Gene Testing
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This is a comprehensive list of genes that are commonly included in nutrigenomic, pharmacogenomic, hormonal, neuropsychiatric, cardiovascular, and detoxification panels. Many of these genes influence health conditions like inflammation, metabolism, neurotransmitter balance, detoxification capacity, hormone conversion, and nutrient utilization. Here's a categorized overview of the genes you listed, including relevance to neurological function and tremor where applicable:
๐ง Neurotransmitter & Brain-Related Genes (Relevant to Tremor, Mood, Dopamine, Serotonin)
- BDNF – Brain-derived neurotrophic factor; involved in neuroplasticity; may influence Parkinson’s risk and mood.
- COMT – Catechol-O-methyltransferase; breaks down dopamine, epinephrine; linked to tremor, anxiety, cognitive processing.
- DRD1, DRD2, DRD3, DRD4 – Dopamine receptor genes; linked to attention, movement disorders, and neuropsychiatric conditions.
- ANK3 – Implicated in bipolar disorder, also linked to neuronal excitability.
- CACNA1C – Calcium channel; implicated in tremor, bipolar, and Parkinson-like symptoms.
- GABRA2 – GABA receptor gene; relates to inhibitory neurotransmission, tremor, alcohol response.
- HTR1A – Serotonin receptor gene; anxiety, depression, SSRI response.
- MAOA (not listed but often tested) – Linked to dopamine and serotonin metabolism.
- DAO, HNMT – Histamine metabolism genes; histamine may modulate tremor, especially in mast cell issues.
๐งฌ Hormone Metabolism & Steroid Pathways
- CYP17A1, CYP19A1 – Steroid hormone synthesis (e.g., estrogen/testosterone conversion).
- SHBG – Sex hormone binding globulin; controls hormone availability.
- PPARG, PPARGC1A – Nuclear receptors regulating insulin sensitivity, adipogenesis, and hormonal signaling.
- DIO2 – Converts T4 to active T3; thyroid hormones can affect tremor.
- SULT1A1, UGT2B15, UGT2B17 – Phase II detox of estrogens, androgens.
๐งช Methylation & Detox Genes (also influence neuroinflammation, nutrient needs)
- MTHFR, MTR, MTRR, BHMT – Methylation cycle; folate, B12 metabolism; impacts homocysteine, mood, and nerve function.
- GSTP1, GSTM1, GSTT1, GSTO2 – Glutathione system; antioxidant defense, detoxification.
- NQO1, SOD2, CAT, GPX1 – Antioxidant enzymes; protect against oxidative stress (a contributor to neurodegeneration).
- NFE2L2 (NRF2) – Master antioxidant response gene.
- EPHX1 – Epoxide hydrolase; detoxification, potential neuroprotection.
๐งฌ Inflammation & Immune Modulation
- TNF, IL6, IL1, IL6R – Cytokine genes; high inflammation linked to Parkinson’s and neurodegeneration.
- HLA – Human leukocyte antigen; autoimmunity susceptibility, MS, etc.
- CRP – C-reactive protein gene; inflammation marker.
- FOXO3, FOXO1 – Longevity genes; also modulate inflammation and stress response.
๐ Pharmacogenetics / Drug Metabolism
- CYP2D6, CYP2C9, CYP2C19, CYP3A4, CYP1A1, CYP1A2, CYP1B1 – Drug metabolism; influence antidepressant, beta-blocker, and anti-epileptic dosing.
- SLCO1B1 – Statin metabolism gene.
- NAT1, NAT2 – Acetylation pathway; detox and drug metabolism.
๐ง Genes That May Be Indirectly Linked to Tremor
These genes do not directly cause tremor, but variants may contribute through neuroinflammation, detox challenges, hormone imbalance, or neurotransmitter disruption:
- COMT, DRD2, CACNA1C, BDNF, GABRA2, MAOA, DIO2, MTHFR, DAO, HNMT, CYP1A2
๐ง What You Could Do:
If you're trying to explore tremor or neurological susceptibility, and you already have this gene list from a report:
- Look at COMT, BDNF, CACNA1C, DRD2, DIO2, GABRA2, MTHFR, DAO, and GSTs.
- Consider a functional medicine interpretation of this genetic data, mapping it to labs like homocysteine, methylmalonic acid, neurotransmitter panels, and advanced detoxification markers.
- Combine this with clinical neurology workup: MRI brain, DaTscan (for Parkinsonian features), and labs like B12, copper, ceruloplasmin, heavy metals, thyroid panel.
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genes — ATG16L1, HLA-DQ2, HLA-DQ8, and NOD2 — are not the same, but they are all immune-related genes and are particularly relevant to inflammatory and autoimmune conditions, especially in the gut.
Here’s a comparison:
๐น ATG16L1
- Function: Involved in autophagy (the body’s process of clearing damaged cells and pathogens).
- Disease association:
- Crohn’s disease – a specific variant (T300A) is strongly associated.
- May influence gut barrier function and susceptibility to infections.
๐น HLA-DQ2 and HLA-DQ8
- Function: Part of the HLA (human leukocyte antigen) system, which presents antigens to immune cells.
- Disease association:
- These two are necessary (but not sufficient) for the development of celiac disease.
- ~90–95% of people with celiac disease have HLA-DQ2.
- ~5–10% have HLA-DQ8.
- Also associated with type 1 diabetes, autoimmune thyroid disease, and other autoimmune conditions.
- Note: They are not causal but increase genetic susceptibility.
๐น NOD2 (CARD15)
- Function: Recognizes bacterial molecules inside immune cells, triggering inflammation.
- Disease association:
- Strongly linked to Crohn’s disease, particularly ileal (small intestine) involvement.
- Mutations lead to impaired bacterial sensing and abnormal immune responses.
- Also involved in innate immunity and gut homeostasis.
๐ง Summary Table:
GeneFunctionAssociated ConditionsNotesATG16L1Autophagy & cellular cleanupCrohn’s disease, gut inflammationWorks with NOD2 in immune regulationHLA-DQ2Antigen presentation (HLA)Celiac disease, T1D, autoimmune thyroiditisCommon in European populationsHLA-DQ8Antigen presentation (HLA)Celiac disease (less common), T1DTest with DQ2NOD2Bacterial recognition (PRR)Crohn’s disease, Blau syndromeDefective bacterial sensing
Here’s a functional medicine summary for the genes ATG16L1, HLA-DQ2, HLA-DQ8, and NOD2, including how they may affect gut health, immunity, and practical guidance on diet, supplements, and lifestyle.
๐งฌ Functional Medicine Interpretation & Action Plan
๐น ATG16L1 (Autophagy Gene)
Function: Regulates autophagy (cellular cleanup, including pathogens and damaged proteins)
Implications of Variants:
- Increased susceptibility to Crohn’s disease
- May impair clearance of intracellular pathogens
- Promotes gut barrier dysfunction and immune hyperreactivity
Functional Strategy:
- Support autophagy:
- Intermittent fasting
- Berberine, resveratrol, curcumin, quercetin
- Gut barrier support:
- L-glutamine, zinc carnosine, collagen peptides
- Probiotics (Lactobacillus plantarum, Bifidobacterium)
- Avoid chronic overfeeding and processed foods
๐น NOD2 (Pattern Recognition Receptor)
Function: Senses bacterial components in the gut to trigger appropriate immune responses
Implications of Variants:
- Associated with Crohn’s disease, especially ileal involvement
- Poor innate immunity → abnormal microbiome responses
- Promotes gut dysbiosis and chronic inflammation
Functional Strategy:
- Enhance innate immunity:
- Beta-glucans (from mushrooms or oats)
- Vitamin D (critical for innate immune signaling)
- Microbiome balancing:
- Avoid antibiotics unless necessary
- Use broad-spectrum probiotics and prebiotics (like PHGG, FOS)
- Limit triggers: High-fat, low-fiber diets worsen outcomes
๐น HLA-DQ2 / DQ8 (Antigen-Presenting Genes)
Function: Present gluten-derived peptides to immune cells
Implications of Presence:
- Strong predisposition to celiac disease (DQ2 > DQ8)
- Risk of non-celiac gluten sensitivity
- Higher risk of autoimmune disorders (e.g., thyroid, T1DM)
Functional Strategy:
- Gluten-free or gluten-minimized diet even if celiac not confirmed
- Test for tTG IgA and total IgA to screen for celiac
- Monitor for other autoimmunity (TPO antibodies, ANA, etc.)
- Gut-healing nutrients: Vitamin A, vitamin D, selenium, omega-3s
๐ฟ Summary of Recommended Supplements
SupplementBenefitDose (Typical)L-glutamineGut barrier repair5–10 g dailyZinc carnosineMucosal healing75 mg twice dailyVitamin DImmune regulation (esp. NOD2)2,000–5,000 IU daily (based on labs)Beta-glucansStimulates innate immunity (NOD2 support)250–500 mg dailyCurcumin/QuercetinAnti-inflammatory, supports autophagy250–500 mg 1–2x/dayProbioticsMicrobiome and immune support10–50 billion CFU/dayResveratrolSupports autophagy and antioxidant defense100–200 mg/day
๐ฅฆ Diet & Lifestyle Recommendations
- Gluten-free or low-gluten diet if HLA-DQ2/8 positive
- Anti-inflammatory, high-fiber diet (rich in vegetables, omega-3s, polyphenols)
- Avoid processed foods, excessive alcohol, NSAIDs
- Practice intermittent fasting (e.g., 16:8 method) to boost autophagy (ATG16L1)
- Manage stress: chronic stress increases intestinal permeability and immune overactivation
๐ฌ Optional Tests to Consider
- Celiac panel: tTG-IgA, total IgA
- Stool test (GI-MAP or Genova GI Effects): gut pathogens, inflammation, secretory IgA
- Zonulin: marker of intestinal permeability (leaky gut)
- Vitamin D, homocysteine, CRP, TPO antibodies
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๐งฌ VDR – Vitamin D Receptor Gene
๐น Function
The VDR gene codes for the vitamin D receptor, which is critical for:
- Binding active vitamin D (calcitriol)
- Regulating expression of hundreds of genes involved in:
- Calcium and bone metabolism
- Immune function
- Hormone production (including thyroid, insulin, sex hormones)
- Detoxification enzymes
- Neurological function and mood
๐น Common VDR Polymorphisms
Some widely studied variants:
- FokI (rs2228570)
Affects how the receptor is translated; F allele = less efficient receptor. - BsmI (rs1544410), ApaI (rs7975232), TaqI (rs731236)
Influence stability of VDR mRNA and receptor expression.
People with certain polymorphisms may have less sensitive or less active vitamin D receptors, meaning they:
- Require higher levels of circulating vitamin D to achieve the same biological effects
- May be more prone to autoimmune, inflammatory, or bone disorders even with “normal” vitamin D levels
๐น Associated Health Implications
SystemPotential Issues if VDR is ImpairedImmune systemAutoimmunity (e.g., Hashimoto’s, MS, lupus), infectionsMood/BrainDepression, anxiety, low serotonin/dopamineEndocrineThyroid dysfunction, insulin resistance, low testosteroneBone healthOsteopenia, osteoporosis, calcium malabsorptionDetox pathwaysLess CYP gene activation for Phase I detox
๐น Functional Medicine Strategy
1. Optimize Vitamin D Status:
- Goal: Serum 25(OH)D between 50–70 ng/mL
- Many with VDR SNPs need 4,000–10,000 IU/day to maintain optimal levels
- Consider using liposomal or emulsified vitamin D3 + K2 for enhanced absorption
2. Synergistic Nutrients:
- Magnesium – cofactor for vitamin D activation (Mg glycinate or malate: 200–400 mg/day)
- Vitamin K2 (MK-7) – directs calcium to bones (90–200 mcg/day)
- Zinc and boron – support vitamin D signaling
3. Immune & Hormone Support:
- Monitor autoimmune markers if there's a family history
- Support with omega-3s, probiotics, curcumin, and resveratrol
- If mood or hormonal symptoms are present: test thyroid, testosterone, estradiol, cortisol
๐ฌ Optional Tests to Run:
- Vitamin D (25-OH) and 1,25(OH)2D (active form)
- Magnesium RBC
- Thyroid panel (with TPO antibodies)
- CRP, homocysteine
- Genetic testing: Nutrigenomic panels (e.g., VDR, MTHFR, CYPs)
๐ Clinical Tip:
If a patient has persistently low vitamin D despite supplementation, suspect:
- VDR SNPs
- Fat malabsorption (consider checking stool elastase, fat-soluble vitamins)
- Magnesium deficiency
- Poor adherence or low-quality D3 supplement
- GNMT, MAT1A, SHMT
Here’s a functional medicine summary of the genes GNMT, MAT1A, and SHMT, which are all involved in methylation, one-carbon metabolism, and homocysteine clearance. These are crucial processes for detoxification, neurotransmitter synthesis, DNA repair, and hormone regulation.
๐งฌ Gene Overview
๐น GNMT – Glycine N-Methyltransferase
- Function: Regulates SAMe (S-adenosylmethionine) levels by converting it to sarcosine.
- Balances methylation demand and protects against excess SAMe buildup.
- Acts as a regulatory buffer in the methylation cycle.
Implications of Variants:
- May contribute to:
- Liver dysfunction, fatty liver
- Hormonal imbalance (estrogen detoxification)
- Cancer risk (due to altered methylation of tumor suppressor genes)
Functional Support:
- Choline, betaine (TMG) – alternative methyl donors
- Support methylation cofactors: B2, B6, B12, folate
- Consider NAC or glutathione if impaired liver detox markers present
๐น MAT1A – Methionine Adenosyltransferase 1A
- Function: Converts methionine to SAMe, the universal methyl donor.
- Vital for initiating methylation reactions in the liver.
Implications of Variants:
- May cause:
- Reduced SAMe production → downstream effects on mood, detox, DNA repair
- Elevated homocysteine
- Increased risk for neurological symptoms, fatty liver, and methylation imbalance
Functional Support:
- Supplement with methionine, SAMe, or methyl-B12 if low methylation suspected
- Monitor homocysteine and support transsulfuration with B6, Mg, zinc
๐น SHMT – Serine Hydroxymethyltransferase
- Function: Converts serine to glycine and transfers a one-carbon unit to tetrahydrofolate (THF).
- Critical for folate cycle, DNA synthesis, and methylation.
Implications of Variants:
- May cause:
- Folate trap or deficiency in active folate forms (especially with MTHFR variants)
- Poor methyl group availability → impaired neurotransmitter synthesis, detox, hormone metabolism
- May exacerbate issues with MTHFR, MTR, BHMT mutations
Functional Support:
- Use 5-MTHF instead of folic acid
- Support serine/glycine balance (protein-rich diet, glycine powder if needed)
- Cofactors: B6, zinc, magnesium
๐งช Summary Table
- GeneKey RoleFunctional IssuesSuggested SupportGNMTSAMe regulation, methyl bufferEstrogen detox, fatty liverCholine, betaine, NAC, liver supportMAT1ASAMe synthesis from methionineLow methylation, high homocysteineSAMe, methyl donors, homocysteine supportSHMTFolate metabolism, one-carbonLow methylation, folate trap5-MTHF, B6, glycine/serine, folate cycle nutrients
๐ฟ Clinical Application
If these genes show polymorphisms, and especially if the patient has symptoms like:
- Fatigue
- Brain fog
- Mood issues
- Hormonal imbalance
- Detox difficulty
- High homocysteine
- Fatty liver (NAFLD)
...then you should support methylation through:
- A methylation-friendly multivitamin with active B vitamins
- Possibly SAMe or TMG
- Liver support nutrients
- Testing: homocysteine, methylmalonic acid (MMA), glutathione, liver enzymes
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Functional Medicine Guide: GNMT, MAT1A, SHMT Genes
๐งฌ Gene Overview
๐น GNMT – Glycine N-Methyltransferase
Function: Regulates SAMe (S-adenosylmethionine) by converting it to sarcosine; acts as a methylation buffer.
Key Concerns:
- Fatty liver, hormonal imbalance
- Cancer risk (due to altered gene methylation)
- Impaired estrogen detox
Support Recommendations:
- Nutrients: Choline, Betaine (TMG), NAC, Glutathione
- Cofactors: B2, B6, B12, Folate
- Lifestyle: Reduce liver-toxic exposures, support methylation
๐น MAT1A – Methionine Adenosyltransferase 1A
Function: Converts methionine to SAMe; initiates the methylation cycle, especially in the liver.
Key Concerns:
- Low SAMe levels
- Elevated homocysteine
- Mood, detoxification, DNA repair issues
Support Recommendations:
- Nutrients: SAMe, Methyl-B12, Methionine
- Cofactors: B6, Zinc, Magnesium
- Monitoring: Homocysteine levels, liver function
๐น SHMT – Serine Hydroxymethyltransferase
Function: Transfers one-carbon units to THF (folate cycle); converts serine to glycine.
Key Concerns:
- Folate cycle disruption (especially with MTHFR variants)
- Low methyl group availability
- Poor detox and neurotransmitter synthesis
Support Recommendations:
- Nutrients: 5-MTHF (not folic acid), Glycine
- Cofactors: B6, Zinc, Magnesium
- Diet: Adequate protein (serine/glycine sources)
๐ฎ Clinical Summary Table
GeneRoleRisk If ImpairedFunctional SupportGNMTSAMe buffer, estrogen detoxFatty liver, hormone imbalanceCholine, TMG, NAC, GlutathioneMAT1ASAMe productionHigh homocysteine, mood issuesSAMe, Methyl-B12, Methionine, B6SHMTFolate metabolismLow methylation, folate trap5-MTHF, B6, Glycine, Serine
๐ฟ Suggested Lab Tests
- Homocysteine
- Methylmalonic Acid (MMA)
- Vitamin B12 and Folate
- Glutathione (GSH/GSSG ratio)
- Liver Enzymes (ALT, AST)
๐ฑ Lifestyle & Diet Tips
- Avoid synthetic folic acid
- Use active B vitamin blends
- Ensure protein intake to support amino acid pathways
- Support liver detox (cruciferous veggies, antioxidants)
- Reduce alcohol and liver stressors
This guide is intended to help patients and practitioners understand the functional implications of GNMT, MAT1A, and SHMT gene variants, and how to address them with personalized nutrition and lifestyle strategies.
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CYP1B1 – Cytochrome P450 1B1
๐น Function
CYP1B1 is part of the cytochrome P450 enzyme family involved in Phase I liver detoxification. It plays key roles in:
- Estrogen metabolism
- Activation of procarcinogens (e.g., polycyclic aromatic hydrocarbons)
- Retinoic acid metabolism (vitamin A)
- Ocular and developmental health
โ ๏ธ Clinical and Functional Implications of CYP1B1 Variants
1. Estrogen Metabolism
- Converts estradiol (E2) to 4-hydroxyestradiol (4-OH-E2) — a potentially carcinogenic metabolite.
- Increased CYP1B1 activity may lead to:
- Elevated 4-OH estrogens → DNA damage → higher breast, prostate, or uterine cancer risk
- Estrogen-dominant symptoms (e.g., fibroids, PMS, endometriosis)
2. Cancer Susceptibility
- CYP1B1 polymorphisms may increase risk for:
- Breast cancer
- Prostate cancer
- Glaucoma (especially congenital or early-onset)
3. Retinoid Pathways & Eye Health
- Mutations can cause primary congenital glaucoma
- Influences vitamin A metabolism → impacts epithelial health and vision
4. Detoxification Imbalance
- May overactivate Phase I detox without sufficient Phase II conjugation, leading to:
- Toxin accumulation
- Increased oxidative stress
- Hormone imbalance
๐ฟ Functional Medicine Support Strategies
GoalStrategyBalance estrogen metabolismUse DIM, calcium-D-glucarate, broccoli seed extract (sulforaphane)Support Phase II detoxCruciferous veggies, methylation cofactors (B6, B12, folate), glutathioneReduce oxidative stressCurcumin, resveratrol, vitamin C, quercetin, seleniumMinimize exposure to toxinsAvoid charred meats, BPA, pesticides, smoking
๐ Suggested Nutrients
- DIM (Diindolylmethane): 100–300 mg/day – promotes 2-OH estrogen metabolism
- Calcium D-glucarate: 500–1000 mg/day – supports glucuronidation of estrogens
- Sulforaphane: from broccoli seed extract – induces Phase II enzymes
- N-acetylcysteine (NAC): 600–1200 mg/day – precursor to glutathione
- Methylated B vitamins: especially B2, B6, B12, 5-MTHF
- Vitamin A (retinyl palmitate or mixed carotenoids) – if eye concerns are present
๐ฌ Optional Labs to Run
- Urinary Estrogen Metabolites (DUTCH or Genova) – assess 4-OH vs 2-OH pathways
- Glutathione (GSH/GSSG ratio)
- 8-OHdG – marker of DNA oxidative damage
- Homocysteine – methylation efficiency
- Liver function tests
๐ Summary
CategoryEffect of CYP1B1 VariantsEstrogen Detox↑ 4-OH estrogen → DNA adducts → ↑ cancer riskCancer Susceptibility↑ Breast, prostate, uterine cancer riskEye HealthLinked to congenital glaucoma, vitamin A metabolismDetox & Oxidative StressOveractive Phase I → need for strong Phase II & antioxidants
Companies that test genes: GeneDx, Invitae, Fulgent, or Blueprint Genetics
Complement C4 and all other complements
ChatGPT said:
Here’s a functional medicine guide to Complement C4 and the broader complement system (C1–C9), with emphasis on clinical significance, autoimmune involvement, and functional support.
๐งฌ Complement System Overview
The complement system is a group of over 30 proteins (C1–C9, regulatory proteins, and split fragments) that work together as part of the innate immune system to:
- Defend against pathogens
- Clear immune complexes
- Regulate inflammation
- Interface with the adaptive immune system
๐น Key Complement Proteins
ComplementPrimary FunctionClinical RelevanceC1q, C1r, C1sStart classical pathwayLow in lupus, Sjögren’sC2Classical pathwayLow in lupus, associated with C3/C4C3Central role (all pathways)Low in SLE, infection risk, immune complex diseaseC4 (C4A, C4B)Classical/lectin pathwaysKey marker in autoimmunity (especially SLE); genetic deficiency linked to lupus, immune dysregulationC5Promotes inflammation (C5a)Deficiency = recurrent infections; high = inflammatory damageC6–C9Membrane attack complex (MAC)Lytic activity → kill bacteria; deficiency = recurrent Neisseria infections
๐ Complement C4 (Focus)
๐ธ Two types: C4A and C4B
- Both play roles in clearing immune complexes and modulating inflammation
- C4A deficiency → More associated with autoimmunity (e.g., lupus)
- C4B deficiency → May predispose to chronic infections
๐ธ Low C4 Levels May Suggest:
- Systemic lupus erythematosus (SLE) or lupus-like autoimmunity
- Chronic inflammation or immune complex disease
- Congenital C4 deficiency (rare, often undiagnosed)
- Complement consumption during active disease
๐งฌ Functional & Genetic Associations
GeneFunctionClinical NotesC4A/C4BClassical pathway complement proteinsCNVs (copy number variations) can lead to low levels or absenceC1Q genesInitiate complement cascadeDeficiency linked to early-onset lupusCFH, CFI, CD55, CD59Complement regulatorsMutations linked to atypical HUS, PNH, and autoimmunity
๐ฟ Functional Medicine Strategies
โ If C4 is low or patient has autoimmune/inflammatory symptoms:
1. Modulate Immune System, Reduce Autoimmunity
- Vitamin D3 – 2,000–5,000 IU/day (immunomodulatory)
- Omega-3s (EPA/DHA) – 2–4 g/day (reduces inflammatory cytokines)
- Curcumin, resveratrol, quercetin – reduce complement activation
- Probiotics – gut-immune axis regulation (Lactobacillus rhamnosus, L. plantarum)
- Glutathione or NAC – antioxidant, supports regulatory T cell function
2. Support Liver Function
- Liver synthesizes complement proteins
- Use: Milk thistle, dandelion, artichoke extract, methylation support (B6/B12/folate)
3. Reduce Triggering Infections
- Identify and manage latent infections: EBV, HSV, Lyme, mycoplasma
- Test and treat gut dysbiosis or leaky gut
๐ฌ Suggested Lab Tests
TestPurposeC3, C4 levelsBasic complement activityCH50 (total hemolytic complement)Measures overall classical pathway functionAH50Alternative pathway functionANA, dsDNA, ENA panelScreen for lupus, Sjögren’sC4A/C4B copy number (genetic)Genetic deficiency evaluationInflammatory markers: CRP, ESRAssess systemic inflammationImmunoglobulins (IgG, IgA, IgM)Rule out immune deficiency
๐ง Summary Table
FindingPossible CauseFunctional SupportLow C4Lupus, chronic inflammation, genetic deficiencyVitamin D, omega-3s, curcumin, liver supportLow C3 & C4Active autoimmune flareAntioxidants, treat infections, immunomodulatorsLow CH50Classical complement deficiencyImmune support, rule out serious infectionsNormal C3, Low C4Classical pathway consumptionAutoimmunity more likely than infection
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