Autoimmune Conditions Glossary: Complete Guide to Autoimmune Diseases

Autoimmune conditions represent a diverse group of disorders in which the immune system, normally protective against foreign invaders, mistakenly attacks the body’s own tissues. These conditions affect millions of people worldwide, with prevalence increasing in developed nations. In Dubai and the UAE, the changing environmental factors, dietary patterns, and genetic diversity of the population create unique considerations for autoimmune disease awareness and management.

The immune system is a complex network of cells, tissues, and organs designed to distinguish self from non-self. When this distinction fails, autoreactive immune cells attack healthy tissues, causing inflammation and damage. Autoimmune diseases can affect virtually any organ system, from joints and skin to glands, nerves, and internal organs.

The exact cause of autoimmune disease is unknown, but it involves complex interactions between genetic susceptibility and environmental triggers. Understanding these conditions is essential for early recognition, appropriate treatment, and optimizing outcomes for affected individuals.

Understanding Autoimmunity

How the Immune System Works

The immune system consists of innate and adaptive components. Innate immunity provides immediate, non-specific defense through physical barriers, phagocytes, natural killer cells, and inflammatory responses. Adaptive immunity involves T and B lymphocytes that provide targeted, long-lasting protection with immunological memory.

T cells include helper T cells (CD4+) that coordinate immune responses and cytotoxic T cells (CD8+) that directly kill infected or abnormal cells. B cells produce antibodies that neutralize pathogens and mark cells for destruction. Regulatory T cells (Tregs) suppress immune responses and maintain tolerance.

Tolerance, the ability to distinguish self from non-self, develops during immune system maturation. Central tolerance in the thymus (for T cells) and bone marrow (for B cells) eliminates most autoreactive lymphocytes. Peripheral tolerance mechanisms (anergy, suppression by Tregs, immune privilege) handle any autoreactive cells that escape central tolerance.

What Goes Wrong in Autoimmunity

Autoimmune diseases develop when self-tolerance fails. This can result from defects in central or peripheral tolerance, molecular mimicry (foreign antigens resembling self-antigens), bystander activation (inflammation releasing hidden self-antigens), or epigenetic changes altering gene expression.

Genetic factors contribute significantly to autoimmune disease risk. Certain HLA (human leukocyte antigen) types are associated with specific conditions: HLA-DR3 and DR4 with type 1 diabetes, HLA-DR4 with rheumatoid arthritis, HLA-B27 with ankylosing spondylitis. Non-HLA genes also contribute, often involving immune regulation.

Environmental triggers vary by condition but include infections (which may trigger molecular mimicry), vitamin D deficiency, smoking, silica exposure, and hormonal factors. The “hygiene hypothesis” suggests that reduced childhood infections may increase autoimmune risk by altering immune development.

Classification of Autoimmune Diseases

Autoimmune diseases can be organ-specific or systemic. Organ-specific diseases affect particular organs: Hashimoto’s thyroiditis (thyroid), type 1 diabetes (pancreas), celiac disease (intestine), multiple sclerosis (nervous system). Systemic diseases affect multiple organs: systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis.

Autoantibodies (antibodies against self-antigens) are present in many autoimmune diseases and aid in diagnosis. Rheumatoid factor (RF) and anti-CCP in rheumatoid arthritis, ANA (antinuclear antibody) in lupus, anti-dsDNA and anti-Smith in lupus, anti-TPO in Hashimoto’s, and anti-gluten antibodies in celiac disease are examples.

Rheumatoid Arthritis

Definition and Overview

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by inflammatory arthritis affecting synovial joints, typically in a symmetrical distribution. It causes progressive joint destruction, deformity, and disability if untreated. RA affects approximately 1 percent of the population worldwide, more commonly women (3:1 ratio).

The pathophysiology involves autoimmune inflammation of the synovium (pannus formation), with infiltration of inflammatory cells, proliferation of synovial fibroblasts, and production of cytokines (TNF-alpha, IL-6, IL-1). Autoantibodies including rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPAs/anti-CCP) are present in most patients.

Symptoms and Diagnosis

The typical presentation involves symmetric polyarthritis of small joints of the hands (MCP and PIP joints) and feet (MTP joints), with morning stiffness lasting more than 30-60 minutes. Joint swelling, warmth, and tenderness are present. Systemic symptoms include fatigue, low-grade fever, and weight loss.

Physical findings include symmetrical joint swelling, ulnar deviation of fingers, swan neck and boutonniere deformities, and rheumatoid nodules (firm, non-tender nodules over extensor surfaces). Extra-articular manifestations include rheumatoid lung disease, pericarditis, scleritis, anemia, and vasculitis.

Diagnosis is based on clinical criteria including joint involvement, serology (RF and anti-CCP), acute phase reactants (ESR, CRP), and duration of symptoms. X-rays show periarticular osteopenia, joint space narrowing, and erosions in established disease.

Treatment and Management

Treatment has been transformed by biologic and targeted synthetic disease-modifying antirheumatic drugs (DMARDs). Early, aggressive treatment within the “window of opportunity” can induce remission and prevent joint damage.

Methotrexate is the anchor drug for RA treatment. Conventional synthetic DMARDs include leflunomide, sulfasalazine, and hydroxychloroquine. Biologic DMARDs target TNF-alpha (etanercept, adalimumab, infliximab), IL-6 (tocilizumab), B cells (rituximab), and T cell costimulation (abatacept). JAK inhibitors (tofacitinib, baricitinib, upadacitinib) are oral options.

Non-pharmacological management includes physical and occupational therapy, exercise programs, and joint protection strategies. Surgery may be needed for severe joint damage.

Systemic Lupus Erythematosus

Definition and Overview

Systemic lupus erythematosus (SLE or lupus) is a chronic multisystem autoimmune disease characterized by autoantibody production and immune complex deposition causing inflammation and tissue damage. Lupus affects approximately 5 million people worldwide, predominantly women (9:1 ratio) of childbearing age.

The pathophysiology involves loss of self-tolerance, production of autoantibodies (particularly antinuclear antibodies, ANA), and immune complex formation depositing in tissues. Multiple genetic loci and environmental triggers (UV light, infections, hormones) contribute to disease.

Symptoms and Diagnosis

Lupus is the “great imitator” with diverse manifestations. Common symptoms include fatigue, fever, joint pain, and rash. The classic malar (“butterfly”) rash spans the cheeks and bridge of the nose. Discoid lesions are thick, scaly plaques.

Renal involvement (lupus nephritis) is common and serious, causing proteinuria, hematuria, and potential kidney failure. Neurologic involvement includes headaches, seizures, and cognitive dysfunction. Cardiopulmonary involvement includes pericarditis, pleuritis, and antiphospholipid syndrome with thrombosis.

Diagnosis uses criteria including clinical manifestations (malar rash, arthritis, serositis, renal disorder, neurological disorder) and immunological findings (ANA, anti-dsDNA, anti-Smith, antiphospholipid antibodies).

Treatment and Management

Hydroxychloroquine (antimalarial) is foundational for most lupus patients, reducing flares and improving survival. Immunosuppressive medications include mycophenolate mofetil, azathioprine, cyclophosphamide, and calcineurin inhibitors for organ-threatening disease. Biologics (belimumab, anifrolumab) are approved for lupus.

Corticosteroids are used for active disease, with dose and duration minimized to reduce side effects. Non-steroidal anti-inflammatory drugs (NSAIDs) help with arthritis and serositis. Anticoagulation is needed for antiphospholipid syndrome.

Lifestyle management includes sun protection, smoking cessation, vaccination, and managing cardiovascular risk. Regular monitoring for disease activity and medication toxicity is essential.

Multiple Sclerosis

Definition and Overview

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system, characterized by demyelination, axonal loss, and gliosis disseminated in time and space. MS affects approximately 2.8 million people worldwide, typically beginning in young adulthood (ages 20-40), and is more common in women.

The cause involves complex interactions between genetic susceptibility and environmental factors. Associated factors include low vitamin D, smoking, adolescent obesity, and Epstein-Barr virus infection. HLA-DRB1*15:01 is the strongest genetic risk factor.

Types and Symptoms

Clinically isolated syndrome (CIS) is the first episode of neurological symptoms suggestive of MS. Relapsing-remitting MS (RRMS) involves discrete attacks (relapses) followed by partial or complete recovery. Secondary progressive MS (SPMS) involves gradual disability accumulation after initial RRMS. Primary progressive MS (PPMS) involves gradual disability from onset without clear relapses.

Symptoms depend on lesion location and include visual disturbances (optic neuritis), sensory symptoms, motor weakness, coordination problems (ataxia), bladder dysfunction, fatigue, and cognitive changes. Heat sensitivity (Uhthoff phenomenon) temporarily worsens symptoms with warm temperatures.

Treatment and Management

Disease-modifying therapies (DMTs) reduce relapse rate and MRI activity in relapsing forms of MS. Options include injectable interferons and glatiramir acetate, oral agents (fingolimod, dimethyl fumarate, teriflunomide, cladribine), and highly effective infusions (natalizumab, ocrelizumab, alemtuzumab).

Acute relapses are treated with high-dose corticosteroids (methylprednisolone), which speed recovery. Symptomatic treatment addresses spasticity, fatigue, bladder dysfunction, pain, and other symptoms. Rehabilitation maintains function.

Type 1 Diabetes

Definition and Overview

Type 1 diabetes is an autoimmune disease characterized by destruction of pancreatic beta cells, resulting in absolute insulin deficiency. It accounts for 5-10 percent of all diabetes cases and typically presents in children and adolescents, though it can occur at any age.

The pathophysiology involves T cell-mediated destruction of beta cells in the pancreatic islets. Autoantibodies (GAD65, IA-2, IAA, ZnT8) are present and serve as markers of autoimmunity. Genetic susceptibility involves HLA-DR3 and DR4. Environmental triggers (viral infections, possibly dietary factors) initiate the autoimmune process.

Symptoms and Diagnosis

The classic presentation includes the “3 Ps”: polyuria (frequent urination), polydipsia (excessive thirst), and polyphagia (increased hunger) with weight loss. Symptoms develop over weeks to months as insulin deficiency becomes severe. Diabetic ketoacidosis (DKA) may be the initial presentation.

Diagnosis is confirmed by hyperglycemia (random glucose >=200 mg/dL with symptoms, fasting glucose >=126 mg/dL, or HbA1c >=6.5 percent). Low or undetectable C-peptide and positive autoantibodies distinguish type 1 from type 2 diabetes.

Treatment and Management

Lifelong insulin therapy is required, typically through multiple daily injections or insulin pump therapy. Blood glucose monitoring, through fingerstick testing or continuous glucose monitoring (CGM), guides insulin dosing. The goal is to maintain blood glucose levels as close to normal as possible while minimizing hypoglycemia.

Diabetes education, nutritional management, and regular physical activity are essential components of care. Screening for other autoimmune conditions (thyroid, celiac) is recommended. Monitoring for and treating diabetes complications (retinopathy, nephropathy, neuropathy, cardiovascular disease) is important.

Celiac Disease

Definition and Overview

Celiac disease is an autoimmune disorder triggered by ingestion of gluten (a protein in wheat, barley, rye) in genetically susceptible individuals. It affects approximately 1 percent of the global population and has diverse manifestations.

The autoimmune response involves CD4+ T cells that recognize gluten peptides when presented by HLA-DQ2 or HLA-DQ8 molecules. These T cells produce inflammatory cytokines that damage intestinal villi. Antibodies against tissue transglutaminase (tTG) and deamidated gliadin peptides are sensitive markers.

Symptoms and Diagnosis

Classic gastrointestinal symptoms include chronic diarrhea, weight loss, abdominal pain, bloating, and steatorrhea. However, many patients have atypical or extraintestinal presentations including iron deficiency anemia, osteoporosis, elevated liver enzymes, dermatitis herpetiformis (itchy rash), neurological symptoms, infertility, and delayed growth in children.

Diagnosis involves serologic testing for tTG-IgA (with total IgA to rule out IgA deficiency). Positive tests require confirmation with duodenal biopsy showing characteristic villous atrophy, crypt hyperplasia, and increased intraepithelial lymphocytes. HLA typing can rule out celiac disease when tests are equivocal.

Treatment and Management

Treatment is a strict, lifelong gluten-free diet. All wheat, barley, and rye products must be eliminated. Naturally gluten-free foods (rice, corn, potatoes, legumes, fruits, vegetables, meats) are allowed. Hidden gluten in processed foods requires careful label reading.

Improvement on a gluten-free diet confirms diagnosis, with symptom resolution typically occurring over weeks to months. Repeat biopsy is not always necessary but may be considered in high-risk patients or those with persistent symptoms. Support from dietitians ensures nutritional adequacy.

Hashimoto’s Thyroiditis

Definition and Overview

Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas. It is an autoimmune condition in which antibodies (anti-thyroid peroxidase, anti-thyroglobulin) attack the thyroid gland, causing progressive destruction and eventual hypothyroidism.

Hashimoto’s affects predominantly women (8:1 ratio) and has strong genetic predisposition. Risk factors include family history, other autoimmune diseases, and certain genetic markers. The disease often presents with goiter and progresses from subclinical to overt hypothyroidism over years.

Symptoms and Diagnosis

Symptoms of hypothyroidism develop gradually and include fatigue, weight gain, cold intolerance, constipation, dry skin, hair loss, muscle weakness, depression, cognitive slowing, menstrual irregularities, and elevated cholesterol. Severe, long-standing hypothyroidism can cause myxedema (non-pitting edema).

Diagnosis is confirmed by elevated TSH with low free T4 (overt hypothyroidism) or normal free T4 with elevated TSH (subclinical hypothyroidism). Positive anti-TPO and/or anti-thyroglobulin antibodies confirm autoimmune etiology.

Treatment and Management

Levothyroxine replacement is the treatment of choice for hypothyroidism. Dosing is individualized to maintain TSH in the target range. Subclinical hypothyroidism may not require treatment if TSH is mildly elevated and antibodies are positive.

Regular monitoring of TSH is essential, particularly when starting or adjusting treatment. Autoimmune thyroid disease may be associated with other autoimmune conditions, warranting awareness and screening as appropriate.

Graves’ Disease

Definition and Overview

Graves’ disease is the most common cause of hyperthyroidism, an autoimmune condition in which stimulating TSH receptor antibodies cause the thyroid to produce excess thyroid hormone. It affects predominantly women and has peak incidence between ages 20-40.

The pathophysiology involves autoantibodies (thyroid-stimulating immunoglobulins) that bind to and activate the TSH receptor, causing thyroid hyperplasia and hyperfunction. The thyroid may enlarge (goiter), and autoimmune ophthalmopathy affects the eyes.

Symptoms and Diagnosis

Symptoms of hyperthyroidism include weight loss despite increased appetite, heat intolerance, sweating, tremor, anxiety, irritability, insomnia, palpitations, diarrhea, menstrual irregularities, and proximal muscle weakness. Physical findings include thyroid enlargement, tachycardia, atrial fibrillation, warm moist skin, and Graves’ ophthalmopathy (proptosis, periorbital edema).

Diagnosis involves suppressed TSH with elevated free T4 and/or free T3. TSH receptor antibodies confirm Graves’ disease. Radioactive iodine uptake and scan shows diffuse increased uptake.

Treatment and Treatment

Three treatment options exist: antithyroid drugs (methimazole, propylthiouracil), radioactive iodine ablation, and thyroid surgery. Choice depends on patient factors, preferences, and local expertise. Antithyroid drugs may be used long-term in some patients but have higher recurrence rates.

Beta-blockers provide symptomatic relief of hyperadrenergic symptoms. Graves’ ophthalmopathy requires ophthalmology management, including steroids, radiation, or surgery for severe cases.

Inflammatory Bowel Disease

Definition and Overview

Inflammatory bowel disease (IBD) includes Crohn’s disease and ulcerative colitis, chronic inflammatory conditions of the gastrointestinal tract. IBD affects approximately 7 million people worldwide and is increasing in prevalence in newly industrialized regions.

Crohn’s disease can affect any part of the GI tract from mouth to anus, most commonly the terminal ileum and colon. It is characterized by transmural inflammation with skip lesions. Complications include strictures, fistulas, and abscesses.

Ulcerative colitis is limited to the colon and rectum, beginning at the anus and extending proximally in a continuous pattern. Inflammation is limited to mucosa and submucosa. Complications include severe bleeding, toxic megacolon, and increased colorectal cancer risk.

Symptoms and Diagnosis

Symptoms include abdominal pain, diarrhea (often with blood), weight loss, fatigue, and fever. Perianal disease occurs in Crohn’s. Extraintestinal manifestations include arthritis, skin lesions, eye inflammation, primary sclerosing cholangitis, and increased thrombosis risk.

Diagnosis involves colonoscopy with biopsy, which is diagnostic and allows disease classification. Imaging (CT enterography, MR enterography) evaluates small bowel disease. Blood tests show inflammation and anemia. Stool tests rule out infection and assess inflammatory markers.

Treatment and Management

Treatment aims to induce and maintain remission. Aminosalicylates (mesalamine) are first-line for mild to moderate ulcerative colitis. Corticosteroids induce remission in moderate to severe disease. Immunomodulators (azathioprine, methotrexate) maintain remission.

Biologic agents have transformed IBD treatment. Anti-TNF agents (infliximab, adalimumab, golimumab), vedolizumab (gut-specific), ustekinumab (anti-IL12/23), and JAK inhibitors (tofacitinib, upadacitinib) are effective options.

Surgery is indicated for complications or refractory disease. Total proctocolectomy is curative for ulcerative colitis. For Crohn’s disease, surgery is not curative but may be necessary for strictures or fistulas.

Other Autoimmune Conditions

Sjogren’s Syndrome

Sjogren’s syndrome is an autoimmune disease characterized by lymphocytic infiltration of exocrine glands, causing dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia). It can occur alone (primary Sjogren’s) or with other autoimmune diseases (secondary Sjogren’s).

Treatment is symptomatic: artificial tears, saliva substitutes, and good oral hygiene. Systemic disease may require hydroxychloroquine, immunosuppressants, or biologics. Increased lymphoma risk requires monitoring.

Systemic Sclerosis

Systemic sclerosis (scleroderma) is characterized by fibrosis, vascular abnormalities, and autoantibodies affecting skin and internal organs. Limited cutaneous scleroderma affects face, hands, and feet; diffuse cutaneous scleroderma involves trunk and proximal limbs.

Raynaud’s phenomenon, skin thickening, and internal organ involvement (pulmonary fibrosis, pulmonary arterial hypertension, renal crisis) define the disease. Treatment involves vasodilators for Raynaud’s, immunosuppressants for inflammatory lung disease, and ACE inhibitors for renal crisis.

Myasthenia Gravis

Myasthenia gravis is an autoimmune disease caused by antibodies against the acetylcholine receptor or related proteins at the neuromuscular junction, causing fatigable muscle weakness. Ocular myasthenia affects eye muscles; generalized myasthenia affects other muscles.

Treatment includes acetylcholinesterase inhibitors (pyridostigmine), immunosuppressants (corticosteroids, azathioprine, mycophenolate), and thymectomy. Acute worsening (myasthenic crisis) requires plasmapheresis or IVIG.

Psoriasis and Psoriatic Arthritis

Psoriasis is a chronic immune-mediated inflammatory disease characterized by well-demarcated, erythematous plaques with silvery scale. Psoriatic arthritis occurs in approximately 30 percent of patients, causing joint inflammation, dactylitis, and enthesitis.

Treatment ranges from topicals and phototherapy for mild disease to systemic agents (methotrexate, cyclosporine, acitretin) and biologics (TNF inhibitors, IL-17 inhibitors, IL-23 inhibitors) for moderate to severe disease.

Frequently Asked Questions

General Autoimmune Questions

Are autoimmune diseases genetic? Autoimmune diseases have genetic components, but they are not directly inherited. Having a family member with an autoimmune disease increases risk, but most people with affected relatives do not develop disease.

Can autoimmune diseases be cured? Most autoimmune diseases are chronic and cannot be cured. However, they can often be effectively managed to achieve remission (no active disease symptoms).

Are autoimmune diseases contagious? No, autoimmune diseases are not contagious. They result from the person’s own immune system attacking their body.

Can stress cause autoimmune disease? Stress does not directly cause autoimmune disease but may trigger flares in susceptible individuals. The relationship between stress and autoimmunity is complex.

Rheumatoid Arthritis Questions

Is rheumatoid arthritis hereditary? Family history increases risk, but most people with RA have no affected relatives. Multiple genes contribute small effects, combined with environmental factors.

Can RA go into remission? Yes, with appropriate treatment, many patients achieve remission (no active disease). Early, aggressive treatment improves the likelihood of remission.

Does cold weather worsen RA? Many patients report increased joint pain in cold, damp weather, though scientific evidence is mixed. Keeping warm may help symptoms.

Lupus Questions

Is lupus contagious? No, lupus is not contagious. You cannot “catch” lupus from someone.

Can people with lupus have normal lives? Yes, with appropriate treatment and lifestyle management, most people with lupus can lead full, productive lives.

Does lupus affect pregnancy? Lupus increases pregnancy risks, but many women with lupus have successful pregnancies with careful management. Pre-conception planning is important.

Multiple Sclerosis Questions

Is MS inherited? Having a first-degree relative with MS slightly increases risk, but most people with MS have no family history. Genetic susceptibility involves multiple genes.

Does vitamin D help MS? Vitamin D deficiency is a risk factor for MS, and vitamin D supplementation may reduce flares in established disease. Adequate vitamin D is recommended for all MS patients.

Is MS fatal? MS itself is rarely fatal. However, complications or comorbidities can reduce life expectancy. Most people with MS have normal or near-normal life expectancy.

Thyroid Questions

Is thyroid disease autoimmune? Hashimoto’s thyroiditis and Graves’ disease are autoimmune conditions. Most hypothyroidism and hyperthyroidism in iodine-sufficient areas are autoimmune.

Do I need thyroid medication forever? Hypothyroidism from Hashimoto’s or thyroidectomy requires lifelong levothyroxine replacement. Subclinical hypothyroidism may resolve or persist.

Diabetes Questions

Is type 1 diabetes different from type 2? Yes, they are completely different diseases. Type 1 is autoimmune, requiring insulin from diagnosis. Type 2 involves insulin resistance and relative deficiency, initially managed with lifestyle and oral medications.

Can diet prevent type 1 diabetes? No, diet cannot prevent type 1 diabetes, which is autoimmune. However, breastfeeding and early introduction of gluten may slightly reduce risk.

Celiac Questions

Is celiac disease an allergy? No, celiac disease is an autoimmune condition, not an IgE-mediated allergy. It involves T cell-mediated damage to the intestine.

Can I ever eat gluten again? A strict gluten-free diet is required for life in celiac disease. Even small amounts cause ongoing intestinal damage.

Key Takeaways

Autoimmune conditions represent a diverse group of disorders where the immune system attacks the body’s own tissues. From organ-specific diseases like type 1 diabetes and Hashimoto’s to systemic conditions like lupus and rheumatoid arthritis, these disorders affect millions and require lifelong management.

The causes of autoimmune disease involve complex interactions between genetic susceptibility and environmental triggers. Understanding these factors helps in risk assessment and potential prevention strategies.

Early diagnosis and treatment are essential for optimizing outcomes. Many autoimmune diseases have effective treatments that can induce remission and prevent organ damage. Newer biologic therapies have transformed care for conditions like rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis.

Living with autoimmune disease requires ongoing medical care, medication adherence, and lifestyle management. Support from healthcare providers, family, and patient organizations improves outcomes.

For Dubai residents, access to rheumatologists, endocrinologists, gastroenterologists, neurologists, and other specialists supports comprehensive autoimmune disease care.

Natural support strategies including balanced nutrition, stress management, adequate sleep, and appropriate exercise complement conventional treatment. Traditional approaches including Ayurveda provide additional perspectives on immune balance and overall wellness.

The field of autoimmunity continues to advance, with new treatments and understanding emerging regularly. Patients benefit from staying informed and working collaboratively with their healthcare providers.

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Related Services

At Healer’s Clinic Dubai, we offer comprehensive autoimmune disease support through our integrated services:

• Consultation and Diagnosis: Our experienced specialists provide thorough autoimmune disease assessments, testing, and personalized treatment plans for all autoimmune conditions.

• Homeopathic Condition Support: Our homeopathic practitioners offer individualized remedies to support immune balance and overall wellness alongside conventional treatment.

• Ayurvedic Immune Balance: Traditional Ayurvedic approaches including specialized diet plans (Agni balancing, Ama reduction), herbal formulations, yoga, and lifestyle guidance support immune health from an ancient wellness perspective.

• Autoimmune Rehabilitation: Our team provides comprehensive approaches for managing autoimmune conditions, including nutritional support, stress management, and complementary therapies.

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Medical Disclaimer: This glossary is provided for educational purposes only and is not intended as a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read in this material. If you think you may have a medical emergency, call your doctor or emergency services immediately.