking isn’t just how we soften the hits. It’s whether we’ve done anything to prepare the brain absorbing them.

Ensuring that the athlete at risk of concussion and resultant future neuropathologies is Vitamin D replete is a safe, low cost, easy to implement measure to potentially change the devastating course that repeated head trauma causes.

To the critics who say “But, but there are no RCT clinical trials…” we are unlikely to ever get RCTs on anything vitamin D and health related as discussed elsewhere. Therefore, the best available evidence as presented here suggests that optimizing vitamin D levels, certainly in vitamin D deficient athletes, may be a lot more than just a hail Mary effort in reducing the disordered neuroimmune response after sport-related head trauma.

This article discusses general research on vitamin D and traumatic brain injury and is provided for educational purposes. It is not medical advice, and it does not diagnose, treat, cure, or prevent any disease, including CTE or concussion. Athletes and parents should consult a qualified healthcare provider before beginning any supplementation regimen, particularly at the higher end of the dosing ranges discussed above.

References

Chahin, M., Mutschler, J., Dzhuleva, S. P., Dieterle, C., Jimenez, L. R., Bhattarai, S. R., Van Steenbergen, V., & Bareyre, F. M. (2025). Repetitive concussions promote microglia-mediated engulfment of presynaptic excitatory input associated with cognitive dysfunction. Communications Biology, 8(1), 335.

Cekic, M., Sayeed, I., & Stein, D. G. (2009). Combination treatment with progesterone and vitamin D hormone may be more effective than monotherapy for nervous system injury and disease. Frontiers in Neuroendocrinology, 30(2), 158–172. https://doi.org/10.1016/j.yfrne.2009.03.004

Cekic, M., & Stein, D. G. (2010). Traumatic brain injury and aging: Is a combination of progesterone and vitamin D hormone a simple solution to a complex problem? Neurotherapeutics, 7(1), 81–90. https://doi.org/10.1016/j.nurt.2009.10.017

Daneshvar D H, Nowinski C J, Abdolmohammadi B, Luster C B, Uretsky M, Martin B M et al. Prevalence of chronic traumatic encephalopathy at death in National Football League players: retrospective population based cohort study, 2008-21 BMJ 2026; 394 :e100418 doi:10.1136/bmj-2026-100418

Giza, C., & Hovda, D. (2014). The new neurometabolic cascade of concussion. Neurosurgery, 75(4), S24–S33. https://doi.org/10.1227/NEU.0000000000000505

Karve, I. P., Taylor, J. M., & Crack, P. J. (2016). The contribution of astrocytes and microglia to traumatic brain injury. British Journal of Pharmacology, 173(4), 692–702. https://doi.org/10.1111/bph.13125

Maroon, J. C., Mathyssek, C. M., Bost, J. W., Amos, A., Winkelman, R., Yates, A. P., Duca, M. A., & Norwig, J. A. (2015). Vitamin D profile in National Football League players. The American Journal of Sports Medicine, 43(5), 1241–1245. https://doi.org/10.1177/0363546514567297

Masbough, F., Kouchek, M., Koosha, M., Salarian, S., Miri, M., Raoufi, M., Taherpour, N., Amniati, S., & Sistanizad, M. (2024). Investigating the effect of high-dose vitamin D3 administration on inflammatory biomarkers in patients with moderate to severe traumatic brain injury: A randomized clinical trial. Iranian Journal of Medical Sciences, 49(10), 643–651. https://doi.org/10.30476/ijms.2023.99465.3156

Nguyen, R. H., Newton, M., Kratofil, R. M., et al. (2025). Imaging a concussion and the ensuing immune response at the blood-brain barrier. Proceedings of the National Academy of Sciences, 122(21), e2414316122. https://doi.org/10.1073/pnas.2414316122

Sailike, B., Onzhanova, Z., Akbay, B., Tokay, T., & Molnár, F. (2024). Vitamin D in central nervous system: Implications for neurological disorders. International Journal of Molecular Sciences, 25(14), 7809. https://doi.org/10.3390/ijms25147809

Scuderi, G. (2012, March 25). Significantly lower levels of vitamin D found in NFL players with muscle injuries. Healio. https://www.healio.com/news/orthopedics/20120325/significantly-lower-levels-of-vitamin-d-found-in-nfl-players-with-muscle-injuries

Sullivan, B. (2026, August 25). At least 25% of former NFL players who died between 2016 and 2021 had CTE, study finds. NPR. https://www.npr.org/2026/08/25/nx-s1-5943168/cte-nfl-concussions-deaths-study

Supple, W. F., Jr. (2026). The Sunlight Solution: Reclaiming vitamin D, reversing the chronic disease epidemic, and making America healthy again (Chapter 23: Concussion, Neuroinflammation, and the Protective Shield of Vitamin D). MAHA Books/Skyhorse.

Weber, J. T. (2012). Altered calcium signaling following traumatic brain injury. Frontiers in Pharmacology, 3, 60. https://doi.org/10.3389/fphar.2012.00060

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The Sunlight Solution was published June 23, 2026 by Skyhorse.

It is essential reading to fully understand and appreciate these articles on how sunlight and vitamin D work to keep you disease-free and thriving. Link on Amazon https://a.co/d/0eH8MzBY

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General Recommendations for Vitamin D for Healthy Adults

The U.S. Institute of Medicine (IOM), now the National Academy of Medicine, recommends a dietary reference intake of 600 IU (International Units) per day for adults up to age 70, and 800 IU for those over 70, to maintain bone health (Institute of Medicine, 2011). However, this amount is orders of magnitude too low considering that the human body “uses” at least 4000 IU vitamin D per day.

However, there is a vast literature on the extraskeletal functions of vitamin D for maintaining optimal functioning of the immune system, muscular system and ideal aging that indicates that optimal levels of serum vitamin D are much, much higher (e.g., Grant et al. 2020).

Based on Blood Levels

A blood test provides a clear picture of vitamin D status. Levels are typically categorized as follows (Holick et al., 2011; Wang et al., 2017):

Link to StarPowerLifeSciences.org for more information

DISCLAIMER: This publication is educational and informational in nature. Nothing published here — including articles, case reports, reader comments, or author responses — constitutes medical advice, a diagnosis, or a treatment recommendation. Dosing figures and administration methods discussed here reflect information from published scientific literature or the personal experiences of individual readers; they are not prescriptions and are not tailored to any individual’s health situation. Always consult a qualified physician or licensed health professional before making any change to your medical care or beginning any self-treatment. The case reports presented reflect the personal experiences of individual contributors and may not be representative of others. We make no claim that any outcome described here is typical or predictable. Statements have not been evaluated by the Food and Drug Administration. Do your own research.

A trajectory that doesn’t look like typical drift

CDC surveillance puts autism spectrum disorder (ASD) prevalence at 1 in 150 children in 2000 and 1 in 36 in 2020 (Maenner et al., 2023). Compare that to the pre-sunscare and sunscreen era of the 1960s, when the rate was closer to 1 in 2,000 — a roughly 55-fold increase in incidence over sixty years, with a tenfold jump since 2000 alone. Numbers moving that fast, that uniformly, don’t look like slow genetic drift. They look like the signature of a fast-moving, near-universal environmental exposure. That factor is chronic vitamin D deficiency during critical windows of neurodevelopment, compounded by neurotoxic sunscreen chemicals absorbed through the skin.

Geography, season, and the “Swedish Disease”

Autism incidence is elevated at sun-starved temperate latitudes relative to equatorial regions, and birth-month effects — a child’s autism risk shifting with the season they were born in — point toward a prenatal exposure that fluctuates across the year, tracking the same seasonal pattern vitamin D levels follow (Lee et al., 2019).

The starkest illustration is a natural experiment: Somali families who relocated to Minnesota or Stockholm, Sweden began seeing autism at rates their communities had never encountered back home — so unfamiliar that the Stockholm Somali community started calling it “the Swedish disease” (as reported in Scientific American, 2015). Same genetic background, same population, radically different sun exposure — and radically different autism rates. Grant and Soles (2009) provide the broader ecological analysis behind this pattern, linking lower-sunlight populations worldwide to higher infantile autism risk.

What’s new: autistic children measurably run low on vitamin D

This is where the newest evidence strengthens the case directly, rather than by geographic proxy. A systematic review and meta-analysis by Wang, et al., 2016, pooling serum 25-hydroxyvitamin D [25(OH)D] data across multiple studies, found that children with ASD have significantly lower circulating vitamin D than age-matched neurotypical controls. A follow-up systematic review and meta-analysis by Wang, Ding, and Wang (2020) reached the same conclusion from a broader and more recent set of studies: lower vitamin D status is consistently associated with ASD. This moves the argument from “autism is more common where sunlight is scarcer” to “autistic children themselves, individually, are measurably vitamin D deficient” — a stronger and more direct form of evidence.

Vitamin D as a working part of brain machinery, not a bystander

Vitamin D receptors (VDRs) and the enzyme that activates vitamin D locally are distributed throughout the brain — cortex, hippocampus, and cerebellum, particularly the midline cerebellar vermis, among them (Buell & Dawson-Hughes, 2008; Eyles et al., 2005). Timing matters as much as presence: Voltas et al. (2025) found that low maternal 25(OH)D across pregnancy predicted poorer visual-motor precision in children, and low third-trimester levels specifically predicted weaker working memory and executive function. Vitamin D governs neuronal differentiation, proliferation, survival, neurotransmitter synthesis, and — most importantly for autism — synaptic plasticity (Eyles, 2021; Ye et al., 2023). Autism has been described by researchers as, at its core, “a disease of the synapses” (Sudarov, 2013), which is precisely the level at which vitamin D operates.

Why the cerebellar vermis specifically

Four things converge in the cerebellar vermis regarding this being a key region involved in autism:

• reduced cerebellar vermis volume is one of the most consistent brain anatomy disruptions in autism (Fatemi et al., 2012),

• the Purkinje cells that populate it carry vitamin D receptors,

• the cerebellum has an unusually long developmental window both before and after birth, and

• animal models with damage confined to the midline cerebellum show behavioral deficits that closely resemble autism.

Eric Courchesne’s early MRI work (2001) first drew attention to abnormal cerebellar growth patterns in autistic children, and Webb et al. (2009) later showed the vermal changes in autism are behaviorally distinct from what’s seen in other forms of developmental delay — this isn’t generic brain difference, it’s specific to autism.

The cellular detail makes the stakes concrete: a Purkinje cell receives roughly 200,000 synapses, compared to 10,000–30,000 for a typical cortical pyramidal neuron (Sudarov, 2013). Autism is consistently associated with fewer Purkinje cells in the vermis. Each one lost represents a disproportionate loss of processing capacity.

The mirror-image case: Williams syndrome

Williams syndrome sits at nearly the opposite behavioral pole from autism — hyper-social, outgoing, minimal social inhibition, instead of withdrawal and repetitive behavior. Amazingly, the cerebellar vermis of a child with Williams Syndrome is, correspondingly, hypertrophic (more cells) rather than atrophic (fewer cells) (Jones et al., 2002). Two conditions with opposite social profiles and opposite vermis anatomy is a striking pattern — suggestive of the vermis’s central role in complex social behavior, and possibly an anatomical site affected in autism.

What’s new: VitD supplementation measurably helps

Jia, et al., (2015), published in Pediatrics, gave vitamin D supplementation to children with ASD and found significant improvement in core autism symptoms — one of the earliest direct interventional signals in this literature.

Far more recent: Tian, Zhu, Liu, and Gao (2025), published in BMC Psychiatry in March 2025, used resting-state functional MRI in preschool children with ASD and found that lower serum 25(OH)D was significantly associated with multiple brain functional abnormalities — and, importantly, children with lower vitamin D had more severe autism symptoms. That’s a dose-relationship inside a single population, not just a cross-study comparison.

And most directly: Javadfar, Soltani, Khamoushi, and Zare (2025), published in BMC Pediatrics in August 2025, ran a double-blind randomized clinical trial giving vitamin D supplementation to children with ASD over fifteen weeks. Serum 25(OH)D rose significantly, inflammatory markers dropped, and — the result that matters most — behavioral symptoms improved significantly in the supplemented group relative to controls. This is the strongest form of evidence: a randomized, blinded, controlled trial showing a measurable symptom benefit from correcting the deficiency.

Related animal research provides a mechanistic thread that helps explain why: vitamin D–deficient animals show impaired prepulse inhibition of acoustic startle (Burne et al., 2004), a sensorimotor gating measure that’s also disrupted in autism, and cerebellar vermis damage independently blocks the related process of startle habituation (e.g., Leaton & Supple, 1986) — two lines of evidence converging on the same circuit.

Sunscreen as a potential teratogen

So far, the idea is that vitamin D is insufficient leading to disrupted brain development. At the same time the same decades that drove vitamin D levels down also introduced a second, largely unexamined exposure: the chemical UV-filter ingredients in modern sunscreens. These aren’t inert skin coatings. A randomized clinical trial by Matta et al. (2019), published in JAMA, found that after a single sunscreen application, all fourteen active ingredients tested were absorbed into the bloodstream at concentrations exceeding the FDA’s own threshold for waiving further safety testing — and several, including oxybenzone, octocrylene, avobenzone, and octinoxate, persisted in circulation for days after use stopped. Because these ingredients are absorbed systemically rather than staying on the skin, they can cross the placenta and reach the fetal bloodstream and brain (Matta et al., 2019; Ruszkiewicz et al., 2017). Neurotoxic sunscreens placed on the mother’s skin end up in her developing baby’s brain.

There are three mechanisms by which these chemicals could act as developmental neurotoxins during critical windows: triggering hyperinflammatory states in the developing brain; generating oxidative stress, to which the fetal brain is especially vulnerable given its high metabolic rate; and acting as endocrine disruptors — several common UV filters, including oxybenzone and octinoxate, have documented estrogenic and antiandrogenic activity (Schlumpf et al., 2004). That endocrine-disrupting property is also proposed as a possible contributor to autism’s roughly 4-to-1 male-to-female ratio (Loomes et al., 2017), through differential effects on male brain organization during development.

Importantly, this mechanism is a combined insult rather than a standalone one. Sunscreen chemicals themselves impair vitamin D synthesis by blocking the UV exposure the skin needs to produce it (Di Nisio et al., 2020), while vitamin D independently helps protect the developing brain against toxic insults from endocrine-disrupting chemicals (Wang et al., 2022). That creates a two-way trap: less sun means less vitamin D and more reliance on sunscreen, and more sunscreen means more circulating teratogenic chemical exposure and still less UV-driven vitamin D synthesis.

The two-hit model: why deficiency plus sunscreen may be worse than either alone

The central mechanistic claim is synergy: a vitamin D–replete fetal brain has full neurotrophic, anti-inflammatory, and antioxidant defenses on hand to absorb a chemical insult like sunscreen exposure without lasting damage. A vitamin D–deficient fetal brain has those defenses running low at the exact moment the insult arrives. In The Sunlight Solution I use the metaphor: a house of cards where deficiency weakens the foundational cards, so a chemical exposure that might do nothing to a well-supported structure is enough to bring it down. Individually, either factor might be subthreshold. Combined, during a narrow developmental window, they may not be. This reframes maternal vitamin D deficiency not as a direct cause of autism, but as the precondition that removes the brain’s capacity to safely tolerate sunscreen-chemical exposure (and other environmental insults) during the periods when it matters most.

The cerebellum keeps developing well past birth — functionally maturing to at least age five (Lyu et al., 2025), maybe even much longer — and Purkinje cells show meaningful regenerative capacity in other species (Bayin et al., 2018; Pose-Méndez et al., 2023). Between 3% and 25% of children diagnosed with autism experience spontaneous remission (Helt et al., 2008), which on its own argues that autism can be “fixed.” Combined with the intervention data above, the chapters frame this postnatal plasticity window as a genuine — if unproven — opportunity: not a cure, but a rationale for taking vitamin D status seriously well past the prenatal period.

What this argument is and isn’t

To be direct about where the solid ground ends: the geographic and seasonal patterns, the Somali natural experiment, and the two deficiency meta-analyses are real, replicated findings — autistic children do run lower in vitamin D than their peers, and that association is well established. The systemic absorption of sunscreen chemicals into the bloodstream, and their persistence for days after use, is also directly documented in a randomized clinical trial (Matta et al., 2019) — that part isn’t speculative. What remains hypothesis is the leap from “these chemicals are absorbed and cross the placenta” to “they act as autism-relevant teratogens in combination with vitamin D deficiency”; no study has yet directly tested sunscreen-chemical exposure against autism outcomes in humans. The 2025 fMRI and RCT data on vitamin D and symptom severity are genuinely new and promising, but still early-stage single studies, not yet a large, replicated evidence base. The Williams syndrome comparison and the full two-hit causal chain (deficiency → weakened Purkinje cell resilience → worsened teratogen or toxin vulnerability → autism) remain hypothesis. This is not a claim that vitamin D deficiency or sunscreen exposure is the sole cause of autism, or that supplementation is a cure. Vitamin D status is a measurable, correctable variable with a growing, increasingly direct evidence base connecting it to both autism risk and autism symptom severity, and that its interaction with everyday chemical exposures like sunscreen deserves far more direct research attention than it currently receives.

References

Buell, J. S., & Dawson-Hughes, B. (2008). Vitamin D and neurocognitive dysfunction: Preventing “D”ecline? Molecular Aspects of Medicine, 29(6), 415–422. https://doi.org/10.1016/j.mam.2008.05.001

Bayin, N. S., Mizrak, D., Stephen, D. N., Lao, Z., Sims, P. A., & Joyner, A. L. (2018). Age-dependent dormant resident progenitors are stimulated by injury to regenerate Purkinje neurons. eLife, 7, e39879. https://doi.org/10.7554/eLife.39879

Burne, T. H. J., Féron, F., Brown, J., Eyles, D. W., McGrath, J. J., & Mackay-Sim, A. (2004). Combined prenatal and chronic postnatal vitamin D deficiency in rats impairs prepulse inhibition of acoustic startle. Physiology & Behavior, 81(4), 651–655. https://doi.org/10.1016/j.physbeh.2004.03.004

Courchesne, E. (2001). Unusual brain growth patterns in early life in patients with autistic disorder: An MRI study. Neurology, 57(2), 245–254. https://doi.org/10.1212/WNL.57.2.245

Di Nisio, A., Rocca, M. S., De Toni, L., et al. (2020). Endocrine disruption of vitamin D activity by perfluoro-octanoic acid (PFOA). Scientific Reports, 10, 16789. https://doi.org/10.1038/s41598-020-74026-8

Eyles, D. W. (2021). Vitamin D: Brain and behavior. JBMR Plus, 5(1), e10419. https://doi.org/10.1002/jbm4.10419

Eyles, D. W., Smith, S., Kinobe, R., Hewison, M., & McGrath, J. J. (2005). Distribution of the vitamin D receptor and 1 alpha-hydroxylase in human brain. Journal of Chemical Neuroanatomy, 29(1), 21–30. https://doi.org/10.1016/j.jchemneu.2004.08.006

Fatemi, S. H., Aldinger, K. A., Ashwood, P., Bauman, M. L., Blaha, C. D., Blatt, G. J., Chauhan, A., Chauhan, V., Dager, S. R., Dickson, P. E., Estes, A. M., Goldowitz, D., Heck, D. H., Kemper, T. L., King, B. H., Martin, L. A., Millen, K. J., Mittleman, G., Mosconi, M. W., … Welsh, J. P. (2012). Consensus paper: Pathological role of the cerebellum in autism. Cerebellum, 11(3), 777–807. https://doi.org/10.1007/s12311-012-0355-9

Grant, W. B., & Soles, C. M. (2009). Epidemiologic evidence supporting the role of maternal vitamin D deficiency as a risk factor for the development of infantile autism. Dermato-Endocrinology, 1(4), 223–228. https://doi.org/10.4161/derm.1.4.9500

Helt, M., Kelley, E., Kinsbourne, M., Pandey, J., Boorstein, H., Herbert, M., & Fein, D. (2008). Can children with autism recover? If so, how? Neuropsychology Review, 18, 339–366. https://doi.org/10.1007/s11065-008-9075-9

Jia, F., Wang, B., Shan, L., Xu, Z., Staal, W. G., & Du, L. (2015). Core symptoms of autism improved after vitamin D supplementation. Pediatrics, 135(1), e196–e198. https://doi.org/10.1542/peds.2014-2121

Javadfar, Z., Soltani, S., Khamoushi, F., & Zare, F. (2025). Effect of vitamin D supplementation on inflammatory status and behavioral symptoms in children with autism spectrum disorders: A double-blind randomized clinical trial. BMC Pediatrics, 25, 615. https://doi.org/10.1186/s12887-025-05985-y

Jones, W., Hesselink, J., Courchesne, E., Duncan, T., Matsuda, K., & Bellugi, U. (2002). Cerebellar abnormalities in infants and toddlers with Williams syndrome. Developmental Medicine & Child Neurology, 44(10), 688–694. https://doi.org/10.1017/s0012162201002766

Leaton, R. N., & Supple, W. F., Jr. (1986). Cerebellar vermis: Essential for long-term habituation of the acoustic startle response. Science, 232(4749), 513–515. https://doi.org/10.1126/science.3961494

Lee, B. K., Gross, R., Francis, R. W., & Fung, S. (2019). Birth seasonality and risk of autism spectrum disorder. European Journal of Epidemiology, 34, 785–792. https://doi.org/10.1007/s10654-019-00506-5

Loomes, R., Hull, L., & Mandy, W. P. L. (2017). What is the male-to-female ratio in autism spectrum disorder? A systematic review and meta-analysis. Journal of the American Academy of Child & Adolescent Psychiatry, 56(6), 466–474. https://doi.org/10.1016/j.jaac.2017.03.013

Lyu, W., Thung, K. H., Huynh, K. M., et al. (2025). Functional development of the human cerebellum from birth to age five. Nature Communications, 16, 6350. https://doi.org/10.1038/s41467-025-61465-y

Maenner, M. J., Warren, Z., Williams, A. R., Amoakohene, B., Bakian, A. V., Bilder, D. A., … Durkin, M. S. (2023). Prevalence and characteristics of autism spectrum disorder among children aged 8 years — Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, 2020. MMWR Surveillance Summaries, 72(2), 1–14. https://www.cdc.gov/mmwr/volumes/72/ss/ss7202a1.htm

Matta, M. K., Zusterzeel, R., Pilli, N. R., Patel, V., Volpe, D. A., Florian, H., … Saraceno, L. L. (2019). Effect of sunscreen application on plasma concentration of active ingredients: A randomized clinical trial. JAMA, 321(21), 2082–2091. https://doi.org/10.1001/jama.2019.5232

Pose-Méndez, S., Candal, E., Adrio, F., et al. (2023). Lifelong regeneration of cerebellar Purkinje cells after induced cell ablation in zebrafish. eLife, 12, e79672. https://doi.org/10.7554/eLife.79672

Ruszkiewicz, J. A., Pinkas, A., Ferrer, B., Peres, T. V., Tsatsakis, A., & Aschner, M. (2017). Neurotoxic effect of active ingredients in sunscreen products, a contemporary review. Toxicology Reports, 4, 245–259. https://doi.org/10.1016/j.toxrep.2017.05.006

Scientific American. (2015, June). Vitamin D and autism. https://www.scientificamerican.com/article/vitamin-d-and-autism/

Schlumpf, M., Cotton, B., Conscience, M., Haller, N., Steinmann, B., & Lichtensteiger, W. (2004). In vitro and in vivo estrogenicity of UV screens. Environmental Health Perspectives, 112(13), 1391–1401. https://doi.org/10.1289/ehp.7050

Sudarov, A. (2013). Defining the role of cerebellar Purkinje cells in autism spectrum disorders. Cerebellum, 12(6), 950–955. https://doi.org/10.1007/s12311-013-0490-y

Supple, W. F. Jr., The Sunlight Solution. Skyhorse Publishing, 2026,

Tian, P., Zhu, X., Liu, Z., & Gao, J. (2025). Effects of vitamin D on brain function in preschool children with autism spectrum disorder: A resting-state functional MRI study. BMC Psychiatry, 25, 198. https://doi.org/10.1186/s12888-025-06534-8

Voltas, N., Cendra-Duarte, E., Canals, J., & Hernández-Martínez, C. (2025). Vitamin D status during pregnancy and child neurocognitive functioning at 4 years. Pediatric Research. Advance online publication. https://doi.org/10.1038/s41390-025-04258-9

Wang, T., Shan, L., Du, L., Feng, J., Xu, Z., Staal, W. G., & Jia, F. (2016). Serum concentration of 25-hydroxyvitamin D in autism spectrum disorder: A systematic review and meta-analysis. European Child & Adolescent Psychiatry, 25(4), 341–350. https://doi.org/10.1007/s00787-015-0786-1

Wang, Z., Ding, R., & Wang, J. (2020). The association between vitamin D status and autism spectrum disorder (ASD): A systematic review and meta-analysis. Nutrients, 13(1), 86. https://doi.org/10.3390/nu13010086

Wang, J., Huang, H., Liu, C., Zhang, Y., Wang, W., Zou, Z., Yang, L., He, X., Wu, J., Ma, J., & Liu, Y. (2022). Research progress on the role of vitamin D in autism spectrum disorder. Frontiers in Behavioral Neuroscience, 16, 859151. https://doi.org/10.3389/fnbeh.2022.859151

Webb, S. J., Sparks, B. F., Friedman, S. D., Shaw, D. W., Giedd, J., Dawson, G., & Dager, S. R. (2009). Cerebellar vermal volumes and behavioral correlates in children with autism spectrum disorder. Psychiatry Research, 172(1), 61–67. https://doi.org/10.1016/j.pscychresns.2008.06.001

Ye, X., Zhou, Q., Ren, P., Xiang, W., & Xiao, L. (2023). The synaptic and circuit functions of vitamin D in neurodevelopment disorders. Neuropsychiatric Disease and Treatment, 19, 1515–1530. https://doi.org/10.2147/NDT.S407731Supple, W. F. (2026). The Sunlight Solution. Skyhorse Books.

Thomas, R., Wang, W., & Su, D. M. (2020). Contributions of age-related thymic involution to immunosenescence and inflammaging. Immunity & Ageing, 17, 2. https://doi.org/10.1186/s12979-020-0173-8

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The Sunlight Solution was published June 23, 2026 by Skyhorse.

It is essential reading to fully understand and appreciate these articles on how sunlight and vitamin D work to keep you disease-free and thriving. Link on Amazon https://a.co/d/0eH8MzBY

i

Included in all posts

General Recommendations for Vitamin D for Healthy Adults

The U.S. Institute of Medicine (IOM), now the National Academy of Medicine, recommends a dietary reference intake of 600 IU (International Units) per day for adults up to age 70, and 800 IU for those over 70, to maintain bone health (Institute of Medicine, 2011). However, this amount is orders of magnitude too low considering that the human body “uses” at least 4000 IU vitamin D per day.

However, there is a vast literature on the extraskeletal functions of vitamin D for maintaining optimal functioning of the immune system, muscular system and ideal aging that indicates that optimal levels of serum vitamin D are much, much higher (e.g., Grant et al. 2020).

Based on Blood Levels

A blood test provides a clear picture of vitamin D status. Levels are typically categorized as follows (Holick et al., 2011; Wang et al., 2017):

Link to StarPowerLifeSciences.org for more information

DISCLAIMER: This publication is educational and informational in nature. Nothing published here — including articles, case reports, reader comments, or author responses — constitutes medical advice, a diagnosis, or a treatment recommendation. Dosing figures and administration methods discussed here reflect information from published scientific literature or the personal experiences of individual readers; they are not prescriptions and are not tailored to any individual’s health situation. Always consult a qualified physician or licensed health professional before making any change to your medical care or beginning any self-treatment. The case reports presented reflect the personal experiences of individual contributors and may not be representative of others. We make no claim that any outcome described here is typical or predictable. Statements have not been evaluated by the Food and Drug Administration. Do your own research.

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We can now explain Finsen’s results, and the explanation is more remarkable than the cure. When ultraviolet light strikes the skin, it doesn’t just make vitamin D. It switches on the body’s own antibiotics — a standing chemical defense that sits on every surface where you meet the outside world. …

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In the context of pharmaceutical development “translation” refers to the eventual application (translation) of preclinical discoveries - usually new drugs - utilizing experimental preparations like lab animals to humans. The issue with vitamin D status is that the lab animals in the preclinical testing are all replete in vitD while the humans in the eventual clinical trials are not. Is this an oversight - which would equate to scientific malpractice - or purposeful?

The Multi-Billion-Dollar Mystery

Every year, pharmaceutical companies invest tens of billions of dollars developing new medicines. Brilliant scientists spend careers in the lab. Promising results pile up. Then those drugs enter human clinical trials—and most of them fail.

Not a little. A lot. About nine out of every ten drugs that reach the first stage of human testing never make it to pharmacy shelves (Sun et al., 2022; Arora et al., 2021). The most common reason isn’t that the drugs turn out to be dangerous. It’s that they…

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This article is the foundational basis for just about every subsequent article that you will read here. It describes a 23 year experiment into the effects of high-dose Vitamin D on health, physiology and behavior. Optimal Vitamin D not only helps keep you exceptionally healthy, it also appears to slow indices of biological aging.

Numbers on a lab report rarely tell the whole story. But sometimes, when you hold them up to the right light, they reveal something remarkable. This is the story of what a comprehensive blood panel drawn in May 2026 appears to be saying about twenty-three years of daily supplementation with high-dose Vitamin D, the StarPower formulation, and what it might mean for the science of biological aging.

This story begins not with longevity research, but with a skin disease.

The Origin: A Skin Problem That Became Something Much Bigger

In the winter of 1982, during my first year of graduate school at Dartmouth, small patches of dry, flaking skin appeared on my elbows and knees. A physician at the student infirmary delivered a verdict that would define the next two decades of my life: psoriasis. I was told it was an autoimmune disease with no cure — only treatments to manage symptoms. What followed was exactly that: a grinding, years-long battle with tar creams, steroids, ointments, and proprietary dermatological concoctions, none of which worked reliably or durably.

Living in Vermont made it worse. Every fall, like clockwork, my skin would begin to deteriorate as the sun moved lower in the sky. At its worst, up to 30 percent of my skin surface was affected. I noticed the condition improved during trips to Florida, and initially attributed this to the salt water — even testing that hypothesis with saltwater soaks at home. The saltwater made it worse.

Finally, in 2003, the obvious answer became unavoidable: it was the sun. Not saltwater. The sun. And what the sun does is produce vitamin D.

In the fall of 2003, I began taking high-dose vitamin D3 supplements. Within nine to ten weeks, my psoriasis was eradicated — completely.

What happened next set the stage for everything that followed. Over that first winter, I experimented with different daily doses, using my skin as a real-time feedback meter — if patches began to return, I needed more; if my skin stayed clear, I had found my threshold. I settled on a dose well above the then-current RDA of 400 IU per day, which I describe in my upcoming book The Sunlight Solution as “the bare minimum to keep your bones from crumbling.” My psoriasis required vastly more than that. No adverse effects appeared in my annual health examinations, so I continued.

That therapeutic dose — refined over time into the StarPower formulation of 5,150 IU vitamin D3, 200 mg calcium carbonate, 200 mg potassium gluconate, and 400 mcg folic acid — became my daily supplement beginning at age 44. I am now 67 as I write this. I developed it to eradicate an autoimmune skin disease. The possibility that it might also slow the aging process was not part of the plan.

That appears it may have been a bonus.

The Biology Behind the Psoriasis Cure

To understand why this matters for aging, it helps to understand why vitamin D eradicated my psoriasis in the first place. Modern immunology now classifies plaque psoriasis as a classic Th17-driven autoimmune disease. Overactive Th17 immune cells migrate to the skin and release large quantities of interleukin-17 and other pro-inflammatory cytokines, causing the characteristic rapid skin cell proliferation and plaque formation (Lowes et al., 2014). The immune system is not broken — it is imbalanced, attacking the body’s own tissues due to a failure of regulatory control.

As I detail in Chapter 10 of The Sunlight Solution, vitamin D is one of the most potent known modulators of exactly this immune imbalance. It directly suppresses Th17 cell activity, dampens their production of destructive cytokines, and simultaneously promotes the growth of regulatory T cells — the immune system’s referees — whose job is to prevent the immune response from turning on healthy tissue (Aranow, 2011; Baeke et al., 2010). Restore vitamin D sufficiency, and you restore the balance that keeps psoriasis, and dozens of other autoimmune diseases, from expressing.

This is not a minor or incidental connection. The pharmaceutical industry has spent billions developing biologic drugs — the “-ab” and “-ib” class medications — that target IL-17, IL-23, and TNF-alpha specifically to treat psoriasis and other autoimmune conditions. As I show in Chapter 31 of The Sunlight Solution, these drugs are, in effect, pharmacological attempts to replicate what adequate vitamin D accomplishes naturally — by chemically manipulating the downstream inflammatory pathways that vitamin D would regulate holistically if it were present in sufficient quantity.

I cured my psoriasis with the upstream intervention. The downstream drugs were never necessary.

What I did not fully appreciate in 2003 — and what my bloodwork from May 2026 now illuminates — is that correcting that immune imbalance for the long term also appears to have profoundly slowed my biological aging.

Chronological Age Versus Biological Age

I am 67 years old. I live in Vermont, 6-ft, 193-lbs, 7% body fat, 125/80 bp, 60 bpm HR. I work out almost daily (~30 minutes max), I eat real food, no consistent junk food, I take no pharmaceuticals, and I have been taking the StarPower Vitamin D formulation every day for twenty-three years, beginning at age 44.

I recently had a comprehensive blood draw through Labcorp that included a complete blood count with differential, a comprehensive metabolic panel, hemoglobin A1c, testosterone, prostate-specific antigen (PSA), high-sensitivity C-reactive protein (hsCRP), and a full urinalysis. The same blood draw also measured my serum 25-hydroxyvitamin D level. I then analyzed these results against established biomarkers of biological aging.

The estimate that came back stopped me in my tracks.

Based on the available markers — weighted against the peer-reviewed literature on blood-based aging biomarkers — my estimated biological age is approximately 51 years, against a chronological age of 67. That is a gap of roughly 16 years.

Here is the arithmetic that intrigues me most: I began taking StarPower at age 44. If my biological age today is approximately 51, then over the 23 years since I started supplementing, I appear to have aged biologically by only about 7 years. Chronological time moved 23 years forward; my biology, by this estimate, moved approximately 7. While this is an observational report and alternative interpretations exist — including confounding lifestyle factors and the inherent imprecision of blood-based biological age estimation — the finding is striking enough to discuss seriously.

This post walks through the key biomarkers, explains why each one is relevant to biological aging, and connects those findings to the science laid out in my upcoming book, The Sunlight Solution (Skyhorse/MAHA Books, 2026).

Vitamin D Status

My vitamin D level [25(OH)D3] came in at 129. Because I am not a sickly person I usually don’t get periodic examinations. I actually don’t get sick. However, over the years when I have had bloodwork done - mainly to know my vitD level - it has been in the 80-110 range. Note: early on, back in my forties, doctors would express alarm at that vitD level as being dangerous; now some doctors are recommending 8000 IU per day. I also use a doctor’s response to my vitD level as a litmus test as to whether it is a smart move to keep them on or not.

The Most Important Single Number for Biological Age: hsCRP

The one result from this entire panel that is the most meaningful indicator of biological age is high-sensitivity C-reactive protein (hsCRP): 0.79 mg/L.

This places me firmly in the low-risk category for future cardiovascular events (the threshold for low risk is below 1.00 mg/L). But its significance extends far beyond heart disease.

The concept of inflammaging — chronic, low-grade, systemic inflammation as a primary driver of aging — was introduced by Franceschi and colleagues in a landmark 2000 paper in the Annals of the New York Academy of Sciences (Franceschi et al., 2000). As I discuss in Chapter 19 of The Sunlight Solution: “Rather than tying aging to a process we can’t control like the passage of time, identifying one of the mechanisms that changes as a function of time, vitamin D and inflammation, enables us to predict and control that mechanism and in turn, control aging.”

Inflammaging is not the dramatic inflammation of a wound. It is a quiet, persistent, subclinical fire that contributes to nearly every major disease of aging — heart disease, type 2 diabetes, cancer, arthritis, and neurodegenerative disorders (Franceschi et al., 2000). The hsCRP test is among the best widely available proxies for this process.

Here is the connection to the psoriasis story that I find most striking: psoriasis is itself an inflammatory disease. The same Th17-driven immune dysregulation that inflamed my skin for twenty-four years — before I corrected it with vitamin D — is the same category of chronic, smoldering inflammation that drives inflammaging and accelerated biological aging. When I fixed my psoriasis, I did not merely clear my skin. I rebalanced my immune system that, if left uncorrected, would have been producing the chronic inflammatory burden that silently ages us from the inside.

A hsCRP of 0.79 at age 67 is uncommon. Most aging individuals accumulate inflammatory burden; it is a biological gauge of the aging process. That mine has not is, I believe, a direct consequence of twenty-three years of optimal vitamin D intake keeping my immune system in the balanced, tolerogenic state it was designed to maintain.

The American College of Cardiology just published a scientific statement in 2025 explicitly identifying hsCRP as a key marker for cardiovascular risk assessment based on its inflammatory predictive power (Mensah et al., 2025). I have been requesting a CRP test for more than twenty years and have consistently found the same result: no systemic inflammation.

Telomeres, Telomerase, and the Biological Clock

To understand why this matters at the chromosomal level, it helps to understand telomeres. Telomeres are the protective caps at the ends of our chromosomes — often compared to the plastic tips on shoelaces. Every time a cell divides, they shorten. When they become critically short, the cell either dies or becomes a senescent “zombie cell” that pumps inflammatory signals into surrounding tissue and damages it. Telomere length is, therefore, one of the most rigorous available biomarkers of biological age (Epel et al., 2004).

The connection to stress is striking. In a landmark 2004 study, Nobel laureate Dr. Elizabeth Blackburn and colleagues found that mothers caring for chronically ill children — a situation of sustained psychological stress — had telomeres so much shorter than lower-stress controls (mothers of healthy children) that it equated to at least a decade of additional aging (Epel et al., 2004). Stress literally ages our chromosomes.

Two findings from the peer-reviewed literature are directly relevant to vitamin D supplements, including the StarPower formulation:

First, a large-scale study involving over 2,000 women found that those with higher serum vitamin D levels had significantly longer telomeres (Richards et al., 2007).

Second — and this is the study that most directly speaks to what long-term supplementation might accomplish — a randomized controlled trial nested within the VITAL study found that taking 2,000 IU of vitamin D3 daily for four years resulted in 140 fewer base pairs of telomere loss compared to placebo, equivalent to nearly three fewer years of chromosomal aging (Zhu et al., 2025). As I write in The Sunlight Solution: “Think about that: They took 2,000 IU vitamin D for four years and only aged one year. We can only imagine the magnitude of the antiaging effect if physiologically relevant quantities (5,000–10,000 IU) of vitamin D3 were used in this study.”

StarPower delivers 5,150 IU VitD3 per day — more than double the VITAL trial dose. I have been taking it for twenty-three years. If a modest dose over four years slows chromosomal aging by a factor of four, what might a higher dose over twenty-three years accomplish? We cannot know from this single case report. But the biological plausibility is real and scientifically grounded.

Vitamin D protects telomeres through two complementary mechanisms. First, by suppressing the chronic inflammation and oxidative stress that damage DNA, it creates a less hostile environment for chromosomes. Second, it appears to upregulate telomerase — the enzyme that can rebuild and extend telomeres (Zarei et al., 2021). As I note in Chapter 19, vitamin D may play a role not merely in protecting telomeres from damage, but in actively repairing them.

Albumin: The Overlooked Longevity Marker

One of the most underappreciated findings in my panel is serum albumin: 4.7 g/dL, near the top of the normal range of 3.9–4.9 g/dL.

Albumin is synthesized in the liver and declines reliably with age. It is one of the strongest independent predictors of all-cause mortality in aging populations, because it reflects the integrated status of protein synthesis, nutritional health, and — most importantly — systemic inflammation. Elevated inflammation suppresses albumin production; low inflammation allows it to remain high. My albumin level, like my hsCRP, is consistent with the biochemical profile of someone significantly younger than 67.

Testosterone: The Hormonal Fingerprint of Youth

My testosterone came back at 523 ng/dL, against a reference range of 264–916 ng/dL — a range calibrated to healthy, nonobese males between 19 and 39 years of age (Travison et al., 2017, as cited by Labcorp). The average testosterone for a man in his late 60s is typically in the 300–400 ng/dL range, and it declines measurably each decade after age 30.

Testosterone at 523 ng/dL places me solidly in the mid-range for men roughly thirty years my junior. This is not merely a vanity metric. Testosterone is a well-established biomarker and driver of biological aging: it maintains muscle mass, supports bone density, regulates metabolic function, and is inversely associated with all-cause mortality. Its preservation is a meaningful signal of delayed biological aging.

As I discuss in Chapter 7 of The Sunlight Solution, vitamin D directly influences testosterone production. Vitamin D receptors are present in the testes, and vitamin D regulates genes involved in sex hormone biosynthesis.

The Athletic Body at 67

I work out almost daily. But I feel the workout is minimal. On alternating days I do 3 sets of 10 of bench press, seated rows and pulldowns for upper body; then leg (quad) extensions, leg press and squats on other days. I use the maximum weight I can do to complete the 10 reps. I do not increase the weight as I’m not trying to gain, only maintain. Each day is preceeded by a 10 minute step climber workout.

The biology behind this relatively easy workout is not mysterious. As I detail in Chapter 21 of The Sunlight Solution, vitamin D receptors (VDRs) have been found directly within the nucleus of human muscle cells (Bischoff et al., 2001). The concept is use-dependent plasticity, as I exercise the muscle an optimal vitamin D environment enables me to maintain (or gain muscle if I wanted to). This makes vitamin D an active manager of muscle function at the genetic level — not a passive bystander. VitD preferentially acts on fast-twitch Type II muscle fibers, the fibers responsible for power, speed, and explosive movement (Sato et al., 2005). Vitamin D deficiency - which is common as we age - leads to measurable atrophy specifically of these power-generating fibers.

Additionally, vitamin D is a natural inhibitor of myostatin — the protein that acts as a brake on muscle growth — vitD is functioning, in effect, as a legal and natural anabolic agent (Garcia et al., 2011). By suppressing myostatin, adequate vitamin D allows for greater muscle protein synthesis and hypertrophy in response to training. So instead of killing myself with hours of weight training, I can do a minimal workout to maintain what I have.

At 67, I remain athletic and muscular at 6-ft, 194 lbs. I can still play baseball. I could dunk a basketball when I was 60. This is not simply genetic luck or lifestyle discipline. It is, I believe, substantially mediated by twenty-three years of vitamin D sufficiency keeping the biological machinery of muscle maintenance and repair running at a level rarely seen in a man of my chronological age. A systematic review found that 56 percent of athletes have inadequate vitamin D levels (Farrokhyar et al., 2015) — meaning the majority of people who train hard are doing so while their fundamental hormonal support system is running on empty.

Of course your mileage may vary on these things but I feel that with optimal vitamin D and minimal weight training the benefits of youth are prolonged. I enjoy the luxury to eat what I want, but I eat to live not live to eat.

Mitochondria: The Cellular Engine of Aging

The “mitochondrial theory of aging” holds that the slow, progressive decline in mitochondrial function — the energy-producing organelles in every cell — underlies most of what we experience as getting older (Harman, 1972). Damaged mitochondria produce less ATP and more reactive oxygen species (ROS), creating a vicious cycle of energy decline and oxidative damage that accelerates aging.

As I discuss in Chapter 22 of The Sunlight Solution, vitamin D plays a direct role in mitochondrial health. The vitamin D receptor (VDR) has been found not only in cell nuclei but inside mitochondria themselves (Matta Reddy et al., 2022). When vitamin D binds to these mitochondrial receptors, it promotes the creation of new, healthy mitochondria (biogenesis), enhances their energy-producing efficiency, and protects them from oxidative damage (Latham et al., 2021).

In essence, twenty-three years of vitamin D sufficiency may have been continuously supporting my cells’ energy production at the very site where aging originates. I feel like I have plenty of energy during the day, and I fall asleep as soon as my head hits the pillow at night. Both phenomenons very likely a result of long-term vitamin D use.

The Aging Skin: Why Supplementation Matters More With Age

There is a further irony in the biology of vitamin D and aging that is particularly pointed in my case. The organ responsible for producing vitamin D from sunlight — the very skin that psoriasis was destroying — loses its efficiency with age regardless. Research by MacLaughlin and Holick (1985) demonstrated definitively that the concentration of 7-dehydrocholesterol, the precursor molecule converted to vitamin D by UVB light, is only about 25 percent as high in the skin of a 70-year-old as in the skin of a young adult. The same amount of sun exposure produces four times less vitamin D.

As I write in Chapter 19: “This age-related decline in cutaneous synthesis creates a biological vulnerability. Just when our bodies need robust defenses against age-related diseases and optimal immune system function, our primary natural mechanism for producing a key hormonal defender falters.”

I began supplementing at 44, motivated by a skin disease; psoriasis. But by doing so, I also stepped ahead of the curve on this age-related decline in cutaneous synthesis — never allowing the vitamin D gap that silently drives inflammaging in most older adults to open in the first place.

What This Is — and What It Is Not

I want to be precise about the claims I am making here.

This is a single-person, N=1 observational report. It cannot prove causation. There are confounding factors: daily exercise, no smoking, no alcohol excess (I do have 1-2 beers most days, some days more), no pharmaceuticals, a reasonable diet. Any or all of these contribute to the biomarker profile observed. The biological age estimate of approximately 51 is derived from blood markers alone — a valid method. However, studies, even case reports like this are few and far between over such a long time span.

What this report represents is a biologically plausible and internally consistent set of findings in a person who has maintained optimal vitamin D — using a specific formulation at a specific dose — for twenty-three years. The markers most strongly associated with inflammaging (hsCRP) (Ferrucci & Fabbri 2018), protein synthesis and longevity (albumin) (Levine et al., 2018), reproductive and metabolic aging (testosterone) (Huang et al., 2025), blood cell health (CBC) (Pyrkov et al., 2021) and organ function (liver enzymes, urinalysis) (Ling et al., 2024) all trend significantly younger than chronological age.

The specific calculation — starting StarPower at 44, biological age now 51, chronological age now 67, implying approximately 7 biological years of aging over 23 chronological years — is a data point, not a proof. But it is a data point that deserves serious attention and, eventually, prospective study with proper controls. For those of you that may be interested in maintaining an active and healthy lifestyle as long as possible maybe my experiences are food for thought.

The Hayflick Limit — the theoretical maximum number of human cell replications before replicative senescence — points to a maximum human lifespan of approximately 122 years (Hayflick & Moorhead, 1961). Most of us fall catastrophically short of that limit not because of genetics but because of chronic inflammation, vitamin D deficiency, and the cascade of immune dysfunction those conditions produce. My data suggest I may be tracking closer to that biological potential than most 67-year-olds.

I started this journey trying to clear my skin. I appear to have accidentally stumbled onto something far larger.

For Readers of This Substack

If you have been following StarPower on Substack for any length of time, none of the underlying science here is new. What is new is seeing it expressed in a single individual’s blood chemistry over a two-decade time horizon — and recognizing that the original motivation had nothing to do with longevity at all.

The takeaways are simple:

Test your vitamin D level. The target range, based on the research reviewed in The Sunlight Solution, is 60–80 ng/mL for general health, with some evidence supporting 80–100 ng/mL for neurological and cancer protection. I have had a serum level of 80-110, now 129, for at least 23 years with nothing but good health and vitality to show for it.

Supplement appropriately. Most adults, particularly those living at northern latitudes, require 5,000–8,000 IU per day to reach and maintain general health levels, especially as cutaneous synthesis declines with age.

Test your hsCRP. This is the single most actionable inflammatory marker available. If it is above 1.0 mg/L, your biological fire alarm is sounding. Optimizing vitamin D is one of the most powerful interventions available to silence it.

Do not wait. The telomere research makes clear that the benefits of vitamin D supplementation are cumulative over years and decades (Zhu et al., 2025). The time to start is not when you are already sick. I started because I was desperate to stop itching and scratching. Twenty-three years later, the numbers suggest that decision was one of the best I ever made.

Vitamin D most likely will not turn back the clock on biological aging but it appears to make it run much slower. My chronological age is 67, yet my biological age is 51. I feel much younger than 51. (The wife was concerned that this was becoming an inadvertent Match profile so no photos are included. But you can find photos of me online elsewhere). By the way, 20 or so years ago she also began taking StarPower for intractable ulcerative colitis - another autoimmune disease. StarPower eradicated her UC in a few weeks and has been managed successfully since then. She takes one StarPower per day I’ll report on her blood value aging analysis in a future report (if she approves).

Note: There is a lot written regarding the importance of co-factors like vitamin K2, magnesium and calcium in conjunction with vitamin D. I include 200 mg calcium carbonate in StarPower “just to be sure” to get enough calcium. The K2 and magnesium were not supplemented, and apparently I get enough in my diet, or their importance over the long term is overstated.

Link to buy StarPower Vitamin D if you’re interested StarPowerLifeSciences

References

Aranow, C. (2011). Vitamin D and the immune system. Journal of Investigative Medicine, 59(6), 881–886. https://doi.org/10.2310/JIM.0b013e31821b8755

Baeke, F., Takiishi, T., Korf, H., Gysemans, C., & Mathieu, C. (2010). Vitamin D: Modulator of the immune system. Current Opinion in Pharmacology, 10(4), 482–496. https://doi.org/10.1016/j.coph.2010.04.001

Bischoff, H. A., Borchers, M., Gudat, F., Duermueller, U., Theiler, R., Stähelin, H. B., & Dick, W. (2001). In situ detection of 1,25-dihydroxyvitamin D3 receptor in human skeletal muscle tissue. Histochemical Journal, 33(1), 19–24. https://doi.org/10.1023/a:1011018602603

Epel, E. S., Blackburn, E. H., Lin, J., Dhabhar, F. S., Adler, N. E., Morrow, J. D., & Cawthon, R. M. (2004). Accelerated telomere shortening in response to life stress. Proceedings of the National Academy of Sciences of the United States of America, 101(49), 17312–17315. https://doi.org/10.1073/pnas.0407162101

Farrokhyar, F., Tabasinejad, R., Dao, D., Peterson, D., Ayeni, O. R., Hadioonzadeh, R., & Bhandari, M. (2015). Prevalence of vitamin D inadequacy in athletes: A systematic review and meta-analysis. Sports Medicine, 45(3), 365–378. https://doi.org/10.1007/s40279-014-0267-6

Ferrucci, L., & Fabbri, E. (2018). Inflammageing: Chronic inflammation in ageing, cardiovascular disease, and frailty. Nature Reviews Cardiology, 15(9), 505–522. https://doi.org/10.1038/s41569-018-0064-2

Franceschi, C., Bonafè, M., Valensin, S., Olivieri, F., De Luca, M., Ottaviani, E., & De Benedictis, G. (2000). Inflamm-aging: An evolutionary perspective on immunosenescence. Annals of the New York Academy of Sciences, 908(1), 244–254. https://doi.org/10.1111/j.1749-6632.2000.tb06651.x

Garcia, L. A., King, K. K., & Ferrini, M. G. (2011). 1,25(OH)2D3 stimulates mechanistically distinct pathways of protein synthesis in C2C12 skeletal muscle cells. The Journal of Steroid Biochemistry and Molecular Biology, 127(3–5), 331–336. https://doi.org/10.1016/j.jsbmb.2011.07.009

Grant, W. B., Lahore, H., & Rockwell, M. S. (2020). The benefits of vitamin D supplementation for athletes: Better performance and reduced risk of COVID-19. Nutrients, 12(12), 3741. https://doi.org/10.3390/nu12123741

Harman, D. (1972). The biologic clock: The mitochondria? Journal of the American Geriatrics Society, 20(4), 145–147. https://doi.org/10.1111/j.1532-5415.1972.tb00787.x

Hayflick, L., & Moorhead, P. S. (1961). The serial cultivation of human diploid cell strains. Experimental Cell Research, 25, 585–621. https://doi.org/10.1016/0014-4827(61)90192-6

Huang W, Deng L, Wen Q et al. (2025). Dynamics of serum testosterone and biological aging in men: insights from Chinese, American, and British populations, eClinicalMedicine, 2025; 82

Latham, C. M., Brightwell, C. R., et al. (2021). Vitamin D promotes skeletal muscle regeneration and mitochondrial health. Frontiers in Physiology, 12, 660498. https://doi.org/10.3389/fphys.2021.660498

Levine, M. E., Lu, A. T., Quach, A., Chen, B. H., Assimes, T. L., Bandinelli, S., Hou, L., Baccarelli, A. A., Stewart, J. D., Li, Y., Whitsel, E. A., Wilson, J. G., Reiner, A. P., Aviv, A., Lohman, K., Liu, Y., Ferrucci, L., & Horvath, S. (2018). An epigenetic biomarker of aging for lifespan and healthspan. Aging (Albany NY), 10(4), 573–591. https://doi.org/10.18632/aging.101414

Lowes, M. A., Suárez-Fariñas, M., & Krueger, J. G. (2014). Immunology of psoriasis. Annual Review of Immunology, 32, 227–255. https://doi.org/10.1146/annurev-immunol-032713-120225

Ling, S., Diao, H., Lu, G., & Shi, L. (2024). Associations between serum levels of liver function biomarkers and all-cause and cause-specific mortality: A prospective cohort study. BMC Public Health, 24, Article 3302. https://doi.org/10.1186/s12889-024-20773-6

MacLaughlin, J., & Holick, M. F. (1985). Aging decreases the capacity of human skin to produce vitamin D3. The Journal of Clinical Investigation, 76(4), 1536–1538. https://doi.org/10.1172/JCI112134

Matta Reddy, A., Iqbal, M., Chopra, H., Urmi, S., Junapudi, S., Bibi, S., Kumar Gupta, S., Nirmala Pangi, V., Singh, I., & Abdel-Daim, M. M. (2022). Pivotal role of vitamin D in mitochondrial health, cardiac function, and human reproduction. EXCLI Journal, 21, 967–990. https://doi.org/10.17179/excli2022-4935

Mensah, G., Arnold, N., Prabhu, S., et al. (2025). Inflammation and cardiovascular disease: ACC scientific statement. Journal of the American College of Cardiology. https://doi.org/10.1016/j.jacc.2025.08.047

Pyrkov, T. V., Avchaciov, K., Tarkhov, A. E., Menshikov, L. I., Gudkov, A. V., & Fedichev, P. O. (2021). Longitudinal analysis of blood markers reveals progressive loss of resilience and predicts human lifespan limit. Nature Communications, 12, Article 2765. https://doi.org/10.1038/s41467-021-23014-1

Richards, J. B., Valdes, A. M., Gardner, J. P., Paximadas, D., Kimura, M., Nessa, A., Lu, X., Surdulescu, G. L., Swaminathan, R., Spector, T. D., & Aviv, A. (2007). Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women. The American Journal of Clinical Nutrition, 86(5), 1420–1425. https://doi.org/10.1093/ajcn/86.5.1420

Sato, Y., Iwamoto, J., Kanoko, T., & Satoh, K. (2005). Low-dose vitamin D prevents muscular atrophy and reduces falls and hip fractures in women after stroke: A randomized controlled trial. Cerebrovascular Diseases, 20(3), 187–192. https://doi.org/10.1159/000087201

Supple, W. F. (2026). The Sunlight Solution: Reclaiming vitamin D, reversing the chronic disease epidemic, and making America healthy again. Skyhorse/MAHA Books. To be published June 23, 2026.

Travison, T. G., Vesper, H. W., Orwoll, E., Wu, F., Kaufman, J. M., Wang, Y., Lapauw, B., Fiers, T., Matsumoto, A. M., & Bhasin, S. (2017). Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe. The Journal of Clinical Endocrinology and Metabolism, 102(4), 1161–1173. https://doi.org/10.1210/jc.2016-2935

Zarei, M., Zarezadeh, M., Hamedi Kalajahi, F., & Javanbakht, M. H. (2021). The relationship between vitamin D and telomere/telomerase: A comprehensive review. The Journal of Frailty & Aging, 10(1), 2–9. https://doi.org/10.14283/jfa.2020.33

Zhu, H., Manson, J. E., Cook, N. R., Bekele, B. B., Chen, L., Kane, K. J., Huang, Y., Li, W., Christen, W., Lee, I. M., & Dong, Y. (2025). Vitamin D3 and marine ω-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITamin D and OmegA-3 TriaL (VITAL) randomized controlled trial. The American Journal of Clinical Nutrition, 122(1), 39–47. https://doi.org/10.1016/j.ajcnut.2025.05.003
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*William F. Supple, Jr., PhD, is the author of The Sunlight Solution (Skyhorse/MAHA Books, 2026) and publishes research and commentary on vitamin D and human health at [StarPower.Substack.com](https://starpower.substack.com).*

*The laboratory results discussed in this article are from a Labcorp panel drawn May 18, 2026. This article is for informational and educational purposes only and does not constitute medical advice. Readers should consult a qualified healthcare professional before making changes to supplementation or health practices.*

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General Recommendations for Vitamin D for Healthy Adults

The U.S. Institute of Medicine (IOM), now the National Academy of Medicine, recommends a dietary reference intake of 600 IU (International Units) per day for adults up to age 70, and 800 IU for those over 70, to maintain bone health (Institute of Medicine, 2011). However, this amount is orders of magnitude too low considering that the human body “uses” at least 4000 IU vitamin D per day.

However, there is a vast literature on the extraskeletal functions of vitamin D for maintaining optimal functioning of the immune system, muscular system and ideal aging that indicates that optimal levels of serum vitamin D are much, much higher (e.g., Grant et al. 2020).

Based on Blood Levels

A blood test provides a clear picture of vitamin D status. Levels are typically categorized as follows (Holick et al., 2011; Wang et al., 2017):

Link to StarPowerLifeSciences.org for more information

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The researchers were looking for changes in two specific areas: the inflammatory immune response and the metabolism of homocysteine (a toxic amino acid often elevated in psoriasis patients).

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Emerging research in the last several years is solidifying the role of vitamin D in cancer prevention and treatment, with numerous studies revealing its ability to hinder cancer cell growth, enhance immune function, and even improve the efficacy of conventional cancer therapies. This growing body of evidence is prompting a fresh look at the potential of this essential nutrient as a key player in oncology.

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Now, new research from the University of South Australia gives strong evidence that vitamin D deficiency is associated with premature death, prompting calls for people to follow healthy vitamin D level guidelines.

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