Vitamin D is a sunshine, fat-soluble essential vitamin and steroid hormone that is synthesized in our skin after exposure to sunlight. There are mainly three sources through which we can get vitamin D:
1. By getting enough sunlight
2. Through vitamin D-rich foods such as egg yolk, fortified dairy products, fortified orange juice and cereals, and fatty fish (like salmon)
3. Through supplements in the form of cholecalciferol (Vitamin D3) or ergocalciferol (Vitamin D2)
The active form of vitamin D is calcitriol or 1,25 dihydroxy vitamin D3, which exerts biological effects by binding to vitamin D receptors (VDR) present in almost every cell of the human body.
IMPORTANCE OF VITAMIN D FOR HEALTH
While vitamin D is traditionally known for its role in bone health, calcium absorption, and phosphate balance, growing evidence shows it also influences several non-skeletal systems.
According to Holick (2007) in The New England Journal of Medicine, vitamin D functions far beyond its traditional role in calcium and bone metabolism. It acts as a hormone that modulates the immune system, enhances muscle performance, regulates mood, and plays an essential role in metabolic and reproductive health.
Furthermore, recent research highlights its role in reducing inflammation, supporting insulin sensitivity, and improving pregnancy outcomes. Given this wide range of effects, vitamin D deficiency is now recognized as a global health concern.
ROLE OF VITAMIN D IN REPRODUCTIVE PHYSIOLOGY
Vitamin D has an important role in the reproductive physiology of both males and females. In males, it supports steroidogenesis, spermatogenesis, and acrosome function.
In females, vitamin D receptors (VDR) and enzymes responsible for its synthesis are found in the ovaries, uterus, and placenta. This suggests vitamin D plays a regulatory role in ovarian functions such as follicular development, luteinization, and egg quality improvement.
To understand how vitamin D influences ovarian function, let’s briefly look at the process of folliculogenesis.
FOLLICULOGENESIS
Folliculogenesis is the process of follicle growth, differentiation, and maturation through the following stages:
• Primordial Follicles: Dormant follicles present at birth in the ovaries, consisting of an oocyte surrounded by granulosa cells.
• Primary Follicles: These develop without FSH and LH influence, with granulosa cells becoming cuboidal.
• Secondary Follicles: Here, granulosa cells proliferate, and theca cells begin androgen production. Under the effect of FSH, aromatase converts androgens into estrogen.
• Antral Follicles: A fluid-filled cavity forms, which continues to expand under the influence of FSH and LH.
• Mature Follicles (Graafian): These are ready to release a fertilizable egg during ovulation.
• Ovulation: Triggered by an LH surge, the egg is released into the fallopian tube.
• Corpus Luteum: The ruptured follicle transforms into the corpus luteum, producing progesterone for early pregnancy maintenance.
• Menstruation: If fertilization does not occur, the corpus luteum degenerates, leading to menstruation.
HOW VITAMIN D SUPPORTS FOLLICULOGENESIS
Emerging evidence indicates that vitamin D affects multiple stages of follicle development:
Early Stages (Primordial to Antral): Granulosa cells in developing follicles secrete Anti-Müllerian Hormone (AMH), a key marker of ovarian reserve.
Research by Dennis et al. (2012, Fertility and Sterility) demonstrated that women with lower serum vitamin D levels tend to have reduced AMH concentrations, suggesting a premature decline in follicle reserves. These findings highlight that adequate vitamin D is crucial for follicle activation, growth, and recruitment during the early stages of ovarian development.
Primary and Secondary Follicular Stages: Vitamin D enhances follicle stimulating hormone (FSH) receptor expression in granulosa cells, thereby improving their sensitivity to FSH. It also stimulates the aromatase enzyme, which converts androgens into estrogens a process essential for follicular maturation.
According to Irani and Merhi (2014, Human Reproduction), this mechanism demonstrates how vitamin D facilitates estrogen biosynthesis and overall follicular responsiveness.
Antral Stage: During the antral phase, vitamin D regulates androgen production through modulation of theca cell function and promotes angiogenesis, ensuring proper nutrient delivery to developing follicles.
Evidence from Thomson et al. (2012, Journal of Clinical Endocrinology & Metabolism) links vitamin D deficiency to polycystic ovary syndrome (PCOS) characterized by elevated androgen levels, insulin resistance, and disrupted follicular development.
Pre-Ovulatory Stage: By increasing luteinizing hormone (LH) receptor expression, vitamin D contributes to final follicle maturation and helps maintain regular ovulatory cycles. This regulatory action underscores its involvement in reproductive hormonal balance.
Luteal Stage: In the luteal phase, vitamin D enhances progesterone synthesis and improves endometrial receptivity, optimizing conditions for embryo implantation.
Findings from Viganò et al. (2016, Reproductive Biology and Endocrinology) support that sufficient vitamin D levels are integral for successful implantation and early pregnancy maintenance.
In summary, vitamin D reduces oxidative stress, lowers androgen levels, improves insulin sensitivity, and supports immune balance all of which promote healthy ovulation and pregnancy outcomes.
VITAMIN D AND IVF (IN VITRO FERTILIZATION)
Several studies show that vitamin D sufficiency is associated with better IVF outcomes. For example, Rudick et al. (Human Reproduction, 2012) found that women with adequate serum vitamin D had higher pregnancy and live birth rates after IVF compared to those who were deficient. The presence of vitamin D seems to improve both oocyte quality and endometrial receptivity, enhancing the chances of implantation.
ADVERSE PREGNANCY OUTCOMES DUE TO VITAMIN D DEFICIENCY
Deficiency of vitamin D during pregnancy has been linked to several complications, including:
1. Preterm birth
2. Preeclampsia (hypertension during pregnancy)
3. Bacterial vaginosis
4. Neonatal mortality
5. Infant asthma
6. Gestational diabetes
According to a meta analysis published in The BMJ (2019), maternal vitamin D deficiency is strongly associated with an increased risk of preterm delivery and preeclampsia.
VITAMIN D AND PREECLAMPSIA
Vitamin D appears to play a preventive role against preeclampsia, a potentially dangerous pregnancy complication characterized by high blood pressure.
According to Wei et al. (2013) in Hypertension, vitamin D deficiency has been shown to impair placental development and immune tolerance, leading to increased inflammation and vascular dysfunction key factors contributing to preeclampsia.
Conversely, multiple clinical studies have demonstrated that vitamin D supplementation during pregnancy can help reduce the risk and severity of preeclampsia by improving endothelial function and modulating inflammatory pathways.
VITAMIN D AND HYPERTENSION
According to Pilz et al. (2016) in Nature Reviews Cardiology, numerous observational studies have demonstrated that low serum vitamin D levels are associated with elevated blood pressure and an increased risk of cardiovascular disease.
However, evidence from interventional trials remains inconclusive, as vitamin D supplementation has shown variable effects on blood pressure regulation across different populations.
Some evidence shows that:
• Vitamin D supplementation lowers blood pressure in older and obese adults.
• Vitamin D3 combined with calcium improves blood pressure in type 2 diabetic patients and elderly women (Forman et al., Hypertension, 2007).
• Vitamin D supplementation reduces diastolic blood pressure in patients with cardiometabolic disorders.
Despite these findings, not all studies confirm a direct cause and effect relationship, suggesting the association between vitamin D and hypertension is complex and influenced by multiple factors.
POSSIBLE MECHANISM OF ACTION
Vitamin D regulates the renin-angiotensin-aldosterone system (RAAS), which plays a central role in blood pressure control.
According to Li et al. (2002) in the Journal of Clinical Investigation, experimental evidence demonstrates that vitamin D suppresses renin gene expression, enhances vasodilation through nitric oxide synthesis, and reduces oxidative stress and inflammation. These mechanisms collectively contribute to the regulation of blood pressure and may help protect against hypertension and preeclampsia.
VITAMIN D AND DIABETES
As reported by Pilz et al. (2016) in Nature Reviews Cardiology, several observational studies indicate that vitamin D deficiency is linked to higher blood pressure and an increased risk of cardiovascular disease.
Nonetheless, findings from interventional studies remain inconsistent, suggesting that the causal role of vitamin D in blood pressure regulation is still uncertain and may depend on individual health status and baseline vitamin D levels.
PRECAUTIONS WHILE TAKING VITAMIN D
Vitamin D supplements can cause nausea or vomiting if taken on an empty stomach. They should be taken with a fatty meal for optimal absorption, along with adequate calcium, magnesium, and vitamin K2 intake.
It’s advisable to avoid taking vitamin D at night as it may interfere with sleep. Over-supplementation can lead to hypercalcemia, kidney stones, muscle weakness, and loss of appetite.
CONCLUSION
In light of current scientific evidence, the importance of vitamin D in reproduction, bone health, diabetes, and cardiovascular diseases is undeniable. Vitamin D deficiency should be considered in infertility assessments and managed to improve reproductive outcomes.
Older adults are especially vulnerable to deficiency, increasing their risk for diabetes and hypertension. Whenever possible, vitamin D should be obtained from sunlight exposure and dietary sources, reserving supplementation for clinically confirmed deficiencies.
FAQs about Vitamin D in Pregnancy, Hypertension, and Diabetes
1. What is the best time to take vitamin D supplements?
Vitamin D should be taken with a fatty meal during the daytime for maximum absorption. It’s better to avoid taking it at night as it might disturb sleep in some individuals.
2. Can vitamin D deficiency cause infertility?
Yes. Research shows that vitamin D deficiency may lower ovarian reserve, reduce AMH levels, and affect follicular development and ovulation, leading to fertility issues.
3. How much sunlight exposure is needed for adequate vitamin D?
About 10–30 minutes of midday sun exposure on arms and legs, at least 2–3 times per week, is generally sufficient. However, this varies based on skin type, climate, and clothing.
4. Is it safe to take vitamin D supplements during pregnancy?
Yes, but always under medical supervision. Studies suggest that maintaining sufficient vitamin D levels during pregnancy may reduce the risk of preeclampsia, gestational diabetes, and preterm birth.
5. Can vitamin D help control blood pressure and diabetes?
Some studies show that vitamin D may improve insulin sensitivity and lower diastolic blood pressure, but the results are inconsistent. Supplementation should always be guided by a healthcare professional.
DISCLAIMER
This article is for educational and informational purposes only and should not be used as a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician, pharmacist, or qualified healthcare provider before starting or changing any supplement or medication, especially during pregnancy or while managing chronic conditions such as hypertension or diabetes.
CALL TO ACTION
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REFERENCES
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9. Pilz S, Verheyen N, Grübler MR, Tomaschitz A, März W. Vitamin D and cardiovascular disease prevention. Nature Reviews Cardiology. 2016;13(7):404–417.
10. Li YC, Kong J, Wei M, Chen ZF, Liu SQ, Cao LP. 1,25-Dihydroxyvitamin D3 is a negative endocrine regulator of the renin–angiotensin system. Journal of Clinical Investigation. 2002;110(2):229–238. 11. George PS, Pearson ER, Witham MD. Effect of vitamin D supplementation on glycaemic control and insulin resistance: a systematic review. Journal of Clinical Endocrinology & Metabolism. 2018;103(10):3356–3368.




