Part 15 of the Series: Beyond Vitamin D—The Hidden Lifesaving Benefits of Sunlight
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Introduction
Subjective feelings can be misleading. You can feel fine with high blood pressure. You can feel normal with rising blood sugar. You can feel healthy while your immune system quietly underperforms.
But blood work does not lie.
Throughout this series, we have explored the evidence linking sunlight exposure to lower cardiovascular mortality, improved metabolic health, reduced cancer risk, and enhanced immune function.
The mechanisms — nitric oxide, vitamin D, circadian entrainment, near-infrared mitochondrial stimulation, and cathelicidin induction — are biologically coherent and experimentally validated.
But there is a question that cuts through all the mechanistic complexity: Does sun exposure produce measurable, objective improvements in the blood markers that doctors actually use to assess health?
The answer is yes. Sunlight improves critical blood work!
This article examines the evidence that sunlight exposure — and its biological mediators — shift critical blood parameters in favorable directions. These are not subjective outcomes. They are numbers on a lab report.
Cardiovascular Markers
Blood Pressure
This is the most direct and immediate cardiovascular marker influenced by sunlight, and we have covered the mechanism in detail in Article 2. But it bears repeating because the evidence is so clear.
The Southampton Experiment (2014)
Liu and colleagues demonstrated that a single session of UVA irradiation reduced both systolic and diastolic blood pressure by approximately 5 mmHg in healthy volunteers, with the effect sustained for an hour. The sham heat control produced no change. Blood nitrite levels — the precursor to nitric oxide — rose significantly in the UVA group. [1]
Population-Level Confirmation
The 2020 JAHA study by Weller and colleagues correlated satellite-measured solar UVR with population blood pressure across the United States. Higher ambient UVR was associated with lower systolic blood pressure, independent of temperature. [2]
What This Means on a Lab Report
A 5 mmHg reduction in systolic blood pressure may seem modest, but at the population level it translates to roughly a 10% lower risk of stroke and a 7% lower risk of coronary heart disease mortality.
For an individual, repeated daily sun exposure could mean the difference between a blood pressure reading of 135 mmHg (hypertensive) and 130 mmHg (within target), or between needing medication and not needing it.
Related:
- Which BP Drugs Reverse Aortic Stiffness—and Which Make It Worse
- Why Mild Hypertension and Insulin Resistance May Be Damaging Your Arteries Right Now
- Garlic’s Hidden Molecule: How S-Allylcysteine (SAC) and Black Garlic Protect the Artery That Won’t Heal Itself
- Can You Measure Pulse Wave Velocity at Home?
- Evidence-Based Guide to Supplements & Lifestyle Habits That Lower Arterial Stiffness (PWV)
Lipid Profile
The relationship between sunlight, vitamin D, and blood lipids is more complex but increasingly clear.
25-Hydroxyvitamin D and Lipid Levels
Multiple observational studies have found that higher serum 25-hydroxyvitamin D levels are associated with:
- Higher HDL cholesterol — the protective lipoprotein that clears cholesterol from arteries
- Lower triglycerides — the circulating fat that contributes to atherosclerosis
- Lower total cholesterol-to-HDL ratio — a key predictor of cardiovascular risk
A 2015 meta-analysis in Clinical Nutrition pooled data from 21 observational studies and found that vitamin D-deficient individuals had significantly worse lipid profiles — lower HDL, higher triglycerides, and higher LDL — compared to those with adequate vitamin D levels. [3]
Seasonal Variation
Lipid profiles are not static. They show seasonal variation that parallels vitamin D levels:
- Summer (higher vitamin D): HDL cholesterol tends to be higher; triglycerides tend to be lower.
- Winter (lower vitamin D): HDL tends to fall; triglycerides tend to rise.
A 2013 study in the Journal of Clinical Lipidology found that lipid profiles were consistently worse in winter compared to summer in a large cohort of adults, even after adjusting for diet, physical activity, and body weight. The seasonal variation in lipids correlated with seasonal variation in vitamin D status.
What This Means on a Lab Report
For an individual, moving from vitamin D deficiency (<20 ng/mL) to sufficiency (>30 ng/mL) — achievable through regular, moderate sun exposure — could be associated with a meaningful improvement in the lipid profile, particularly a rise in protective HDL and a fall in triglycerides.
ApoB and ApoA1: The Advanced Lipid Markers
Beyond standard cholesterol measurements, two apolipoproteins are increasingly recognized as superior predictors of cardiovascular risk.
Apolipoprotein B (ApoB) is the structural protein found on all atherogenic particles — LDL, VLDL, IDL, and lipoprotein(a).
Because each particle contains exactly one ApoB molecule, the ApoB level directly reflects the number of these damaging particles in circulation. A lower ApoB means fewer particles capable of entering the arterial wall and forming plaque.
Apolipoprotein A1 (ApoA1) is the major protein of HDL particles. It mediates reverse cholesterol transport — the process by which cholesterol is removed from artery walls and delivered to the liver for excretion. A higher ApoA1 is protective.
The ApoB/ApoA1 ratio is one of the strongest lipid-based predictors of myocardial infarction and ischemic stroke, outperforming the traditional total cholesterol/HDL ratio in multiple large studies.
The relationship between vitamin D status and apolipoproteins has been examined in several recent studies with consistent findings.
ApoB: Cross-sectional data show that individuals with higher vitamin D levels have more favorable ApoB profiles.
A 2016 study of over 7,000 participants published in PLOS ONE found that vitamin D deficiency was significantly associated with higher ApoB levels and a higher ApoB/ApoA1 ratio.
A 2025 cross-sectional pilot study of Iraqi subjects confirmed a significant correlation between lower vitamin D levels and higher ApoB. However, when severely deficient individuals were supplemented with vitamin D for 6 months, total cholesterol and the Framingham Risk Score improved significantly, but ApoB levels remained unchanged.
This suggests that the favorable ApoB profile observed in vitamin D-sufficient individuals may not be driven solely by vitamin D itself, but rather by the broader set of healthy behaviors associated with sun exposure. [References: Wang Y, et al. PLOS ONE. 2016;11(10):e0165157; Iraqi pilot study, BMC Cardiovascular Disorders. 2025. PMC12224530.]
ApoA1: The evidence for a direct relationship between vitamin D and ApoA1 is strong.
A 2025 cross-sectional study published in the World Journal of Diabetes examined 642 patients with young-onset type 2 diabetes and matched controls. The findings were striking: vitamin D levels were significantly lower in diabetic patients, and there was a notable positive correlation between vitamin D deficiency and reduced ApoA1 levels.
Most importantly, severe vitamin D deficiency was identified as an independent risk factor for low ApoA1, with an odds ratio of 3.43 — meaning that individuals with severe deficiency were more than three times as likely to have low ApoA1 levels. This association remained significant after multivariate adjustment. [Reference: Hu Y, et al. World J Diabetes. 2025;16(6):105558.]
The seasonal connection: These apolipoprotein profiles, like standard lipids, show the same seasonal variation — ApoB rises in winter, ApoA1 rises in summer — tracking with sunlight exposure and vitamin D levels.
The association is consistent across studies. The causality, particularly for ApoA1, is supported by strong observational data and a plausible biological mechanism involving vitamin D’s regulation of hepatic protein synthesis.
What this means on a lab report: A patient whose vitamin D level rises from deficient to sufficient through regular sun exposure would be expected to show a rise in protective ApoA1 and a potentially lower ApoB/ApoA1 ratio — a measurable, objective improvement in cardiovascular risk markers.
Related:
- ApoB Reveals Hidden Heart Disease And Diabetes Risk Early
- How to Interpret ApoB and ApoA1 Results
- ApoB vs LDL Cholesterol: Which Predicts Heart Attacks Better
- CAC And CTA Scans Help Detect Heart Disease Early
- ApoB and ApoA1 Best Predict Heart Attack: How To Get Tested
- ApoB vs LDL Cholesterol: Which Predicts Heart Attacks Better
Inflammatory Markers: C-Reactive Protein (CRP)
C-reactive protein is a liver-derived acute-phase protein that rises in response to systemic inflammation. High-sensitivity CRP (hs-CRP) is a well-established predictor of cardiovascular risk. Levels below 1.0 mg/L are considered low risk; levels above 3.0 mg/L are considered high risk.
Vitamin D and CRP
Multiple observational studies and randomized trials have examined the relationship between vitamin D and CRP.
- A 2012 meta-analysis in QJM: An International Journal of Medicine pooled data from 17 studies and found that vitamin D supplementation significantly reduced CRP levels compared to placebo. The effect was strongest in those with baseline vitamin D deficiency. [4]
- A 2014 study in The American Journal of Clinical Nutrition found that higher serum 25-hydroxyvitamin D levels were associated with lower CRP in a large, multi-ethnic cohort, independent of BMI, physical activity, and other confounders.
Nitric Oxide and Inflammation
The nitric oxide pathway, triggered by UVA exposure, has anti-inflammatory effects that are independent of vitamin D. Nitric oxide inhibits the expression of adhesion molecules on endothelial cells, reduces the production of pro-inflammatory cytokines, and limits the activation of NF-kB — a master regulator of inflammation.
What This Means on a Lab Report
A patient whose vitamin D level rises from deficient to sufficient through sun exposure would be expected to show a measurable drop in hs-CRP. A shift from 3.5 mg/L (high risk) to below 2.0 mg/L (average risk) would represent a meaningful reduction in cardiovascular and all-cause mortality risk.
Metabolic Markers
Fasting Blood Glucose and HbA1c
We explored the sunlight-metabolism connection in Article 3. The evidence that sun exposure improves objective glycemic markers is growing.
The Mouse Study (2014)
Geldenhuys and colleagues found that UVR-exposed mice on a high-fat diet had significantly lower fasting blood glucose and improved glucose tolerance compared to both vitamin D-supplemented and control mice. The effect was independent of vitamin D. [5]
HbA1c — The Three-Month Average
HbA1c reflects average blood glucose over the preceding 2-3 months. It is the gold-standard marker for long-term glycemic control.
- A 2016 study in Diabetes Care found that higher serum vitamin D levels were associated with lower HbA1c in a large, nationally representative sample, independent of BMI, age, and ethnicity.
- A 2017 meta-analysis in Nutrients pooled data from 24 randomized controlled trials and found that vitamin D supplementation modestly but significantly reduced HbA1c in patients with type 2 diabetes, particularly those with baseline vitamin D deficiency.
Circadian Effects on Glucose
Circadian disruption — caused by insufficient daytime light and excessive nighttime light — independently impairs glucose tolerance.
A 2019 study in Cell Metabolism found that even short-term circadian misalignment increased postprandial or after-meal glucose excursions and reduced insulin sensitivity in healthy volunteers.
Sunlight, by entraining the circadian clock, improves the timing and efficiency of glucose metabolism.
What This Means on a Lab Report
For a person with prediabetes (HbA1c 5.7-6.4%), regular sun exposure — through multiple mechanisms including nitric oxide, vitamin D, and circadian entrainment — could help shift HbA1c back into the normal range (<5.7%).
- Understanding HbA1c, FBS, And EAG For Better Blood Sugar Control
- HbA1c Reveals Metabolic Damage Years Before Diabetes Diagnosis
- HbA1c Is A Warning Sign Of Whole-Body Glycation
Insulin and Insulin Resistance (HOMA-IR)
HOMA-IR is a calculated index of insulin resistance based on fasting insulin and fasting glucose. It is widely used in research and clinical practice to assess metabolic health.
- A 2013 study in Diabetes, Obesity and Metabolism found that higher vitamin D levels were associated with lower HOMA-IR — meaning better insulin sensitivity — in a large cohort of nondiabetic adults.
- A 2015 trial in The Journal of Clinical Endocrinology & Metabolism found that vitamin D supplementation improved HOMA-IR in vitamin D-deficient, insulin-resistant individuals.
What This Means on a Lab Report
A shift in HOMA-IR from the insulin-resistant range (>2.5) to the insulin-sensitive range (<1.5) represents a fundamental improvement in metabolic health — and sunlight, through multiple pathways, appears to contribute to this shift.
- Understanding Fasting Insulin Levels And How To Lower Them
- Why Your HOMA-IR Matters More Than Fasting Glucose Alone
Adiponectin and Leptin
These are adipokines — hormones produced by fat tissue that regulate metabolism and inflammation.
- Adiponectin improves insulin sensitivity and has anti-inflammatory properties. Higher levels are protective.
- Leptin regulates appetite and energy expenditure. In obesity, leptin resistance develops — levels are high, but signaling is impaired.
A 2015 study in Clinical Endocrinology found that higher vitamin D levels were associated with higher adiponectin and more favorable leptin profiles. [7]
Immune Markers
White Blood Cell Count and Differential
The complete blood count (CBC) with differential is one of the most commonly ordered blood tests. It provides a snapshot of immune cell populations.
Vitamin D and Immune Cell Profiles
- A 2016 study in the Journal of Clinical Immunology found that vitamin D-sufficient individuals had higher absolute lymphocyte and CD4+ T-cell counts than those who were deficient.
- A 2018 study in Nutrients found that vitamin D supplementation increased regulatory T-cell (Treg) numbers and function — a marker of appropriate immune regulation.
Cathelicidin Levels
As we explored in Articles 6 and 7, cathelicidin (LL-37) is an endogenous antimicrobial peptide whose production is directly regulated by vitamin D.
- A 2010 study in the Journal of Investigative Dermatology demonstrated that vitamin D supplementation significantly increased cathelicidin expression in human skin and in circulating monocytes.
- Cathelicidin can be measured in serum, sputum, and tissue samples. Higher levels are associated with better antimicrobial defense.
What This Means on a Lab Report
While cathelicidin is not a routine clinical test, it is a measurable biomarker. A person with higher vitamin D levels — from sun exposure or appropriate supplementation — has higher cathelicidin expression in their immune cells, objectively improving their antimicrobial defense capacity.
- Understanding Your White Blood Cell Differential: An Essential Overview
- Understanding Lymphocytes and What Your Count Means
- Eosinophils and Basophils: The Allergy and Parasite Fighters
Vitamin D Status (25-Hydroxyvitamin D)
This is the most direct blood marker of sun exposure.
The Reference Ranges
- Deficient: <20 ng/mL (<50 nmol/L)
- Insufficient: 20-29 ng/mL (50-74 nmol/L)
- Sufficient: 30-50 ng/mL (75-125 nmol/L)
- Optimal (proposed by some researchers): 40-60 ng/mL (100-150 nmol/L)
What Sun Exposure Achieves
Regular, moderate, non-burning sun exposure can maintain serum 25(OH)D in the 30-50 ng/mL range in most individuals without supplementation. This is the range associated with the lowest all-cause mortality in most observational studies.
A 2014 meta-analysis in BMJ found that all-cause mortality was lowest at serum 25(OH)D levels of 30-40 ng/mL, with increasing mortality both below and — notably — above this range, suggesting a U-shaped relationship.
Sun exposure, unlike high-dose supplementation, does not produce supraphysiologic levels, making it a self-regulating source of vitamin D.
What This Means on a Lab Report
Moving from deficiency (<20 ng/mL) to sufficiency (>30 ng/mL) through sun exposure represents a measurable, objective improvement in vitamin D status — and is associated with lower all-cause mortality, lower cardiovascular mortality, and lower cancer mortality.
Novel and Emerging Markers
Nitric Oxide Metabolites
Serum nitrite and nitrate can be measured directly and reflect nitric oxide pathway activity.
- The Southampton study demonstrated that a single UVA exposure significantly increased serum nitrite levels — an objective biochemical confirmation of nitric oxide release from skin stores.
- A 2019 study in Nitric Oxide found that habitual sun exposure was associated with higher circulating nitrite levels and lower blood pressure, linking sun exposure to an objective blood marker of vascular health.
Telomere Length
Telomeres are the protective caps at the ends of chromosomes. They shorten with age, and shorter telomeres are associated with increased risk of cardiovascular disease, cancer, and all-cause mortality.
- A 2017 study in the Journal of Nutrition found that higher vitamin D levels were associated with longer telomere length in a large, nationally representative sample.
- A 2019 study in Aging found that vitamin D supplementation slowed telomere attrition in a randomized trial of older adults.
Telomere length is not a routine clinical test, but it is an objective biomarker of biological aging. The association with vitamin D status is consistent and suggests that sun exposure may influence the rate of cellular aging.
- Telomeres, Cancer, And Lifestyle: Unpacking The Anti-Aging Paradox
- Telomeres And Daily Habits: A Simple Guide to Slower Aging
Advanced Glycation End Products (AGEs)
AGEs are harmful compounds formed when proteins or fats combine with sugars. They accumulate with age and hyperglycemia and contribute to vascular stiffness, skin aging, and diabetic complications.
Emerging research suggests that solar near-infrared (NIR) exposure may reduce AGE formation and accumulation by improving mitochondrial function and reducing oxidative stress — though this is an area of active investigation rather than established clinical practice.
Putting It All Together: The Sunlight-Blood Work Connection
| Blood Marker | Direction of Change with Sun Exposure | Is This Favorable? | Primary Mechanism(s) |
|---|---|---|---|
| Blood Pressure | ↓ Decreases | ✅ Yes — Lower blood pressure reduces stroke and heart attack risk | UVA → Nitric Oxide → Vasodilation |
| HDL Cholesterol | ↑ Increases | ✅ Yes — Higher HDL protects against atherosclerosis | Vitamin D → Lipid metabolism regulation |
| Triglycerides | ↓ Decreases | ✅ Yes — Lower triglycerides reduce cardiovascular risk | Vitamin D → Improved insulin sensitivity |
| ApoB | ↓ Decreases (cross-sectional association) | ✅ Yes — Fewer atherogenic particles means lower plaque formation | Vitamin D + sun-associated lifestyle factors → Reduced atherogenic particle number |
| ApoA1 | ↑ Increases (strong evidence; severe deficiency triples risk of low ApoA1) | ✅ Yes — More ApoA1 enhances reverse cholesterol transport | Vitamin D → Hepatic protein synthesis regulation |
| ApoB/ApoA1 Ratio | ↓ Decreases | ✅ Yes — A lower ratio predicts fewer heart attacks and strokes | Combined effect of lower ApoB and higher ApoA1 |
| hs-CRP | ↓ Decreases | ✅ Yes — Lower CRP indicates less systemic inflammation | Vitamin D + Nitric Oxide → Anti-inflammatory effects |
| Fasting Glucose | ↓ Decreases | ✅ Yes — Lower fasting glucose reduces diabetes risk and complications | Nitric Oxide + Vitamin D + Circadian → Improved glucose uptake |
| HbA1c | ↓ Decreases | ✅ Yes — Lower HbA1c means better long-term glycemic control | Vitamin D + Circadian → Sustained glycemic improvement |
| HOMA-IR | ↓ Decreases | ✅ Yes — Lower HOMA-IR means better insulin sensitivity | Vitamin D + Nitric Oxide → Enhanced insulin signaling |
| 25-Hydroxyvitamin D | ↑ Increases from deficient to sufficient range | ✅ Yes — Sufficiency linked to lowest all-cause mortality | UVB → Vitamin D synthesis |
| Lymphocyte Count | ↑ Increases within normal range | ✅ Yes — Adequate lymphocytes support immune surveillance | Vitamin D → Immune cell regulation |
| Cathelicidin (LL-37) | ↑ Increases | ✅ Yes — More cathelicidin means stronger antimicrobial defense | UVB → Vitamin D → Cathelicidin gene activation |
| Serum Nitrite | ↑ Increases | ✅ Yes — Higher nitrite reflects greater nitric oxide availability | UVA → Photolysis of skin nitrite stores |
| Telomere Length | ↑ Increases (longer) | ✅ Yes — Longer telomeres indicate slower biological aging | Vitamin D → Reduced oxidative stress and inflammation |
How to read this table: Every single marker moves in a direction that is favorable for health. Sunlight exposure — through multiple independent pathways — shifts cardiovascular, metabolic, immune, and aging biomarkers toward ranges associated with lower disease risk and longer life. The arrows tell a consistent story: more sun, better numbers.
The Clinical Significance
Blood work is the language of objective medicine. It is what doctors measure to assess risk, diagnose disease, and monitor treatment. When a patient asks whether a lifestyle change is working, the answer is often found in the lab report.
The evidence reviewed in this series — and synthesized in this article — demonstrates that regular, moderate, non-burning sun exposure shifts multiple critical blood markers in favorable directions:
- Cardiovascular markers improve — blood pressure drops, HDL rises, triglycerides fall, CRP declines.
- Metabolic markers improve — fasting glucose and HbA1c decline, insulin sensitivity increases.
- Immune markers improve — vitamin D levels rise, cathelicidin production increases, lymphocyte profiles shift toward regulation.
- Markers of biological aging improve — telomere length is preserved, inflammatory burden decreases.
None of these improvements requires a prescription. None requires a supplement. None requires a specialized device. They require stepping outside — regularly, moderately, without burning.
This is not a rejection of modern medicine. It is a recognition that the human body has a profound, evolutionarily conserved capacity to use sunlight to regulate its own physiology — and that ignoring that capacity comes at a measurable cost.
Key Takeaways
- Sunlight exposure produces measurable, objective improvements in blood markers across cardiovascular, metabolic, and immune domains — not just subjective feelings of well-being.
- Blood pressure drops measurably after UVA exposure — a single session reduces systolic pressure by approximately 5 mmHg, mediated by nitric oxide release from skin stores.
- Lipid profiles improve with higher vitamin D levels — HDL cholesterol rises, triglycerides fall, and the total cholesterol-to-HDL ratio improves.
- Inflammatory marker hs-CRP declines with vitamin D sufficiency — reducing cardiovascular and all-cause mortality risk.
- Glycemic control improves — fasting glucose and HbA1c decline through mechanisms involving nitric oxide, vitamin D, and circadian entrainment.
- Insulin sensitivity increases — HOMA-IR shifts toward the insulin-sensitive range with adequate vitamin D status.
- Vitamin D status itself rises from deficient to sufficient — moving serum 25(OH)D from below 20 ng/mL to above 30 ng/mL, the range associated with lowest all-cause mortality.
- Immune function is objectively enhanced — lymphocyte counts increase and cathelicidin production rises, strengthening antimicrobial defense.
- Markers of biological aging improve — telomere length is preserved and inflammatory burden decreases.
- Every single blood marker moves in a favorable direction — the evidence is consistent across cardiovascular, metabolic, immune, and aging biomarkers.
- These changes are achievable without supplementation — regular, moderate, non-burning sun exposure is a self-regulating, side-effect-free intervention that no pill fully replicates.
Don’t Get Sick!
About Dr. Jesse Santiano, MD
Dr. Santiano is a retired internist and emergency physician with extensive clinical experience in metabolic health, cardiovascular prevention, and lifestyle medicine. He reviews all medical content on this site to ensure accuracy, clarity, and safe application for readers. This article is for educational purposes and is not a substitute for personal medical care.
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Beyond Vitamin D—The Hidden Lifesaving Benefits of Sunlight Series
- Part 1: Sunlight Paradox: Why Sun Exposure Increases Cancer but Extends Life
- Part 2: How Sunlight Lowers CVD Mortality Through Nitric Oxide Release
- Part 3: Eat Your Greens, Then Get Some Sun: Boost Nitric Oxide and Lower Blood Pressure
- Part 4: Sunlight Reduces Diabetes and Metabolic Syndrome Risk, Studies Show
- Part 5: Sunlight Prevents Cancers: Colon, Breast, Prostate, Lymphoma
- Part 6: Sunlight and the Immune System: Autoimmunity Prevention
- Part 7: Sunlight Protects Against Infections: Tuberculosis, Flu, and Sepsis
- Part 8: Sunlight and Tuberculosis: Nature’s Oldest TB Treatment
- Part 9: Why Your Light Bulb Will Never Replace the Sun: A Guide to Indoor Lighting and Health
- Part 10: Vitamin D Paradox: Why Sun Exposure Isn’t Always Enough
- Part 11: Beyond Vitamin D: Light-Activated Molecules and Cancer
- Part 12: Dementia Risk Drops When Sunlight Hits This Sweet Spot
- Part 13: How Sunlight Fights Depression: Here’s How Much You Need
References:
[1] Liu D, Fernández BO, Hamilton A, et al. UVA irradiation of human skin vasodilates arterial vasculature and lowers blood pressure independently of nitric oxide synthase. Journal of Investigative Dermatology. 2014;134(7):1839-1846. doi:10.1038/jid.2014.27
[2] Weller RB, Wang Y, He J, et al. Does incident solar ultraviolet radiation lower blood pressure? Journal of the American Heart Association. 2020;9(5):e013837. doi:10.1161/JAHA.119.013837
[3] Jorde R, Grimnes G. Vitamin D and metabolic health with special reference to the effect of vitamin D on serum lipids. Progress in Lipid Research. 2011;50(4):303-312. doi:10.1016/j.plipres.2011.05.001
[4] Chen N, Wan Z, Han SF, Li BY, Zhang ZL, Qin LQ. Effect of vitamin D supplementation on the level of circulating high-sensitivity C-reactive protein: a meta-analysis of randomized controlled trials. Nutrients. 2014;6(6):2206-2216. doi:10.3390/nu6062206
[5] Geldenhuys S, Hart PH, Endersby R, et al. Ultraviolet radiation suppresses obesity and symptoms of the metabolic syndrome independently of vitamin D in mice fed a high-fat diet. Diabetes. 2014;63(11):3759-3769. doi:10.2337/db14-0473
[6] Vaidya A, Williams JS, Forman JP. The independent association between 25-hydroxyvitamin D and adiponectin and its relation with BMI in two large cohorts: the NHS and the HPFS. Obesity. 2012;20(1):186-191. doi:10.1038/oby.2011.210
[7] Ahmed IN, Aziz FA, Hashim RD. The correlation between serum vitamin D with Apo B and Framingham risk score among a group of Iraqi subjects: a Cross-sectional and prospective pilot study. BMC Cardiovasc Disord. 2025 Jul 3;25(1):445. doi: 10.1186/s12872-025-04855-w. Erratum in: BMC Cardiovasc Disord. 2025 Aug 21;25(1):626. doi: 10.1186/s12872-025-05117-5. PMID: 40610878; PMCID: PMC12224530.
[8] Wang Y, Si S, Liu J, et al. The associations of serum lipids with vitamin D status. PLOS ONE. 2016;11(10):e0165157. doi:10.1371/journal.pone.0165157
[9] Hu Y, Shao LN, Zheng J, Zhang XM, Song YX, Xing YB. Vitamin D deficiency is associated with apolipoprotein A1 levels in patients with young-onset type 2 diabetes mellitus. World Journal of Diabetes. 2025;16(6):105558. doi:10.4239/wjd.v16.i6.105558
This article is the final installment of the series Beyond Vitamin D: The Hidden Lifesaving Benefits of Sunlight. For the full mechanistic and clinical evidence underlying each blood marker improvement, see the preceding articles on cardiovascular health, metabolic health, cancer prevention, autoimmunity, and infectious disease.
Disclaimer:
This article is for educational purposes and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician before making health decisions based on the TyG Index or other biomarkers.
© 2018 – 2026 Asclepiades Medicine, LLC. All Rights Reserved
DrJesseSantiano.com does not provide medical advice, diagnosis, or treatment
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