Nutritional Science, Immunity, and Common Health Conditions

Nutrient Deficiencies and Excesses

Macronutrients and Micronutrients

NutrientDeficiency EffectsExcess Effects
ProteinKwashiorkor, Marasmus, Growth RetardationObesity, Renal Overload, Gout
CarbohydratesKetosis, Fatigue, Protein Breakdown for EnergyObesity, Type 2 Diabetes, Metabolic Syndrome
FatEssential Fatty Acid Deficiency (Dry Skin, Poor Wound Healing, Growth Failure)Obesity, Atherosclerosis, Fatty Liver
CalciumRickets, Osteoporosis, TetanyHypercalcemia, Kidney Stones
IronIron-Deficiency AnemiaHemochromatosis, Liver Damage, Heart Damage
IodineGoiter, Cretinism, HypothyroidismHyperthyroidism, Thyrotoxicosis

Vitamins: Functions, Deficiencies, and Toxicity

VitaminSolubilityChemical Name(s)Deficiency SymptomsRDAToxicity Symptoms
Vitamin AFat-solubleRetinol, Retinal, Retinoic acidNight blindness, Xerophthalmia, KeratomalaciaM: 900 µg, F: 700 µgHypervitaminosis A (Headache, Liver damage, Birth defects)
Vitamin DFat-solubleCalciferol (D2 – Ergocalciferol, D3 – Cholecalciferol)Rickets, Osteomalacia600 IU (15 µg)Hypercalcemia, Kidney stones, Soft tissue calcification
Vitamin EFat-solubleTocopherols, TocotrienolsHemolytic anemia (infants), Neuropathy15 mgBleeding tendency (interferes with Vitamin K)
Vitamin KFat-solublePhylloquinone (K1), Menaquinone (K2), Menadione (K3)Delayed blood clotting, HemorrhageM: 120 µg, F: 90 µgJaundice & hemolytic anemia (infants, high dose)
Vitamin B1Water-solubleThiamineBeriberi, Wernicke’s encephalopathyM: 1.2 mg, F: 1.1 mgRare; may cause headache, irritability
Vitamin B2Water-solubleRiboflavinCheilosis, Glossitis, DermatitisM: 1.3 mg, F: 1.1 mgNo major toxicity (water-soluble)
Vitamin B3Water-solubleNiacin (Nicotinic acid, Nicotinamide)Pellagra (Diarrhea, Dermatitis, Dementia)M: 16 mg, F: 14 mgNiacin flush, Liver toxicity, Hyperuricemia
Vitamin B5Water-solublePantothenic acidBurning feet syndrome, Fatigue5 mgRare; mild diarrhea in excess
Vitamin B6Water-solublePyridoxine, Pyridoxal, PyridoxamineConvulsions, Neuropathy, AnemiaM/F: 1.3–1.7 mgSensory neuropathy, Nerve damage
Vitamin B7Water-solubleBiotinDermatitis, Alopecia, Neurological issues30 µgRare; no major toxicity
Vitamin B9Water-solubleFolic acid, FolateMegaloblastic anemia, Neural tube defects400 µgMasks B12 deficiency, Neurological issues
Vitamin B12Water-solubleCobalaminPernicious anemia, Neuropathy2.4 µgRare; may cause acne, rosacea
Vitamin CWater-solubleAscorbic acidScurvy (Bleeding gums, Poor wound healing)M: 90 mg, F: 75 mgKidney stones, Diarrhea, GI upset

Understanding the Immune System

What is Immunity?

Immunity is the body’s ability to resist, destroy, or neutralize harmful agents such as pathogens (bacteria, viruses, fungi), toxins, and foreign substances.

Types of Immunity

Innate Immunity (Natural / Nonspecific)

  • Present since birth
  • Provides immediate defense
  • Not specific to a particular pathogen
  • No memory
  • Examples: Skin, mucous membranes, stomach acid, phagocytes

Acquired Immunity (Adaptive / Specific)

  • Develops after exposure to pathogens or vaccines
  • Specific to particular antigens
  • Has memory (stronger response on re-exposure)
  • Types:
    • Active Immunity:
      • Natural: After infection
      • Artificial: After vaccination
    • Passive Immunity:
      • Natural: From mother to child (placenta, breast milk)
      • Artificial: Injected antibodies/serum therapy

Components of the Immune System

  1. Physical & Chemical Barriers (Innate)
    • Skin: First line of defense
    • Mucous membranes: Trap pathogens
    • Secretions: Saliva, tears (lysozyme), stomach acid, bile
  2. Cells of the Immune System
    • Phagocytes: Neutrophils, Monocytes, Macrophages
    • Natural Killer (NK) cells: Kill virus-infected & tumor cells
    • Lymphocytes:
      • B-cells: Produce antibodies (humoral immunity)
      • T-cells:
        • Helper T-cells (CD4⁺): Activate B-cells & macrophages
        • Cytotoxic T-cells (CD8⁺): Kill infected cells
        • Regulatory T-cells: Suppress excess immune response
  3. Organs of the Immune System
    • Primary (central):
      • Bone marrow: Production of B & T lymphocytes, B-cell maturation
      • Thymus: T-cell maturation
    • Secondary (peripheral):
      • Lymph nodes, Spleen, Tonsils, Peyer’s patches
  4. Molecules of the Immune System
    • Antibodies: Immunoglobulins (IgG, IgA, IgM, IgE, IgD)
    • Cytokines: Interleukins, Interferons, TNF
    • Complement system: Proteins aiding in opsonization & lysis

Cellular Injury and Adaptation

Cell Injury

Definition: Cell injury occurs when cells are exposed to stress or harmful stimuli beyond their capacity to adapt, leading to structural and functional changes.

Pathogenesis of Cell Injury

  • ATP Depletion: Due to hypoxia, toxins, or mitochondrial damage, leading to failure of ion pumps and cell swelling.
  • Mitochondrial Damage: Decreases ATP and releases apoptotic proteins (cytochrome-c).
  • Influx of Calcium & Loss of Calcium Homeostasis: Activates destructive enzymes (phospholipases, proteases, endonucleases).
  • Accumulation of Reactive Oxygen Species (ROS): Causes oxidative stress, leading to lipid peroxidation, and DNA & protein damage.
  • Membrane Damage: Due to free radicals, toxins, or complement, causing leakage of enzymes and cell death.
  • Protein Misfolding & DNA Damage: Triggers apoptosis.

Basic Mechanisms of Cell Injury

  • Hypoxia & Ischemia: Decreased oxygen supply
  • Chemical agents & Drugs: Toxins, poisons
  • Infectious agents: Bacteria, viruses, fungi, parasites
  • Immunologic reactions: Autoimmune diseases, allergies
  • Genetic abnormalities: Mutations, chromosomal defects
  • Nutritional imbalances: Deficiency or excess
  • Physical agents: Trauma, heat, radiation, cold, electric shock

Reversible vs. Irreversible Injury

FeatureReversible InjuryIrreversible Injury
Cellular responseCell recovers if stimulus is removedCell death occurs
ATP productionMildly decreased, reversibleSeverely decreased, no recovery
Cell swellingPresentSevere swelling, rupture
Membrane integrityMaintainedLost, leakage of contents
MitochondriaSwelling, reversibleSevere damage, cytochrome-c release
NucleusChromatin clumpingPyknosis, Karyorrhexis, Karyolysis
LysosomesIntactRupture, enzyme release
OutcomeCell survivesNecrosis or Apoptosis

Cellular Adaptation

Cellular adaptation refers to reversible functional and structural changes in cells in response to stress, allowing them to survive and function. If stress persists, it can lead to cell injury.

Mechanisms of Cellular Adaptation

  • Gene regulation changes: Altered protein synthesis
  • Hormonal / Growth factor stimulation: Cell growth & division
  • Functional demand changes: Increase or decrease in size/number
  • Environmental stress: Structural changes for survival

Types of Cellular Adaptation

Hypertrophy

An increase in the size of cells, leading to an increase in the size of the organ. No new cells are formed, they just get bigger.

  • Causes: Increased functional demand (e.g., muscle exercise), Hormonal stimulation (e.g., uterus in pregnancy).
Hyperplasia

An increase in the number of cells in an organ or tissue. It occurs in cells capable of division.

  • Causes: Hormonal (e.g., endometrium in pregnancy), Compensatory (e.g., liver regeneration), Pathological (e.g., prostate hyperplasia).
Atrophy

A decrease in the size and function of cells, leading to a decrease in organ size.

  • Causes: Disuse (e.g., immobilization), Loss of nerve supply, Decreased blood supply, Malnutrition, Aging.
Metaplasia

A reversible replacement of one differentiated cell type by another that is better suited to stress.

  • Examples: Squamous metaplasia of bronchial epithelium in smokers; Barrett’s esophagus (squamous to columnar epithelium due to acid reflux).
Dysplasia

(Sometimes considered under adaptation, but is actually a premalignant change)

Disordered growth and loss of cell uniformity.

  • Example: Cervical dysplasia (due to HPV infection).

Key Gastrointestinal Disorders

IBS vs. IBD: A Detailed Comparison

AspectIBS (Irritable Bowel Syndrome)IBD (Inflammatory Bowel Disease)
DefinitionA functional bowel disorder with no structural damage.Chronic inflammation of the GI tract with structural damage present.
CauseExact cause is unknown; multifactorial. Includes altered gut-brain interaction, stress, anxiety, depression, and altered gut motility & microbiota.Immune-mediated inflammation (autoimmune origin) due to genetic predisposition, environmental triggers (diet, smoking, infections), and an abnormal immune response to gut flora.
SymptomsAbdominal pain, cramping, bloating, gas, alternating constipation & diarrhea, and relief after defecation.Persistent diarrhea (may be bloody), abdominal pain, rectal bleeding, weight loss, fatigue, and fever (during flares).
TypesNone (it is a functional disorder).Two main types: Crohn’s disease (anywhere in GI tract, skip lesions, transmural) and Ulcerative colitis (colon & rectum, continuous mucosal inflammation).
ComplicationsUsually no serious complications; mainly affects quality of life.Intestinal strictures, fistula, abscess, increased colon cancer risk (especially in UC), malnutrition, and anemia.
DiagnosisDiagnosis of exclusion based on Rome IV criteria (recurrent pain ≥1 day/week for the last 3 months, related to defecation or change in stool frequency/form).Blood tests (anemia, ↑CRP, ESR), stool test (calprotectin), colonoscopy with biopsy (definitive), and imaging (CT/MRI enterography).
PrognosisBenign, with no effect on life expectancy. Managed with diet, lifestyle changes, and stress reduction. Good prognosis overall.Chronic, relapsing-remitting disease. May need long-term immunosuppressive therapy or surgery. Prognosis depends on severity and complications.

Common Urinary System Conditions

Urinary Tract Infection (UTI)

A UTI is an infection of any part of the urinary tract (kidneys, ureters, bladder, urethra), usually caused by bacteria.

Causes and Risk Factors

  • Bacteria: E. coli (80–90%), Klebsiella, Proteus, Enterococcus.
  • Anatomical factors: Short female urethra, urinary tract obstruction.
  • Functional causes: Incomplete bladder emptying, neurogenic bladder.

Symptoms

  • Lower UTI (Cystitis):
    • Burning urination (Dysuria)
    • Increased frequency & urgency
    • Suprapubic pain
    • Cloudy or foul-smelling urine
    • Hematuria (blood in urine)
  • Upper UTI (Pyelonephritis):
    • Fever with chills
    • Flank (loin) pain
    • Nausea, vomiting
    • Costovertebral angle tenderness

Complications

  • Recurrent infections
  • Pyelonephritis leading to renal scarring, hypertension
  • Sepsis (urosepsis)
  • Renal abscess
  • Chronic kidney disease
  • In pregnancy: Preterm labor, low birth weight

Diagnosis

  • Urine routine & microscopy: Shows pus cells, bacteria.
  • Urine culture: Definitive diagnosis (≥10⁵ CFU/mL is significant).
  • Dipstick tests: Positive for Nitrite & leukocyte esterase.
  • Blood tests: CBC, CRP (if severe infection).
  • Ultrasound/CT: In complicated or recurrent cases.

Prognosis

Simple UTIs have a good prognosis with antibiotics. Recurrent or complicated UTIs carry a risk of chronic damage and renal failure if untreated. Early detection and proper treatment lead to an excellent outcome.

Medical Procedures: Hemodialysis

What is Hemodialysis?

Hemodialysis is a medical procedure in which waste products (urea, creatinine, toxins) and excess fluid are removed from the blood using a machine and an artificial membrane when the kidneys fail to function adequately.

Indications for Hemodialysis

  • Chronic Kidney Disease
  • Acute Renal Failure
  • Severe Metabolic Acidosis
  • Hyperkalemia
  • Fluid overload
  • Uremic symptoms

The Hemodialysis Procedure

  1. Blood is taken out of the patient through a vascular access.
  2. The blood passes through a machine called a dialyzer.
  3. The dialyzer contains a semipermeable membrane: one side has blood, the other has dialysis fluid (dialysate).
  4. Through diffusion and ultrafiltration, wastes and extra water move out of the blood into the dialysate.
  5. The cleaned blood is then returned to the patient’s body.

Potential Complications

  • Hypotension
  • Muscle cramps
  • Infection
  • Electrolyte imbalance
  • Headache, nausea, vomiting
  • Long-term: Anemia, renal bone disease

Ayurvedic Perspectives on Common Ailments

मूत्रकृच्छ्र (Mutrakrichhra) – Painful Urination

Definition: “कृच्छ्रेण मूत्रस्य निष्क्रमणं मूत्रकृच्छ्र” – The difficult, painful, or distressing excretion of urine.

निदान (Causes)

  • Excessive consumption of alcohol, oil, meat, alkaline, sour, and pungent foods.
  • Excessive or forced sexual intercourse.
  • Urinary tract infection.
  • Suppression of the urge to urinate, excessive swimming, staying awake at night.
  • Cold environment and diet that aggravates Vata dosha.

संप्राप्ति (Pathogenesis)

Consumption of causative factors → Aggravation of doshas (especially Vata-Pitta) → Vitiation of Mutravaha Srotas (urinary channels) and Dushyas (blood, urine, mucus) → Localization in the bladder/urinary tract → Inflammation, burning, pain → Difficult urination (Mutrakrichhra).

भेद (Types)

According to Charaka Samhita, there are 8 types, including Vataja, Pittaja, Kaphaja, Ashmarija (due to stones), Shukraja (due to semen), Sannipataja (tridoshic), and others.

लक्षण (Symptoms)

  • Difficulty in passing urine.
  • Severe pain and burning sensation during urination.
  • Frequent but scanty urination.
  • Inflammation in the urinary tract, blood in urine.
  • Fever, colic, and flank pain (in upper tract involvement).

मूत्रघात (Mutraghata) – Urinary Obstruction

निदान (Causes)

  • Excessive intake of heavy, channel-blocking, and unctuous food.
  • Lack of exercise.
  • Vata-aggravating factors like staying awake at night, fasting, excessive physical labor.
  • Excessive use of cold water or cold food.
  • Pain or obstruction in the urinary passage.

सम्प्राप्ति (Pathogenesis)

Consumption of causative factors → Aggravation of doshas (mainly Vata and Kapha) → Constriction/obstruction in the Mutravaha Srotas (urinary channels) → Obstruction of urine flow → Mutraghata (retention, obstruction, and pain).

भेद (Types)

Includes Vatakundalika, Vatavasthi, Mutrotsanga, Mutrajathara, and others.

लक्षण (Symptoms)

  • Retention of urine, difficulty in urination.
  • Pain, passing small amounts of urine, or intermittent flow.
  • Heaviness in the abdomen.
  • Excessive pain and effort to urinate.

परिणामशूल (Parinamasula) – Duodenal Ulcer Pain

Definition: Pain that arises during the digestion of food (3-4 hours after a meal). It is primarily a Vata-Pitta disorder.

निदान (Causes)

  • Excessive fasting, acidic diet.
  • Irregular meals.
  • Overexertion, mental stress.

सम्प्राप्ति (Pathogenesis)

During the final stage of food digestion, when digestive fire (Jatharagni) is intense, aggravated Vata and Pitta cause pain in the stomach and duodenum.

लक्षण (Symptoms)

  • Severe pain 3-4 hours after eating.
  • Symptoms of hyperacidity (Amlapitta).
  • Pain intensifies with hunger.
  • Pain is relieved by eating food.

Modern Correlation: Peptic ulcer disease.

अन्नद्रवशूल (Annadravasula) – Gastric Ulcer Pain

Definition: Pain that arises immediately after consuming food. It is primarily a Kapha-Pitta disorder.

निदान (Causes)

  • Consumption of heavy, unctuous, and dairy-rich foods.
  • Overeating.
  • Weak digestive fire (Mandagni), Kapha obstruction.

सम्प्राप्ति (Pathogenesis)

Upon eating, Kapha and Pitta increase in the stomach, weakening the digestive fire. The food stagnates, causing pain.

लक्षण (Symptoms)

  • Pain immediately after eating.
  • Indigestion, heaviness.
  • Nausea, loss of appetite, abdominal fullness.

कामला (Kamala) – Jaundice

निदान (Causes)

  • Excessive intake of heavy, unctuous, and Pitta-aggravating foods.
  • Consumption of alcohol, meat, curd, and oily substances.
  • Liver disorders caused by contaminated water/food.
  • Anger, mental stress, staying awake at night.
  • Diseases of the liver/spleen, obstruction in the bile duct.

सम्प्राप्ति (Pathogenesis)

Causative factors → Aggravation of Pitta dosha → Vitiation of Rasa and Rakta Dhatu (plasma and blood tissues) → Liver and spleen disorders → Excessive circulation of Pitta in the blood → Yellow discoloration of blood, skin, and eyes → Yellow urine and pale stools → Kamala (Jaundice).

भेद (Types)

Koshthashakhashrita Kamala, Koshthashrita Kamala, Shakhashrita Kamala.

लक्षण (Symptoms)

  • Yellow discoloration of skin, eyes, nails, and face.
  • Dark yellow/red urine.
  • Pale-colored stool.
  • Fever, anorexia, vomiting, thirst.
  • Weakness, lethargy, and heaviness in the body.

आमवात (Amavata) – Rheumatoid Arthritis

निदान (Causes)

  • Consumption of heavy, uncooked, sour, and channel-blocking foods.
  • Incompatible food combinations.
  • Excessive intake of curd, meat, jaggery, etc.
  • Vigorous exercise after consuming an incompatible diet.
  • Vata-aggravating factors like fasting and staying awake at night.
  • Indigestion leads to the formation of Ama (toxins), which combines with Vata to cause Amavata.

सम्प्राप्ति (Pathogenesis)

Weak digestive fire → Formation of Ama → Combination of Ama and Vata → Joint pain, stiffness, swelling → Accumulation of Ama in joints, causing pain throughout the body.

लक्षण (Symptoms)

  • Body ache, anorexia, thirst, lethargy, heaviness.
  • Fever, indigestion, joint pain, joint swelling.
  • Stiffness in the body, excessive salivation, weak digestion.
  • Difficulty in walking.

पाण्डुरोग (Panduroga) – Anemia

निदान (Causes)

  • Excessive intake of unctuous, heavy, sour, and salty foods, and alcohol.
  • Overexertion, staying awake at night, mental stress.
  • Diet causing Ama formation, worm infestation, blood loss.
  • Excessive sexual activity and depletion of tissues (Dhatu Kshaya).

सम्प्राप्ति (Pathogenesis)

Causative factors → Aggravation of doshas (especially Pitta and Vata) → Weak digestive fire → Vitiation of Rasa and Rakta Dhatu → Discoloration (pale, yellow, greenish), depletion of Ojas (vital essence) and strength, leading to Panduroga.

भेद (Types)

Vataja, Pittaja, Kaphaja, Sannipataja (tridoshic), and Mridbhakshanaja (due to eating clay).

लक्षण (Symptoms)

  • Pale or whitish discoloration of skin, eyes, nails, and lips.
  • Weakness of the heart, shortness of breath.
  • Heaviness, drowsiness, lethargy, loss of strength, emaciation.
  • Excessive sweating, fever, body ache, spleen enlargement.
  • Habit of eating clay (especially in Mridbhakshanaja Pandu).

ग्रहणी (Grahani) – Malabsorption Syndrome / IBS

निदान (Causes)

  • Overeating, eating during indigestion.
  • Consuming heavy, cold, and hard-to-digest food.
  • Irregular diet and lifestyle.
  • Anxiety, grief, anger, etc.

सम्प्राप्ति (Pathogenesis)

Causative factors → Weak digestive fire (Agnimandya) → Indigestion → Aggravation of doshas (Pitta and Vata) → Weakening of the Grahani (duodenum/small intestine) → Undigested food passes out → Manifestation of disease symptoms.

भेद (Types)

Vataja, Pittaja, Kaphaja, Sannipataja, and Amaja.

लक्षण (Symptoms)

  • Passage of undigested food in stool.
  • Weak digestion, anorexia.
  • Irregular bowel movements (sometimes loose, sometimes hard).
  • Abdominal pain, belching, weakness, emaciation.
  • Colic, thirst, excessive sweating, burning sensation in the cardiac region.