Vitamin B1 (Thiamine)

 Sources: Whole grains, pork, legumes, nuts

 Functions:
o Coenzyme in carbohydrate metabolism (as TPP)
o Nerve impulse conduction
 Deficiencies:
o Beriberi (wet: cardiovascular, dry: neurological)
o Wernicke-Korsakoff syndrome (mainly in alcoholics)
o Fatigue and irritability

Vitamin B2 (Riboflavin)

 Sources: Milk, eggs, green leafy vegetables

 Functions:
o Coenzyme in redox reactions (FAD, FMN)
o Supports skin and eye health
 Deficiencies:
o Cheilitis (cracked lips)
o Glossitis (inflamed tongue)
o Corneal vascularization

Vitamin B3 (Niacin)

 Sources: Meat, fish, peanuts, whole grains

 Functions:
o Coenzyme in redox reactions (NAD, NADP)
o Supports DNA repair and stress response
 Deficiencies:
o Pellagra (diarrhea, dermatitis, dementia)
o Weakness
o Mental confusion

Vitamin B5 (Pantothenic Acid)

 Sources: Meat, whole grains, legumes

 Functions:
o Component of Coenzyme A (CoA)
o Fatty acid metabolism
 Deficiencies:
 o Fatigue
o Burning foot syndrome
o Nausea and cramps

Vitamin B6 (Pyridoxine)

 Sources: Poultry, fish, bananas, fortified cereals

 Functions:
o Amino acid metabolism (transamination)
o Neurotransmitter synthesis
 Deficiencies:
o Peripheral neuropathy
o Sideroblastic anemia
o Irritability and depression

Vitamin B7 (Biotin)

 Sources: Egg yolk, liver, nuts

 Functions:
o Coenzyme in carboxylation reactions
o Fatty acid synthesis
 Deficiencies:
o Dermatitis
o Hair loss (alopecia)
o Neurological issues (depression, hallucination)

Vitamin B9 (Folate)

 Sources: Leafy greens, legumes, fortified grains

 Functions:
o DNA synthesis and repair
o Red blood cell formation
 Deficiencies:
o Megaloblastic anemia
o Neural tube defects in fetus
o Fatigue

Vitamin B12 (Cobalamin)

  Sources: Animal products (meat, dairy, eggs)
 Functions:
o DNA synthesis
o Maintenance of myelin sheath
 Deficiencies:
o Pernicious anemia
o Neuropathy
o Glossitis

Vitamin C (Ascorbic Acid)

 Sources: Citrus fruits, strawberries, bell peppers

 Functions:
o Collagen synthesis
o Antioxidant activity
 Deficiencies:
o Scurvy (bleeding gums, poor wound healing)
o Anemia (due to iron absorption issues)
o Fatigue

Vitamin A (Retinol)

 Sources: Liver, dairy, orange vegetables (carrots, sweet potatoes)

 Functions:
o Vision (component of rhodopsin)
o Epithelial cell maintenance
 Deficiencies:
o Night blindness
o Xerophthalmia (dry eyes)
o Increased infection risk

Vitamin D (Cholecalciferol/D2-D3)

 Sources: Sunlight, fortified dairy, fish liver oils

 Functions:
o Calcium and phosphate homeostasis
o Bone mineralization
 Deficiencies:
o Rickets (in children)
o Osteomalacia (in adults)
 o Hypocalcemia

Vitamin E (Tocopherol)

 Sources: Nuts, seeds, vegetable oils

 Functions:
o Antioxidant (protects cell membranes)
o Immune support
 Deficiencies:
o Hemolytic anemia (in newborns)
o Neuromuscular problems (ataxia)
o Retinopathy

Vitamin K

 Sources: Leafy greens, broccoli, gut microbiota

 Functions:
o Synthesis of clotting factors (II, VII, IX, X)
o Bone metabolism (via osteocalcin)
 Deficiencies:
o Bleeding/hemorrhage
o Easy bruising
o Osteopenia

Roles in Chronic Disease Development:

Nutrigenomics

 Explores how diet can activate or suppress genes linked to chronic diseases.
 Examples:
o Diets rich in polyphenols (like green tea, berries) may downregulate genes linked
to inflammation and cancer.
o High-fat diets can upregulate genes related to insulin resistance and obesity.

Nutrigenetics

 Helps identify individuals genetically predisposed to conditions based on how they

metabolize certain nutrients.
 Examples:
 o Individuals with APOE4 gene variant are more sensitive to saturated fat intake,
increasing risk of cardiovascular disease.
o Lactose intolerance from variations in the LCT gene affects dairy digestion and
dietary planning.

Their Combined Role in Chronic Disease:

Disease Nutrigenomics Role Nutrigenetics Role

Diet affects expression of fat FTO gene variants linked to higher
Obesity
storage/metabolism genes obesity risk
Sugar-rich diets influence insulin TCF7L2 gene variant increases
Type 2 Diabetes
gene expression diabetes risk
Cardiovascular Diets high in trans fats alter APOE polymorphisms affect lipid
Disease cholesterol metabolism genes metabolism and heart disease risk
Cruciferous vegetables may activate Variants in detoxifying enzymes (e.g.,
Cancer
tumor suppressor genes GST genes) affect cancer risk

Nutrigenomics vs. Nutrigenetics:

Aspect Nutrigenomics Nutrigenetics
Study of how diet affects gene Study of how genetic variations
Definition
expression affect response to diet
Influence of nutrients on genome, How individual genes influence
Focus
transcriptome, proteome nutritional needs or disease risk
Understand how diet modifies Personalize diets based on genetic
Goal
genetic function makeup
Omega-3 fatty acids reducing A person with MTHFR mutation
Example
inflammation-related genes requiring more folate

Clinical Application & Importance:

 Enables personalized nutrition (precision diet plans).

 Prevents or manages chronic diseases through targeted dietary interventions.
 Encourages early screening for genetic risks.
 Promotes healthier lifestyle choices based on genetic predisposition.
Genome-nutrient interaction disorders are conditions that result from the way specific genes
interact with dietary nutrients, leading to health problems. These interactions can cause
nutrient metabolism issues or increase disease risk depending on genetic mutations or
polymorphisms.

Here are key examples of genome-nutrient interaction disorders:

1. Phenylketonuria (PKU)

 Gene Involved: PAH gene (phenylalanine hydroxylase)

 Nutrient Affected: Phenylalanine (an amino acid)
 Mechanism: Mutation in PAH leads to inability to convert phenylalanine into tyrosine.
 Effect: Phenylalanine builds up, causing brain damage if untreated.
 Dietary Management: Strict low-phenylalanine diet; avoid high-protein foods.

2. Lactose Intolerance

 Gene Involved: LCT gene (lactase)

 Nutrient Affected: Lactose (milk sugar)
 Mechanism: Reduced expression of the LCT gene leads to decreased lactase enzyme.
 Effect: Inability to digest lactose, leading to bloating, gas, diarrhea.
 Dietary Management: Avoid dairy or use lactose-free products or lactase supplements.

3. Celiac Disease

 Gene Involved: HLA-DQ2 and HLA-DQ8

 Nutrient Affected: Gluten (protein found in wheat, barley, rye)
 Mechanism: Autoimmune reaction to gluten causes inflammation and damage in the
small intestine.
 Effect: Malabsorption, diarrhea, weight loss, anemia, nutrient deficiencies.
 Dietary Management: Strict gluten-free diet.

4. Hereditary Hemochromatosis

 Gene Involved: HFE gene (most commonly C282Y mutation)

 Nutrient Affected: Iron
  Mechanism: Increased iron absorption from the intestine despite adequate levels.
 Effect: Iron overload → liver cirrhosis, diabetes, heart disease.
 Dietary Management: Avoid iron supplements, reduce red meat intake, therapeutic
phlebotomy.

5. MTHFR Mutation (Methylenetetrahydrofolate Reductase)

 Gene Involved: MTHFR gene (e.g., C677T variant)

 Nutrient Affected: Folate (Vitamin B9) and Vitamin B12
 Mechanism: Poor folate metabolism → impaired DNA methylation and homocysteine
buildup.
 Effect: Increased risk of neural tube defects, cardiovascular disease, and miscarriages.
 Dietary Management: Supplementation with methylated folate and B12.

6. Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency

 Gene Involved: G6PD gene

 Nutrient/Trigger Affected: Fava beans, certain drugs, oxidative foods
 Mechanism: Reduced G6PD enzyme causes red blood cells to break down under
oxidative stress.
 Effect: Hemolytic anemia
 Dietary Management: Avoid trigger foods (like fava beans) and certain medications.

Nutrient
Disorder Gene Effect Management
Involved
Phenylketonuria Brain damage Low-phenylalanine
PAH Phenylalanine
(PKU) from buildup diet
GI discomfort,
Lactose Intolerance LCT Lactose Lactose-free diet
bloating
HLA-
Celiac Disease Gluten Intestinal damage Gluten-free diet
DQ2/DQ8
Hereditary Limit iron,
HFE Iron Iron overload
Hemochromatosis phlebotomy
Neural tube Methylated folate, B12
MTHFR Mutation MTHFR Folate, B12
defects, CVD risk supplements
Fava beans,
G6PD Deficiency G6PD Hemolytic anemia Avoid triggers
oxidants
🔷 PURINE BIOSYNTHESIS

Purines (adenine & guanine) are built on a ribose phosphate scaffold.

Key Enzymes:

1. PRPP Synthetase (Ribose Phosphate Pyrophosphokinase)

o Function: Converts ribose-5-phosphate to PRPP (phosphoribosyl
pyrophosphate).
o Regulation: Activated by Pi, inhibited by purine nucleotides.
2. Amidophosphoribosyltransferase
o Function: Converts PRPP to 5-phosphoribosylamine (committed step).
o Regulation: Inhibited by AMP, GMP.
3. GAR Synthetase, FGAR Amidotransferase, etc.
o Function: Multi-step additions to build the purine ring on PRPP.
o (GAR = glycinamide ribonucleotide, FGAR = formylglycinamidine
ribonucleotide)
4. Adenylosuccinate Synthetase
o Function: Converts IMP to AMP precursor.
o Regulation: Feedback inhibition by AMP.
5. IMP Dehydrogenase
o Function: Converts IMP to XMP → precursor to GMP.
o Inhibition: Target of immunosuppressive drug mycophenolate mofetil.

🔶 PYRIMIDINE BIOSYNTHESIS

Pyrimidines (cytosine, thymine, uracil) are synthesized first, then attached to ribose phosphate.

Key Enzymes:

1. Carbamoyl Phosphate Synthetase II (CPS II)

o Function: Forms carbamoyl phosphate from glutamine, CO₂, and ATP.
o Location: Cytosol
o Regulation: Inhibited by UTP, activated by PRPP.
2. Aspartate Transcarbamoylase (ATCase)
o Function: Combines carbamoyl phosphate with aspartate → carbamoyl
aspartate.
3. Dihydroorotase
o Function: Cyclizes carbamoyl aspartate → dihydroorotate.
4. Dihydroorotate Dehydrogenase
o Function: Converts dihydroorotate to orotate.
o Unique: Occurs in mitochondria (rest are cytosolic).
5. OMP Decarboxylase (in bifunctional UMP synthase)
o Function: Converts orotidine monophosphate (OMP) → UMP.
Conversion Enzymes (Shared)

 Ribonucleotide Reductase: Converts ribonucleotides (NDPs) → deoxyribonucleotides

(dNDPs).
 Thymidylate Synthase: Converts dUMP → dTMP (requires folate).
 PRPP Amidotransferase: Common to both purine and pyrimidine pathways indirectly
via PRPP availability.

Pathway Key Enzymes Notes

PRPP synthetase, Amidophosphoribosyltransferase,
Built on PRPP
Purine Synthesis GAR synthetase, IMP dehydrogenase,
directly
Adenylosuccinate synthetase
Pyrimidine CPS II, ATCase, Dihydroorotase, Dihydroorotate Ring made first, then
Synthesis dehydrogenase, UMP synthase added to PRPP
For deoxynucleotide
Shared/Conversion Ribonucleotide reductase, Thymidylate synthase
production

🦴 CALCIUM (Ca²⁺)

1. Sources

 Dairy: Milk, cheese, yogurt

 Fish: Sardines, salmon (with bones)
 Vegetables: Broccoli, kale, bok choy
 Fortified foods: Orange juice, cereals
 Supplements: Calcium carbonate, calcium citrate

2. Absorption

 Location: Mainly in the duodenum and proximal jejunum

 Regulation:
o Enhanced by Vitamin D (calcitriol)
o Affected by age, estrogen, and stomach acidity

3. Functions
  Bone and teeth formation (99% stored in bones as hydroxyapatite)
 Muscle contraction
 Nerve impulse transmission
 Blood clotting (cofactor in coagulation)
 Enzyme cofactor in many reactions

4. Regulation

 Parathyroid Hormone (PTH):

o Increases blood calcium by:
 Stimulating bone resorption
 Increasing renal reabsorption
 Activating Vitamin D (↑ intestinal absorption)
 Vitamin D (Calcitriol):
o Increases calcium absorption from the gut
 Calcitonin:
o Lowers blood calcium by inhibiting bone resorption

5. Deficiency

 Causes: Vitamin D deficiency, hypoparathyroidism, malabsorption

 Effects:
o Children: Rickets (soft bones)
o Adults: Osteomalacia, osteoporosis
o Tetany (muscle spasms, cramps)
o Seizures in severe cases

6. Toxicity (Hypercalcemia)

 Causes: Hyperparathyroidism, excess Vitamin D, malignancy

 Effects:
o Nausea, vomiting, constipation
o Kidney stones
o Mental confusion
o Cardiac arrhythmias

7. Clinical Notes
  Hypocalcemia: Low serum calcium → Chvostek’s & Trousseau’s signs
 Osteoporosis: Treated/prevented with calcium + vitamin D

🩸 IRON (Fe)

1. Sources

 Heme Iron (better absorbed): Meat, poultry, fish

 Non-Heme Iron: Legumes, spinach, whole grains, nuts
 Fortified cereals, molasses

2. Absorption

 Location: Duodenum (mostly)

 Enhanced by:
o Vitamin C (reduces Fe³⁺ to Fe²⁺)
o Acidic pH
 Inhibited by:
o Phytates (grains)
o Oxalates (spinach)
o Calcium, tannins (tea)

3. Functions

 Hemoglobin (Hb): Oxygen transport in blood

 Myoglobin: Oxygen storage in muscle
 Cytochromes: Electron transport chain (ATP production)
 Enzymes: Catalase, peroxidase

4. Regulation

 Hepcidin (liver hormone):

o ↓ Iron absorption & release from stores
o Increased during inflammation or iron overload
 Ferritin: Storage form of iron
 Transferrin: Transport protein in blood
5. Deficiency

 Causes: Chronic blood loss, poor intake, pregnancy, malabsorption

 Effects:
o Iron-deficiency anemia (microcytic, hypochromic)
o Fatigue, pallor, breathlessness
o Koilonychia (spoon nails), Pica (craving non-food)
o Restless leg syndrome

6. Toxicity (Iron Overload)

 Acute: Accidental overdose → vomiting, GI bleeding, shock

 Chronic: Hemochromatosis (genetic or transfusion-related)
o Iron deposits in liver, pancreas, heart → cirrhosis, diabetes, cardiomyopathy

7. Clinical Notes

 Iron studies:
o Serum ferritin: Storage (↓ in deficiency, ↑ in inflammation)
o TIBC: ↑ in deficiency
o Transferrin saturation: ↓ in deficiency
 Iron therapy:
o Oral: Ferrous sulfate
o IV: Ferric carboxymaltose (when oral fails or rapid correction needed)

Feature Calcium (Ca²⁺) Iron (Fe)

Main Sources Dairy, leafy greens, fortified foods Meat, legumes, fortified grains
Main Role Bones, nerves, muscle, clotting Oxygen transport (Hb), enzymes
Absorbed In Duodenum, jejunum Duodenum
Enhanced By Vitamin D Vitamin C, low pH
Stored As In bones Ferritin (in liver, spleen, marrow)
Deficiency Effects Rickets, osteoporosis, tetany Microcytic anemia, fatigue
Toxicity Effects Kidney stones, confusion, arrhythmias Liver damage, diabetes, organ failure
🥦 Nutrition and Disease: Overview

Nutrition refers to the intake of food and nutrients required for growth, maintenance, and health.
Poor nutrition — whether due to deficiency, excess, or imbalance — is a major risk factor for
numerous diseases, especially chronic non-communicable diseases (NCDs).

🔄 How Nutrition Affects Disease

1. Malnutrition

 Undernutrition: Inadequate intake of calories, protein, or micronutrients.

 Overnutrition: Excess intake of calories, fat, sugar, or specific nutrients.
 Imbalanced nutrition: Disproportionate intake (e.g., high carbs, low fiber).

2. Mechanisms of Disease Development

 Nutrient deficiency → impaired cellular function, immunity, development

 Oxidative stress from poor diet → DNA damage, aging, cancer
 Inflammation triggered by excess fat/sugar → chronic diseases
 Hormonal disruption (e.g., insulin resistance from high sugar)

🩺 Diseases Related to Nutrition

🔹 1. Nutrient Deficiency Disorders

Nutrient Disease Symptoms

Iron Iron-deficiency anemia Fatigue, pallor, pica
Vitamin D Rickets (children), Osteomalacia Bone pain, deformities
Vitamin A Night blindness, xerophthalmia Vision loss, dry eyes
Iodine Goiter, cretinism Thyroid enlargement, mental retardation
Protein Kwashiorkor, marasmus Edema, wasting

🔹 2. Non-Communicable Diseases (NCDs)

a. Cardiovascular Disease (CVD)

 Caused by: High saturated fats, trans fats, salt, low fiber
 Nutritional role: Omega-3 fats, fruits, and vegetables reduce risk
 Related conditions: Hypertension, atherosclerosis, stroke
b. Type 2 Diabetes Mellitus

 Caused by: Excess sugar intake, obesity, high glycemic index foods
 Prevention: Low GI diet, fiber, weight control, physical activity

c. Obesity

 Energy intake > energy expenditure

 Leads to: Diabetes, hypertension, CVD, sleep apnea, fatty liver

d. Cancer

 Linked to: Low antioxidants, high red/processed meats, alcohol

 Diets rich in fruits, vegetables, and fiber are protective

e. Osteoporosis

 Inadequate calcium and vitamin D

 Leads to fragile bones, fractures, especially in the elderly

🔹 3. Infectious Disease and Immunity

 Undernutrition → weak immune system → increased susceptibility to infections like:

o Tuberculosis
o HIV/AIDS
o Respiratory infections
 Nutrients like vitamins A, C, E, zinc, selenium support immunity

🔹 4. Mental and Cognitive Disorders

 Omega-3 fatty acids, B vitamins, iron essential for brain health

 Deficiencies linked to:
o Depression
o Cognitive decline
o Developmental delays in children

🧬 Role of Nutrigenomics & Nutrigenetics

 Study of how genes interact with nutrients

 Explains individual differences in disease risk based on diet
  Example: MTHFR gene mutation → need for methylated folate

🏥 Clinical Nutrition in Disease Management

 Used to prevent, treat, or manage disease through diet:

o Medical nutrition therapy for diabetes
o Renal diets (low protein, sodium, potassium)
o Cancer patients may need high-calorie, high-protein diets

🌍 Public Health and Nutrition

 Nutritional policies to prevent disease:

o Fortification (iodized salt, folic acid in grains)
o Food labeling laws
o School feeding programs
o Obesity prevention campaigns

🔑 Summary Table
Aspect Examples/Details
Nutrient Deficiencies Anemia, Rickets, Goiter, Night blindness
Diet-related NCDs Obesity, Diabetes, Heart Disease, Cancer
Infectious Diseases Malnutrition weakens immunity → TB, HIV, diarrhea
Brain Health B12, Omega-3, Iron, Folate → affect cognition and mood
Prevention Strategies Balanced diet, physical activity, supplementation, public health policies

1. De Novo vs. Salvage Pathway of Nucleotide Synthesis + Hyperuricemia + Nutrigenomics

A. Five Differences Between De Novo and Salvage Pathways of Nucleotide Synthesis

 Feature De Novo Pathway Salvage Pathway
Synthesizes nucleotides from scratch
1. Starting Uses preformed bases/nucleosides
(CO₂, NH₃, amino acids, ribose-5-
Material from degraded DNA/RNA
phosphate)
2. Energy Highly energy-intensive (many ATP
Less energy-demanding
Requirement equivalents used)
3. Enzymes Involves multiple enzymes (e.g. PRPP
Key enzymes: HGPRT, APRT
Involved synthetase, amidotransferase)
Predominates in rapidly dividing cells Found in most tissues, especially
4. Occurrence
(e.g. cancer, embryonic) brain
5. Clinical Targeted by anticancer drugs (e.g. Defects lead to diseases like
Relevance methotrexate, 5-FU) Lesch-Nyhan syndrome
B. Two Diseases Associated with Hyperuricemia

1. Gout:
oA metabolic disorder characterized by elevated serum uric acid levels.
oMonosodium urate crystals deposit in joints, leading to acute inflammatory
arthritis—commonly at the big toe (podagra).
o Risk factors include alcohol, red meat, obesity, and purine-rich foods.
2. Lesch-Nyhan Syndrome:
o X-linked recessive disorder caused by deficiency of HGPRT enzyme in the
salvage pathway.
o Results in accumulation of uric acid, neurologic symptoms, and self-mutilation
behaviors.
o Characterized by hyperuricemia, aggressive behavior, intellectual disability.

C. Biochemical Mechanism of Allopurinol in Hyperuricemia Treatment

 Allopurinol is a structural analog of hypoxanthine.

 It inhibits xanthine oxidase, the enzyme that catalyzes:
o Hypoxanthine → Xanthine → Uric Acid.
 By blocking this step, it:
o Reduces uric acid formation.
o Increases levels of more soluble xanthine/hypoxanthine (easily excreted).
 Especially useful in gout and Lesch-Nyhan syndrome management.

D. Five Principles of Nutrigenomics

1. Genotype Influences Nutrient Response: Each person’s genetic makeup affects how
they metabolize and respond to nutrients.
2. Nutrients Affect Gene Expression: Nutrients and bioactive food compounds can switch
genes on or off.
 3. Diet-Gene Interaction: The interaction of diet with the genome can influence disease
risk and health outcomes.
4. Personalized Nutrition: Nutrition should be tailored based on genetic predisposition to
optimize health.
5. Epigenetic Modifications: Diet can cause heritable changes in gene expression without
altering the DNA sequence.

E. Applications of Nutrigenomics

1. Personalized Diet Plans to prevent chronic diseases like diabetes, hypertension, or

obesity.
2. Identification of Disease Risk based on nutrient-gene interactions (e.g., folate
metabolism & MTHFR gene).
3. Targeted Therapy using food as medicine in metabolic syndromes.

2. Thiamine Deficiency, Wernicke-Korsakoff, Vit C Functions, B12 Deficiency

A. Thiamine (Vitamin B1) Deficiency

 Thiamine is essential for carbohydrate metabolism.

 Coenzyme for:
o Pyruvate dehydrogenase (PDH)
o α-ketoglutarate dehydrogenase (TCA cycle)
o Transketolase (PPP)
 Deficiency States:
o Dry Beriberi: Peripheral neuropathy, muscle wasting.
o Wet Beriberi: High-output heart failure, edema.
o Wernicke-Korsakoff syndrome: Classic in chronic alcoholism.

B. Wernicke-Korsakoff Syndrome

 Caused by severe thiamine deficiency, especially in alcoholics.

 Two-phase disorder:
o Wernicke's encephalopathy (acute): Confusion, ataxia, ophthalmoplegia.
o Korsakoff’s psychosis (chronic): Memory loss, confabulation.
 Pathophysiology: Damage to mammillary bodies and thalamus due to disrupted glucose
metabolism in thiamine-deficient brain.
C. Six Functions of Vitamin C (Ascorbic Acid)

1. Collagen synthesis (hydroxylation of proline/lysine)

2. Antioxidant (reduces ROS)
3. Iron absorption (keeps iron in ferrous form)
4. Catecholamine synthesis
5. Wound healing
6. Immunity enhancement

D. Drug-Induced Vitamin B12 Deficiency

 Proton pump inhibitors (PPIs) and H2 blockers reduce gastric acid → decreased B12
absorption.
 Metformin interferes with calcium-dependent absorption in ileum.
 Nitrous oxide inactivates B12 → neurological deficits.
 Chronic alcoholism and GI surgeries (e.g., gastrectomy) also reduce intrinsic factor or
absorption.

3. Protein Energy Malnutrition (PEM) and Starvation Biochemistry

A. Energy Generation in PEM

 Marasmus: Caloric deficiency.

 Kwashiorkor: Protein deficiency with adequate carbs.
 Body breaks down:
o Adipose tissue → free fatty acids
o Skeletal muscle → amino acids (gluconeogenesis)
o Liver increases ketone production, gluconeogenesis.

C. Biochemical Basis of Symptoms

 Oedema (Kwashiorkor): ↓ Plasma proteins → ↓ oncotic pressure → fluid leakage into

tissues.
 Fat Loss: Lipolysis due to energy demand.
 Muscle Wasting: Muscle catabolism for gluconeogenesis.
 Recurrent Infections: ↓ Immunoglobulin & lymphocyte production.
 Anemia: Protein deficiency → ↓ hemoglobin synthesis + micronutrient deficiency.

4. Food Preservatives and Toxicants (The “Sha YKYK” Part)

A. Food Preservatives

 Added to prolong shelf life, prevent spoilage.

 Types:
o Antimicrobials: Sodium benzoate, sorbic acid.
o Antioxidants: BHA, BHT, ascorbate.
o Chelating agents: EDTA.
 Safe in regulated amounts but long-term exposure raises safety concerns.

B. Food Toxicants

 Naturally occurring or contaminant substances harmful to health.

 Examples:
o Aflatoxins: From molds (hepatotoxic, carcinogenic)
o Cyanogenic glycosides: Cassava
o Heavy metals: Lead, mercury
 Effects include liver damage, neurotoxicity, cancer risk.

5. Minerals & Trace Elements: Calcium, Phosphorus, Sodium

A. Definitions

 Minerals: Inorganic elements required in >100 mg/day (e.g., calcium, phosphorus).

 Trace elements: Needed in smaller amounts (e.g., zinc, iron, selenium).

B. Calcium

 Background: Most abundant mineral in the body.

 Sources: Dairy, leafy greens, tofu.
 Deficiency: Rickets (children), osteomalacia, tetany.
 Adverse Effects: Kidney stones, hypercalcemia (arrhythmia, mental confusion).

C. Phosphorus

 Background: Vital for ATP, nucleic acids, bone.

 Sources: Meat, dairy, legumes.
 Deficiency: Rare, but can lead to weakness, bone pain.
 Adverse Effects: Hyperphosphatemia in renal failure → soft tissue calcification.
D. Sodium

 Background: Regulates extracellular fluid, nerve impulse.

 Sources: Salt, processed foods.
 Deficiency: Hyponatremia → confusion, seizures.
 Excess: Hypertension, cardiovascular risk.

E. Hormonal Regulation of Calcium (3 Hormones)

1. Calcitriol (Vitamin D):

o ↑ Calcium absorption from gut.
o Mobilizes Ca²⁺ from bone.
o ↑ Renal reabsorption of Ca²⁺.
2. Parathyroid Hormone (PTH):
o Stimulated by low serum calcium.
o ↑ Bone resorption.
o ↑ Renal Ca²⁺ reabsorption, ↓ phosphate reabsorption.
o Stimulates calcitriol synthesis.
3. Calcitonin:
o Secreted by thyroid C cells.
o ↓ Bone resorption (inhibits osteoclasts).
o Opposes PTH—protects against hypercalcemia.