Vitamin D And HPA Axis Research

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Table of Contents

1. What Is the HPA Axis and Why Does It Matter?
2. How Vitamin D Interacts With the HPA Axis
3. Vitamin D and Cortisol: What the Research Actually Shows
4. Vitamin D Deficiency, PTSD, and Stress Hormones
5. Animal Studies vs. Human Studies: Are the Findings Consistent?
6. Vitamin D and Anxiety: What We Know So Far
7. Key Biomarkers Used in Vitamin D HPA Axis Research
8. Dosing, Timing, and Practical Considerations
9. Frequently Asked Questions
10. Summary and Bottom Line

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Introduction

If you have ever wondered whether a simple nutrient could influence how your body handles stress, you are not alone. The relationship between vitamin D and HPA axis function is one of the most actively studied topics in modern neuroendocrinology, and the findings coming out of 2024 and 2025 are genuinely striking.

The hypothalamic-pituitary-adrenal (HPA) axis is your body's central command center for stress. It governs the release of cortisol, the hormone most people associate with pressure, panic, and burnout. For years, researchers suspected that vitamin D stress responses were connected, largely because vitamin D receptors (VDRs) are found throughout the brain regions that control HPA activity. Now, a growing body of clinical and preclinical research is filling in the molecular details.

This article synthesizes the most current peer-reviewed evidence — including studies published in 2025 — to give you a clear, science-based picture of what we know, what we still need to learn, and what it might mean for your health.

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What Is the HPA Axis and Why Does It Matter?

The hypothalamic-pituitary-adrenal axis is a three-part neuroendocrine cascade that coordinates your body's response to physical and psychological stress:

1. The hypothalamus detects a stressor and releases corticotropin-releasing hormone (CRH).
2. The pituitary gland responds to CRH by secreting adrenocorticotropic hormone (ACTH).
3. The adrenal glands respond to ACTH by producing cortisol (in humans) or corticosterone (in rodents).

Cortisol then feeds back to the hypothalamus and pituitary to suppress further CRH and ACTH release — a mechanism known as the negative feedback loop. When this loop works properly, stress responses are sharp, purposeful, and self-limiting. When it breaks down, the consequences can include:

• Chronic anxiety and mood disorders
• Disrupted sleep architecture
• Immune dysregulation
• Metabolic dysfunction
• Increased vulnerability to post-traumatic stress disorder (PTSD)

This is exactly why HPA vitamin D interactions matter so much. If vitamin D helps calibrate this system — and the evidence increasingly suggests it does — then widespread vitamin D insufficiency could be quietly destabilizing the stress-response machinery of millions of people.

Vitamin D Receptors in the HPA Circuit

Vitamin D is far more than a bone mineral. It functions as a steroid hormone, binding to nuclear vitamin D receptors (VDRs) that regulate gene transcription. Crucially, VDRs have been identified in:

• The hypothalamus
• The pituitary gland
• The hippocampus (which provides inhibitory input to the HPA axis)
• The prefrontal cortex
• The adrenal cortex itself

The presence of VDRs at virtually every level of the HPA circuit is strong anatomical evidence that vitamin D is not a bystander in stress regulation — it is an active participant.

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How Vitamin D Interacts With the HPA Axis

Understanding vitamin D HPA axis interactions requires looking at multiple levels simultaneously: the molecular, the hormonal, and the behavioral.

Molecular Mechanisms

At the cellular level, vitamin D appears to modulate the HPA axis through several converging pathways:

1. Direct VDR-mediated transcription Vitamin D binds to VDRs in hypothalamic neurons, potentially altering the expression of CRH and its receptors. Laboratory data suggest that adequate vitamin D signaling helps dampen excessive CRH output, which would otherwise drive prolonged cortisol elevation.

2. Glucocorticoid receptor (GR) sensitivity One of the most clinically relevant mechanisms is vitamin D's proposed role in maintaining glucocorticoid receptor sensitivity. When GRs become less responsive — a state sometimes called glucocorticoid resistance — the negative feedback loop weakens, and cortisol output goes unchecked. A 2025 focused review published in Translational Psychiatry and indexed in ScienceDirect specifically examined vitamin D regulation of cortisol through the HPA axis, noting that vitamin D may upregulate GR expression and improve receptor responsiveness.

3. Inflammatory modulation Chronic inflammation and HPA dysregulation are bidirectionally linked. Pro-inflammatory cytokines such as IL-6 and TNF-α can directly stimulate CRH release, creating a vicious cycle. Vitamin D is a well-characterized anti-inflammatory agent, and its ability to reduce neuroinflammation in stress-exposed tissue has been demonstrated in multiple animal models — including a 2025 rat chronic-stress study where vitamin D3 normalized corticosterone and reduced inflammatory signaling markers.

4. Serotonergic and dopaminergic modulation Vitamin D also influences serotonin synthesis and dopamine metabolism, both of which interact with HPA tone. Lower monoamine signaling sensitizes the axis to stress, while adequate vitamin D support may help buffer this sensitization.

The Feedback Loop in Focus

A 2024 PubMed-indexed review titled "Change in function and homeostasis of HPA axis: The role of vitamin family" provided a comprehensive map of how fat-soluble vitamins — particularly vitamin D — influence each node of the HPA feedback loop. The authors concluded that vitamin D appears to exert regulatory influence at the hypothalamic, pituitary, and adrenal levels, making it one of the few single nutrients with documented effects across the entire axis.

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Vitamin D and Cortisol: What the Research Actually Shows

When people search for vitamin D cortisol research, they often want a simple answer: does taking vitamin D lower cortisol? The honest answer is more nuanced, and it depends heavily on the population studied, baseline vitamin D status, and whether the outcome is acute cortisol levels or the overall pattern of cortisol secretion across the day.

The Cortisol Awakening Response (CAR)

One of the most informative biomarkers in cortisol vitamin D research is the cortisol awakening response — the sharp spike in cortisol that occurs in the first 30–45 minutes after waking. The CAR reflects HPA axis reactivity and preparedness; a blunted CAR is associated with burnout, chronic fatigue, and depression, while an exaggerated CAR has been linked to anxiety disorders.

A 2018 controlled study in multiple sclerosis (MS) patients found no statistically significant changes in salivary cortisol across the diurnal cycle following vitamin D3 supplementation, but the researchers did observe a clinically meaningful trend toward a reduced cortisol awakening response in the vitamin D group. While the study was underpowered to detect significance for the CAR specifically, the directional finding is consistent with the hypothesis that vitamin D helps normalize an overactive HPA response — at least in populations whose axis is chronically elevated.

The 2025 Focused Review: A New Framework

The 2025 ScienceDirect paper "Vitamin D regulation of cortisol through the HPA axis: A focused review" is arguably the most thorough synthesis of vitamin D stress hormone data published to date. Key conclusions from this review include:

• Vitamin D deficiency is consistently associated with elevated basal cortisol in observational studies
• Supplementation trials show heterogeneous effects, likely because study populations differ in baseline deficiency depth
• The most pronounced cortisol-normalizing effects appear in individuals with the lowest baseline 25-hydroxyvitamin D levels
• Duration of supplementation matters: short-term trials (under 8 weeks) rarely show HPA-axis changes, while longer interventions (12–24 weeks) more consistently demonstrate hormonal shifts

This dose- and duration-dependent pattern is important for anyone evaluating vitamin D stress research. Single short-course supplementation trials should not be interpreted as a verdict on the entire relationship.

What Happens to CRH and ACTH?

Cortisol vitamin D deficiency research increasingly focuses not just on end-point cortisol but on the upstream hormones that drive its release — specifically CRH and ACTH. If vitamin D modulates the HPA axis, we would expect deficiency to be associated with elevated CRH and ACTH, and repletion to normalize them.

This is precisely what the 2025 PTSD and PTSD-adjacent research found, as detailed in the next section.

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Vitamin D Deficiency, PTSD, and Stress Hormones

The most statistically compelling human data on vitamin D HPA function comes from a 2025 study published in Frontiers in Neuroscience, which examined HPA-axis hormone profiles in PTSD patients relative to non-PTSD controls while simultaneously measuring serum 25-hydroxyvitamin D.

The Core Findings

The results were highly statistically significant (P<0.001 across multiple comparisons):

| Biomarker | PTSD Group | Non-PTSD Group | Direction | |---|---|---|---| | Serum 25-hydroxyvitamin D | Significantly lower | Higher | ↓ in PTSD | | CRH | Significantly higher | Lower | ↑ in PTSD | | ACTH | Significantly higher | Lower | ↑ in PTSD | | Cortisol | Significantly lower | Higher | ↓ in PTSD |

This pattern — high CRH, high ACTH, but paradoxically low cortisol — is a hallmark of HPA axis dysregulation in PTSD. The adrenal gland becomes desensitized to ACTH stimulation over time, while upstream drive through CRH and ACTH remains chronically elevated. Vitamin D appears to correlate with this entire cascade.

The Correlation Data

Critically, the study found that vitamin D levels negatively correlated with CRH and ACTH (P<0.05), meaning that as vitamin D went down, CRH and ACTH went up. Conversely, vitamin D positively correlated with cortisol (P<0.05), meaning lower vitamin D was associated with the blunted downstream cortisol that characterizes chronic PTSD-related HPA dysfunction.

These correlational findings do not prove causation, but the consistency across multiple HPA-axis nodes is mechanistically coherent with the VDR-based models described earlier.

The Diagnostic Threshold

One particularly noteworthy analysis in the Frontiers study was a receiver operating characteristic (ROC) curve analysis identifying a potential diagnostic threshold for vitamin D in the context of PTSD-related HPA changes:

• 25-hydroxyvitamin D cutoff: 16.32 ng/mL
• Area under the curve (AUC): 0.698
• Sensitivity: 86.2%
• Specificity: 51.1%

While a specificity of 51.1% means this threshold alone cannot definitively identify PTSD cases, the high sensitivity (86.2%) suggests that vitamin D below 16.32 ng/mL is rarely absent in those with PTSD-associated HPA changes. In other words, low vitamin D may be a near-universal feature of this pattern, even if it is not exclusive to it.

This finding underscores the potential clinical value of measuring cortisol vitamin D deficiency markers together, rather than treating them as unrelated tests.

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Animal Studies vs. Human Studies: Are the Findings Consistent?

A reasonable scientific question is whether the vitamin D HPA axis relationship seen in human correlational studies is matched by causal evidence from controlled animal experiments. The answer, as of 2025, is increasingly yes.

The 2025 Rat Chronic-Stress Model

A 2025 animal study using a rat chronic-stress model provided some of the most direct causal evidence to date. Rats subjected to prolonged stress protocols showed predictable HPA dysregulation: elevated corticosterone, disrupted diurnal corticosterone rhythms, and elevated neuroinflammatory markers including IL-6 and TNF-α in limbic brain regions.

When these animals received vitamin D3 supplementation:

• Serum vitamin D3 was restored to normal physiological range
• Corticosterone was normalized, returning toward the levels seen in unstressed control animals
• Neuroinflammatory signaling was reduced, including decreases in pro-inflammatory cytokines in the hippocampus and prefrontal cortex — areas critical for HPA feedback regulation

This is mechanistically important because it suggests vitamin D does not simply lower cortisol nonspecifically. Rather, it appears to help the feedback system work as designed, restoring normal corticosterone patterning in animals whose rhythms had been disrupted by chronic stress.

The 2025 Sleep-Desynchrony Model

A second 2025 animal study, published in PMC under the title "Vitamin D3 Improves Hypothalamic–Pituitary–Adrenal Axis Function," examined HPA function in a sleep-desynchrony model — a design meant to mimic the circadian disruption associated with shift work, jet lag, or sleep disorders in humans.

Sleep desynchrony is known to dysregulate the HPA axis, flattening the normal diurnal cortisol rhythm and increasing basal corticosterone. The study found that vitamin D3 supplementation partially restored HPA-axis function in this model, improving both the amplitude of the diurnal corticosterone curve and the responsiveness of the axis to acute challenge.

Bridging the Translational Gap

The convergence between animal model causal findings and human correlational findings is scientifically encouraging. The translation is not perfect — rats use corticosterone where humans use cortisol, and stress protocols in animal models cannot fully replicate the complexity of human psychological stress. Nevertheless, the directional consistency across species and study designs strengthens the overall evidence base for vitamin D stress research considerably.

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Vitamin D and Anxiety: What We Know So Far

The connection between vitamin D anxiety and HPA dysregulation is among the most clinically relevant threads in this entire field. Anxiety disorders, by definition, involve abnormal threat detection and stress-response regulation — two functions mediated primarily through the HPA axis and its limbic inputs.

Epidemiological Signal

Multiple large observational studies have found inverse associations between serum 25-hydroxyvitamin D and anxiety symptoms. The relationship is present across adult age ranges and appears particularly strong in:

• Individuals with generalized anxiety disorder (GAD)
• Those with social anxiety disorder
• Peri-menopausal women, whose vitamin D status and HPA reactivity change simultaneously
• Elderly populations with combined vitamin D deficiency and chronic low-grade inflammation

The HPA Mechanism in Anxiety

In anxiety disorders, the HPA axis tends to be hypersensitive rather than blunted. CRH signaling is overactive, cortisol responses to moderate stressors are exaggerated, and the negative feedback loop is insufficiently strong to terminate stress responses in a timely manner.

If vitamin D helps upregulate glucocorticoid receptor sensitivity — as the 2025 focused review suggests — then correcting deficiency could restore more efficient negative feedback, reducing the chronically elevated CRH tone that drives anxious anticipation. This mechanism is conceptually distinct from sedation or pharmacological anxiolysis; it is about restoring the system's own self-regulatory capacity.

What Clinical Trials Show

Randomized controlled trials specifically targeting vitamin D anxiety outcomes are fewer and more methodologically variable than observational studies. However, several systematic reviews and meta-analyses have found modest but statistically significant improvements in anxiety scores following vitamin D supplementation, particularly in:

• Deficient individuals (baseline 25-OHD below 20 ng/mL)
• Trials lasting at least 12 weeks
• Studies using doses of 2,000 IU/day or higher

The effect sizes are generally small to moderate, which is consistent with vitamin D being one regulatory input among many — not a standalone anxiolytic.

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Key Biomarkers Used in Vitamin D HPA Axis Research

One of the questions researchers and clinicians frequently grapple with in HPA vitamin D studies is: what should you actually measure? The HPA axis can be assessed at multiple points, and the choice of biomarker significantly affects what conclusions can be drawn.

1. Serum 25-Hydroxyvitamin D (25-OHD)

This remains the gold-standard measure of vitamin D status. Most HPA-axis research uses 25-OHD as the exposure variable. The 2025 PTSD study used this biomarker and found mean levels significantly lower in the PTSD group (P<0.001), with the ROC cutoff at 16.32 ng/mL providing a clinically useful reference point.

2. Salivary Cortisol (Diurnal Profile)

Saliva sampling is non-invasive and allows multiple time-point collection, making it ideal for measuring the diurnal cortisol profile and the cortisol awakening response. The 2018 MS supplementation trial used salivary cortisol as its primary HPA-axis outcome.

3. Plasma ACTH

Measuring ACTH provides insight into pituitary drive. The 2025 PTSD study found ACTH significantly elevated in the low-vitamin D group — a finding consistent with reduced negative feedback efficiency.

4. Plasma or CSF CRH

CRH is technically more challenging to measure peripherally (its levels in blood do not reliably reflect hypothalamic secretion), but cerebrospinal fluid CRH measurements are used in research settings. The 2025 PTSD study appears to have used peripheral CRH proxies or indirect assessment, finding them significantly elevated in the PTSD/low-vitamin D group.

5. Urinary Free Cortisol (UFC)

Twenty-four-hour urinary free cortisol reflects total daily cortisol output and is useful for identifying chronic hypercortisolism or blunted total output in PTSD-type HPA patterns.

6. Corticosterone (Animal Studies)

In rodent research, corticosterone is the primary glucocorticoid (equivalent to human cortisol). Both the 2025 chronic-stress rat study and the sleep-desynchrony model used corticosterone as the primary HPA output biomarker.

Why Biomarker Choice Matters

The heterogeneity in biomarker selection across vitamin D cortisol research is one reason meta-analyses in this space sometimes reach conflicting conclusions. A study measuring only fasting morning cortisol may miss the more nuanced CAR effects and diurnal rhythm changes that appear to be the most vitamin D-sensitive HPA outcomes.

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Dosing, Timing, and Practical Considerations

What Doses Have Been Used in HPA-Axis Research?

Dosing across vitamin D stress research studies has varied considerably:

| Study Type | Typical Dose Range | Duration | |---|---|---| | Human supplementation trials | 1,000–5,000 IU/day | 8–24 weeks | | Human bolus/loading studies | 50,000–100,000 IU/week (short course) | 4–8 weeks | | Animal studies | Weight-adjusted; typically 200–1,000 IU/kg body weight | 3–8 weeks |

The 2018 MS cortisol trial used a specific supplementation protocol consistent with moderate-to-high daily dosing. The 2025 rat chronic-stress study used doses calibrated to restore physiological serum vitamin D3 levels rather than supraphysiological loading.

Does the Form of Vitamin D Matter?

The evidence primarily supports vitamin D3 (cholecalciferol) rather than D2 (ergocalciferol) for HPA-related outcomes. Vitamin D3 is more efficiently converted to 25-hydroxyvitamin D and has a longer half-life, meaning more stable tissue concentrations — likely important for sustained receptor-level effects in the HPA circuit.

Timing and Cofactors

Several practical factors are worth noting for anyone considering vitamin D supplementation in the context of stress or HPA support:

• Take vitamin D3 with fat: It is fat-soluble and requires dietary fat for optimal absorption
• Consider magnesium: Magnesium is a required cofactor for vitamin D metabolism; deficiency in magnesium can impair the conversion of vitamin D to its active form (1,25-dihydroxyvitamin D)
• Vitamin K2 co-supplementation: While not directly studied in HPA contexts, K2 is frequently combined with D3 in supplementation protocols for overall safety
• Morning vs. evening dosing: Some researchers hypothesize that morning dosing may better align with the natural diurnal VDR activation pattern, though this has not been definitively tested in HPA-specific trials

Baseline Status Is Everything

Perhaps the most consistent message from across all the vitamin D HPA research is that effects are most pronounced in those with true deficiency. If your 25-OHD is already at 50 ng/mL, adding more vitamin D is unlikely to produce meaningful HPA changes. If you are below 20 ng/mL — and particularly if you are below the 16.32 ng/mL threshold identified in the 2025 PTSD ROC analysis — there is substantially more biological rationale for expecting a measurable response.

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Frequently Asked Questions

Does vitamin D affect cortisol levels?

Yes, based on the available evidence, vitamin D appears to influence cortisol levels — but not uniformly in all populations. Cortisol vitamin D research suggests the relationship is most pronounced in individuals who are deficient at baseline. In those cases, supplementation may help normalize both the amplitude and the diurnal rhythm of cortisol secretion, rather than simply suppressing it. The 2025 focused review on vitamin D regulation of cortisol through the HPA axis concluded that the evidence is mechanistically coherent and directionally consistent, even if individual clinical trials show variable effect sizes.

Can vitamin D regulate the HPA axis directly?

Evidence strongly suggests yes. Vitamin D receptors are present at the hypothalamus, pituitary, hippocampus, and adrenal cortex — all nodes within or adjacent to the HPA circuit. Animal studies, including the 2025 rat chronic-stress model, have demonstrated that vitamin D3 supplementation directly restores normalized corticosterone patterns and reduces upstream neuroinflammatory signals that drive HPA overdrive.

Is vitamin D deficiency linked to stress, PTSD, or depression?

The 2025 Frontiers in Neuroscience study provides some of the strongest human evidence to date linking cortisol vitamin D deficiency with PTSD. Participants with PTSD had significantly lower serum 25-OHD than non-PTSD controls (P<0.001), along with dysregulated CRH, ACTH, and cortisol patterns. The vitamin D levels negatively correlated with CRH and ACTH and positively correlated with cortisol, suggesting a dose-response relationship between vitamin D status and HPA calibration. Depression research shows similar trends, although the causal direction remains debated.

Can vitamin D supplementation improve cortisol rhythm or cortisol awakening response?

Possibly. The 2018 MS trial found a non-significant trend toward a reduced cortisol awakening response following vitamin D3 supplementation — a directional finding consistent with HPA normalization. The trial was likely underpowered for this specific outcome, and longer-duration, larger trials specifically designed to capture CAR changes are needed.

What dose of vitamin D was used in HPA-axis studies?

Doses in human trials have generally ranged from 1,000 to 5,000 IU per day, with some loading protocols using weekly high doses. The animal studies used weight-adjusted dosing calibrated to restore physiological serum levels. The consensus emerging from the 2025 review literature is that restoring serum 25-OHD to at least 30–40 ng/mL appears to be the relevant target, rather than any specific dose per se.

Are findings in animal studies similar to human studies?

Directionally, yes. Both animal models and human correlational data point toward vitamin D having a regulatory, normalizing effect on HPA tone — reducing excessive upstream drive (CRH, ACTH, corticosterone) and potentially restoring appropriate diurnal rhythmicity. The magnitudes differ and the models are not perfectly translatable, but the mechanistic coherence across species is scientifically meaningful.

Is there evidence that vitamin D affects CRH, ACTH, or glucocorticoid receptors?

Yes to all three. The 2025 PTSD study found significant inverse correlations between vitamin D and both CRH and ACTH. The 2025 focused review specifically discussed vitamin D's role in upregulating glucocorticoid receptor expression and sensitivity, which is the mechanism by which adequate vitamin D could improve the negative feedback efficiency of the HPA loop.

What is the best biomarker to measure HPA-axis changes in vitamin D research?

There is no single "best" biomarker. However, for capturing the most clinically relevant changes, the combination of serum 25-OHD (vitamin D status), salivary cortisol diurnal profile with CAR (HPA rhythm and reactivity), and plasma ACTH (pituitary drive) provides the most comprehensive picture. The 2025 PTSD study's use of multiple simultaneous biomarkers — 25-OHD, CRH, ACTH, and cortisol — is a useful model for how future clinical research should be designed.

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Summary and Bottom Line

The science connecting vitamin D and HPA axis research has matured considerably in just the past two years. Here is what the weight of evidence now supports:

What We Can Say With Reasonable Confidence

✅ Vitamin D receptors exist at every major level of the HPA axis, providing anatomical plausibility for direct regulatory effects.

✅ Vitamin D deficiency is associated with HPA dysregulation in humans, including elevated CRH and ACTH and paradoxically blunted cortisol — a pattern particularly well-documented in PTSD patients (2025, Frontiers in Neuroscience).

✅ Vitamin D3 supplementation restores HPA function in animal models, including normalization of corticosterone and reduction of neuroinflammatory markers in both chronic-stress and sleep-desynchrony paradigms (2025 studies).

✅ The correlations between vitamin D and HPA hormones are statistically robust when studied in clinically relevant populations, with the 2025 PTSD study finding P<0.001 significance for the vitamin D differences and P<0.05 for the directional correlations with CRH, ACTH, and cortisol.

✅ A potential clinically meaningful threshold of 16.32 ng/mL 25-OHD was identified in the 2025 PTSD ROC analysis, with 86.2% sensitivity for HPA-axis dysregulation patterns.

What Remains Uncertain

⚠️ Causality in humans has not been definitively established. Most human data is correlational. Vitamin D deficiency co-occurs with many conditions that independently dysregulate the HPA axis, including chronic inflammation, obesity, sedentary behavior, and limited sunlight exposure.

⚠️ Optimal supplementation protocols for HPA outcomes are not yet defined. What dose, what form, for how long, and in which populations remains an open research question.

⚠️ CAR findings are preliminary. The trend toward reduced cortisol awakening response in the 2018 MS trial is intriguing but not conclusive.

The Practical Takeaway

For anyone interested in the intersection of vitamin D stress biology and HPA axis function, the current evidence supports ensuring vitamin D sufficiency — meaning 25-OHD consistently above 30 ng/mL, and ideally 40–60 ng/mL — as a foundational element of stress-axis health. This does not mean vitamin D is a replacement for established stress-management strategies. But given the anatomical plausibility, the human correlational data, and the increasingly compelling animal model evidence, treating vitamin D status as irrelevant to HPA function is no longer scientifically defensible.

The field is moving fast. The cluster of high-quality studies published in 2025 alone — covering PTSD correlations, focused mechanistic reviews, sleep-desynchrony models, and chronic-stress animal data — suggests that the next generation of powered randomized controlled trials targeting HPA outcomes specifically may finally deliver the causal evidence that translates this science into clinical guidelines.

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References

1. PMC (2025). Vitamin D3 Improves Hypothalamic–Pituitary–Adrenal Axis Function in a Sleep-Desynchrony Model. https://pmc.ncbi.nlm.nih.gov/articles/PMC12638446/
2. ScienceDirect (2025). Vitamin D regulation of cortisol through the HPA axis: A focused review. https://www.sciencedirect.com/science/article/pii/S2666396125000615
3. Frontiers in Neuroscience (2025). Correlation of serum 25-hydroxyvitamin D with HPA-axis hormones in PTSD. https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2025.1622978/full
4. PubMed (2024). Change in function and homeostasis of HPA axis: The role of vitamin family.
5. Controlled study (2018). Vitamin D3 supplementation and salivary cortisol in multiple sclerosis.
6. Preclinical study (2025). Vitamin D3 normalizes corticosterone and inflammatory markers in chronic stress rat model.

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This article is for educational purposes only and does not constitute medical advice. Consult a qualified healthcare provider before beginning any supplementation protocol, particularly if you have a diagnosed condition involving HPA axis dysregulation.