Download Specific Nutrient Deficiencies

Global Health Fellowship
Nutrition Module
Ramona Sunderwirth, MD MPH
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Calcium & Vit D
Iodine
Zinc
Vit A
Thiamine (Vit 1)
Niacin
Vit C
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Evidence shows that energy deficits more general than
protein deficit in community & hospitals
1ary protein deficiency:
 Staple food cassava or plantain
 Mothers feed inappropriate foods (sugar water)
 A major precipitating factor in Kwashiorkor
Sufficient carbs in diet spares protein from being used as
substrate for glucose
Varied diet, proteins from plants & animal sources increases
NPU
 Variety & balance
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Long chain PUFAs
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alfa-linolenic & linoleic acids only available in diets
Requirements EFA small
gross deficiencies in bowel resection
 s/p weaning in many communities: cognitive impairment ,
(-) impact on community development
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Good intake of LC-PUFAs beneficial to health
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Breast milk critical source on LC-PUFAs
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Major influence on brain development
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Absorption
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Dietary
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Non dairy diets in Africa: low Ca
Rural African mothers: low Ca in breast milk
Deficiency
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Aided by Vit D, regulated Parathyroid hormone
Stunting in children
Ca deficient Rickets rare
Sources
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Milk, dairy products, fish (bones), beans, peas, dark green leaves, nuts,
millet
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Function
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Sources
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Fat soluble vit, stimulates intestinal Ca absorption
Fortified food products richest source Vit D
Fish oils, egg yolks, mushrooms
Animal products (fatty parts, liver)
Vit D in diet: cholecalciferol or ergocalficerol
Converted to active form 1,25-dihydroxyvit D3 in skin, liver & kidney
Requires ultraviolet light
Deficiency
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Interaction of low dietary sources + lack exposure sunlight
Rickets
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↓Sun exposure, ↓ Ca nutritional requirements
↓serum Ca → induce ↑ PTH secretion → osteoclasts
↑ resorb bone → demineralization of bone & cartilage
at sites of rapid growth & remodeling
#Limited exposure to sun
*limited sun exposure:
poor air quality
live > 37TH parallel
cultural, social habits, dress codes
darkly pigmented skin
#Nutritional deficiencies
*breast milk low in Vit D, weaning diets (low in fats/oils)
* inadequate intake Ca (↑consumption polished rice), Phosphate
* diets w/ ↑ content phytate (wheat - binds Ca in gut)
* ↓ energy supplies, growth outstrips Ca availability
#Genetic causes
*Vit D-dependent rickets type 1&2
#Malabsorption (repeated GI infections)
#Chronic renal, liver disease
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Early
Craniotabes, head asymmetry,
frontal bossing, delayed closing ant fontanelle
 Delayed tooth eruption, abnormal formation
enamel, cavities
 Rachitic rosary
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Late
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Pigeon chest irregularity, Harrison groove
Motor delays, hypotonia (muscle weakness)
Classic limb abnormalities
 Genu varum, genu valgum, windswept deformities
 Fraying, widening, cupping metaphysis long bones, fxs
 Lordosis, kyphosis, scoliosis
 Narrow pelvis: obstructed labor
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Muscles
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Delayed motor development
Tetany, carpopedal & laryngeal spasm
Convulsions
Pneumonia
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2ary defective immune function
Thorax deformity (restrictive airway)
Cor pulmonale
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Biochemistry
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Radiology
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Serum Ca: Nl or ↓
Serum Ph: ↓
Alkaline Phosphatase: ↑
Hydryxyproline excretion: ↑
Radius/ulna: widened, cupped, frayed ends
Costochondral junctions: widened
Osteopenia
Bone biopsy
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Inadequate mineralization
Excessive volume of osteoid tissue
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Sunlight or ultraviolet light
Calciferol
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Tetany
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IV Ca Gluconate 10%solution ( 5-10ml)
PO Ca Chloride 1g q 6 h ( in milk)
Ca supplements
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PO or IM Vit D2: 150K i.u. once
PO calciferol: 3K i.u. (75mg) QD x 1 mo
Cod liver oil (75 i.u./ml or 1.8mg/ml) QD x 1mo
Milk or Ca lactate tab 5g TID
Healing
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6 wks Vit D treatment biochemical changes reverses
Bones heal more slowly, may never become normal
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Community Health Education
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Need for sunlight & animal foods (eggs)
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Fish oil for children at risk:
premies/infants/patients
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Iodine > thyroid hormones
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Regulation of growth, development & metabolism
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Commonest thyroid disease is goiter, response to
insufficient I intake
All body systems vulnerable to I deficiency
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CNS (fetal life & infancy-3yr age)
Milder degrees of MR affect whole populations
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Hypothyroidism → Goiter
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Subclinical I deficiency
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Loss energy
Brain damage
Iodine deficiency in pregnancy → cretinism infants (MR + stunted
growth)
Endemic Goitre
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Soil deficient
Marginal I deficient areas, precipitated by consumptions of goitrogenic
agents in food: poorly cooked roots (cassava)/leaves
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Fetus
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Neonate
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Abortions, stillbirths,
congenital malformations
↑PNM, neurological &
myxoedematous cretinism
NN hypothyroidism
Child & adolescent
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Retarded mental &
physical development
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Adult
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Goitre
I-induced hyperthy (IIH)
All ages
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Goitre, Hypothy
Impaired mental function
↑ susceptibility nuclear
radiation
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I content water & food reflects levels in soil & groundwater
I sources: animal>fruits/vegetables
Goitergens
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Thiocyanate ( from cassava)
Selenium deficiency, high levels fluoride
Soil erosion
Inland, mountainous areas w/ poor soils & hi rainfall +
coastal areas, large cities
Public Health Problem
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Reduces potential of whole community
Low achievement, poor quality life, blunted ambition
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Urinary iodine
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Thyroid size (goitre surveys)
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Most useful/reliable indicator I status
24hr or random (30 samples) urine collection
Related to recent dietary I intake
100mico gm/l satisfactory
Palpation, ultrsound (more reliable)
“Total Goitre Rate”, schoolchildren
TSH NN screening programs
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For early detection of congenital NN hypothyroidism
Useful epi information severity of I deficiency, not cost effective to
monitor IDD programs
Mild
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Goitre
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Moderate
Severe
5-19%
20-29%
>30%
Median Urinary I
50-99
20-49
<20
TSH > 5mU/L
3-19%
20-39%
>40%
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Consumption of adequate amounts I (150microgm/d)
 Sea fish, kelp
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Supplementation programs
 Iodization of water or salt
 Direct administration I oil: IM or PO
 Iodine solutions (Lugol’s iodine): regular PO dose
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Iodization of all salt for human consumption
 Sustainable , costs borne by consumer
 K iodate recommended (more stable)
 20-40mg I/kg salt
 Monitoring essential
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Function
Cell replication & growth
 Stabilizing fct in organic compounds (cell membranes)
 Bone & muscle (total body content: 2-3gm)
 No known correlation btw intakes & plasma levels
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Sources
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Animal products, seafood, cereals (outer layers)
Absorption impaired by phytates, protein acts as
anti-phytate, aids absorption
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Deficiency
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Growth retardation (IUGR)
cell mediated immunity
wound healing
Replacement
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Strong evidence supports low dose supplementation
 Reducing diarrhea
 Reducing mortality
 Children in several areas of developing world
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Careful in administration in early recovery phases severe
malnutrition w/ chronic diarrhea
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Retinols
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Retinol: preformed Vit A
 Most active form
 Found in animal sources
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Beta-carotenes
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Provitamin A (converted to Vit A in intestines)
Plant source of retinol from which mammals make 2/3 of
their Vit A
Carotenoids
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Largest group
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Functions
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Cell differentiation (eye, mouth, gut, respiratory tract,
immune cells, reproduction & growth)
Vision (retinal rod & cone cells) & maintenance of integrity
of conjunctiva & cornea
Sources
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Retinol: animal products, liver
Carotenoids: yellow, red fruits/vegetables & leaves
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Deficiency Syndromes
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3rd most common nutritional deficiency in world
S. & SE Asia, Africa & S. America
 Night, complete blindness & Xerophthalmia in malnourished
adults & children
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500K preschool school children/yr blind
Chronic illnesses can deplete tissue Vit A
Disorders w/ fat malabsorption
 CF, celiac disease, cholestatic liver disease, Crohn’s, pancreatic
insufficiency
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Xerophthalmia
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Inadequate fct of lacrimal glands
Night blindness
Bitot’s spots →corneal xerosis →keratomalacia
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Poor bone growth
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Dermatological problems
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Hyperkeratosis, follicular hyperkeratosis, destruction of
hair follicles and replacement w/ mucus secreting glands
Impairment of humoral & cellular immune system
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Effects on phagocytes & T cells
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Community wide administration of Vit A
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WHO recommended: beneficial effects on immunity
↓ U5MR by 25%
Replacement : q4-6 mos
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Infants 50K IU PO
Infants 6-12mo: 100K IU PO
Mothers: 200K IU PO w/in 8 wks delivery
Pregnant or women of reproductive age: small doses 10K IU/d or 25K
IU wkly
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Hi dose supplementation
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Children at hi risk Vit A deficiency:
*measles, diarrhea, respiratory diseases, severe malnutrition
(single dose if no supplement in 1-4 mo)
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Reduces complications & mortality
Treatment Xerophthalmia
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3 doses at age specific doses
1st immediately on diagnosis, 2nd the next day,
3rd dose 2 weeks later
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Functions
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Co factor for many reactions: amino acid & carbohydrate metabolism,
requirements of Vit related to carbohydrate intake
Catalyst in pyruvate → acetyl CoA
Role in initiation nerve impulse propagation
Transketolation of pentose phosphate pathway (WE, WKS)
Found in skeletal muscle, liver, heart, kidney, brain
½ life 10-20d, cont. supplementation required
Sources
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Yeast, legumes, pork, rice, cereals
Hi cooking temperatures, canning, pasteurization can destroy thiamine
(denatured at hi pH/temperature)
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Beriberi
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Infantile
Adult
 Wet or Dry
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Wernicke-Korsakoff syndrome
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Apparent between ages 2-3 mos
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Fulminant cardiac syndrome
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Cardiomegaly, tachycardia, cyanosis, dyspnea
Loud piercing cry, vomiting
Aseptic meningitis
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Vomiting, nystagmus, purposeless movements
Seizures, normal CSF
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Dry
Symmetrical peripheral neuropathy
 Sensory & motor distal extremities
 Acidotic, often w/ chronic diarrhea
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Wet
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Neuropathy
Cardiac: cardiomegaly, cardiomyopathy, CHF (hi output),
peripheral edema & tachycardia
Complication of Bariatric surgery & TPN
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Polyneuropathy w/ burning sensation extremities,
weakness, falls
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Wernicke’s encephalopathy (WE)
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Acute syndrome, emergent treatment required
Nystagmus, ophthalmoplegia, ataxia, confusion
Chronic alcoholics w/ thiamine deficiency
Wernicke’s Korsakoff syndrome (WKS)
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Chronic neurological condition, consequence of WE
Impaired short term memory & confabulation
Otherwise grossly normal cognition
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Blood thiamine concentration
ITKA erythrocyte thiamine tranketolase
Transketolase urinary thiamine excretion
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Requirements:
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RDA 1.2-1.4mg/d
Treatment Beriberi
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Bed rest
IV or IM 50-100mg/d x 7-14 d
PO of 10mg/d till full recovery
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Epi:
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Endemic in maize eating populations Central & S. Africa
Subsist on maize (deficient in tryptophan) & lots alcohol
Prisoners, refugees, poor urban/rural
Functions
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Niacinamide & nicotinamide: incorporated into NAD &
NADP
Function in many reactions : glycolysis, fatty acid/
carbohydrate/protein synthesis & metabolism, respiration
& detoxification
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Sources
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Plant & animal foods: yeast, meats,
cereals, legumes, seeds, dairy products
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Any hi protein diet of 100g/d (tryptophan → niacin)
Deficiency
Common in poorer countries w/ local diet cereal, corn,
sorghum
 Alcoholics, complication bariatric surgery/anorexia
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3 D’s
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Dermatitis
 Photosensitive, hyperpigmentation/roughening skin
 Forearms, & around neck (“Casal’s Collar)
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Diarrhea
 Smooth red & painful tongue, esophagitis, vomiting
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Dementia
 Insomnia, anxiety, confusion, disorientation, delusions,
hallucinations (like DT)
 Dementia, encephalopathy,
 Acute, precipitated by acute infection (typhoid)
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Carcinoid syndrome
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INH prolonged use
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Tryptophan → 5-OH tryptophan & serotonin (rather than
nicotinic acid)
Isoniazid depletes stores of pyridoxal phosphate, which
↑production tryptophan, precursor niacin
Hartnup Disease
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Autosomal recessive congenital disorder
Defect of membrane transport in intestinal & renal cells
responsible for absorption tryptophan
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Nicotinamide
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Chlorpromazine (for confusion)
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50mg TID PO
25-50 mg
Requirements
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14-18 NE (niacin equivalents) /day
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Epi
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Functions
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Laborers in S. Africa, S. Sudanese migrants
Prisoners, constant threat to refugees
Patients w/ severe malabsorption, alcoholics, drug addicts
Scurvy develops > 6mo severe deficient diet
Cofactor, enzyme complement, co substrate, antioxidant in many
reactions & metabolic processes (copper, iron, folic acid, Vit E)
Collagen synthesis
Fatty acid transport (mitochondial membrane w/ carnitine)
Neurotransmitters (synthesis of norepi & dopamine)
Prostaglandin metabolism, attenuating inflammatory response
Sources: Vegetable & fruit
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Marginal deficiency
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Signs
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Bleeding gums, retarded wound healing
Peri follicular hemorrhage (early)
Bruises, petechiae, coiled hairs, hyperkeratosis
Subperiosteal hemorrhages (very painful)
Arthralgias, Sjogren’s syndrome
Generalized systemic symptoms
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Weakness, malaise, joint swelling, edema,
Depression, neuropathy
Vasomotor instability
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Leukocyte ascorbic test
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Plasma concentration
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<0.2mg/dL
Xrays in infants
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Best test to prove deficiency
Knees: atrophic b ones, white line (calcified cartilage at metaphysis &
epiphysis)
Treatment
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Children: 100mg ascorbic acid TID x 1 week, the QD x several weeks till
full recovery
Adults: 300-1000mg QD x 1mo
Improvement constitutional symptoms 24 hr, skin in wks
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Principles of Medicine in Africa, Ed E. Parry,
R. Godfrey. 3rd Ed. Cambridge 2004
Clinical Manifestations of malnutrition in
children, Overview of water soluble vitamins
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