MINERALS- Classification ,function, deficiency and sources.

MINERALS
Presenter : SARUMATHI .M

Minerals are natural compounds present and utilized within the body.
The minerals are needed by the body in small amounts and help the
body to function properly and stay strong.
Iron, calcium, potassium, and sodium are some of essentital minerals.
Body need small amounts of 16 minerals to maintain normal body
function and good health.
INTRODUCTIO
N

The 16 minerals which are
essential for human body are
1. Calcium
2. Phosphorous
3. Magnesium
4. Sodium
5. Potassium
6. Chloride
7. Sulfur
8. Iron
9. Manganese
10. Copper
11. Iodine
12. Zinc
13. Fluoride
14. Selenium
15. Chromium
16. molybdenum

MACRO MINERALS
CALCIUM
Calcium makes up between 1.5 -2 % of body
weight accounting for 1200-1600g of the
typical adult male body.
Almost 99 % of this calcium is found in the
hard tissues of the body namely the bones
and teeth. The rest is distributed in blood and
soft tissues, such as muscles,the liver and the
heart.
Calcium content of the blood plasma is
maintained within a narrow range of 9-11
mg/dl, rarely varied by more than 3 %. when
levels in the plasma begin to fall, bone
calcium is mobilized.

Sources :-
Dairy Sources (High in Calcium & Well Absorbed ✅)
🥛 Milk (Cow, Buffalo, Goat) – ~300 mg per cup
🧀 Cheese (Cheddar, Mozzarella, Parmesan)
🥣 Yogurt & Curd
🍼 Fortified Plant-Based Milk (Soy, Almond, Oat Milk – if fortified)
Plant-Based Sources 🌿 (Good for Vegans & Lactose Intolerant)
🥬 Leafy Greens (Kale, Bok Choy, Turnip Greens – High Absorption ✅)
🌰 Sesame Seeds (Til) & Tahini
🥜 Almonds & Brazil Nuts
🥦 Broccoli (Surprising but well-absorbed!)
🍊 Oranges & Figs (Good fruit sources)
🍚 Ragi (Finger Millet) – Best grain source!

Seafood Sources (Rich in Absorbable Calcium)
🐟
🐟 Sardines & Canned Salmon (with bones!)
🦐 Shrimp & Crabs
🦑 Shellfish & Oysters
Calcium-Fortified Foods 🍞 (Extra Calcium Added)
🥖 Calcium-Fortified Bread & Cereals
🥤 Fortified Juices (Orange Juice, Soy Milk, Almond Milk)
🥄 Fortified Tofu (Set with Calcium Sulfate)

Age Group Calcium Needed (mg/day)
Infants (0-12 months)
Children (1-9 yrs)
500mg
600 mg
Adolescent (10-17 yrs) 800 mg
Women 600 mg
Pregnant & Lactating
Women
1200-1300 mg

BIOAVAILABILITY:-
Bioavailability is the amount of a nutrient that is absorbed and used by the
body from food or supplements. It's a measure of how well the body can
access and use nutrients.
Bioavailability means how much calcium from food is actually absorbed
and used by our body.
Different foods have different bioavailability:
• Milk (high bioavailability) → 30-35% absorbed
→
• Spinach (low bioavailability) → Only 5% absorbed (because of oxalates)
→
• Broccoli (high bioavailability) → 50-60% absorbed
→

FUNCTION:-
1. Bone and Teeth Formation 🦴🦷
• Calcium Hydroxyapatite Formation:
• In bones and teeth, calcium combines with phosphate to form calcium
hydroxyapatite (Ca10(PO4)6(OH)2), which gives structural strength.
• Bone Remodeling:
• Bones are dynamic and continuously undergo resorption and
deposition.
• Osteoblasts (bone-forming cells) deposit calcium in bones.
• Osteoclasts (bone-resorbing cells) release calcium into the blood when
needed.
• Role of Vitamin D & Hormones:
• Vitamin D increases calcium absorption in the intestines.
• Parathyroid hormone (PTH) increases blood calcium by stimulating
osteoclasts.
• Calcitonin (from the thyroid) lowers blood calcium by inhibiting
osteoclasts.

2. Muscle Contraction 💪
Calcium and Actin-Myosin Interaction:
• Nerve signals (action potential) trigger calcium release from the
sarcoplasmic reticulum (SR) in muscle cells.
• Calcium binds to troponin, causing a conformational change.
• This moves tropomyosin, exposing binding sites on actin for myosin.
• Myosin heads attach to actin, forming cross-bridges, leading to muscle
contraction.
• When calcium is pumped back into the SR, muscles relax.
3. Nerve Transmission ⚡
Calcium in Synaptic Transmission:
• When a nerve impulse reaches the axon terminal, voltage-gated calcium
channels open.
• Calcium enters the presynaptic neuron.
• This triggers the release of neurotransmitters (e.g., acetylcholine,
dopamine, GABA) into the synaptic cleft.
• Neurotransmitters bind to receptors on the postsynaptic neuron,
propagating the signal.

4. Blood Clotting (Coagulation) 🩸
Calcium as a Coagulation Factor:
• Platelets at the injury site release signaling molecules.
• Calcium activates clotting factors (e.g., factor IV), which promote fibrin clot formation.
• Prothrombin Thrombin
→ , and Fibrinogen Fibrin
→ , forming a stable clot.
5. Enzyme Activation
Acts as a cofactor for various enzymes, such as those involved in metabolism.
6. Hormone Secretion
Regulates the release of hormones, including insulin and parathyroid hormone.
• PTH Increases blood calcium (stimulates bone resorption).
→
• Calcitonin Decreases blood calcium (promotes bone formation).
→
• Vitamin D Enhances calcium absorption from food.
→
7. Cell Signaling
Involved in intracellular signaling pathways that regulate various cellular functions.
8. Maintaining Heart Function
Helps regulate heartbeat and prevent abnormal heart rhythms.
9. Regulation of pH Balance
Works with other minerals to maintain acid-base balance in the body.

Absorbtion
Calcium is absorbed by two distinct
mechanism,
• Passive diffusion
• Active transport
Type Energy Needed?
Vitamin D
Required?
Where It Happens?
When It
Happens?
Active
Transport
✅ Yes (ATP needed) ✅ Yes
Duodenum (1st part of
intestine)
When
calcium is
low
Passive
Diffusion
❌ No (happens
naturally)
❌ No
Jejunum & Ileum (later
parts of intestine)
When
calcium is
high

• In normal adult, 95% of calcium from a
low calcium diet is absorbed by the
active process
• On an average 30-40 percent of the
dietary calcium is absorbed in adults.
Growing children, pregnant and
lactating women absorb 50-60% of
calcium.
• The efficiency of calcium absorbtion
decreases to 20-30% after 45 years of
age in women and 60 years in men.
Estrogen enhances calcium absorption
declines after menopause.
• Calcium absorbtion decreases to about
10% in elderly.

FACTORS FAVORING ABSORPTION:-
Vitamin D (from sunlight & food) ☀️
Acidic foods (like citrus fruits) 🍊
✔️
Lactose (in milk) 🥛
✔️
FACTORS DEPRESSING ABSORPTION:-
🚫Oxalates (found in spinach, tea, and chocolate) bind calcium and form calcium oxalate and
prevent absorption.
🚫 Phytates (found in whole grains, nuts, and beans) can block calcium absorption.
🚫 Too much caffeine or soda can reduce calcium levels.
🚫 High salt intake makes the kidneys flush out more calcium.
🚫Steatorrhea
🚫Emotional instability
🚫Increased gastrointestinal motility
🚫Lack of exercise
🚫Drugs - antocoagulants, cortosone, and thyroxine

Deficiency disorder
Osteoporosis
• Osteoporosis is a progressive bone disease characterized by decreased bone density and mass,
leading to fragile bones that are more prone to fractures. The condition occurs when bone
resorption (breakdown) exceeds bone formation, making bones weak and porous. It is often
called a “silent disease” because it usually has no symptoms until a fracture occurs.
• Common in postmenopausal women and elderly individuals.
Causes
• Bone mass peaks around the age of 30, after which bone resorption outpaces
formation.
• Postmenopausal women experience rapid bone loss due to decreased estrogen
levels.
• Estrogen deficiency (in postmenopausal women) and testosterone deficiency
(in men) contribute to osteoporosis.
• Hyperthyroidism and excessive thyroid hormone replacement can accelerate
bone loss.
• Parathyroid hormone (PTH) imbalance can cause increased calcium resorption
from bones.

• Lack of weight-bearing and resistance exercises weakens bones
over time.
• Prolonged bed rest or immobility accelerates bone loss.
• Chronic kidney disease (CKD) affects calcium and phosphorus
balance.
• Rheumatoid arthritis (RA) and other inflammatory conditions can
contribute to bone loss.
• Gastrointestinal disorders (e.g., celiac disease, Crohn’s disease)
reduce nutrient absorption.
• Corticosteroids (e.g., prednisone) cause bone loss by reducing
calcium absorption and increasing bone resorption.
• Prolonged use of proton pump inhibitors (PPIs) affects calcium
absorption.
• Anticonvulsants can alter vitamin D metabolism.

• Smoking interferes with bone remodeling.
• Excessive alcohol intake reduces calcium absorption.
• High caffeine and sodium intake can lead to calcium loss.

2. Osteomalacia (in Adults) & Rickets (in Children)
Osteomalacia is a metabolic bone disorder characterized by defective bone
mineralization, leading to soft and weak bones in adults. It occurs due to
insufficient calcium and phosphate deposition in the bone matrix, primarily
caused by vitamin D deficiency. This condition increases the risk of fractures,
bone pain, and muscle weakness.
Causes:-
• Inadequate Sun Exposure
• Poor Dietary Intake – Lack of vitamin D-rich foods (e.g., fish, fortified dairy,
eggs).
• Malabsorption Disorders – Conditions like celiac disease, Crohn’s disease,
cystic fibrosis, or gastric bypass surgery reduce vitamin D absorption.
• Chronic Liver Disease – The liver converts vitamin D into its active form;
dysfunction can impair this process.
• Kidney Disease – The kidneys convert vitamin D into its biologically active form
(calcitriol); renal failure leads to deficiency.

3. Hypocalcemia (Low Blood Calcium Levels)
• Symptoms: Muscle cramps, tingling in fingers, seizures, and irregular
heartbeats.
• Often caused by Vitamin D deficiency, kidney disease, or
hypoparathyroidism.
4. Tetany
• Severe muscle spasms and cramps due to very low calcium levels.
• Can cause difficulty in breathing and neurological disturbances.
5. Dental Problems
• Weak tooth enamel, delayed tooth development in children, and
increased risk of cavities.
6. Neuromuscular and Cognitive Issues
• Memory problems, depression, irritability, and confusion in severe
deficiency cases.

MINERALS- Classification ,function, deficiency and sources.

INTRODUCTION
Iron is a part of haemoglobin, the oxygen-carrying component of
the blood. Iron-defecient people tire easily because their bodies are
starved for oxygen. Iron is also part of myoglobin, which helps
muscle cells store oxygen.
Without enough iron, ATP (the fuel the body runs on) cannot be
properly synthesized. As a result ,some iron deficient people
become fatigued.

FUNCTIONS:-
1. Oxygen Transport & Storage
• Hemoglobin is the protein in red blood cells (RBCs) that carries oxygen. Each
gram of hemoglobin contains about 3.34 mg of iron.
• Iron binds to oxygen and helps transport it through the blood.
• Myoglobin is another iron-containing protein found in muscles. It stores
oxygen in muscles, so it's available when needed for energy production,
especially during exercise.
2. Role in Energy Production
• Iron is part of many enzymes that help release energy from food.
• The haeme group (iron-containing part of hemoglobin) plays a role in
breaking down nutrients and producing ATP (the body's energy molecule).
• Iron + Copper help in energy production by supporting an enzyme called
cytochrome oxidase, which is needed for cellular respiration.

3. Formation of Red Blood Cells (RBCs)
• Red blood cells are made in the bone marrow.
• Immature RBCs, called erythroblasts, grow and develop into mature RBCs.
• During this process, they:
• Make hemoglobin (which needs iron).
• Use vitamin B and copper to complete hemoglobin formation.
4. Life Cycle of Red Blood Cells
• RBCs live for 120 days and then get old or damaged.
• They are broken down in the spleen, liver, and bone marrow.
• The useful parts of RBCs are recycled:
• Iron is saved and reused to make new RBCs (stored as ferritin and
haemosiderin in the liver and spleen).
• Amino acids from the globin protein are reused to build new proteins or for
energy.
• The haeme group (non-reusable part) is converted into bilirubin, which is
excreted through bile.

ABSORBTION AND METABOLISM
Haeme iron, found in animal-based foods, is absorbed in the intestine by
specialized cells called enterocytes. After digestion, the haeme enters these cells,
where the iron is released from its haeme structure through an enzymatic process.
The released iron (in its ferrous form) quickly binds with a protein called apoferritin,
forming ferritin. Ferritin has two main roles:
• Storage: It acts as a temporary store of iron within the cell.
• Transport: It helps move the iron from the surface of the cell (brush border) to the
opposite side (basolateral membrane), where it can enter the bloodstream.
Unlike non-haeme iron, the absorption of haeme iron is not significantly affected by the
food you eat or the digestive juices. Its absorption rate is relatively high—around 25%.
In the body, most iron is recycled rather than lost. On average, only 1–3 mg of iron from
food is absorbed daily to meet the body’s needs.

ICMR Recommended Dietary Allowance of Iron
GROUP IRON (mg/day)
Man 17
Woman 21
Pregnancy 35
Lactating 25
Infants (0-12 months) 46µg/Kg
Children
1-3 years 9
4-6 years 13
7-9 years 16
Boys
10-12 years 21
13-15 years 32
16-17 years 28
Girls
10-12 years 27
13-15 years 27

Sources
Animal-Based Iron Sources
Contains heme iron (easily absorbed). Bioavailability: 15-35%.
• Red meat (e.g., beef, lamb, mutton)
• Poultry (e.g., chicken, turkey)
• Fish and seafood (e.g., salmon, tuna, shellfish like clams, oysters, and mussels – particularly
rich)
• Liver and organ meats (e.g., chicken liver, beef liver)
• Egg yolk (less than meat but still a source)
• Consuming sprouted pulses regularly increases bio-availabilty of iron. It increases the
content of vitamin C and B-Complex vitamins in the grains.
• Consuming GLV with Vitamin C increases the absorbtion of non-haeme

Plant-Based Iron Sources
Contains non-heme iron (less bioavailable, ~2-20%). Absorption improves with vitamin C or an
acidic medium.
Legumes and Pulses
• Lentils, chickpeas, black beans, kidney beans, soybeans
Whole Grains
• Quinoa, oats, brown rice, fortified cereals
Nuts and Seeds
• Pumpkin seeds, sesame seeds, flaxseeds, cashews, almonds
Vegetables
• Spinach, kale, broccoli, beet greens, Swiss chard
Dried Fruits
• Raisins, apricots, prunes
Other Sources
• Tofu, tempeh
• Dark chocolate (high cocoa percentage)

Factors Influencing Bioavailability
Enhancers (boost absorption of non-heme iron):
• Vitamin C: Citrus fruits, bell peppers, strawberries
• Organic acids: Tomatoes, vinegar
Inhibitors (reduce absorption of non-heme iron):
• Phytates: Found in whole grains, legumes
• Polyphenols: Coffee, tea, wine
• Calcium: Found in dairy products
• Oxalates: Spinach, rhubarb

Iron Deficiency Anaemia
When there is an insuffiency of iron for the formation of haemoglobin,the RBC
becomes pale ( hypochromic ) and small (microcytic) . Most common form of
anaemia affecting mainly women in their reproductive years, infants and
children.
Prevalence and Causes
• Children between the ages of 6 and 59 months, a majority (70%) are
anaemic. Nearly 75% of women in india are anaemic.
• Among pregnant women 50% are anaemic .
• Maternal deaths every year due to nuyritional anaemia is about 24%.

Causes
1. Inadequate Iron Intake:
• Poor dietary intake of iron-rich foods (e.g., vegetarians or low-income populations).
• Lack of bioavailable heme iron (found in meat, poultry, and fish).
• Exclusive breastfeeding beyond 6 months without supplementation.
2. Increased Iron Demand:
• Pregnancy and lactation: Higher iron requirements due to fetal growth and milk
production.
• Infancy and adolescence: Rapid growth phases increase demand for iron.
3. Blood Loss:
• Chronic blood loss:
• Heavy menstrual bleeding (menorrhagia).
• Gastrointestinal bleeding (e.g., ulcers, hemorrhoids, colorectal cancer,
hookworm infestation).
• Frequent blood donation or injury-related blood loss.

4. Malabsorption
Diseases affecting the gastrointestinal tract:
Celiac disease, Crohn’s disease, or infections.
Post-gastric surgeries (e.g., gastric bypass).
Antacids or proton pump inhibitors reducing stomach acidity (needed
for iron absorption).
5. Parasitic Infections
Hookworm (Ancylostoma and Necator species): Major cause in
developing countries due to blood loss in the gut.
Schistosomiasis and malaria also contribute to iron depletion.
6. Socioeconomic and Lifestyle Factors
Poverty and food insecurity.
Unawareness of iron-rich dietary sources.
Cultural dietary practices limiting consumption of iron-rich foods.

Clinical findings
General Symptoms (Due to Reduced Oxygen Delivery)
• Fatigue: Persistent tiredness or lack of energy.
• Pallor: Pale skin, mucous membranes (e.g., conjunctiva, nail
beds).
• Dyspnea on exertion: Shortness of breath during physical
activity.
• Dizziness or lightheadedness: Due to reduced oxygen
supply to the brain.
• Palpitations: Feeling of irregular or rapid heartbeat.

2. Specific Signs (Due to Iron Deficiency)
• Pica: Craving for non-nutritive substances (e.g., ice, clay,
dirt).
• Koilonychia: Spoon-shaped, brittle nails.
• Glossitis: Smooth, inflamed tongue with a burning
sensation.
• Angular Stomatitis: Cracks or sores at the corners of the
mouth.
• Cheilitis: Dry, chapped lips.
• Hair loss
3. Neurological and Cognitive Symptoms
• Restless Leg Syndrome (RLS): Uncomfortable sensation in
the legs, relieved by movement.

4. Severe or Chronic IDA Symptoms
• Tachycardia: Increased heart rate due to compensatory mechanisms.
• Cardiac murmurs: Resulting from increased cardiac output.
• Heart failure (rare): Severe, prolonged anemia can lead to high-
output cardiac failure.
5. Laboratory Findings in Clinical Diagnosis
• Peripheral Blood Smear:
• Microcytic (small-sized), hypochromic (pale) red blood cells.
• Complete Blood Count (CBC):
• ↓ Hemoglobin, hematocrit, and red blood cell indices (MCV,
MCH, MCHC).
• Iron Studies:
• ↓ Serum iron and ferritin levels (early markers of iron depletion).
• ↑ Total Iron Binding Capacity (TIBC).

Iron Overload
HAEMOCHROMATOSIS
• It is an inborn error of metabolism. There is a failure to control iron absorption
from small intestines.
• The excess iron is then deposited in the tissues.
• The characteristics features are an enlarged and cirrhotic liver, pancreatic
diabetes, a slate-grey discolouration of skin and hypogonadism .
• The disease is fatal if the iron content is not reduced.
SIDEROSIS
Siderosis is the accumulation of iron in body tissues, which can result from
occupational exposure to iron dust (e.g., in welders) or excessive iron deposition
due to repeated blood transfusions or iron overload conditions.

NATIONAL PROGRAMS TO PREVENT
ANAEMIA, LBW AND INFANT MORTALITY
• Anaemia Mukt Bharat (AMB)
• Integrated Child Development Services (ICDS)
• Mid-Day Meal Scheme (MDM)
• Janani Suraksha Yojana (JSY)
• Pradhan Mantri Matru Vandana Yojana (PMMVY)
• Kilkari Program
• Supplementary Nutrition Program (SNP) under ICDS
• Reproductive, Maternal, Newborn, Child, and Adolescent Health (RMNCH+A)
• National Health Mission (NHM)
• India Newborn Action Plan (INAP)
• Universal Immunization Program (UIP)
• Home-Based Newborn Care (HBNC)
• Sick Newborn Care Units (SNCUs)
• Janani Shishu Suraksha Karyakram (JSSK)

INTRODUCTION
Iodine is an essential trace element required for the synthesis of thyroid
hormones, which regulate the body's metabolic processes. A deficiency
in iodine can lead to a range of disorders collectively known as Iodine
Deficiency Disorders (IDD).
• Essential for normal growth, development, and brain function.
• A trace mineral, accounting for 0.00004% of body weight.
• Total body iodine: 15–23 mg
• 75% stored in the thyroid gland.
• Remainder in salivary, mammary, gastric glands, and kidneys.
• Circulates as free iodide ions (I⁻) or protein-bound iodine (PBI).

FUNCTION
Iodine is essential for synthesizing triiodothyronine (T3) and thyroxine (T4), which are thyroid
hormones that regulate growth and development.
• Metabolic Rate: Thyroid hormones stimulate the metabolic rate by as much as 30%,
increasing oxygen use and heat generation.
• Brain Development: Critical for normal brain development, increasing brain cell proliferation
and regulating brain function processes. Vital from the 4th month of intrauterine life to the
third year of postnatal life.
• Hypothyroidism: Insufficient thyroid hormones lead to defective brain development and
impaired brain function.
• Nutrient Conversion: Regulates the conversion of carotene into active vitamin A, protein
synthesis, and carbohydrate absorption from the intestine.
• Cholesterol Levels: Hypothyroidism is linked to high cholesterol levels, while
hyperthyroidism leads to low cholesterol levels.
• Reproduction: Thyroxine is essential for reproduction.

Absorption & Metabolism
Iodine is found in food as iodide ions, free inorganic iodine, or covalently bonded iodine atoms
within organic compounds.
Absorption Process:
• Iodide ions are rapidly absorbed in the small intestine.
• Distributed throughout the extracellular fluid.
• Free iodine is reduced to iodide ions and absorbed.
Excretion:
• Iodine is removed through the kidneys and excreted in urine.
• One-third of absorbed iodine is taken up by the thyroid gland.
• The remainder is lost through perspiration and feces.
• Excretion protects against toxic levels.
Thyroid Gland Process:
• Iodide entering the thyroid gland is oxidized back to iodine.
• Combines with tyrosine residues within the iodine-storage protein thyroglobulin.

Hormone Regulation Loop:
• Hypothalamus detects a fall in blood thyroxine levels.
• Releases thyroxine-releasing factor (TRF) into the plasma.
• TRF travels to the pituitary gland.
• Stimulates the release of Thyroid Stimulating Hormone
(TSH) into the plasma.
• TSH is transported to the thyroid gland.
• Stimulates the production of T3 and T4 from thyroglobulin.
TRF Pituitary TSH Thyroid T3+T4

Hormone Release:
• An enzyme acts on thyroglobulin to release iodine-containing
tyrosine residues.
• T3 and T4 are released into blood plasma in a ratio of four T4
molecules for each T3 molecule.
• They travel to every cell in the body to regulate energy release
processes, determining the overall metabolic rate.
• Iodine Status: Excess iodine intake is primarily excreted
through urine; urinary iodine is a good measure of iodine
status.

Recommend
ed Dietary
Allowances

Upper Limit of Iodine Intake
Excess iodine can be harmful and may inhibit the synthesis of thyroid hormones, known as
the Wolff-Chaikoff effect.
Wolf-Chaikoff effect: Iodine-induced hypothyroidism that depends on the level of iodine intake
before exposure to iodine excess. Commonly encountered among newborns as neonatal
chemical hypothyroidism when pregnant women receive high doses of iodine via iodized oil
injections.
Sources of Iodine
The National Institute of Nutrition has established a database on the iodine content of Indian
foods.
• Water:
• Goitrous areas: 3-16 μg/L
• Non-goitrous areas: 5-64 μg/L
• Bovine Milk: 11-13 μg/100g
• Fish: 28-55 μg/100g
• Certain types of fish (cod/haddock): 175 μg/100g
• Egg: ~50 μg/100g, concentrated more in the white portion

Daily Intake of Iodine from Different Food
Groups in Indian Diet
Food Group
Percentage of Daily
Intake
Cereals 40%
Milk and Milk
Products
37%
Flesh Foods 11%
Pulses 10%

• Regional Diets: Iodine content ranges from 170-300 μg/day.
• Non-Endemic Areas: 60-75% of iodine needs are met by the iodine present in diet,
and the rest through the iodine content of water.
• Endemic Goitre Areas: Iodine deficiency exists in the soil, water, and locally grown
foods.
• Non-Goitre Areas: Diet provides nearly 200 μg iodine daily, meeting the body's
requirements.
• Soil Content: The iodine content of food depends on the iodine content of the soil.
• Rich Sources: Seafood (marine fish, shellfish) are rich sources of iodine.
• Animal Products: Milk, meat, or eggs are richer in iodine when animals consume
iodine-rich foods.
• Other Sources: Legumes and cereal grains.
• Plant Foods:
• Millet sorghum: 73 μg/100g
• Black gram (pulses): 48 μg/100g
• Mustard: 55 μg/100g
• Poor Sources: Fruits and vegetables

Losses During Cooking
Iodine in foods is lost in varying amounts during cooking.
• Loss Range: 40-70% loss of iodine in various preparations using iodized salt.
• Indian Cooking Processes: Lower iodine content by 37-70%.
• Frying: 20% reduction
• Grilling: 23% reduction
• Boiling: 58% reduction
• Specific Food Losses:
• Cereals during boiling: 30-60% loss
• Frying of vegetables: 25-52% loss
• Steaming: 30% loss
• Fish frying or grilling: 20% loss
• Fish boiling: 58% loss
Since the population's mean requirement is 100-150 μg/day, food sources are more
important contributors to iodine intake than water intake.

IODINE CONTENT
OF SOME
COMMON INDIAN
FOODS µg /100 IN
GOITROUS AND
NON-GOITROUS
REGION

Iodine Deficiency Disorders (IDD)
Wide variety of physical and neurological disorders associated with iodine deficiency.
Recognized by WHO as the most preventable cause of brain damage.
Incidence
• Global Problem: Major global public health problem.
• At Risk: About 1.5 billion people worldwide are at risk of IDD.
• India: Over 200 million are in India.
• Iodized Salt Access: 68% of households globally have access to iodized salt.
• Developed Countries: Problem virtually eliminated through iodine fortification.
• Persistent Problem: Major nutritional problem in Latin America, Africa, and Asia.
Regional Incidence
• North America and Australia: No IDD
• India, Asia, and South America: IDD is decreasing with control programs
• Africa: IDD likely to be a persistent problem due to a lack of control programs

Endemic Areas in India
• Along the slopes, foothills, and plains adjacent to the Himalayas (over
2400 km).
• Pockets in the Aravalli Hills (Rajasthan), Subvindhya hills (Madhya
Pradesh), Narmada Valley (Gujarat), hilly areas of Odisha, Andhra
Pradesh, tea estates of Karnataka and Kerala, and districts of
Aurangabad and Pune in Maharashtra and Kolli hills in Salem district.
• Coastal areas are relatively free of goitre.
• Overall prevalence of total goitre among 6 to 11-year-old children was
about 4%, below the cutoff to indicate endemicity. Higher proportion
in Maharashtra (11.9%) and West Bengal (9%) in 2003-04.

Etiology
Factors responsible for IDD are classified as environmental and intrinsic factors.
Environmental Factors
Iodine deficiency is a disease of the soil where the environmental deficiency results in
the manifestation of iodine deficiency disorders in human beings and livestock
populations.
• Elevated Regions: Likely to occur in elevated regions subject to higher rainfall with
runoff into rivers.
• Rainfall Impact: High rainfall, snow, and flooding increase the loss of soil iodine,
which has often been denuded by past glaciation.
• Iodine Content: Causes low iodine content of food for humans and animals.
• Seawater Source: Seawater contains large quantities of iodine (50-60 μg/L).
• Enrichment Process: Seawater evaporates to form clouds, which condense as rain
and enrich the top layers of soil with iodine.

• Food Chain: Food crops grown on this soil and animals grazing on the
plants assimilate iodine.
• Water Source: Water from deep wells can provide a major source of
iodine.
• No State/UT is Free: A significant increase in goitre prevalence has
been reported from hitherto non-endemic regions.
• Risk Population: More than 200 million people are at risk of IDD in
the country.
• Affected Population: About 71 million people suffer from IDD.
• Endemic Belt: Classical endemic belt of IDD is known to exist in the
sub-Himalayan belt, but several studies have shown that IDD endemic
pockets exist in peninsular India as well.
• Water Iodine Levels: Iodine-deficient areas have water iodine levels
below 2 μg/L; in India, the levels range from 0.1 - 1.2 μg/L.
• Delhi Example: In Delhi, water iodine levels are 9 μg/L, and it is not an
iodine-deficient area.

Goitrogens
Substances that interfere with
iodine metabolism, affecting
various stages of thyroid hormone
homeostasis.
• Enzyme Interference: Interfere
with iodine uptake, oxidation, and
thyroxine to triiodothyronine
conversion. The enzymes include
NADPH-oxidase, thyroid
peroxidase, and 5'-deiodinase.
Classes of Goitrogens
Class Substances Mechanism
Class I
Thiocyanate,
isothiocyanate,
cyanogenic
glycosides
Inhibit iodine
uptake by the
thyroid gland
Class II
Thiourea,
thionamides,
flavanoides
Affect the stages of
organification and
coupling in
thyroxine synthesis
Class III
Excess iodine,
lithium
Interfere at the
stage of proteolysis
necessary for
thyroxine utilization

sources
• Sources: Tapioca, sorghum, finger millets, okra, sweet potato, almonds, peaches,
soyabeans, bamboo shoots, lima beans, cassava, cabbage, cauliflower, and other
vegetables belonging to the brassicae family.
• Cassava: Significant due to being a dietary staple in many tropical countries.
• Groundnuts: Contain arachidoside, which interferes with iodine use.
• Seasonal Variation: Seasonal and regional variation in thiocyanate content.
• Cooking Effect: Action of goitrogens may become inactive after cooking.
• Other Substances: The antibiotic sulphonamide reduces the conversion of iodine to
iodide. Para-amino benzoic acid has a similar potentially goitrogenic effect.
• Recommendations: People in goitrous areas should avoid goitrogens, while those
in non-goitrous areas can include them in moderation. Goitrogens cannot be used
as staple foods.

Intrinsic Factors
Rare congenital defects can occur in hormone synthesis and secretion. Peripheral resistance to
thyroid hormones can also result in goitre.
The Spectrum of IDD
IDD covers a myriad of consequences of iodine deficiency at all stages of human growth and
development. Except for certain types of goitre, Iodine Deficiency Disorders are permanent
and incurable.
Fetal Development
• Thyroid and Pituitary: Developed by the end of the first 12 weeks of gestation.
• Hypothalamus: Develops from the 10th to 30th weeks.
• TSH Detection: Between 18 and 22 weeks, TSH can be detected in the blood, stimulating the
thyroid.
• T4 Increase: Followed by a surge in T4.
• T3 Levels: T3 remains low because the 5-deiodinase enzyme removes the inner-ring 5 iodine
atom to form reverse T3, which has no hormonal activity.
• Birth Preparation: Just before birth, there is a decline in this enzyme with a rise in 5-
deiodinase enzyme acting change prepares the organism for the transition from intrauterine
to extrauterine life.
• Iodine Deficiency Impact: Failure of this conversion to produce sufficient T3 in iodine

Spectrum
of IDD in
Different
Age
Groups

Goitre
Non-neoplastic (tumour), non-inflammatory, and non-
toxic enlargement of the thyroid gland.
• Cause: Compensatory adaptation to a lack of iodine
required for thyroid hormone synthesis.
• Stimulus: Abnormally high level of TSH, brought about
by low plasma levels of thyroid hormones.
• TSH Effect: Excessive TSH causes an increase in both
the number and size of the cells of the thyroid gland.
• Symptoms: Simple goitre is a painless condition, but if
uncorrected, it can lead to pressure on the trachea,
causing difficulty in breathing.
• Treatment: Administration of appropriate doses of
iodine results in a slow reduction in the size of the
thyroid gland.
• Prevalence: More common among adolescents, young
adults, and school-age children.
• Gender: More females are affected than males.

Cretinism
Endemic cretinism is associated with severe iodine
deficiency during intrauterine life.
Associated Conditions: Mental deficiency, deaf-
mutism, and spastic paralysis of legs in varying
degrees.
Types of Cretinism
Neurological Cretinism:
• Manifestations: Mental retardation,
deaf-mutism, squint, spastic diplegia
(spastic rigidity affecting the lower
limbs leading to characteristic gait),
and brisk reflexes.
• Stunting: Not a regular feature.
• Cause: Inner ear or cochlea and brain
development during the second
trimester of pregnancy; iodine
deficiency during this critical time.

Myxoedematous Cretinism:
• Manifestations: Hypothyroidism signs (coarse and dry skin, swollen
tongue, deep hoarse voice, apathy, and mental deficiency), associated
skeletal growth retardation, and weak abdominal muscles.
• Other Symptoms: Do not usually suffer from spasticity, goitre, or
deaf-mutism.
• Regional Prevalence:
• Neurological cretinism is seen in areas with environmental iodine
deficiency.
• Myxoedematous cretinism results from iodine deficiency later in
pregnancy combined with continuing iodine deficiency during
the infant's first few years of life.
• Myxoedematous cretinism is also seen predominantly in areas
where goitrogens are consumed commonly (e.g., tapioca-eating
populations in Zaire, Africa).

Hypothyroidism
Characterized by coarse and dry skin, husky voice, and delayed tendon reflexes.
• Hormone Levels: Low serum T4, normal T3, and elevated TSH levels.
• Commonality: Common among adults.
• Impact on Children: Recent studies show that iodine deficiency or mild maternal
hypothyroidism can affect neuropsychological development in children.
Psychomotor Defects
Studies have shown that children from iodine-deficient areas show poor scores on IQ
tests and impaired school performance, along with poor motor coordination.
Impaired Mental Function
Communities residing in iodine-deficient areas usually exhibit reduced mental
function, low intelligence levels, and a high degree of apathy, reflected in a lack of
initiative and decision-making capacity.

Dietary Sources and Recommended Intake
Iodine Content in Foods
Food
Iodine
Content
(µg/100g)
Iodized Salt 3000-4000
Seaweed 200-2000
Codfish 100-150
Milk 50-100
Eggs 12 - 30
Spinach 10 - 20
Rice (Non-Goitrous
Areas)
40
Rice (Goitrous
Areas)
10
Recommended Daily Allowance (RDA)
Age Group RDA (µg/day)
Adults 140
Pregnant Women 220
Lactating Women 280
Infants (0-6 months) 100
Children (1-3 years) 90

Prevention
National IDD Control Programme
• History: Started in the 1960s as the National Goitre Control Programme and later renamed as National
IDD Control Programme.
• Implementation: Since April 1992, implemented by the Dept. of Health, Govt. of India.
• Iodized Salt Consumption: About 71% of households in India consume iodized salt.
Salient Features
• Liberalized production of iodized salt.
• Ensuring accessibility of iodized salt at a rate comparable to non-iodized salt.
• Manufacturers are being supplied potassium iodate free of cost or paid at subsidy.
• Arranging and supervising the transport of salt by the Salt Commissioner in consultation with the Ministry
of Railways.
• Ensuring the use of iodized salt in goitre-endemic areas while banning the sale of non-iodized salt under
the provision of the PFA Act.
• Establishing goitre control cells in all States and Union Territories for proper monitoring and
implementation of NIDDCP.
• Imparting training in undertaking simple surveys in States.

Essential Components
• Iodine Fortification
• Monitoring and Surveillance
• Manpower Training
• Mass Communication
Iodine Fortification
Providing iodine to the community is the only way to combat the
problem of IDD. Fortification of food items is practiced in different
parts of the world.
Criteria for Selection
• Should be consumed by a high proportion of the population
• Unrelated to socio-economic status
• Low potential for excessive intake
• No change in consumers' acceptability

Technical Criteria
• Centrally processed
• Minimal segregation of fortificant and vehicle
• Minimal regional variation
• Good masking quality
• Simple, low-cost technology
• Good shelf life
• High bioavailability
Iodized Salt
Common salt has been selected as a suitable vehicle for fortification of iodine
to control IDD.
• Technology: Simple, involving either dry mixing or spray mixing of salt with
an iodine source.
• Benefits: Economical, convenient, and effective means of mass prophylaxis
in endemic areas.

Fortification of Salt
• Dr. Venkatesh Mannar: President of Micronutrient Initiative, improved the lives of billions by
salt iodization. He helped establish salt iodization plants in more than 50 countries, providing
4 billion people access to iodized salt.
• Fortificant: Salt is fortified with potassium iodate.
• Double Fortified Salt: The National Institute of Nutrition developed double-fortified salt with
iron and iodine.
• Iodization Level: Fixed under the Prevention of Food Adulteration Act, not less than 30 ppm
at the production point and not less than 15 ppm of iodine at the consumer level on a dry
weight basis.
• Effectiveness: Goitre endemias of mild to moderate degree can be effectively controlled by
using iodized salt.
• Coverage: Studies in 2019 showed that 76.3% of Indian households consumed adequately
iodized salt. Tamil Nadu ranked lowest in coverage (61.9%).
• Regulations: In places where the ban is enforced, non-iodized salt must be sold with the
caption "not fit for human consumption" on the wrapper.
• Test Kits: Available to find the iodine content of the salt.
• Ban Enforcement: A total ban by all states can effectively help in liberating the country from
iodine deficiency disorders.

Double Fortified Salt (DFS)
Iodine deficiency disorders and iron deficiency anemia are widely prevalent and often coexist in
the country.
• Recommendation: Fortification of food with iodine and iron as a strategy to prevent and
control these two deficiency disorders.
• Technology: NIN developed a suitable technology for dual fortification of common salt with
iodine and iron.
• Stability: The stability of iodine is satisfactory in DFS, with very little loss of iodine in six
months.
• Effectiveness: Iodization would be an effective program even in non-IDD-endemic areas due
to the decline in iodine absorbed by food crops from the soil.
• Cost: An effective, low-cost (about 30 paise per person a year), long-term, and sustainable
solution.
• Distribution: The Salt Corporation is involved in mass production of iodized salt and making
it available to rural people at an affordable price through fair price shops. About 71% of
households in India consume iodized salt.
Highlight
Salt fortified with vitamins A, B12, iron, zinc, folic acid, along with iodine, is available in the
market.

Iodine Content
• Raw Foods: Estimated iodine content of raw foods consumed
in a day in non-goitrous areas is 170-300 μg, of which 30-70% is
lost during cooking.
• Daily Intake: Daily iodine intake from diets is low (100-160 μg).
• Salt Intake: The average salt intake among adults is about 10
g/day, and at the current level of fortification (15-30 ppm), the
iodized salt provides an additional amount of about 100 μg.
• Safety: The total intake of iodine is much below the safe limit
and is unlikely to cause any harmful effects, even in
populations who are not iodine deficient.

Do's and Don'ts for Iodized Salt
Do's
• Use iodized salt to save yourself from goitre and other Iodine Deficiency Disorders.
• Insist on iodized salt only.
• Always store iodized salt in a container with a lid and keep it away from direct
sunlight/heat and moisture.
Don'ts
• Never store iodized salt near fire.
• Never use ordinary, unlined jute bags for transport of iodized salt.
• Never store in the open or in a damp, poorly ventilated godown.
• Avoid transporting in open trucks or in open railway wagons.
• Never store iodized salt for more than six months.

Iodized Oil
Oil fortified with iodine is available for oral or intramuscular injections.
• Production: France is the only country in the world that produces iodized oil from poppy seed
oil for injection (Lipiodol) and oral (Oriodol) administration on a commercial scale.
• Dosage and Duration:
• Intramuscular injection of 1 ml of iodized oil containing 480 mg of iodine can maintain
a satisfactory iodine supply for 2-3 years.
• An oral dose of 1 ml can give protection for one year.
• Use Cases: In severe cases of cretinism and mental retardation, supplementation of iodized
oil should be given.
• Production Innovation: Scientists at the National Institute of Nutrition, Hyderabad, have
successfully developed a process to produce iodized oil with safflower oil.
• Challenges: Compared to salt, direct contact must be made with each subject receiving the
oil. It is very expensive and requires extensive manpower to carry out the program.
• Primary Use: For areas where the magnitude of the problem is large and severe and iodized
salt is not available. This is the best method of preventing new cases of cretinism and mental
retardation.
• Phasing Out: Once the iodized salt distribution program is well established, the iodized oil
program can be slowly phased out in these states.

Iodized Water
Iodine added directly to drinking water can correct iodine
deficiency.
• Iodine Level: At least 150 μg/L of iodine should be present
in the drinking water.
• Methods: Iodization is achieved through a public water
supply or through a common well.
• Iodiators: Canisters containing iodine crystals are
connected to main water pipes, and a fraction of the water
is diverted through them.

Excess Intake of Iodine
The Expert Committee of ICMR-2020 set the maximum acceptable daily
intake at 1100 μg/day.
• Adaptation: People exposed to excess iodine may remain normal
through adaptive mechanisms.
• Adverse Effects: May be seen in susceptible individuals and patients
with pre-existing abnormalities of the thyroid gland.
• Potential Diseases: Might contribute to the development of Hashimoto
thyroiditis, iodide and colloid goitre, and thyroid carcinoma.
• Prophylaxis Programs: There is little indication that iodine in the
amounts consumed through prophylaxis programs influences the
development of any of these thyroid diseases.

PHOSPHORUS
PRESENTER: SARUMATHI M

FUNCTIONS
1. Mineralization of Teeth and Bones
• Phosphorus, along with calcium, is a major component of hydroxyapatite, the
mineralized structure that provides strength to bones and teeth.
• About 85% of the body's phosphorus is stored in bones and teeth, contributing to
their density and durability.
• It plays a crucial role in bone remodeling, a continuous process where old bone
tissue is replaced with new tissue.
2. Facilitation of Energy Transactions
• Phosphorus is a key component of adenosine triphosphate (ATP), the body's
energy currency.
• ATP stores and releases energy required for muscle contractions, nerve
transmission, and metabolic reactions.
• It is also a part of creatine phosphate, which helps rapidly generate ATP during
high-intensity physical activity.

3. Absorption and Transport of Nutrients
• Phosphorus is involved in the activation of B-complex vitamins, which
are essential for energy metabolism.
• It plays a role in phosphorylation reactions, which modify nutrients
(like glucose) to facilitate their absorption and utilization.
• Phospholipids, which contain phosphorus, form cell membranes,
allowing proper transport of nutrients in and out of cells.
4. Regulation of Protein Activity
• Many proteins and enzymes require phosphorylation (attachment of a
phosphate group) to become active or inactive.
• This process helps regulate metabolic pathways such as glycolysis,
glycogen metabolism, and lipid metabolism.
• Phosphorus is also involved in cell signaling, allowing cells to
communicate and respond to external stimuli.

5. Component of Essential Body Compounds
Phosphorus is a vital part of:
• Nucleic acids (DNA & RNA) – Essential for cell growth, repair, and
replication.
• Phospholipids – Major components of cell membranes, aiding in structural
integrity and function.
• Enzymes and coenzymes – Required for various biochemical reactions.
• Second messengers (cAMP, cGMP) – Play a role in hormone signaling and
cellular communication.
6. Regulation of Acid-Base Balance
• Phosphates act as buffers in the blood, helping to maintain the body's pH
balance.
• The phosphate buffer system prevents drastic changes in pH, which is essential
for enzyme function and overall homeostasis.
• This function is particularly important in the kidneys, where phosphorus helps in
excreting excess hydrogen ions, thereby regulating acid-base balance.

ABSORPTION AND METABOLISM
Phosphorus Regulation in Blood Plasma
• The normal blood phosphorus level is 2.5–4.5 mg/dL (or 2.5–4.5 mg/100
mL).
• Phosphatases are enzymes that help regulate phosphorus by removing
phosphate groups from molecules.
• Vitamin D, parathyroid hormone (PTH), and renal function play key
roles in phosphorus homeostasis.
Role of Vitamin D in Phosphorus Metabolism
• Active vitamin D (calcitriol) enhances phosphorus absorption in the
intestine.
• It also promotes renal reabsorption of phosphorus, preventing its loss in
urine.
• Helps in bone mineralization by maintaining calcium-phosphorus
balance.

Parathyroid Hormone (PTH) and Phosphorus
• PTH increases renal excretion of phosphorus (via urine) while increasing calcium
absorption.
• It does this by reducing phosphorus reabsorption in the kidneys, leading to
phosphaturia (increased phosphorus excretion in urine).
• PTH stimulates bone resorption, releasing both calcium and phosphorus into the blood.
Phosphorus Excretion
• 90% of phosphorus is excreted via the kidneys, regulated by PTH.
• 10% is excreted via the GI tract, including bile and feces.
Hypophosphatemia (Low Blood Phosphorus, <2.5 mg/dL)
Causes:
• Diarrhea & Laxative Abuse Increased loss of phosphorus through the GI tract.
→
• Hyperparathyroidism Excess PTH leads to phosphorus excretion in urine.
→
• Vitamin D Deficiency Reduces phosphorus absorption from the intestines.
→
Hyperphosphatemia (High Blood Phosphorus, >4.5 mg/dL)
• Can occur in kidney failure, where phosphorus excretion is impaired.
• May result in calcium-phosphate deposits in soft tissues.

Factors Affecting Phosphorus
Absorption
Enhancing Absorption:
• Vitamin D (Calcitriol) – Increases phosphorus absorption by stimulating
active transport.
• Acidic pH – Enhances solubility and absorption of phosphorus.
• Presence of Calcium in Optimal Ratios – Helps in bone mineralization.
Inhibiting Absorption:
• Excessive Calcium Intake – High calcium-to-phosphorus ratio leads to
precipitation, reducing absorption.
• Phytates (from plant foods like grains and legumes) – Bind to
phosphorus, making it less bioavailable.
• Iron, Aluminum, and Magnesium Excess – Form insoluble phosphate salts
that are excreted.

Dietary
Sources of
Phosphoru
s
Rich sources:
Animal-Based: Meat, poultry, fish, eggs, dairy
(milk, cheese, yogurt)
Plant-Based: Nuts, seeds, legumes, whole grains
Beverages: Soft drinks and processed foods
(contain phosphoric acid)
Bioavailability:
Phosphorus from animal sources is more
bioavailable (absorbed easily) than plant sources.
Phytates in plant-based foods can reduce
phosphorus absorption.

Daily
Requireme
nts (RDA)
Infants (0-6 months): 100 mg
Infants (7-12 months): 275 mg
Children (1-3 years): 500 mg
Adolescents (10-12 years): 850 mg
Adolescents (13-17 years): 1000 mg
Men & Women (18+ years): 1000 mg
Pregnant & Lactating Women: 1000 & 1200
mg

Deficiency of
Phosphorus
(Hypophosphatemia)
Causes:
Malnutrition or prolonged starvation
Chronic kidney disease (CKD)
Alcoholism
Certain medications (e.g., antacids containing
aluminum)
Symptoms:
Weakness, fatigue
Bone pain or soft bones (osteomalacia)
Loss of appetite
Muscle weakness

Excess Phosphorus & Health
Risks (Hyperphosphatemia)
Causes:
• Chronic kidney disease (kidneys cannot excrete excess phosphorus)
• High intake from processed foods and soft drinks
• Excessive supplementation
Health Risks:
• Bone loss & Calcium imbalance (high phosphorus can reduce calcium absorption, leading to
osteoporosis)
• Heart disease risk (linked to vascular calcification)
• Kidney problems

Phosphorus & Kidney
Health
• In chronic kidney disease (CKD), phosphorus levels
need to be controlled to prevent complications like
bone disease and heart problems.
• CKD patients should limit high-phosphorus foods
and opt for phosphorus binders if prescribed.

MAGNESIUM
PRESENTER : SARUMATHI M

COMPOSITION :-
Total body magnesium: 20–25 g
• Distribution:
• 60–70% in bones Contributes to bone crystal structure and mineralization.
→
• 25–30% in muscles Essential for muscle function.
→
• 6–8% in soft tissues Involved in enzyme activity.
→
• ~1% in extracellular fluid Regulates physiological functions like nerve
→
signaling and muscle contractions.

Functions of Magnesium
• Bone Health: Structural component of bone crystals, working alongside calcium and
phosphorus.
• Cell Membrane Stability: Found in phospholipids, helping maintain cell membrane
integrity.
• Nucleic Acids & Protein Synthesis: Essential for DNA, RNA, and protein synthesis.
• Neuromuscular Function:
• Helps regulate muscle membrane electrical potential, preventing excessive nerve
excitability.
• Deficiency may contribute to neurological dysfunctions, including seizures, muscle
spasms, and tremors.
• Alzheimer’s Disease:
• Magnesium deficiency has been linked to neurodegenerative diseases, including
Alzheimer's, due to its role in neuroprotection and cognitive function.

Absorption of Magnesium
• Occurs mainly in the small intestine through:
• Passive Diffusion (when intake is high).
• Carrier-Mediated Transport (when intake is low, enhancing absorption efficiency).
Absorption Rate:
• 50–70% from a self-selected diet.
• 25–35% absorption efficiency (varies based on dietary intake, body needs, and
competing nutrients like calcium).
Hormonal Regulation of Magnesium
• Calcitropic Hormones (Parathyroid Hormone, PTH)
• Enhances renal reabsorption of magnesium, preventing excessive loss.
• Stimulates magnesium absorption in the gut alongside calcium.

Magnesium Deficiency
(Hypomagnesemia)
Causes:
• Inborn Errors of Absorption Genetic disorders affecting magnesium uptake.
→
• Chronic diarrhea & malabsorption syndromes.
• Excessive alcohol intake Increases urinary magnesium loss.
→
• High calcium intake Can compete with magnesium for absorption.
→
• Symptoms:
• Neurological: Confusion, muscle cramps, seizures, and tremors.
• Cardiovascular: Arrhythmias and high blood pressure.
• Metabolic: Insulin resistance and increased risk of osteoporosis.
Recommended Intake
• 370 mg/day (varies by age, gender, and physiological conditions).
• Good sources: Nuts, seeds, whole grains, leafy greens, legumes, and dairy.

GROUP MAGNESIUM mg/d
MAN 440
WOMAN 370
PREGNANT 440
LACTATING 400
INFANT
0-6 m
6-12 m
CHILDREN
1-3 Y
4-6 Y
7-9 Y
BOYS
10-12 Y
13-15 Y
16-18 Y
GIRLS
10-12 Y
13-15 Y
30(AI)
75(AI)
90
125
175
240
345
440
250
340

INTRODUCTI
ON
Sodium (Na) is an essential mineral and
electrolyte that plays a crucial role in
maintaining fluid balance, nerve function, and
muscle contraction. It is primarily found in
extracellular fluid and is vital for homeostasis.
Sodium is naturally present in foods, but it is
often consumed in excess through processed
and packaged foods.

Absorption of Sodium
Sodium absorption occurs primarily in the small intestine through active transport mechanisms, mainly in the
duodenum and jejunum.
 Sodium is absorbed in the small intestine through active transport and passive diffusion.
 Aldosterone regulates sodium levels by promoting its retention.
 Renin helps maintain sodium balance by controlling blood pressure and fluid retention.
 Once absorbed, sodium enters the bloodstream and is distributed in extracellular fluid.
RAAS and Sodium Regulation
 Low blood pressure or sodium Kidney releases renin
→ .
 Renin activates angiotensin I ACE converts it into angiotensin II.
→
 Angiotensin II constricts blood vessels & signals adrenal glands to release aldosterone.
 Aldosterone increases sodium and water retention → Raises blood volume & pressure.
End Result: Sodium is reabsorbed, potassium is excreted, blood volume increases, and blood pressure is
maintained.

Excretion of Sodium
Sodium balance is tightly regulated by the kidneys, which filter sodium and adjust its reabsorption and
excretion to maintain homeostasis.
Routes of Excretion:
Urine (Primary Route):
• The kidneys regulate sodium levels through glomerular filtration, reabsorption in the tubules, and
excretion in urine.
• Hormones like aldosterone (from the adrenal glands) promote sodium reabsorption, while atrial
natriuretic peptide (ANP) increases sodium excretion.
Sweat:
• Sodium is lost through perspiration, especially during exercise, in hot climates, or in fever conditions.
Feces:
• A small amount of sodium is lost through stool, but this increases in cases of diarrhea or malabsorption
syndromes.
Other Minor Losses:
• Vomiting, excessive sweating, and certain medical conditions can lead to significant sodium loss.

1. Metabolism of Sodium
• Sodium is absorbed in the small intestine and transported into the
bloodstream.
• It is primarily regulated by the kidneys, which adjust excretion
through urine.
• The Renin-Angiotensin-Aldosterone System (RAAS) controls sodium
retention and excretion.
• Some sodium is lost through sweat and feces.
2. Regulation of Sodium Balance
• Aldosterone (from adrenal glands) increases sodium reabsorption in
the kidneys.
• Renin (from kidneys) helps control sodium levels and blood pressure.
• Antidiuretic hormone (ADH) regulates water balance, indirectly
affecting sodium concentration.
• Atrial Natriuretic Peptide (ANP) promotes sodium excretion when
levels are high.

3. Distribution of Sodium in the Body
• Extracellular Fluid (ECF): 90-95% of body sodium is in plasma and
interstitial fluid.
• Intracellular Fluid (ICF): A small amount is present inside cells.
• Bones: Stores a minor portion, released when needed.
4. Functions of Sodium
• Maintains fluid and electrolyte balance.
• Regulates blood pressure and blood volume.
• Essential for nerve impulse transmission and muscle contraction.
• Helps in glucose and amino acid absorption in the intestines.

5. Deficiency of Sodium (Hyponatremia)
• Causes: Excessive sweating, diarrhea, vomiting, kidney disease, or low salt intake.
• Symptoms: Weakness, nausea, confusion, muscle cramps, and in severe cases, seizures or
coma.
6. Daily Sodium Requirements
• WHO: 2000 mg/day (~5g salt).
≤
• ICMR: 2400 mg/day for adults.
• AHA (Ideal Limit): 1500 mg/day (max 2300 mg/day).
8. Excess Sodium (Hypernatremia)
• Causes: High salt intake, dehydration, kidney dysfunction.
• Symptoms: High blood pressure, swelling (edema), thirst, and kidney strain.
• Risks: Hypertension, heart disease, osteoporosis, and kidney damage.

POTASSIUM

Compositio
n :-
1. Potassium in the Body
• Found as positively charged ions (K⁺), either
free or bound in salts.
• Total body potassium: ~250 g, mainly in
intracellular fluid (ICF).
• Distribution:
• 98% inside cells (skeletal muscles contain
80% of total potassium).
• 2% in extracellular fluid (ECF) (~80 mmol).
• Bones contain only 7% (negligible storage).
• Na⁺/K⁺ Ratio:
• Intracellular Fluid: 1:10 (Potassium
dominant).
• Extracellular Fluid: 28:1 (Sodium
dominant).

2. Functions of Potassium
• Essential for cell function, growth, and glycogen synthesis.
• Regulates osmotic balance between ICF and ECF.
• Maintains acid-base balance by adjusting potassium levels based on
acidity/alkalinity.
• Plays a key role in nerve impulse transmission and muscle contraction.
• Involved in the release of insulin from the pancreas.
• Acts as a muscle relaxant (opposes calcium’s muscle-contracting effects).
• Helps regulate blood pressure—a 1:1 sodium-to-potassium intake ratio
may protect against hypertension.
• Supports heart function and is crucial for cardiac muscle activity.

3. Absorption and Excretion of
Potassium
• Daily Intake: 50–150 mmol (5–10 g KCl) from diet.
• Absorption: Passive diffusion; distributes evenly in body fluids.
• Excretion:
• Urine: 40–90 mmol/day, depending on intake.
• Feces: Minimal under normal conditions.
• Tissue Breakdown: Potassium loss increases during muscle breakdown (2.7
mmol potassium per gram of nitrogen loss).

4. Potassium Deficiency
(Hypokalemia)
Causes:
• Diuretics, severe diarrhea, malnutrition, or excessive losses.
• In severe diarrhea, 10-30% of body potassium may be lost, especially in infants and
adults with acute conditions.
• Symptoms:
• Muscular weakness, mental confusion.
• ECG changes, cardiac arrhythmias, and sudden death.
• Paralytic ileus (especially in children).
• Treatment:
• Dietary intake is usually insufficient for correction.
• Potassium supplements are needed for drug-induced or diarrhea-related losses.

5. Recommended Dietary Allowances (RDA) of Sodium
and Potassium (ICMR 2020)
1 g of salt (NaCl) contains 39% sodium; 2000 mg sodium =
5 g salt.
Group
Sodium
(mg/day)
Potassium
(mg/day)
Na⁺/K⁺ Molar
Ratio
Adult Man 2000 3500 1:01
Adult Woman 2000 3500 1:01
Infants (0-6
months)
500 900 1:01
Infants (7-12
months)
650 1100 1:01
Children (1-3 years) 1000 1750 1:01
Children (4-6 years) 1300 2250 1:01

6. Sources
of
Potassiu
m
Whole Grains and Cereals:
• Bajra: 365 mg/100g
• Ragi: 443 mg/100g
• Whole wheat: 366 mg/100g
Legumes and Pulses:
• Black gram dal: 1157 mg/100g
• Green gram whole: 1177 mg/100g
• Soybean: 1613 mg/100g
Fruits and Dried Fruits:
• Banana: 306 mg/100g
• Dates (dry, pale brown): 804 mg/100g
• Raisins (dry, black): 1105 mg/100g
• Tamarind pulp: 836 mg/100g

7. Potassium
Toxicity
(Hyperkalemi
a)
• Toxicity Risk: Can occur from excess
potassium salt intake (10–18 g KCl).
• Symptoms:
• Can lead to cardiac arrest and fatal
arrhythmias.
• Individuals with renal failure are at high
risk.
• Upper Limit: 140 mmol/day (10 g KCl) is
the tolerable intake.

CHLORIDE

INTRODUCTION
Chloride is an essential electrolyte present in the body, primarily found in
the form of chloride ions (Cl⁻). It is the major anion of the extracellular fluid
(ECF) and plays a key role in maintaining fluid balance, acid-base balance,
and nerve function. Chloride is mostly consumed in the diet as sodium
chloride (NaCl), commonly known as table salt. It is also an essential
component of gastric hydrochloric acid (HCl), which is crucial for digestion.
Since chloride metabolism is closely linked to sodium, its absorption,
excretion, and regulation follow a similar pattern.

1.
Chloride
in the
Body
• Found in the body as chloride ions (Cl⁻),
mainly in extracellular fluid (ECF).
• Total body chloride content (~2150 mmol
in a 60 kg man).
• Highest concentrations: Cerebrospinal
fluid and gastric secretions.
• Lower concentrations: Muscle and nerve
tissue.

2. Absorption and Excretion
• Chloride absorption parallels sodium (Na⁺) to maintain electrical
neutrality in body fluids.
• Kidneys regulate chloride levels—excreting excess or reabsorbing it
efficiently when intake is low.
• Chloride loss occurs due to:
• Sweating, diarrhea, vomiting (especially excessive vomiting).
• Salt restriction—first reducing chloride in urine, then in tissues.
• Vomiting-induced loss should be replaced quickly.

3. Functions of Chloride
• Maintains acid-base balance in body fluids.
• Essential for secretion of gastric hydrochloric acid (HCl).
• Chloride Shift:
• Movement of Cl⁻ into and out of red blood cells (RBCs).
• Maintains electrical neutrality as RBCs transport oxygen and carbon dioxide.
• In the Central Nervous System (CNS):
• Specific chloride channels linked to benzodiazepine receptors.
• Chloride entry into cells causes hyperpolarization, leading to neuroinhibition
4. Chloride Deficiency
• Rare under normal conditions (dietary intake usually exceeds requirement).
• Losses occur under the same conditions as sodium deficiency—vomiting, diarrhea,
excessive sweating.
5. Sources of Chloride
• Main source: Common salt (NaCl).
• Found naturally in sodium-rich foods like processed foods, canned foods, and sauces.

Aspect Deficiency (Hypochloremia) Toxicity (Hyperchloremia)
Causes
- Prolonged vomiting (loss of HCl)
- Excess chloride-rich IV fluids
(e.g., saline)
- Chronic diarrhea - Dehydration
- Excessive sweating - Renal failure
- Use of diuretics (loop, thiazide) - Certain medications
- Metabolic alkalosis - Metabolic acidosis
Symptoms
- Muscle weakness - Fluid retention
- Lethargy or fatigue - High blood pressure
- Dehydration - Weakness, fatigue
- Hypoventilation
- Deep, rapid breathing
(Kussmaul respiration)
- Low blood pressure - Mental confusion
- Confusion or convulsions (severe cases)
Clinical Signs
- Serum chloride < 96 mEq/L - Serum chloride > 106 mEq/L
- Often with low sodium or potassium - Often with low bicarbonate
Normal
Requirement
~2.3 g/day for adults -
Main Sources
Table salt (NaCl), processed foods, cheese,
seaweed, tomatoes, celery, olives

Element Metabolism
Physiologic
Function
Clinical Application Sources
Manganese
Absorbed poorly.
Excretion mainly by
intestine.
Enzyme component
in general
metabolism.
Low serum levels in
diabetes, protein-energy
malnutrition, inhalation
toxicity.
Cereals, whole
grains, legumes,
soybean, leafy
vegetables.
Chromium
Absorbed in
association with zinc.
Excretion mainly by
kidney.
Associated with
glucose metabolism,
improves faulty
glucose uptake by
tissues.
Potentiates insulin action
in diabetes. Lowers
serum cholesterol, LDL
cholesterol.
Cereals, whole
grains, animal
proteins, Brewer’s
yeast.
Cobalt
Absorbed as
component of food
source, vitamin B₁₂.
Elemental form shares
transport with iron,
stored in liver.
Constituent of
vitamin B₁₂.
Functions with
vitamin. Increases
biological effect of
insulin.
Deficiency only
associated with
deficiency of vitamin B₁₂.
Vitamin B₁₂ source.
Selenium*
Absorption depends on
solubility of compound
form. Excreted mainly
by kidney.
Constituent of
enzyme glutathione
peroxidase.
Synergistic
antioxidant with
vitamin E, structural
component of teeth.
Marginal deficiency when
soil content is low.
Deficiency secondary to
parenteral nutrition
(TPN), malnutrition.
Varies with soil.
Seafood, legumes,
whole grains, low-fat
meat, dairy,
vegetables. High
bioavailability from
cereals and millets.

Element Metabolism
Physiologic
Function
Clinical Application Sources
Zinc
Absorbed in small
intestine. Competes
with copper and iron
for absorption.
Excreted via feces,
minimal loss in urine.
Cofactor for over
300 enzymes.
Supports immune
function, wound
healing, growth,
DNA synthesis, and
taste.
Deficiency leads to
growth retardation,
delayed wound healing,
impaired immunity,
dermatitis, hypogeusia.
Meat (esp. red
meat), shellfish
(oysters), legumes,
whole grains, nuts,
seeds, dairy, eggs.
Copper
Absorbed in small
intestine, stored in liver.
Excretion mainly via
bile. Absorption
decreases with excess
zinc.
Enzyme cofactor;
aids iron
metabolism,
connective tissue
formation, nervous
system function, and
melanin production.
Deficiency may cause
anemia, neutropenia,
bone abnormalities,
neurological disorders.
Seen in Menkes disease.
Organ meats,
shellfish, nuts,
seeds, cocoa,
legumes, whole
grains.
Fluoride
Absorbed in stomach
and small intestine.
Deposited in bones and
teeth. Excreted in urine.
Strengthens enamel,
reduces dental
caries, supports
bone mineralization.
Deficiency dental
→
caries. Excess →
dental/skeletal fluorosis.
Important in community
water fluoridation.
Fluoridated water,
tea, seafood,
toothpaste (topical
effect).
Component of

MINERALS- Classification ,function, deficiency and sources.

More Related Content

What's hot (14)

Similar to MINERALS- Classification ,function, deficiency and sources. (20)

More from Sarumathi Murugesan (20)

Recently uploaded (20)

MINERALS- Classification ,function, deficiency and sources.