Arrow BackHealth Report — July 21, 2025

Vitamin Deficiency

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Thyroid Dysfunction

Hormonal Imbalance

The use of the Diadia Health interpretive results received are intended for informational purposes only, and are not a substitute for medical advice. This includes all instances, in which the interpretive results are generated by using Artificial Intelligence. You should consult your primary care physician or other qualified healthcare provider for medical advice, diagnosis or treatment.

Vitamin D Deficiency with Micronutrient Imbalances

A condition characterized by clinically low vitamin D levels accompanied by imbalances in several key micronutrients required for optimal metabolism and cellular function.

Your vitamin D deficiency and broader micronutrient imbalances represent a foundational physiological challenge affecting multiple body systems. Vitamin D functions as a hormone with receptors throughout your body, influencing calcium metabolism, immune function, and cellular signaling. Your deficiency is clinically significant, with levels falling below both optimal and laboratory reference ranges, indicating a serious shortfall in this crucial nutrient.

  • Genetic Vitamin D Metabolism Impairment: Your CYP2R1 rs10741657 GG genotype significantly reduces the activity of vitamin D 25-hydroxylase, the enzyme responsible for converting vitamin D to its circulating form. This genetic variant creates a fundamental inefficiency in your vitamin D metabolism, explaining why your levels are so low despite potential adequate intake. Research shows this genotype is associated with approximately 20% lower vitamin D levels, creating a personalized requirement for higher supplementation doses to achieve optimal status.

  • Beta-Carotene Conversion Defect: Your BCMO1 rs12934922 AT and rs7501331 CT genotypes create a compound heterozygous state that significantly impairs your ability to convert beta-carotene from plant foods into active vitamin A. This explains your below-optimal vitamin A levels despite potentially adequate carotenoid consumption. These variants reduce conversion efficiency by 30-40%, creating a specific need for preformed vitamin A rather than relying on plant precursors.

  • Magnesium Depletion Affecting Vitamin D Activation: Your below optimal RBC magnesium indicates intracellular magnesium deficiency, which directly impairs vitamin D activation. Magnesium is required as a cofactor for all steps of vitamin D metabolism, including the conversion to the active 1,25-dihydroxy form. Your deficiency creates a compounding effect where even with vitamin D supplementation, activation may remain impaired without addressing magnesium status.

  • Genetic Fatty Acid Metabolism Dysregulation: Your FADS1 rs174537 GG genotype creates increased activity of fatty acid desaturase enzymes, resulting in enhanced conversion of omega-6 fatty acids to inflammatory compounds. This directly contributes to your elevated omega-6:3 ratio and creates a pro-inflammatory state that can worsen hormone signaling, including vitamin D receptor function.

These drivers interact synergistically, creating a perfect storm of nutrient imbalances. Your magnesium deficiency impairs vitamin D activation, while your genetic vitamin D conversion inefficiency creates higher baseline needs. The inflammatory state from your fatty acid imbalance may impair cellular responses to what little active vitamin D you have, while your vitamin A deficiency compounds this by affecting vitamin D receptor function. Conventional approaches often focus on simple vitamin D supplementation without addressing these genetic factors, conversion issues, or cofactor depletions. By targeting these specific drivers through genetically-informed dosing of vitamin D, adding preformed vitamin A, optimizing magnesium status, and addressing your omega fatty acid balance, you can create a comprehensive approach to resolving these foundational nutrient imbalances and their widespread effects on your health.

Vitamin D deficiency with micronutrient imbalances represents a low-level cause in the physiological hierarchy, focusing on fundamental building blocks that support higher-level systems. Despite this lower hierarchical position, it has profound upstream effects on your high-level neuroendocrine function. Your micronutrient deficiencies, particularly vitamin D and magnesium, directly impact your thyroid function by impairing hormone conversion and receptor sensitivity. Similarly, these deficiencies affect your hormonal balance by influencing sex hormone metabolism, binding protein regulation, and receptor function. There's a bidirectional relationship with your thyroid condition - your thyroid dysfunction may affect nutrient absorption and utilization, while nutrient deficiencies impair thyroid function, creating a challenging cycle. These nutrient issues represent foundational factors that, when corrected, can positively influence multiple downstream systems simultaneously. Addressing your genetically-influenced nutrient needs will likely improve thyroid function, hormone balance, metabolic parameters, and even kidney function through multiple mechanistic pathways. This explains why, though hierarchically lower-level, these nutrient imbalances represent a high-impact intervention point for your overall health picture.
  • Your suboptimal sleep quality strongly connects to your vitamin D deficiency and magnesium insufficiency. Vitamin D receptors are present throughout brain regions that regulate sleep, and deficiency directly impairs normal sleep architecture. Your below optimal RBC magnesium further compounds sleep issues, as magnesium is essential for GABA production and function - the primary inhibitory neurotransmitter needed for quality sleep. This dual deficiency creates a neurochemical environment highly conducive to sleep disruption.
  • Your night awakenings strongly support vitamin D and magnesium deficiencies. Magnesium deficiency creates neuronal hyperexcitability that directly triggers nighttime awakenings by reducing the threshold for arousal. Your low vitamin D compounds this effect by disrupting circadian signaling in the brain and reducing melatonin effectiveness. The combination creates a perfect storm for sleep maintenance insomnia with characteristic middle-of-night awakenings as you're experiencing.
  • Your shortened REM sleep strongly connects to your micronutrient deficiencies, particularly magnesium and vitamin D. Magnesium deficiency directly impairs GABA and melatonin pathways that regulate REM sleep duration and quality. Vitamin D deficiency further disrupts the neurological timing mechanisms controlling REM cycles. Your combined deficiencies create neurotransmitter imbalances that specifically impair your brain's ability to maintain normal REM sleep duration.
  • Your ovulation-related water retention connects to your vitamin and mineral imbalances. Magnesium deficiency directly affects renal handling of sodium and water, predisposing you to fluid retention. Your vitamin D deficiency compounds this by altering aldosterone responsiveness and vascular permeability. These deficiencies create a physiological environment where normal hormonal fluctuations during ovulation trigger excessive fluid shifts into tissues, manifesting as your cyclical swelling.

POTENTIAL DOWNSTREAM EFFECTS

Subclinical Hypothyroidism with Autoimmune Component, Female Hormonal Imbalance with Androgen Insufficiency, Sleep Disturbances, Fluid Retention

POTENTIAL CAUSED BY

Genetic Predispositions, Dietary Patterns, Aging

Recommended Action Steps

Genetics
Lifestyle
Nutrition
Supplements
Medical Steps

For Vitamin D Deficiency with Micronutrient Imbalances

  • You need specific vitamin D supplementation protocols tailored to your CYP2R1 rs10741657 GG genotype, which reduces vitamin D 25-hydroxylase activity by approximately 20%. This requires both higher loading doses (10,000 IU daily for 8 weeks) and maintenance doses (5,000-7,000 IU daily) compared to standard recommendations, with more frequent monitoring to ensure optimal blood levels are achieved and maintained.
  • You require preformed vitamin A supplementation due to your compound heterozygous BCMO1 variants (rs12934922 AT and rs7501331 CT), which reduce your ability to convert beta-carotene to active vitamin A by 30-40%. This explains your suboptimal vitamin A status despite potentially adequate plant-based carotenoid intake and necessitates direct retinol supplementation rather than beta-carotene to bypass this genetic limitation.
  • You should implement specific omega-3 fatty acid interventions to counter your FADS1 rs174537 GG genotype, which creates increased activity of fatty acid desaturase enzymes leading to enhanced conversion of omega-6 to inflammatory compounds. This requires higher direct intake of preformed EPA/DHA (2,000-3,000mg daily) rather than relying on ALA conversion, which would not adequately address your genetic predisposition to inflammation.
  • You need to adopt a comprehensive absorption-focused supplement strategy with your TMPRSS6 rs4820268 AG genotype, which affects iron regulatory hormone hepcidin and moderately restricts iron absorption. This genetic variant contributes to your below-optimal iron status and requires using highly bioavailable iron forms (bisglycinate), strategic timing away from absorption inhibitors, and potentially vitamin C co-supplementation to maximize absorption despite your genetic limitation.

Detailed Insights

Supporting Biomarkers
Genetic Evidence
Conflicting Biomarkers

vitamin d

Low Levels

•

31.3 ng/mL

STRONG EVIDENCE

Your vitamin D is below both optimal and laboratory ranges, indicating a clinically significant deficiency. This severe deficiency has wide-ranging implications for your immune function, calcium metabolism, hormonal regulation, and cellular signaling pathways. Vitamin D receptors are present throughout your body, and your insufficient levels can contribute to inflammatory processes, reduced calcium absorption, hormonal imbalances, and impaired immune function.

magnesium rbc

Low Levels

•

6 ng/mil RBC

STRONG EVIDENCE

Your RBC magnesium is below optimal, indicating intracellular magnesium deficiency. RBC magnesium is a more sensitive indicator of your long-term magnesium status than serum levels. Magnesium is a critical cofactor for over 300 enzymatic reactions including ATP production, vitamin D activation, and hormone synthesis. Your deficiency can significantly impact energy production, neuromuscular function, and the activation of vitamin D, compounding the effects of your vitamin D deficiency.

vitamin a

Low Levels

•

48.7 ug/dL

MODERATE EVIDENCE

Your vitamin A is below optimal, contributing to a pattern of fat-soluble vitamin deficiencies alongside your vitamin D deficiency. Vitamin A plays crucial roles in immune function, cellular differentiation, and thyroid hormone metabolism. Your insufficient level can compromise mucosal barrier integrity, reduce thyroid hormone receptor sensitivity, and impair immune regulation, potentially contributing to the hormonal imbalances observed in your biomarker profile.

omega 3 index

Low Levels

•

7.9 % by wt

MODERATE EVIDENCE

Your omega-3 index is below optimal, indicating insufficient levels of these essential anti-inflammatory fatty acids. The omega-3 index reflects your long-term omega-3 status and cell membrane composition. Your low levels are associated with increased inflammatory potential, reduced cell membrane fluidity, and impaired cellular signaling. This deficiency can affect your hormonal balance, neurotransmitter function, and contribute to chronic, low-grade inflammation.

omega 6 3 ratio

High Levels

•

5.2

MODERATE EVIDENCE

Your omega-6:3 ratio is above optimal, indicating a pro-inflammatory imbalance in essential fatty acids. This elevated ratio creates a metabolic environment favoring inflammatory processes and can exacerbate hormonal imbalances. The imbalance affects your eicosanoid production, shifting toward pro-inflammatory mediators that can impact thyroid function, hormone receptor sensitivity, and immune regulation, potentially contributing to your observed thyroid dysfunction and hormonal patterns.

iron

Low Levels

•

67 ug/dL

MODERATE EVIDENCE

Your iron is below optimal, adding to the pattern of multiple micronutrient deficiencies. Iron is essential for oxygen transport, energy production, and as a cofactor for numerous enzymes including those involved in thyroid hormone metabolism. Your deficiency can contribute to impaired thyroid function, reduced cellular energy production, and compromised immune function, creating a synergistic negative effect when combined with your other nutrient deficiencies.

Toggle Action Items

Optimize Vitamin D Status

Take high-dose vitamin D3 with K2 to correct your significant deficiency and support multiple body systems.

Your CYP2R1 GG genotype reduces vitamin D conversion by 20%, requiring higher supplementation. Correcting this deficiency will improve sleep quality, energy, and hormonal balance within 4-6 weeks.

This plan targets your genetic vitamin D conversion defect while supporting thyroid function. High-dose vitamin D3 with K2 will rapidly improve cellular metabolism, while optimized thyroid medication enhances conversion of T4 to T3.

  • Vitamin D3+K2 10,000 IU daily with meals
  • NP Thyroid 75mg daily on empty stomach
  • Magnesium glycinate 400mg daily in divided doses