BIOCHEM ● BIOCHEMISTRY SHIFT

Common Nutritional Disorders in the Philippines

#4
Vheejay B. Tampol, R.N.D., M.D. May 2, 2022

● Updating Survey of Nutritional Status of Children & Other

LECTURE OUTLINE
Population
I. Present State of Nutrition in the Philippines ○ Conducted in–between the 5 year period of the NNS every 2-3 years
A. Department of Science & Technology – Food & Nutrition Research ○ Goal: rapidly assess the nutritional status of the Philippines
Institute (DOST–FNRI) ○ Latest: 6th Updating Survey in 2015
B. National Nutrition Survey (NNS) ● In 2018, instead of having the 9th NNS, DOST decided to conduct an
1. Data Collectors expanded national nutrition survey.
2. Components of the NNS
3. Uses of the Survey Results
II. Nutrition Assessment
A. Anthropometry
B. Anthropometric Measurements in Adults
III. Malnutrition
A. Overview
B. Markers of Malnutrition Risk
C. Protein–Energy Metabolism (Marasmus and Kwashiorkor)
D. Impacts of Malnutrition in the Body
E. Management
IV. Malnutrition–Related Syndromes Figure 1. History Background of the NNS and Updating Survey
A. Refeeding Syndrome
B. Frailty 1. DATA COLLECTORS
C. Cachexia
● Registered Nutritionist–Dietitians (RNDs)
V. Obesity and Related Metabolic Disorders ● Registered Medical Technologists (RMTs)
A. Obesity ● Registered Nurses (RNs)
B. Obesity and Diabetes Mellitus Type II ● Other allied health professionals
C. Obesity and Dyslipidemia
D. Obesity and Insulin Resistance
E. Obesity and Metabolic Syndrome 2. COMPONENTS OF THE NNS
F. Health Implications of Obesity
Table 1. Components of the NNS
VI. Most Common Micronutrient Deficiencies in the Philippines
A. Vitamin A Deficiency 1978 NNS 2013 NNS
B. Iodine Deficiency Anthropometry
C. Iron–Deficiency Anemia Biochemical
Dietary
I. PRESENT STATE OF NUTRITION IN THE PHILIPPINES
Clinical & Health
A. DEPARTMENT OF SCIENCE & TECHNOLOGY – FOOD & Socio–Economic
NUTRITION RESEARCH INSTITUTE (DOST–FNRI) Government Program
● EXECUTIVE ORDER 128, SECTION 22 Food Security
○ Mandated to undertake research that defines the citizenry’s Maternal
nutritional status, with reference to malnutrition problems, its IYCF
causes and effects and identify alternative solutions to them. Salt Survey
ADDITIONAL INFORMATION:
Executive Order No. 128 – Reorganizing the National Science and 1. ANTHROPOMETRY
Technology Authority by then President Corazon Aquino (s. 1987) ○ Physical growth (height and weight)
● Section 22 – Food Nutrition Research Institute. The Food Nutrition ■ Weight - using bathroom weighing scale or stadiometer
Research Institute, presently existing, is hereby reorganized and shall ■ Height - using measurement boards (children) or stadiometer
have the following functions: (older individuals)
○ [a] Undertake research that defines the citizenry’s nutritional ○ Body Composition – using tape measure
status, with reference particularly to the malnutrition problem, its ■ Mid Upper Arm Circumference
causes and effects, and identify alternative solutions to them; ■ Waist Circumference
○ b] Develop and recommend policy options, strategies, programs ■ Hip Circumference
and projects, which address the malnutrition problem for ○ Identify prevalence of:
implementation by the appropriate agencies; ■ Underweight
○ [c] Disseminate research findings and recommendations to the ■ Underheight
relevant end-users. ■ Thinness
■ Overweight
B. NATIONAL NUTRITION SURVEY (NNS) ■ Obesity
● EXECUTIVE ORDER 352
○ Designated statistical activity that will generate critical data for 2. BIOCHEMICAL
decision–making of the government and the private sector ○ Collection of human fluid samples
○ Comprehensive survey conductive every 5 years since 1978 ■ Blood (e.g. blood extraction for assessment of Vitamin A and
● Latest NNS: 8th NNS in 2013 iron deficiency)
■ Urine (e.g. measurement of iodine levels in urine
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 1
 ○ Identify prevalence of: → Specifically goal number 2 ( having a country with zero
■ Vitamin A deficiency hunger) and goal number 3 (having a country with good
■ Iron–Deficiency Anemia health and well being)
■ Other nutrient deficiencies ○ Philippine Development Plan (PDP)
○ Collected by registered medical technologists ■ National plan that guides the decision making plan for the next
decade
3. DIETARY ○ Philippine Plan of Action for Nutrition (PPAN)
○ Perform 24-hr food recall and food weighing ■ Normally sends targets for prevalence and certain laboratory
○ Collected by registered nutritionist–dietitians parameters that should be achieved every time the national
nutrition survey is being conducted
4. CLINICAL AND HEALTH ○ The Food Fortification Program
○ Involves ■ The compliance of the food manufacturing industries
■ BP measurement ○ 2018 Expanded National Nutritional Survey (ENNS)
■ Blood collection ■ Sample size:
■ Face-to-face interview → 45, 957 households
○ Identify prevalence of → 159, 926 individuals (interviewed and subjected to the
■ Elevated BP components ENNS)
■ High Fasting Blood Glucose ■ Results:
■ Dyslipidemia → Target goal of SDG 2: By 2030, end hunger and ensure
■ Behavioral Risk Factors access by all people, in particular the poor, people in
→ Smoking vulnerable situations, including infants, to safe, nutritious
→ Alcohol Consumption and sufficient food all year round.
→ Physical Activity
→ Unhealthy Diet ● Where are we in terms of the prevalence of malnutrition among
○ Collected by registered nurses and medical technologists children?

5. OTHERS
○ Data is primarily collected through face-to-face interviews
○ FOOD SECURITY
■ Assess for food security of at the household and individual level
■ Identify coping mechanisms and strategies
○ GOVERNMENT PROGRAM PARTICIPATION
■ Assess the household’s and member’s participation in selected
nutrition and related government programs
○ SOCIO–ECONOMIC CHARACTERISTICS OF
HOUSEHOLDS/INDIVIDUALS Figure 2. Prevalence of Malnutrition in Children
■ Identify/predict purchasing power by assessing:
→ Education ● Where are we in terms of prevalence of overweight among children,
→ Occupation adolescents and adults?
→ Type of Housing, Wall and Roof
→ Ownership of Different Types of appliances
○ INFANT AND YOUNG CHILD FEEDING
■ Identify feeding practices of Filipino children 0-23 months old
■ Identify other related factors affecting feeding practices
○ MATERNAL HEALTH AND NUTRITION
■ Determines the health and nutrition of mothers with children 0-3
years old

3. USES OF THE SURVEY RESULTS Figure 3. Prevalence of Overweight children, adolescents and adults
● To address nutrition problems by crafting policies & interventions
○ Micronutrient Supplementation ● Where are we in terms of the prevalence of Anemia?
○ RA 8976 – Philippine Food Fortification Act of 2000
■ Mandate all food manufacturers to voluntarily fortify common
food items of average FIlipino consumers
→ Chips are fortified with iron
→ Pancit Canton is fortified with Vitamin E
→ Rice is fortified with B vitamins
○ RA 8172 – Asin Law
■ Mandates all Filipinos should ideally use iodized salt in
preparation of food items
○ RA 10351 – Sin Tax Law
■ Increase tax imposed in distilled spirits to deter the general
population from buying alcoholic beverages Figure 4. Prevalence of Anemia
○ School Feeding Law
○ The First 1000 Days Law ● Where are we in terms of prevalence of Vitamin Deficiency?
■ Government is mandated to support all children from the time
they are born up to 2 years old
■ This is a critical period for provision of needed nutrients to
ensure maximum potential and growth
○ AO 2015–0014 – National Policies on Infant and Young Children

● For planning, targeting, implementing nutrition & related

intervention programs, goals & commitment
○ Sustainable Development Goal (SDG)
■ Each country is trying to achieve a certain goal Figure 5. Prevalence of Vitamin A Deficiency

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 2
● Where are we in terms of iodine status? ○ Familial factors
○ Ethnicity
■ e.g.: races/ group of people that will have a relatively higher
head circumference
○ Environment
■ e.g.: presence of war, famine, or natural disasters could impact
the accessibility of food

● In children and adolescents:

Figure 6. Iodine Status Based on Age Group
Figure 7. Urinary Iodine concentration, <50 mcg/L
● Where are we in terms of other nutrition parameters?
○ WHO International Growth Standards
■ For children aged <24 months (<2 years)
○ CDC Growth Charts
■ For children aged 24 months to 18 years
○ Height and Weight measurements are recorded as percentiles
■ Reflect the percentage of the total population of children of the
same sex who are at or below the same height or weight at a
certain age
■ When using a growth chart, weight or height (or combination of
the two) of a specific child is compared to the general
population of children
→ Growth charts are designed based on a specific number
of children/adolescents whose height and weight are
recorded to reflect a certain baseline
○ Children’s growth at every age can be monitored by mapping data
on growth curves:
■ Height-for-Age
→ Low values: chronic undernutrition (labeled as: stunted)
■ Length-for-Age
→ For those who cannot yet stand
■ Weight-for-Age
→ Low values: undernutrition/underweight
■ Weight-for-Length
→ Good measure of acute undernutrition (labeled as: with
wasting)

Figure 8. Other nutrition parameters

● Where are we in terms of implementation of Tobacco control?

○ SDG 3 (Good Health and Well-Being)
■ Target goal: Strengthen the implementation of the World Health
Organization Framework Convention on Tobacco Control in all
countries, as appropriate .

Figure 9. Other nutritional parameters

II. NUTRITION ASSESSMENT

Figure 10. Length-for-Age and Weight-for-Age percentiles (Boys)
A. ANTHROPOMETRY
EXPLANATION
● Obtaining physical measurements of an individual, comparing them to
● Length-for-Age and Weight-for-Age percentiles
standards that reflect the growth & development of that individual, & using
○ Y-axis: different measures for weight (lbs/kg) and height (in/cm)
them for evaluating overnutrition, undernutrition or the effects of nutrition
○ X-axis: Age in months
interventions over a period of time.
○ Find the intersection of the age and the weight or height of the
● Require training in the proper techniques using calibrated Instruments.
infant
Measurements of accuracy can be established by several clinicians
■ Example: 6 month-old infant weighing 6kg
taking the same measurement & comparing the results
→ Intersection falls below the 10th percentile. Which
○ Average of the results are usually the one recorded and interpreted.
means Weight-for-Age of the infant is relatively low
● Includes:
(undernourished).
○ Height/Length
○ Weight
○ Girth Measurements
○ Skinfold Thickness
○ Circumference Measurements (e.g.: head)
● When doing anthropometric assessments, always consider the impact of:
○ Birth weight
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 3
 ● Different weighing scales for other groups
○ Salter weighing scale
■ Used in a community setting with a diaper pouch where the
infant is placed
○ Automated weighing scale
■ In the clinical setting
● Recorded on the age and gender appropriate growth grid
● Use of BMI as a screening tool to identify those who are overweight and
obese

FIgure 11. Head circumference-for-Age and Weight-for-Length

EXPLANATION
● Head circumference-for-Age and Weight-for-Length percentile
○ Weight-for-Length Figure 12. Formula for BMI computation and Interpretation of BMI percentiles
■ X-axis: Length (cm/in) for Children and Teenagers
■ Y-axis: Weight (lbs/kg) EXPLANATION
○ Head circumference-for-Age ● Metric formula unit: kg/m2
■ X-axis: Age in months ● Imperial formula unit: lbs/in2
■ Y-axis: Head circumference (in/cm) ● The BMI is compared to the age of the child or adolescent to determine
■ Example: 12 month-old infant with a head circumference whether they are underweight, normal, overweight, or obese.
of 46cm
→ Find the intersection. It falls between 50-75 percentile. B. ANTHROPOMETRIC MEASUREMENTS IN ADULTS
→ After recording the equivalent percentile, a specific table ● BMI is used to assess the nutritional status
of interpretation is used to know whether it is normal, ● For hospitalized patients:
below, average or above average. ○ Measure the patient’s height to confirm their last recorded
measurement
1. LENGTH OR HEIGHT OF CHILDREN ○ Measure weight (at admission, current, and usual)
● Determined by the age of the child ○ Determine percentage of weight change over time (weight pattern)
● Recumbent length measurements ○ Determine percentage above or below usual or ideal body weight
○ Used for infants and children <2 or <3 years of age
○ Measured using a length board by two people 1. HEIGHT MEASUREMENTS IN ADULTS
■ Has 2 ends, the top part is immovable. Only the end that ● Direct and Indirect method
touches the feet of the child can be adjusted by another
clinician while the other holds the head of the infant, touching DIRECT METHOD
the upper board. ● Use of a Stadiometer
■ A tape measure is present in the other side of the board ● Adult is able to stand or recline flat
○ Recorded on the birth to 24 month growth grids to identify the ○ Tape measures can also be used
percentile rank
INDIRECT METHOD
● In the field of nutrition, as long as the child can already stand properly the
normal measures for height can be utilized ● For adults who cannot stand or stand straight
● Standing height ○ Scoliosis
○ For children capable of standing ○ Kyphosis
○ Measured using a rod or a stadiometer ○ Cerebral Palsy
■ Can also measure the weight ○ Muscular Dystrophy
○ Recorded on the 2 to 20-year growth grids ○ Contractures (burns)
● Sitting height ○ Paralysis
○ For children who cannot stand ○ Bedridden patients
○ Normally measure the arm span ● Knee-height measurements
● Recording on the proper growth grids provides a record of a child’s gain ● Arm span
in height over time and compares the child’s height with that of other ● Recumbent Length using a tape measure
children of the same age ○ Comatose
● Long-term nutritional adequacy is reflected by the rate of length or height ○ Critically ill
gain ○ Unable to move

2. WEIGHT IN CHILDREN AND ADOLESCENTS 2. HEIGHT MEASUREMENTS IN ADULTS

● More sensitive measure of nutritional adequacy than height ● Actual body weight (ABW)
● Reflects more recent nutritional intake ○ Weight measured obtained at the time of examination
● Provides a rough estimate of the overall fat and muscle reserves ○ Influenced by changes in the individual’s fluid status
■ Weight loss: Dehydration or Suboptimal Food Intake

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 4
 ○ % of Weight Loss is indicative of the extent & severity of an
individual’s illness
○ Benchmarks for evaluating weight loss
■ Defined by the Academy of Nutrition & Dietetics (AND) &
American Society of Parenteral and Enteral Nutrition (ASPEN)
as
→ Significant Weight Loss
→ Severe weight loss
■ Computed as:
% weight loss = 𝑈𝑠𝑢𝑎𝑙 𝑤𝑒𝑖𝑔h𝑡 − 𝑎𝑐𝑡𝑢𝑎𝑙 𝑤𝑒𝑖𝑔h𝑡 x 100
​ 𝑢𝑠𝑢𝑎𝑙 𝑤𝑒𝑖𝑔h𝑡
​ Figure 13. Classification of obesity as recommended by
Table 2. Weight Loss Definition the Asia-Pacific Task Force
● Asia-Pacific Task Force Recommendation
SIGNIFICANT WEIGHT LOSS SEVERE WEIGHT LOSS ○ Range of BMI is narrower
5% loss in a month >5% loss in a month ■ Helps push an individual to be more aware or vigilant of their
weight, height, and overall BMI or degree of adiposity
7.5 % loss in 3 months >7.5 % loss in 3 months ✓ NOTE: It would be better to use Asia-Pacific classification when dealing
with Filipino population
10 % loss in 6 months >10 % loss in 6 months

✓ NOTE: It would depend on the severity of weight loss whether the patient 4. CIRCUMFERENCE MEASUREMENTS IN CHILDREN
would be discharged and managed as an outpatient or should be admitted in a
● Useful in healthcare settings in which measurements are recorded
malnutrition ward for aggressive treatment. Those who are in severe weight
periodically (monthly or quarterly)
loss must be confined to determine if the cause is purely dietary related alone
○ Every 3 months
or other underlying conditions.
● Tracked overtime to identify trends & potential risk factors for chronic
conditions
● Usual Body Weight (UBW)
○ Another method to calculate an individual’s current or actual body
● Head Circumference (HC)
weight using % of UBW
○ Useful in children < 3 years old
○ Computed as:
○ Indicator of non-nutritional abnormalities
% weight loss = 𝐴𝐵𝑊 x 100 ■ Ex. congenital disorders
𝑈𝐵𝑊 ○ Affected by severe undernutrition
○ Use UBW instead of abw for those experiencing involuntary weight
loss
○ Depends on the memory of the patient's UBW, so it can be
unreliable and affects the accuracy of the computation

3. BODY MASS INDEX (BMI) or QUETELET INDEX

● Expressed as 𝑊 𝐻2
● Used to determine whether an adult’s weight is appropriate for height
● Indicates overnutrition or undernutrition
● Accounts for the differences in body composition by defining the level of
adiposity and relating it to height, eliminating dependence on the frame
size
● May also be calculated from nomogram
● Plotting computed BMI to determine the nutrition status
● Has the least correlation with the body height but with highest correlation
with independent measures of body fat
● Other measures of body fat is underwater weighing and dual x-ray
absorptiometry (more accurate but expensive and not ideal)
● Good way to assess adiposity of a person
● Important to remember:
○ BMI values tend to increase with age
○ Risk of mortality is increased in older adults with BMI <23 Figure 14. Measuring Head Circumference

Table 3. Classification of adult underweight, overweight and obesity ● Mid–Upper Arm Circumference (MUAC)
according to BMI ○ Measured in “cm” halfway between the acromion process of the
CLASSIFICATION BMI RISK OF COMORBIDITIES scapula and olecranon process at the tip of elbow
○ Measured when assessing nutritional status of children aged 6-59
Low (but risk of other clinical months of age
Underweight <18.50
problem increased) ■ Good measure of protein composition and fat stores of body
○ Can be compared to the WHO standards to determine malnutrition
Normal 18.50 - 24.99 Average
○ Ex: 3 years, 12 cm, low the yellow marker → falls below red zone
Overweight: ≥ 25.00 ■ Tape measure is coded (for MUAC) with red, yellow, and green
→ Green - normal MUAC value
Pre-obese 25.00 - 29.99 Increased
→ Yellow - alarming
Obese Class I 30.00 - 34.99 Moderate → Red - presence of malnutrition
● Further verify by performing anthropometric or
Obese Class II 35.00 - 39.99 Severe biochemical parameters
Obese Class III ≥ 40.00 Very severe

✓ NOTE: Obese Class I is known to have normal interpretation as overweight

while Obese class II is known as morbid obesity
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 5
 Figure 15. Boundaries of Mid-Upper Arm Circumference

Figure 18. Boundaries of Hip Circumference

c. WAIST–TO–HIP RATIO
● Divide the WC/HC
● Used as benchmark for metabolic syndrome
● Consistent within findings of research predicting all cause fo CVD
mortality

Figure 16. Measuring Mid-Upper-Arm Circumference (MUAC)

5. CIRCUMFERENCE MEASUREMENTS IN ADULTS

● Mid-Upper arm Circumference (MAC) Figure 19. WHO cut-off points and risk of metabolic complications
○ Similar method to the ones used for children
○ Different table of interpretation d. WAIST–TO–HEIGHT RATIO
● Waist and Hip Circumference
● Waist-to-Hip Ratio ● Divide the WC/ height
● Waist-to-Height Ratio ● Measure of distribution of adipose tissue
● Higher the values, greater the risk of acquiring metabolic syndrome and
a. WAIST CIRCUMFERENCE (WC) other obesity-related atherosclerotic CVDs
● Obtain by measuring the distance around the narrowest area of the ○ May be interpreted that fats within the body are prominent and
waist, between lower rib, iliac crest and above umbilicus (halfway to iliac widespread
crest, midpoint)
○ Using a stretchable tape measure at the level of the umbilicus →
read the value
● Non-stretchable tape measure check → read value
● Excess body fat around the abdomen out of proportion to total body fat
→ risk factor for chronic diseases associated with obesity and metabolic
syndrome
● Abdominal Obesity
○ WC: ideal way to assess the risk/prevalence of developing obese
● Waist circumference (WC)
○ Indicator of supplementary BMI
Figure 20. Interpretation of Waist-to-Height Ratio by Gender

III. MALNUTRITION

A. OVERVIEW
● A gradual decline in nutritional status which leads to a decrease
in functional capacity and other complications
● Worldwide public health concern with medial, social and
economical impacts
○ Example: Labor force having obese as the prevalent
Figure 17. Combined recommendations of BMI and WC cut off points made complication → decrease in economical productivity
from overweight or obesity and association with disease risk ● In the developed world (e.g. Canada), common among:
○ hospitalized patients (ICU, CCU)
● Higher cut off more than 1.02 cm, values fall between very high to ○ elderly population (living in home for the aged)
extremely high disease risk
○ Still varies on obesity classification B. MARKERS OF MALNUTRITION RISK
● SIGNIFICANT RISK:
b. HIP CIRCUMFERENCE (HC) ○ Unintentional weight loss of 10% of body weight within the
● Measured at the widest area of hips at the greatest protuberance of the preceding 3-6 months
buttocks ○ BMI <18.5 kg/m2
● Identify the area of the great trochanter, palpate tip of bone ○ Course of Acute Illness: Inability to eat for >5 days
● Once palpated, non stretchable tape measures around the hip
● Becomes more meaningful when it is compared to the weight C. PROTEIN–ENERGY MALNUTRITION
management → Waist-Hip Ratio (WH4) ● Most common form of malnutrition in the world
● Prevalent in developing countries among infants and young
children
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 6
● Classified into 2 types: ● Due to inadequate intake of protein with adequate energy intake
○ Marasmus (Acute Form of Undernutrition)
○ Kwashiorkor ○ Relatively high carbohydrate content in the diet
○ Change of balance in the three macromolecules
1. MARASMUS ○ Lowering of protein content was complemented by a rise in
either the fat or most of the time, carbohydrate
● Latin word (1650s) which means “wasting away of the body” ● May occur in a background of marasmus
● Greek word marasmos: a wasting away, withering or decay ● Often precipitated by condition of increased protein demand (e.g.
● Due to inadequate intake of both protein and energy Infections or after Trauma)
● Develops over months/ years ● Visceral tissues are not spared
● Loss of muscle tissue and subcutaneous fat ○ Main differentiating factor from marasmus
● Preservation of the synthesis of visceral proteins (e.g. Albumin) ○ Decreased albumin production in the liver
● Early stages of marasmus:no findings of edematous due to ○ Hypoalbuminemia
normal levels of albumin which controls osmotic pressure in blood ● Signs and Symptoms
○ Plump due to edema
■ Appears fat but it is edema
○ Dry, brittle hair
○ Diarrhea
■ High carbohydrate content of the diet
■ Sugar has an osmotic effect on the enterocytes
○ Dermatitis of various forms
■ Lack of protein
○ Retarded growth
● Hallmark: Edema due to low conc. of plasma albumin & loss of
oncotic pressure or vice versa
○ Edema may mask the weight loss
● Complications: Dehydration, Hypoglycemia, Hypothermia,
Electrolyte Disturbances, Septicemia

Figure 21. Marasmus.

DESCRIPTION:
1. Upper and lower extremities show the “cheek and bones
appearance”
2. Balding on some areas of the skull due to decreased protein synthesis
in the body
3. Child shows some form of ascites, explaining why abdomen is
enlarged
4. Most likely, the child has been experiencing chronic marasmus for
several years

● In the early onset of marasmus, ascites is not yet present due to

preservation of visceral proteins
● Signs and Symptoms
Figure 22. Kwashiorkor
○ Infants: thin, wasted appearance; small for age
■ Weight-Age values that matches undernutrition
■ Height-Age values is also low D. IMPACTS OF MALNUTRITION IN THE BODY
■ Chronic undernutrition in the past, and presently acute ● In the immune system:
undernutrition ○ Reduced number of T lymphocytes
○ Children: permanently stunted in physical & mental ○ Decreased cell-mediated immune response
development ○ Defects in generation of phagocytic cells,such as the
■ If not addressed, may cause them to die due to neutrophils, immunoglobulins, interferon, other components
complications from infections of the immune system
■ Nutrients help in the proper development of the ○ Secondary infections are the usual cause of death in PEM,
immune system; the body can’t launch a proper not starvation
immune response against pathogens found in ■ The superimposed bacterial, viral, and fungal infections
contaminated food and water
● Consequences of Protein–Calorie Malnutrition:
2. KWASHIORKOR ○ Decreased protein synthesis
○ Decreased activity of Na+/K+-ATPAse
● A native Ghanian word that mean “illness striking a child ○ Decreased glucose transport
when the 2nd child is born OR deposed child” ○ Fatty liver, liver necrosis, liver fibrosis
○ The first child is the one that normally suffers ○ Depression, apathy, mood changes
○ Frequently befalls a child when a baby replaced him at the ○ Hypothermia
breast, and weaning food were inadequate to meet his ○ Compromised ventilation
nutritional needs ○ Compromised immune system, impaired wound healing
○ Initially, the first child will have a relatively normal diet, but ○ Risk of wound breakdown
when the second child is born– from the relatively high ○ Decreased cardiac output
protein, normal carbohydrate, normal fat, and normal energy ○ Decreased renal function
diet– it shifts to a more carbohydrate diet, low protein, and ○ Loss of muscle strength
relatively low energy content ○ Anorexia
○ Because the focus of the mother is no longer on the first
child – the focus of the mother is now on breastfeeding the
second child
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 7
 E. MANAGEMENT C. CACHEXIA
● Combined with adequate water, good sanitation & adequate basic ● Weight loss predominantly related to disease (esp. Cancer or Sepsis)
health care ● Predominant loss of muscle (life-threatening)
● In famine areas, malnutrition treatment uses standard ○ Main feature of cachexia is sarcopenia or muscle wasting
preparations:
● Characterized by:
○ Formula 100 therapeutic milk (F100): a liquid diet with an
energy content of 100 kcal/100mL ○ Anorexia
○ Composed of dried skimmed milk, oil, sugar & a mix of ○ Muscle protein breakdown occurring earlier than in common PEM
vitamins & minerals without iron due to increased muscle catabolism & reduced muscle protein
● Community feeding programs: synthesis
○ Use life-sustaining general rations”: food packages that ● Other characteristics:
provide at least 2100 kcal/8786 kJ per day ○ Insulin resistance related to to increased glucocorticoid
■ More than enough to produce a positive energy
secretion (cortisol) from the zona fasciculata
balance
○ Contains grains, legumes, and vegetable oil ● Increased activity of pro inflammatory cytokines: TNF-α, INF-γ, IL-6
● Depends on the underlying conditions as well. If there is an ○ Stimulate the NF -κβ pathway: increased protein degradation
ongoing infection, antibiotics will be needed to help manage the through the ubiquitin proteasome pathway (proteins are
infection pre-maturely degraded because they are being tagged by ubiquitin)
○ Hypothalamic effects: increased BMR, lethargy and anorexia
IV. MALNUTRITION–RELATED SYNDROMES ● Common Laboratory Results with Nutritional Implications:
○ Increased plasma C-reactive protein (CRP)
A. REFEEDING SYNDROME
○ Hypoalbuminemia
● Develops as a normal consequence of inappropriate feeding of
○ Anemia
malnourished person
○ Ex. You’ve become very excited in correcting the problem so the
tendency is that you compute and then you prepare without actually V. OBESITY AND RELATED METABOLIC SYNDROMES
looking into the tolerability of the food or preparations → impacts the A. OBESITY
px’s biochemically
● An epidemic in the developed world
● Due to a major shift of fluid and electrolytes between the intracellular ● Defined in terms of body mass index (BMI)
and extracellular compartments
● Blood profile: decreased plasma magnesium, phosphate, potassium Table 4. Classification of BMI
brought about by increased insulin secretion
CLASSIFICATION BMI RANGE
○ The diet and preparation given are high in carbohydrates →
stimulates beta cells of the pancreas → more insulin Ideal Body Weight < 24.99
Overweight 25.00 – 29.99
B. FRAILTY
Obese 30.00 – 40.00
● A multisystem deterioration associated with age
○ Common among elderly population Morbidly Obese > 40.00
● Affects the nervous, endocrine, musculoskeletal, and immunologic
systems ● For Filipino patients, use Asia-Pacific BMI Classification
● Risk is increased by the presence of chronic diseases ○ Narrower values & aggressive impact in management
● Main feature: sarcopenia ● Genetic factors contribution: 30 - 70%%
● 3 Levels of Genetic influences:
○ Loss of muscle mass/ muscle wasting
○ Monogenic Obesity
○ After age 50: 1-2% loss of muscle/year ○ Polygenic predisposition to Obesity
○ If more than 2%, you are classified as sarcopenic ○ Monogenic resistance to Obesity
■ Adjust your diet specifically protein → chance to decrease the
possibility of developing certain frailty related complications 1. MONOGENIC OBESITY
● Other characteristics:
● Single genetic defects
○ Anorexia ● Strongly linked to obesity, irrespective (regardless) of environmental &
○ Lack of appetite behavioral influences
○ Weight loss ● Obey classical Mendelian inheritance
○ Exhaustion ● Exceedingly rare in the general population
■ Normally, mistaken for iron deficiency anemia
○ Slowness of gait
○ Low Daily Energy Expenditure
○ Muscular weakness
○ Higher levels of TNF-α and Interleukin-6
● Osteoporosis increases the risk of falls
● May be associated with deficiencies of:
○ Micronutrients
○ Vitamins (B6 and other B vitamins)
○ Amino acids
○ Some minerals
● On a cellular level, protein abnormal unfolding, misfolding, and
aggregation of proteins

Figure 23. The leptin appetite suppression pathway

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 8
● Leptin
○ Hormone produced by adipocytes
○ Leptine receptor
○ Suppresses appetite
■ In the hypothalamus, it will express a leptin receptor → leptin
binds to this receptor → stimulate the hypothalamus →
produces substances → will suppress appetite (specifically
POMC & CART)
■ Absence of the leptin receptor → arcuate nucleus of the
hypothalamus will not be inhibited → produce peptides (NPY &
AgRP) → increased appetite
○ Most overweight individuals overproduce Leptin
○ Defects in both the leptin gene and leptin receptor gene are very
rare in the human population
● Leptin Appetite Suppression Pathway
○ Amount of leptin increases as the fat stores increases
○ Appetite Suppressing Hormones - in response to the binding of
leptin to leptin receptors
■ POMC: Proopiomelanocortin
■ CART: Cocaine - and amphetamine-regulated transcript
○ Appetite Stimulating Neuropeptides - shis will be released if there Figure 24. Effect of TNFα on the expression of enzymes involved in
is NO leptin receptor activation fatty acid and triglyceride synthesis in the liver
■ NPY: Neuropeptide Y EXPLANATION:
■ AgRP: Agouti-Related Protein ● TNFα will mimic insulin
○ Normally, Insulin is stimulatory to SREBP-1c (produced in RER)
2. POLYGENIC PREDISPOSITION TO OBESITY ● SREBP-1c translocates in the Golgi apparatus → Packaged into a
vesicle so that it can be transported and protected against the impact of
● Presence of common polymorphisms in certain genes that proteases
increase the risk of obesity BUT only in those persons who ● SREBP-1c bound to vesicle passes through the nuclear membrane →
consume excess calories for prolonged periods of time Vesicle is cleaved by proteases
● In most cases, predisposition is relatively weak ● SREBP-1c would then bind to a Sterol-regulatory element (SRE)
● Common among general population ● SRE is located 5’ upstream on the genes responsible for the synthesis
of your
3. MONOGENIC RESISTANCE TO OBESITY ○ Acetyl CoA carboxylase
○ FA synthase
● Genetic polymorphisms that predispose to leanness even in persons
○ G3P acyltransferase
who consume excess calories over prolonged periods of time
● In summary, this figure tells us why TNFα, being a mimicker of
● Relatively rare in the general population
insulin, can also do the same thing to your SREBP-1c
● Even if you don’t have high insulin but because of the upregulation of
TNFα the same effects are achieved which are the elevation of the ff
B. OBESITY AND DIABETES MELLITUS TYPE II enzymes:
● 80% of people with Type 2 diabetes are overweight ○ Acetyl CoA carboxylase
● Incidence of Type 2 diabetes has increased in parallel with the incidence ○ FA synthase
of obesity ○ G3P acyltransferase
● In obesity, the increased number and/or size of adipocytes lead to ● These enzymes allow the synthesis and release of your FFAs and
increase endocrine activity TAGs into the circulation
○ Adipocytes - not just a storage, it is an endocrine organ that
produces hormones (adipokines) - pro-inflammatory effects in the
● Results of the mechanism of TNFα :
body
○ Increased circulating FFAs
■ Increased FFA influx to the liver
Fat-Engorged Adipocytes:
■ Increases fatty acyl CoA available for TAG synthesis & acetyl
○ Overproduction of:
CoA available for lipogenesis
■ Leptin
■ Increased production of TAG-rich VLDL
→ hormone responsible in signalling your brain to stop eating
→ Expected due to inc. lipogenesis
further
■ Decreased clearance of VLDL
■ Resistin
→ VLDL contains TAG that cannot be released to the
■ Cytokines or Adipokines
peripheral tissue because of inactivated lipoprotein lipase,
→ (TNFα)
a secondary effect of the activation of hormone-sensitive
lipase.
TUMOR NECROSIS FACTOR (TNFα) ■ Increased TAGs in the circulation
● With strong paracrine effect on adipose tissue
○ Can activate nearby adipose cells C. OBESITY AND DYSLIPIDEMIA
● Stimulates hormone-sensitive lipase ● Elevated TAGs
○ Increases FFA in the circulation ● Decreased HDL levels
○ Inhibits lipoprotein lipase ● Increased risk for CVD due to the factors mentioned above
■ Decrease clearance rate of TAG-rich VLDL from the circulation
○ Activates SREBP-1c D. OBESITY AND INSULIN RESISTANCE
■ transcription factor that increases enzymes for FA & TAG ● Organs involved:
Biosynthesis
○ Skeletal muscle
○ Decreases HDL levels, decreasing the expression and activity of:
○ Liver
■ Lecithin: Cholesterol Acyltransferase (LCAT)
● Increased circulating FFAs stimulate PKC-θ
■ ATP-binding cassette (ABCA1 & ABCG1)
○ Catalyze serine phosphorylation of the insulin receptor 1& 2
■ Apo A-1 & Apo A-IV
substrates (instead of tyrosine phosphorylation)
→ Needed in the synthesis of HDL ○ Interferes with Insulin stimulation of the PKB signaling pathway

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 9
 ● In the liver:
○ Interferes with the ability of insulin to downregulate gluconeogenesis

Figure 27. PI3k-PKB signaling pathway in the liver

● The primary impact of PKC-θ is to downregulate glycolysis and

upregulate gluconeogenesis
○ Increased gluconeogenesis, decreased glycolysis
● Early stages of obesity:
Figure 25. Mechanisms involved in insulin resistance in muscle and liver ○ The pancreas will compensate for the insulin resistance by
overproducing insulin. Overtime, one to two decades, the pancreas
● PKC-θ inhibits normal activity of Insulin receptor Substrates 1 and 2 → loses the ability to do this, called decompensation. This mimics
affects PI3K signaling pathway type 1 DM.
○ PI3K signaling pathway decreases gluconeogenesis and increases ○ Hyperglycemia ensues once the pancreas becomes fully
glycolysis decompensated.
○ Increased risk of several types of cancer due to increased cell
● Inhibition of PI3K
proliferation because of high levels of sugar.
○ Inc. gluconeogenesis and decrease glycolysis
○ Stimulation of SNS
■ Increased FFAs competitively inhibits
■ Sodium and water retention
→ Glucose uptake by both GLUT 2 in the liver, GLUT 4 in ■ Hypertension (impact of aldosterone)
the skeletal muscle ■ Vasoconstriction
■ Hyperglycemia results due to
→ decreased uptake in the muscle and liver
→ Increased production of glucose in the liver E. OBESITY AND METABOLIC SYNDROME
● FFAs competitively inhibit the entry of glucose using the GLUT 2 in the ● The condition that exists between the onset of insulin resistance and the
liver GLUT 4 in the skeletal muscle. This results to hyperglycemia due development of Type 2 Diabetes
to: ● Not universally accepted since the defining conditions do not occur
○ Decreased uptake in the muscle and in the liver simultaneously in a given person
○ Increased production of glucose in the liver through ● WHO definition is the presence of:
gluconeogenesis ○ Abdominal obesity
○ Dyslipidemia
● In the muscles: ■ Elevated TAG-rich VLDL & decreased HDL
○ Interference in the ability of insulin to stimulate translocation of the ○ Hypertension
GLUT4 transporter to the membrane. ○ Insulin resistance
○ Insulin would activate the PI3K-PKB signaling pathway which would ○ Modest increase in FBS (Fasting Blood Sugar)
stimulate translocation of GLUT4 from the cytoplasm to the cell ○ Prothrombotic state
membrane, but in the presence of PKC-θ which is stimulated by ○ Proinflammatory state, an elevated C-reactive protein
FFAs, the process is stopped.

Figure 26. PI3k-PKB signaling pathway in the muscles

Figure 28. Schematic of the metabolic response to obesity over time.
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 10
● Being overweight stimulates TNF-alpha increasing FFAs which contribute ■ Normal immune cells such as the resident
to insulin resistance. Once other factors have been met, metabolic macrophages/neutrophils are either deficient in that area or not
syndrome can develop: responding as expected
○ Elevated Insulin ○ Blindness
○ Normal blood sugar ■ Most familiar
○ High triglycerides ■ Most important preventable causes of blindness in humans
○ Low HDL ■ Earliest signs:
○ High Blood Pressure → Loss of sensitivity to green light
● Pancreas will start compensating by producing more insulin, causing → Impairment to adapt to dim light
hyperinsulinemia. → Night blindness
● If there is no management your metabolic syndrome can develop into ■ With progression to deficiency this can lead to further
Type 2 DM, which will show: impairment of the ability to adapt to dim light and then that’s
○ Pancreas will stop compensating, dropping insulin level when one can have night blindness
○ High Blood Sugar ○ Increased susceptibility to cancer
○ High Triglycerides ■ Related to a deficiency of beta-carotenes or whole family of
○ Low HDL carotenoid, which are normally transformed in the body to other
○ High Blood Pressure Vitamin A forms
● Prognosis of Type 2 DM depends on the compliance of the patient to ■ Decreased protection from free oxygen radicals (carotenoids)
medications. ■ Structure of carotenoid
→ A lot of double bonds: easily a good target of free oxygen
F. HEALTH IMPLICATIONS OF OBESITY radicals
→ Instead of the free oxygen radical damaging the double
● Primary risk factor in:
bonds of polyunsaturated fatty acids in the cell membrane,
○ Coronary Heart Disease
Vitamin A would be sacrificed for this purpose
○ Hypertension
■ Decreased regulation of cell growth due to lack of retinol and
○ Diabetes Mellitus
retinoic acid
● Associated with:
○ Inflammatory diseases
○ Some cancers 1. MILD DEFICIENCY
○ Bone and joint disorders (ex. osteoarthritis) ● Night blindness: earliest symptoms for most cases
○ Breathing disorders ● Follicular hyperkeratosis (roughly keratinized skin resembling
■ Higher rates of bronchial asthma exacerbation goosebumps
● Majority are reversible ○ Described as having chicken skin
● Nutritional therapy aims to reduce weight to ideal body weight ○ If you touch the surface of the skin, you will see goosebumps
● A short-term weight gain is observed when dieting due to the retention of wherein you won’t see any hair growing in that area
water that is produced during the catabolism of fats ○ Sign of excessive keratin synthesis due to the downregulation of the
○ Discuss possible complications gene responsible for keratin production
○ Because of the lack of retinoic acid or retinol
VI. MOST COMMON MICRONUTRIENT DEFICIENCIES ● Anemia
IN THE PHILIPPINES ○ A non-iron related type of anemia which can be checked by a CBC
● Vitamin A deficiency ● Increased susceptibility to infection and cancer
● Iodine deficiency disorders ○ Patients can manifest mild to moderate types of infection
● Iron deficiency anemia ○ Early onset of cancer

A. VITAMIN A DEFICIENCY
● Three main causes:
1. Inadequate Dietary Intake
■ Common among all types of deficiencies
■ Number one consideration
2. Severe Liver Damage
■ Vitamin A is a fat soluble vitamin, much of its storage is in the
liver
3. Fat Malabsorption Syndromes/Diseases
■ Absorption of Vitamin A requires presence of normal amounts
of fat as part of the chyme
● Clinical manifestations
○ Lack of mucus secretion and drying of epithelial tissues
Figure 29. Follicular hyperkeratosis
■ Failure to synthesize glycoproteins (Retinyl Phosphate)
■ Due to the lack of this form of Vitamin A (Retinyl Phosphate), 2. SEVERE DEFICIENCY
this will affect the normal ability of the body to produce
glycoproteins ● Xerophthalmia: progressive keratinization of the cornea
○ Excessive keratin synthesis (Horny Keratinized Surface) ● Infections: Succumb to many types of infections
■ Failure to downregulate the synthesis of keratin ● Eye hemorrhages: Keratinization as an area of bleeding
■ Deficiency of two forms of Vitamin A (Retinol &/or Retinoic ● Loss of vision
Acid) which are involved in downregulation of keratin synthesis ○ Severe Vitamin A deficiency with Xerophthalmia
○ Anemia ○ Most of the time are permanently blinded
■ Lack of transferrin
■ Related also to lack retinol &/or Retinoic Acid
○ Increased susceptibility to infections
■ Due to the increased keratinization of mucosal cells lining the
RT, GIT, and GUT
■ The excessive keratin can easily causes the development of
fissures in the mucosal membranes
→ Allows fast entry of microorganisms in the systemic
circulation

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 11

Figure 30. Keratin already obscuring the whole vision
3. MANAGEMENT
Figure 31. Schedule for taking Vitamin A supplements
EXPLANATION
● Table from the WHO on the schedule for taking Vitamin A
● Recommended dose of VItamin A depending on the age group
● Unit: Retinol equivalents
● Depending on the condition, several doses that can be given
● Most of these are oral administration
● Ranges from 15, 000 - 30, 000, or even as high as 200,000 retinol
equivalent per day, depending on the associated situation
Figure 32. Latest revision for Vitamin A supplementation
EXPLANATION
● More specifically introduced for children with Vitamin A deficiency age 6
- 59 months of age
● Major revision: inclusion of children who are HIV +
● Basic doses: 100,000 IU or 30 mg retinol equivalents for the younger
ones and for the older ones, 200,000 IU (60 mg RE) Vitamin A
○ Frequency:
■ Younger age group: 1x a month
■ Older age group: every 4 - 6 months
→ Assumption is we are also correcting the diet of the
child, diet is also important source of Vitamin A
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO
● Medical Nutrition Therapy
○ Consume the recommended daily amount of Vitamin A
○ Prevent further derangements of existing levels of Vitamin A, it is
best to plan a diet that meets the daily recommended amount of
Vitamin A
■ Follow 2015 PDRI recommendations
Figure 33. PDRI recommendations of daily Vitamin A intake
EXPLANATION
● Seen in figure x, the amount of Vitamin A as expressed in micrograms
of Retinol equivalent is more or less the same for the age group
● For 0 - 5 months old it’s 380 μg per retinol equivalence
● Increases to 400 μg when you enter 6 - 11 months old until 6 - 9 years
old
● But when you enter the first stage of adolescence, 10 - 12 years old, it
further rises to 500 per retinol equivalent and this value is maintained
for adolescent females aged 13 - 15
○ For males, more significant increase to 700 - 800
● For adolescents (males) aged 19 - 70 years old, the amount
recommended is 700 μg per retinol equivalent
○ For females it’s 100 μg per retinol equivalence lesser, but you
have to add 300 - 400 μg per retinol equivalence if the female
enters the state of pregnancy or lactation respectively
B. IODINE DEFICIENCY
● Most common cause of preventable mental retardation and brain
damage in the world
● Present in nearly 1⁄3 of the world’s school-age children
● Manifestations in children:
○ Goiter
○ Poor school performance
○ Or a combination of the two
● During pregnancy, severe iodine deficiency leads to:
○ Cretinism - extreme and irreversible mental and physical retardation
○ IQ is around 20 (Normal:100)
○ Can survive until adulthood but cannot reach their maximum linear
growth potential
○ Can be prevented with prompt diagnosis and treatment
■ Pregnant women are normally screened for the concentration
of iodine in urine
12
 Figure 34. Cretinism
EXPLANATION
● Infants with cretinism can survive into adulthood but they cannot reach
their maximum growth or linear growth potential
● In severe cases, they will have mental retardation which will limit the
ability to engage in variou societal activities

1. CAUSES OF DEFICIENCY STATES

● Inadequate Dietary Intake
● Excessive consumption of goitrogens
○ Goitrogen
■ Substance that enlarges the thyroid gland
■ Causes toxic goiter
■ Forms a complex with iodine which prevents its uptake via the
Na/I symporter
■ Lack of iodination of your thyroglobulin thereby decreasing the
production of T3 and T4
■ Occur naturally in cabbage, kale, brussel sprouts, cauliflower,
broccoli, kohlrabi Figure 36. PDRI recommendations of iodine intake
● Antithyroid Drugs EXPLANATION
○ Certain drugs can prevent the thyroid from taking up and ● For 0 - 5 months old to 3 - 5 years old, regardless of gender, 90 μg
concentrating iodine or incorporating iodine to thyroglobulin should be consumed per day
● For 6 - 12 years old, regardless of gender, 120 μg should be consumed
2. GOITER
per day
● One of the basic physical manifestations of iodine deficiency ● For 13 years old onward 150 μg should be maintained
● An enlargement of the thyroid gland due to: ● 100 μg per day should be added for pregnant women to prevent
○ Iodine deficiency (Simple Goiter) development of cretinism
○ Malfunction of the gland
● May be the earliest and most obvious sign of iodine deficiency
○ Normally when you see patients coming in the clinic with goiter you C. IRON–DEFICIENCY ANEMIA
already have an idea that you have to rule out whether it is dietary or ● Characterized by the production of microcytic, hypochromic erythrocytes
non-dietary related ○ Microcytic - small than normal
○ Confirm hypothyroidism with signs and symptoms: ○ Hypochromic - Diminished level of circulating hemoglobin
■ Sluggishness ● Last stage of iron deficiency
■ Weight Gain ○ A person has already been experiencing iron deficiency for several
month or years before clinical manifestations appear
● Represent the end point of a long period of iron deprivation

1. CAUSES OF DEFICIENCY STATES

● Inadequate dietary intake secondary to a poor diet without
supplementation
● Inadequate absorption resulting from diarrhea, achlorhydria, intestinal
disease such as celiac disease, atrophic gastritis, partial or total
gastrectomy, or drug interference
● Inadequate utilization secondary to chronic gastrointestinal disturbances
● Increased iron requirement for growth of blood volume, which occurs
during infancy, adolescence, pregnancy, and lactation, and which is not
being matched with intake
● Increase excretion because of excessive menstrual blood (in females);
hemorrhage from injury; or chronic blood loss from a bleeding ulcer,
Figure 35. Advanced case of Goiter. Anterior portion of neck is obstructed bleeding hemorrhoids, esophageal varices, regional enteritis, celiac
disease, Crohn’s disease, ulcerative colitis, parasitic or malignant disease
3. MANAGEMENT ● “Increased destruction” of iron from iron stores into the plasma and
● Eat iodine rich foods defective iron use caused by a chronic inflammation or other chronic
● Use iodized salt disorders
● Consume the recommended daily amount of dietary iodine (set by PDRI)
2. SIGNS AND SYMPTOMS
● Reflection of a malfunction of a variety of body organ systems
○ Iron is a trace mineral that is utilized by almost all cells because of
its importance in hemoglobin production
○ Heme portion of hemoglobin will not be produced properly and affect
oxygen metabolism (especially the delivery of oxygen to peripheral
tissues)
(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 13
● Musculoskeletal system: Decreased work performance & exercise
tolerance
● Neurologic: Fatigue, anorexia, pica, pagophagia, abnormal cognitive
development in children
○ Pica - consumption of non-food items (ex. soil)
○ Pagophagia - ice eating
● Growth abnormalities
● Early onset epithelial disorders
● Reduction in gastric acidity
● Reduced immunocompetence
○ A possible sign of early iron deficiency
○ Especially defects in cell-mediated immunity and the phagocytic
activity of neutrophils
■ Iron is utilized in the synthesis of phagocytic cells specifically
neutrophils and macrophages
○ Results to frequent infections
● Restless Leg Syndrome (RLS)
○ With leg pain or discomfort
○ May result from a lack of iron in the brain that alters dopamine
production and movement
○ Can also be caused by:
■ Glutamate imbalance (excessive glutamate production)
■ Pregnancy state - compress the circulation of blood especially
in the lower extremities
■ Any form of peripheral neuropathy (Vit B6 or B12 deficiency)
■ Fibromyalgia
■ Smoking
● Severe Cases:
○ Defects arise in the structure and function of the epithelial tissues
(especially of the tongue, nails, mouth and stomach)
○ Skin may appear pale in people with lighter complexions
○ Inside of the lower eyelid may be light pink instead of red regardless
of skin tone (Pale Palpebral Conjunctiva)
○ Atrophy of the lingual papillae
○ Burning sensation and erythematous tongue redness
○ Glossitis: completely smooth, waxy, and glistening appearance of
tongue
○ Angular stomatitis
○ A form of dysphagia (difficulty swallowing)
○ Gastritis leading to hypochlorydia (low stomach acid)
■ Problem in the absorption of certain minerals and vitamins (ex.
B12) because of the reduction in gastric acid
○ Koilonychia (Spoon-shaped nails)
● Progressive and Untreated cases lead to:
○ Cardiovascular and respiratory changes
○ Cardiac or respiratory failure
3. ORAL IRON SUPPLEMENTATION
● One of the major treatments
● Form given: Inorganic iron (Fe2+) on an empty stomach
● Frequency & Duration: 3x a day for 3-6 mos
○ At least 3 months because the lifespan of an RBC is about 3 mos
around 90-120 days
● Dosage:
○ Adults: 50-100 mg elemental Fe, 3x a day
○ Children: 2-6 mg/kg BW divided into 3 doses per day
● Use of Micronutrient Powders (MNPs) containing iron may be useful
methods of home food fortification for children under age 2
○ Can be added to semisolid foods without affecting its sensory appeal
● Chelated Iron (combined with amino acids or Krebs cycle intermediaries)
○ Includes ferrous fumarate, succinate, aspartate and bisglycinate
○ Best form to give if budget is not an issue
○ More bioavailable than non chelated iron
○ Less affected by inhibitors of iron absorption (ex.Phytate, oxalate,
phosphate, and calcium)
○ Less GIT disturbances than elemental iron (esp. Ferrous
Bisglycinate)
○ Can be given at a lower dose to reduce costs
● Oral Iron Supplement Side Effects (GIT-related):
○ Nausea
○ Epigastric discomfort
○ Distention
○ Heartburn
○ Diarrhea or constipation
○ Darkening of the stool
○ If GIT-related side effects occur, advise patient to take the iron
supplements with meals
○ Disadvantage: Sharply reduces iron absorbability
ROLE OF VITAMIN C SUPPLEMENTATION
● Enhances iron absorption at standard doses
○ Vit. C can reduce the ferric form of iron and convert it into ferrous
○ In the intestinal lining you only have a divalent metal transporter
which would only allow divalent cations such as ferrous
■ Ferrous (Fe2+) - present in meat
■ Ferric (Fe3+) - present in fruits and vegetables
● But at higher doses it may also increase gastric irritation by intensifying
oxidative stress in GIT
○ Can further increase the amount of oxidized iron
● Better alternative: Consume vitamin C-rich food/drinks (ex. Orange juice)
together with your iron supplement
EFFECTS OF ORAL IRON SUPPLEMENTATION
● Effects can be readily achieved if there is absorption of 10-20 mg of
Fe/day
○ Permits RBC production to increase approx 3x the normal rate
○ In the absence of blood loss, hemoglobin concentration to rise at
a rate of 0.2 g/dL daily
● Increased reticulocytosis is seen within 2-3 days BUT affected persons
may report subjective improvements in mood and appetite sooner
● Hemoglobin level will begin to increase by day 4
● Iron therapy should be continued for 4-6 months, even after restoration of
normal hemoglobin levels, to allow for repletion body iron reserves
(specifically Ferritin)
POSSIBLE CAUSES OF FAILURE TO CORRECT ANEMIA
VIA ORAL IRON SUPPLEMENTATION
● Patient may not be taking the supplemental iron as prescribed due to
gastric distress
● Bleeding may be continuing at a rate faster than the erythroid marrow can
replace RBCs
○ Internal bleeding - peptic ulcer disease or esophageal varices
● Supplemental iron is not being absorbed, possibly as a result of
malabsorption secondary to steatorrhea, celiac disease, or hemodialysis
○ Shift to parenteral iron administration

Table 5. Advantages and Disadvantages PARENTERAL IRON ADMINISTRATION

FORM ADVANTAGES
Most commonly studied
FERROUS SULFATE
Least expensive
CARBONYL IRON Generally well-tolerated
(SLOW IRON) with few GI side effects
Better absorbed
CHELATED IRON Fewer side effects
Less constipating
● Best used for patients who are receiving erythropoietin
DISADVANTAGES
○ EPO - stimulates bone marrow to undergo erythropoiesis
● Replenishment of iron stores by this route is faster
Most constipating
○ More expensive and carries additional risk
● 3 Forms that can be given
Slow rate of ○ Iron Dextran (MOST COMMON)
solubilization which ○ Iron Sucrose
slows absorption ○ Ferric Gluconate
■ Alternative to Iron Bisglycinate
More expensive

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 14
 4. MEDICAL NUTRITION THERAPY Table 6. PDRI Requirements for Iron
AGE GROUP MALE (in mg) FEMALE (in mg)
FORMS OF DIETARY IRON
INFANTS (in months)
● Heme iron (Ferrous)
○ Meat-fish-poultry (MFP) factor 0-5 0.4 0.4
○ Organic form of iron in meat, fish, and poultry
○ Approximately 15% is absorbable 6-11 10 9
○ Part of the heme molecule CHILDREN (in years)
● Non heme iron (Ferric)
○ Also found in some MFP + legumes, grains vegetables, herbs, and 1-2 8 8
fruits 3-5 9 9
○ Approximately 3-8% is absorbable
○ Depending on the presence of enhancing factors (ex. Vit.C, MFP) 6-9 10 9
10-12 12 20
BIOAVAILABILITY OF DIETARY IRON
13-15 19 28
● Depends on the iron status of an individual
○ With IDA: 20-30% of dietary iron is absorbed 16-18 14 28
○ Without IDA: 5-10% of dietary iron is absorbed ADULTS
○ Body adjusts depending on the demand or need of the cells
19-29 12 28

GOOD SOURCES OF IRON 30-49 12 28

● Contain a substantial amount of iron in relation to its calorie content 50-59 12 10
● Contributes at least 10% of the Fe RDA
60-69 12 10
● Best sources:
○ Liver kidney, beef, dried fruits, dried peas and beans, nuts, dark >70 12 10
green leafy vegetables, fortified whole-grain breads, muffins,
cereals, nutrition bars PREGNANT +10
● About 1.8 mg of iron must be absorbed daily to meet the needs of LACTATING +2
80-90% of adult women, adolescent boys and girls

APA REFERENCES
INHIBITORS OF DIETARY IRON ABSORPTION
● Batch 2024. (2021). Common nutritional disorders in the Philippines.
● Inhibitors that form a complex with iron thereby preventing its absorption [PDF]
across the enterocyte ● Tampol, V. (2022). Common nutritional disorders in the Philippines.
○ Carbonates [Lecture Video on Panopto]
○ Oxalates
○ Phosphates FREEDOM WALL
○ Phytates - in whole grain breads, cereals, legumes
○ Vegetable fiber YOWN FINAL TRANS NA!!! Nakapaglagay na din ako ng something
● If iron supplements are taken with meals: tea and coffee can reduce iron sa Freedom Wall ahaha.
absorption by 50% through the formation of insoluble iron compounds
with tannins Thank you po, Section C for allowing me to serve you all. Thank
● Iron in egg yolk is poorly absorbed because of the presence of phosvitin you for your cooperation in the last 5 months. Vice Chief of Trans
Patrick, Serge Ry and Colonel Nyel, thank you. Trans group leaders,
thank you. Thank you everyone. Ily all. Sa uulitin :))
MANAGEMENT
● Consume the recommended daily amount of dietary iron – Trans Chief Marly

(TWG) MARTIN M, MOSQUEDA, NAZAR, NEBRES, NERI, NERY, NG, NICOLAS, NIERRA, NIEVA, OCAMPO, ORTEGA; (TEG) MARTIN M, MERCADO 15