epidemiology- nutrition

Epidemiology-Nutrition

Mbongue N. Germaine S., Msc.Ph.D. (finalization)

Muenster University of Applied Sciences, Germany/ Charité-Universitätsmedizin Berlin, Germany /University of Dschang

Cameroon

Course outline

• Major public health relevant nutritional problems

• Case study: developing countries• Protein Energy Malnutrition (Dr. Zambou)• Micronutrient deficiency (Mbongue)• Obesity (Mbongue)

Vitamin A

• What is Vitamin A– Is a lipid soluble organic compound, essential in

the diet in small amounts and that are involved in fundamental functions in the body

– Vitamin A includes provitamin A carotenoids, that are dietary precursors of retinol

Functions of Vitamin A

• Vision:– Released all-trans retinol is converted to all-trans retinol,

which can be transported across the inter photoreceptor matrix to the retinal epithelial cell to complete the visual cycle.

– Inadequate retinal available to the retina results in impaired dark adaptation known as ‘Night blindness

Functions of Vitamin A

• Gene expression:• Vitamin A may interacts with thyroid hormone and

vitamin D to influence gene transcription.• Through the stimulation and inhibition of transcription

of specific genes, retinoic acid plays a major role in cellular differentiation, the specialization of cells for highly physiological roles.

• Integrity of epidermal and mucosal surfaces, and thus the physical barrier against the environment

Function of Vitamin A

• Red blood cell production:– Red blood cells, like all blood cells, are derived from

precursor cells called stem cells, which are dependent on retinoids for normal differentiation into red blood cells.

Functions of Vitamin A

• Nutrient interaction: – Vitamin A and Zinc

• Zinc deficiency is thought to interfere with vitamin A metabolism in several ways. Zinc deficiency results in decreased synthesis of retinol binding protein(RBP),which transports retinol through the circulation to tissues (e.g.,the retina). (health consequencies of zn deficiency on Vitamin A unclear)

– Vitamin A and Iron• Vitamin A supplementation has been shown to have

beneficial effects on iron deficiency anemia and improve iron nutritional status among children and pregnant women.

Functions of Vitamin A

• Immunity:– Vitamin A and retinoic acid (RA) play a central role

in the activation of macrophages and differentiation of white blood cells (moncytes), that play critical roles in the immune response.

• Growth and development:– Retinol and retinoic acid are essential for embryonic

development and has been found to regulate expression of the gene for growth hormone

Micronutrient deficiencyworld wide

• Statistics:– 2 billion cases of vitamin and mineral deficiency in

both developing and developed countries (WHO 2000)

– Examples: Vitamin A, Fe, Vitamin B12, Iodine, Folic acid, Zn

• Main examples:– Vitamin A deficiency– Fe-deficiency– Iodine deficiency

Micronutrient deficiency in Developing countries

Vitamin A deficiency

• Statistics:– 14 Mio children under 5 years (WHO)– 6 to 7 Mio new cases yearly – Prevalence: South and East Asia, part of Africa and

Latin America, middle East

Vitamin A deficiency

• Vulnerable group:– Pregnant women– Lactating mothers– Preschool children

Vitamin A deficiency

• Clinical features:– Xerpthalmia:

• Night blindness• Bitot's spots: Foamy accumulations on the conjunctiva

(inner eyelids), that often appear near the outer edge of the iris

• Corneal xerosis: Dryness, dullness or clouding (milky appearance) of the cornea

• Keratomalacia: Softening and ulceration of the cornea. sometimes followed by perforation of the cornea, leading to permanent blindness.

Vitamin A deficiency

• Clinical features– Low levels of blood vitamin A– Malnutrition in children– Increased infection rate– Decreased growth rate– Increase rate of fatigue

Vitamin A deficiency

• Determinants:– Nutritional habit

• Low dietary intake (e.g. maternal undernutrition)• Nutritional habits differs from the north to the south of

the country.• Westernization of local meals

– Geographical and regional variation• Palm oil, green vegetable for example rich in Vitamin A

is scarce in the northern region compared to the south

Vitamin A deficiency

• Determinants:– High rates of infections e.g. diarrheas, Measles

and HIV/AIDS – Infection stimulates a vicious cycle, since

inadequate vitamin A leads to a poor nutritional status with increased severity and likelihood of death from infectious disease.

Vitamin A deficiency

• Determinants:– GIT disorders: Malabsorption of vitamin A by the

body due to sprue, celiac disease, obstructive jaundice, cirrhosis, giardiasis, cystic fibrosis

– Poverty• Animal products which are a rich source of Vitamin A

are expensive for a majority in developing countries

Vitamin A deficiency

• Consequences :– Xerophthalmia : major cause of blindness in young

children• 20% of survivors being totally blind • 50-56% of survivors being partially blind

– Childhood diseases– Maternal and 20-30% childhood mortality– Increases HIV-mother to child transformation

(MTCT) (needs further investigation)

Vitamin A deficiency

• Daily requirement:• Babies 0-12 months:

– 0.5-0.6 mg retinol eq./day

• Children under 1-5:– 0.6 - 0.7 mg retinol eq./day

• Pregnant women: – 1.1 mg retinol eq./day

• Breast feeding mothers: – 1.5 mg retinol eq. /day

• RNI: 700ug (no official RNI) since amount depends on fat content of food

Eq. =equivalent, RNI: required nutrient intake

Sources of Vitamin A

– Free retinol is not generally found in foods. Retinyl palmitate, a precursor and storage form of retinol, is found in foods from animals.

– Plants contain carotenoids, some of which are precursors for vitamin A (e.g.,Alpha-carotene and B-carotene).

– Common sources are: oil, fortified cereal, egg, butter, whole milk, sweet potato, carrot etc.

Sources of Vitamin A

Vitamin A deficiency

• Intervention:– Vit A intake through food such as egg, whole milk,

liver, dark green vegetable, red palm oil– RDA of 0.9 mg is present in:

• 3l whole milk, 200g margarine, 8 eggs, 2-3 kg meat, 200g thon fish, 5-10g liver, 150g caviar,

Vitamin A deficiency

• Intervention:– Supplementation (treatment with palmitate-

30mg)• Short-term solution• Liquid gelatin filled capsule given orally or intravenously• Reducing child mortality to 23% overall• Reducing Measles infection to about 50%

Vitamin A deficiency

• Intervention– Fortification

• Medium –term solution• Increase nutrient in specific food (margarine, oil, sugar,

carotenoid- rich bananas)• Requires commitment from government , food

industry, legislation, consumer and research facilitators

Food fortification

Vitamin A fortified cereals

Vitamin A-deficiency

• Intervention:– Diet diversification

• Long term solution• Should run parallel to short term solution• Increases variety and frequency of micronutrient rich

food• Modifies food production, consumption and

distribution• Cost effective and would’t lead to hypervitaminose• Long term commitment from participants

Vitamin A deficiency

• Intervention:– Diet diversification

• Through education of the population, home garden and improved methods of preparation and preservation

– Nutritional Education• Long term commitment from the participants• Education of mother and children on how to eat a well

balanced diet• Improved local access to VA-rich food• Requires economic, political, operational, behavioral

sustainability

Iron deficiency

Iron deficiency

• Statistics:– Over 2 billion people world wide suffer from some

form of iron deficiency– 25% of the world’s children under age 3 have Fe-

deficiency anemia with higher rates in developing countries

– Africa & South Asia have the highest overall incidence of anemia, followed by Latin America & East Asia

Fe-types

• Iron intake and absorption– Two forms of iron occurs in the diet:

• Hem (organic): greater absorption than non-hem iron• Sources include: meat, liver, fish and eggs• Non-hem (inorganic)• Sources include: cereals, legumes, green vegetable,

nuts, dried fruits and chocolate

Fe-intake and absorption

• Iron intake and absorption– Iron absorption is tightly controlled to match the

body’s need, as iron is toxic to cells because of its pro-oxidant properties

– Ingested iron not immediately required remains in the enterocytes, and is shed at the end of their life cycle in the faeces

– Up to 25-30 mg of iron is transported in the body per day from sites of absorption or release for storage or utilization

Iron stores in the body

– Iron stores in the body:• Hemoglobin: 60% (total of 4g) of body’s iron content• Bone marrow: 15%• Ferritin (in liver): contains up to 4000 atoms of iron• Functional enzymes• Muscles (as myoglobin)• In circulation: attached to transferrin

Factors influencing Fe absorption

• The absorption of Fe from food is influenced by multiple factors:o Form of Fe: Hem Fe from animal sources is better

absorbed than non-hem Fe from plant origino The absorption of non-hem iron can be improved when a

source of hem iron is consumed in the same meal.o Fe absorption-enhancing food: e.g. Ascorbic acid-rich fruits

and vegetable (orange, orange juice, grape, spinach, fruits); lean beef, liver.

Maria Kapsokefalou and Dennis D. Miller 1993. J.Nutr.

Fe-absorption: factors affecting absorption of non-hem iron

Factors promoting absorption Factors inhibiting absorption

Vitamin C Phytate (in whole cereal grain)

Citric acid Polyphenols (in tea, coffee and nuts)

Lactic acid Oxalic acid (in tea, spinach)

Fructose Phosphate (in egg yolk)

Peptides from protein sources, especially meat

Calcium, Zinc

These enhance the solubility of the iron, facilitating absorption

These either bind with iron, making it less soluble, or compete for binding site

Fe-deficiency stages

• Pre-latent– Reduction in iron stores without reduced serum in

iron level• Hb (N), MCV (N), iron absorption (), transferin

saturation (N), serum ferritin (), marrow iron ()

• Latent– iron stores are exhausted, but the blood

hemoglobin level remains normal• Hb (N), MCV (N), TIBC (), serum ferritin (), transferrin

saturation (), marrow iron (absent)

Fe-deficiency stages

• Iron deficiency anemia– blood hemoglobin concentration falls below the

lower limit of normal• Hb (), MCV (), TIBC (), serum ferritin (), transferrin

saturation (), marrow iron (absent)

Fe-deficiency anemia

• Iron deficiency anemia (IDA):o Is the most common nutritional deficiency in the world,

with a range of pathological consequences.o These can include changes to the digestive tract, loss of

appetite, reduced work capacity and eventually heart failure

o IDA can also affect the function of white blood cells, reducing their ability to destroy invading organisms

Iron def. anaemia

• Prevalence:oThe most affected are young children between

8 and 16 months and women of reproductive ages

oIn dev. countries:About 40% women between 15 and 40 years of agee.g. 32% in Cameroon

Ray Yip and Usha Ramakrishnan 2002. Journal of Nutritional

Fe-deficiency

• Vulnerable group:– Women of reproductive age– Pregnant and lactating women– Malaria infected persons– Vegetarians– Sick persons (tuberculosis, HIV/AIDS, Malaria)

Causes of Fe def. anaemia

• Low dietary Fe intakeo Food of animal sources such as beef, fish, poultry,

liver are rich sources of iron • Not all causes of anaemia are nutritional in origin; yet

anaemia linked to iron and/or folic acid deficiency is among the world’s major nutritional disorders

Causes of Fe def. anaemia

• Iron absorption inhibitors in food such as:oPhytatesoOxalatesoCarbonatesoPhosphates oDietary fibresoOthers Fe- inhibitors : milk, eggs and tea, coffee

Reduces the bioavailability of Fe in the body, a single cup of tea taken with meal reduces iron absorption by up to 11%.

Morck et al. 1983. Am.J. Nutr.

Causes of Fe def. anaemia• Parasitic infections such as:

oMalariao HIV/AIDSo Hookwormo Schistosomiasis o Tuberculosis

WHO 2009; Nutrition Topics: Iron deficiency anaemia

Causes of Fe def. anaemia

• Chronic bleeding :oMenstrual blood loss (20mg to 60mg)o Gastrointestinal tract (stomach/intestinal cancer,

haemorrhoids)o Blood in sputum (rare) Tuberculosiso Urinary blood loss (rare)

Ray Yip and Usha Ramakrishnan 2002. Journal of Nutrition

Causes of Fe def. anaemia

• Increased Fe utilization:o Pregnancyo Lactationo Infancyo Adolescence

Fe-deficiency anemia

• Signs and symptoms:– Dry pale skin– Fatigue– Dizziness– Headache– Irritability– palpitation– Etc.

Iron deficiency anemia

Angular cheilosis or stomatitis

Fe- deficiency anemia

• Consequences:– Reduces work capacity, thus productivity, earnings

& ability to care for children– Contributes to 20% of all maternal deaths– Retards fetal growth, causes low birth weight (LBW)

& increases infant mortality– Impairs ability to resist disease; in childhood,

reduces learning capacity– Learning disabilities and psychomotor development– Inability to maintain body temperature

Iron deficiency

• RDA:– Men: 8.7 mg– Women: 14.8 mg

• Dietary sources:– beef, liver, fish, dairy products, Green vegetables,

lentils– For 15 mg : 350 g nuts, 750g lean meat, 100g pig

liver, 400g spinach, 200g leguminous fruits

Dietary sources of Iron

Hem iron: Beef

Non-hem iron: Lentils

Interventions to control Fe def. anaemia

• Supplementation: o Fe could be supplied to the vulnerable group in

the form:TabletsCapsulsSyrups

Interventions to control Fe def. anaemia

• Fortification: o Fe could be added to food commonly used by a

significant proportion of the target population e.g.Fe-rich saucesZinc- rich wheatB-carotene-rich riceIodized salt etc.

Interventions to control Fe def. anaemia

• Education: o To improve dietary practices o To enhance bioavailability of iron

consumedo To enable introduction of greater

diversity of iron sources into diet

Interventions to control Fe def. anaemia

• Control of diseases such as:o Malaria, diarrhoea and parasitic infections

• Deworming: o May contribute to achieving at least 7 out of the 8

Millenium Development Goals (MDG)

Thinking beyond deworming, Lancet 2004

Fe- depletion– Failure to supply sufficient iron to the body will result

in a depletion, which passes through several stages:• Normal status: serum ferritin >15µ/l and hemoglobin >

120/130g/l (women/men)• Ferritin stores depleted (< 15µg/L), but sufficient iron

recycled to maintain normal RBC production• Depletion of functional iron: transferrin saturation begins to

fall (critical value <16 % ), as less iron is transported• Hemoglobin concentration falls (<80fL), hypochromic RBCs

are produced, typical of iron deficiency anemia (IDA)

Iodine deficiency

Iodine

• Iodine is an important trace element– 80%of the iodine in the body(15 milligrams in

adult) is present in the thyroid gland where it is used in the synthesis of several thyroid hormones.

– The remainder is distributed throughout tissues particularly in the mammary, salivary, gastric glands and in the kidneys.

Iodine deficiency

• Statistics:– 30% of the world’s population live in iodine

deficient areas– 1 billion persons exposed– 200 million persons affected (goitres)– 26 million cases of mental problems– 6 million cases of cretinism

• Classification:– 3 categories:

oMild : iodine intake of 50-99 µg/dayoModerate : iodine intake of 20-49 µg/dayo Severe: iodine intake of < 20 µg/day

Iodine deficiency

WHO/UNICEF/ICCIDD 1994. Geneva

Iodine deficiency

• It is the leading cause of preventable intellectual impairment– It is associated with a variety of clinical disorders

called ”Iodine deficiency disorders” (IDD)– IDD is known to be a significant health problem in

in 118 countries, IDD affects 740 million people (13% of world population), 30% of remainder are at risk

Iodine deficiency disorders

• Can lead to:– Endemic cretinism– Hypothyroidism– Mental retardation– Reproductive failure– Endemic goiter– Childhood mortality– Socioeconomic retardation

Hypothamalus

TSH T3 T4

Hypofysis

- SomatostatinTSHRF

T4 T3

I pool

Iodine disorder regulation

Importance of the problem

0.0

0.5

1.0

1.5

2.0

2.5

Iodine Iron Vitamin A

People(billions)

1.6

2.0

0.8

Population at risk of deficiency - Global

Source: UNICEF (2002)

Iodine

• Vulnerable group:– Pregnant women– Preschool children – Adults

• Clinical features:– Goiter– Dosage of iodine in urine– TSH dosage– Prevalence of cretinism

Province Population Site Surveyed Clinical Prevalence

Mean Population At Risk

Extreme North

1,880,866 MokoloDoukoula

36%75%

56.5% 1,880,862

North 833,103 Pitoa 12.5% 12.5% 227,701

Adamawa 491,042 Vina 45% 45% 491,042

North West 1,237,804 WumJakiriDjittin/OkuOshie

13.3%45.9%41.4%64.0%

44.4% 1,237,804

West 1,331,201 BamougoumBafangMboudaNoun

29%5.4%502%65%

13.3%65%

347,942287,375

Littoral 1,351,827 Edea ? ? ?

South West 840,883 LimbeTikoMamfe

0.2%2.8%12.6%

1.5% 30,00072,000

Centre 1,655,540 EsekaAkonolingaEfok

13.5%16.5%6.22%

12% 506,000

East 516,733 Batouri 14.5% 14.5%

South 377,237 Ebolowa 6.0% 6.0% 56,585

TOTAL 10,516,236 21 Sites AV 26.25% ---- 5,654,044

Community diagnosisTABLE II: ESTIMATES OF POPULATION AT RISK OF IDD IN CAMEROON IN 1991

Iodine deficiency

• Determinants:– Low iodine uptake in plants: soil dependent

(erosion, wash away)– Low intake of iodine in food : plant dependent– Goitrogens

• Cassava: linnamarin, thiocyanate, Brassica family• Blocs uptake of Iodine at the thyroid, competitive

inhibition• polutants

Iodine deficiency and foetus

• Consequences:– Brain development:

• fast between 3-5 months pregnancy and from third trimester till end of second year

• Maternal T4 essential for first 24 weeks• Foetal T4 starts at 24 weeks• 30% cord blood is of maternal origin

Iodine deficiency and neonates

• Consequences– Perinatal and infant mortality– Low birth weight– Poor brain development due to lack of needs T4– ID mental retardation, retarded motor

development. – General IQ decrease of 15 Points

Iodine deficiency and adults

• Consequences:– lack of energy– apathy, slow brains– goitre and mechanical complications– nodular thyroid– hyperthyroidism– pregnancy and cretinism

Iodine deficiency

• Consequences:– Endemic goiter

• Enlargement of thyroid gland• most obvious clinical manifestation of iodine deficiency

caused by dietary deficiency of iodine.• The minimum amount of iodine required to cover the

turnover of the thyroid gland is 50 microgram/day.• Below this the thyroid gland will begin to enlarge

markedly at puberty particularly in girls

Iodine deficiency

• Consequences:– Endemic goiter:

• This enlargement is considered as a compensatory mechanism to trap more iodine.

• In some patients large goiter may cause pressure on the trachea & esophagus which cause difficulty in breathing, irritative cough, voice changes & some time may affect swallowing

Iodine deficiency

• Consequences– Hypothyroidism

• could be mild – low thyroid hormone level, low BMR, low

productivity, slower mental function, low physical growth

• or severe – classical myxoedema

Iodine deficiency

• Consequences– Endemic cretinism

• Iodine deficiency during pregnancy can lead to birth of cretinous child.

• The infant may appear normal at birth but slow to grow & development

• small in size mentally dull• retarded in reaching normal developmental milestones

• Consequences:– Endemic cretinism (two types exists)

• Neurological– severe motor and mental deficit– cerebral palsy– deafness, mutism– euthyroid

Iodine deficiency disorder

Iodine deficiency disorder

• Consequences– Endemic cretinism

• Myoedematous– severe mental deficit – hypothyroid, destruction of the thyroid– Iodine deficiency combined with goitrogens and Se deficiency

Iodine-consequence summaryTable 1. The Spectrum of Iodine Deficiency Disorders, IDD.Fetus Abortions Stillbirths

Congenital anomaliesIncreased perinatal mortalityEndemic cretinism

Neonate Neonatal goiter Neonatal hypothyroidismEndemic mental retardationIncreased susceptibility of the thyroid glandto nuclear radiation

Child and Goiter adolescent (Subclinical) hypothyroidismImpaired mental functionRetarded physical developmentIncreased susceptibility of the thyroid glandto nuclear radiation

Adult Goiter with its complications HypothyroidismImpaired mental functionSpontaneous hyperthyroidism in the elderlyIodine-induced hyperthyroidismIncreased susceptibility of the thyroid glandto nuclear radiation

Adapted from Hetzel (1), Laurberg et al. (52, 171) and Stanbury et al. (158).

Recommended daily allowance (RDA)

• The RDA : o Children from 0-6 months: 50 µg/day o Children from 6 months to 6 years: 90 µg/dayo Children from 7 years to 10 years: 120 µg/dayo Adolescent und adulthood: 150 µg/dayo Pregnancy and lactation: 200-300 µg/day

WHO 1996. Geneva

Iodine-control

• Intervention:– Supplementation: Injections, oral (Iodine capsule)– Food fortification e.g.:

• Iodized bread• Iodized water• Iodized salts

– changing food habits

Assessment of iodine concentration in school aged children

Table 5. Epidemiological criteria for assessing iodine nutritionbased on median urinary iodine concentrations in school-aged childrenMedianurinaryiodine

Iodine intake(µg/L)

Iodine nutrition

< 20 Insufficient Severe iodine deficiency20-49 Insufficient Moderate iodine deficiency50-99 Insufficient Mild iodine deficiency100-199 Adequate Optimal200-299 More than adequate Risk of iodine-induced

hyperthyroidism within 5-10 yearsfollowing introductionof iodized salt in susceptible

> 300 Excessive Risk of adverse health consequences(iodine-induced hyperthyroidism,autoimmune thyroid diseases)

From WHO/UNICEF/ICCIDD (2)

Food Vehicle Fortifying agent

Salt Iodine, iron

Wheat and corn flours, bread. pasta, rice Vitamin B complex, iron, folic acid, Vitamin B12

Milk, margarine, yoghurts, soft cheeses Vitamins A and D

Sugar, monosodium glutamate, tea Vitamin A

Infant formulas, cookies Iron, vitamins B1, B2, niacin, vitamin K, folic acid, zinc

Vegetable mixtures amino acids, proteins Vitamins, minerals

Soy milk, orange juice Calcium

Juices and substitute drinks Vitamin C

Ready-to-eat breakfast cereals Vitamins and minerals

Diet beverages Vitamins and minerals

Enteral and parenteral solutions Vitamins, minerals

Table 2 Widely Used Fortified Foods

Adapted from: Office of Dietary Supplements, National Institutes of Health. Vitamin D and healthful diets. Dietary Supplement Fact Sheet.

Control of complication

• Need for intensive follow up• Changing consumption patterns in salt• Variations in salt consumption • Transient hyperthyroidism

Micronutrient Deficiency Prevalence Major Deficiency Disorders

Iodine 2 billion at risk

Goiter, hypothyroidism, iodine deficiency disorders, increased risk of stillbirth, birth defects infant mortality, cognitive impairment

Iron 2 billionIron deficiency, anemia, reduced learning and work capacity, increased maternal and infant mortality, low birth weight

Zinc Estimated high in developing countriesPoor pregnancy outcome, impaired growth (stunting), genetic disorders, decreased resistance to infectious diseases

Vitamin A 254 million preschool childrenNight blindness, xerophthalmia, increased risk of mortality in children and pregnant women

Folate (Vitamin B6) Insufficient dataMegaloblastic anemia, neural tube and other birth defects, heart disease, stroke, impaired cognitive function, depression

Cobolamine (Vitamin B12) Insufficient data Megaloblastic anemia (associated with Helicobacter pylori induced gastric atrophy

Thiamine (Viamin B1)Insufficient data, estimated as common in developing countries and in famines, displaced persons

Beriberi (cardiac and neurologic), Wernicke and Korsakov syndromes (alcoholic confusion and paralysis)

Riboflavin (Vitamin B2) Insufficient data, est. to be common in developing countries

Non specific – fatigue, eye changes, dermatitis, brain dysfunction, impaired iron absorption

Table 1 Micronutrients Deficiency Conditions and Their Worldwide Prevalence

Niacin (Vitamins B3)Insufficient data, estimated as common in developing countries and in famines, displaced persons

Pellagra (dermatitis, diarrhea, dementia, death)

Vitamin B6Insufficient data, estimated as common in developing countries and in famines, displaced persons

Dermatitis, neurological disorders, convulsions, anemia, elevated plasma homocysteine

Vitamin C Common in famines, displacedpersons

Scurvy (fatigue, hemorrhages, low resistance to infection, anemia)

Vitamin D Widespread in all age groups, low exposure to ultra violet rays of sun

Rickets, osteomalacia, osteoporosis, colo rectal cancer

Calcium Insufficient data, estimated to be widespread

Decreased bone mineralization, rickets, osteoporosis

Selenium Insufficient data, common in Asia, Scandinavia, Siberia

Cardiomyopathy, increased cancer and cardiovascular risk

Fluoride Widespread Increased dental decay, affects bone health

Source: Adapted from Allen L et al.: Table 1.2 pp 6-10.2

Public Health in the 21st century

• Includes: – Adoption of Food Fortification Recommended

Guidelines by WHO member states particularly addressing:

• iodized salt, flour fortification (iron, vitamin B complex, folic acid, and vitamin B12), milk with vitamin D, and others according to local conditions

Public Health in the 21st century

• Includes:– Regulation and incentives, both technical and

possibly financial, provided to food producers, manufacturers and marketers

• to implement, promote and monitor food fortification policies and their public acceptance.

Public Health in the 21st century

• Includes: – Encouragement of national health systems to adopt and

finance vitamin and mineral supplementation policies for vulnerable groups

– Promotion of low fat foods in the food industry, marketing, and consumer education

– Regulation to ban use of transfats and high salt content in manufactured foods and incorporation of nutritional educational measures.

• Includes: – Promotion of unsweetened drinks and reduction

of high sugar and salt content in food particularly in schools, institutions, as well as national and community organizations

– Implementation and promotion by national and international agencies of nutrition strategies with monitoring and review mechanisms

Public Health in the 21st century

• Includes: – Promotion of national food security and nutrition

advisory boards • to link ministries of health, industry, and agriculture

with food manufacturers’ associations and academic and public representatives

• to monitor implementation of nutritional status, the evolving science of nutrition, epidemiology and health, health food laws and their regulation, and implementation

Public Health in the 21st century

• Includes:– Monitoring of nutrition status in the population

with technical and financial assistance by national ministries of health in periodic national nutrition and health surveys

Public Health in the 21st century

Includes: – Promotion of nutrition education in school

systems, professional education and• training programs for physicians, nurses, and other

health professionals, among other social and educational professions, as well as for the general public.

Public Health in the 21st century

Impact on health

• Improving vitamin-A status o Reduces mortality rates by 23% on average.o Prevents 1.3–2.5 million deaths per yearo Saves hundreds of thousands of children from irreversible

blindness• Improving iron status

o Increases levels of national productivity by 20%o Reduces maternal mortality; iron-deficiency anemia

contributes to 20% of all maternal deaths• Improving iodine status

o Prevents mental retardation and brain damage

Nutrition related diseases

Definition

• Excessive accumulation of body fat.– In men: 15% of total weight– In women: 25% (reflecting hormonal differences

and needs between the sexes)– Excessive accumulation of fat may exceed 50% of

total weight contributing to major pathological consequences

Obesity and overweight

– Causes:• Reduced level of physical activity• Passive overconsumption as a result of increased

snacking on energy-dense foods and drinks, a process fuelled by advertising

• Reduced consumption of food and vegetable• High consumption of processed food

Obesity

• Vulnerable group– Children– adults

Measurement of body fat

– Measuring body fat is not a straight forward process. Several simple surrogate measurements are used to categorize overweight and obesity. These are:

– Body mass index– Waist circumference– waist hip ratio.– MUAC-middle upper arm circumference

BMI

Reference :16 – 17 underweight18 – 25 Normal weight26 – 30 pre-obese31 – 38 Obesity

31 – 34 WHO I35 – 38 WHO II39 – 41 WHO III

BMI with least mortality according to age

Age (year) BMI (kg/m2)

19-24 19-24

25-34 20-25

35-44 21-26

45-54 22-27

55-64 23-28

>65 24-29

According to Andres et al., based on data from the Metropolitan Life Insurance

Middle arm muscle circumference (MAMU or MUAC)

• Indication: gives information on the (Muscle) protein reserve

• During malnutrition upper arm muscles swell faster than other groups of muscles

• Practical use:– Patients is standing– Measurement: triceps skin fold and arm circumference – MAMU =AMC – (0.314 x TSF)– AMC=arm muscle circumference (cm), TSF triceps- skin

fold thickness (mm)

MUAC-interpretation

• 90 % > standard is the norm

• Table: Interpretation of MUAC in (cm) (Morgan)% standard

100 90 80 70 60 50 40

Men 25.5 23.0 20.0 18.0 15.0 12.5 10.0

Women 23.0 21.0 18.5 16.0 14.0 11.5 9.0

interpretation

Adequate limit severe deficiency

MUAC-disadvantages

• Acute changes in protein reserve cannot be assessed

• Error source: false measurement technique: upper arm edema

Waist circumference

• Indication: measurement of either waist circumference, or waist/Hip ratio and blood pressure at first as well as following patient visit

• Recommendation: at least 1x yearly• Interpretation: studies show that waist cir.

Correlates more with risk of disease compared to w/h

Waist circumference

• Table: Waist circumference (cm) and obesity related conditions ( WHO, 2000)

Low risk Increse risk High risk

men < 94 94 - 102 => 102

women < 80 80 - 88 = > 88

Waist / Hip ratio (W/H)

• Indication: recommended at first and follow-up patient visit (at least 1x yearly)

• Practical use (internet)• Normal value:

1. Men: upper limit: 0.95 (85 % of men have w/h b/w 0.85 and 1.0

– Women: upper limit: 90% (90 % of women have w/h b/w 0.65 and 8.84

– Compare: obesity

Prevalence of overweight and obesity

Global prevalence has been rising steeply over the last 20years in most countries; there are now more overweight than undernourished people across the globe.• Overweight and obesity combined now affects

65% of men and 56% of women in the U.K. • The figures represent a doubling of prevalence in

women and a tripling in men since 1980

Prevalence of overweight and obesity

• Obesity affects 22% of men and 23% of women in UK.

• Rates of overweight and obesity are increasing among children and adolescents.

• In general obesity increases with age• Obesity in more prevalent in lower socio-economic

groups in western countries.• However, in some parts of the world, such as India

it is more common among the more afluent groups

Public Health concerns• Consequences:

– Regarding this trends relates to the parallel increase in risk of associated diseases

– Obesity is directly responsible for some 6 % of all deaths in the western world and reduces life expectancy by an average of 9 years.

– It is associated with substantial morbidity, in terms of physical, metabolic and psychological consequences

– The associated financial cost of obesity are estimated to account for 2-8% of health care budgets in the west, and after diabetes, constitute the second greatest area of expenditure in these budgets.

N.B. Development of overweight and obesity

– Weight gain occurs when energy intake exceeds energy output over a period of time.

– This represents a positive energy balance, such that the energy supplied to the body as food is not used and therefore stored in adipose tissue.

– A reduction in energy intake, an increase in energy output, or both are needed to remove the stored energy, create a negative energy balance and reduce body weight

External influences on energy intake

• Food availability– Both the quantity and the nature of the food available

to people in many parts of the world has changed substantially in the last decade

– Changes include:• Greater choice with more variety encouraging intake;• Food on sale around the clock;• Improved preservation methods, so food can always be

made available;• Many food require little preparation, so can be eaten

immidiately.

N.B. Control of Energy balance

• Physiological control mechanism exist,– To regulate both energy intake and output.– For humans in modern society, both intake and output are

subject to a variety of external influences.– These interact with or override the internal regulatory

mechanisms, creating a challenge to the maintenance of energy balance

– In addition, the relative importance of these influences varies, as a result of the underlying genetic make-up of the individual, dietary complexity and environmental variables.

External influences on energy intake

Food Quantity and Quality– Dietary surveys suggests that energy intakes in the

U.K. have fallen since 1970s.– Recorded intakes are frequently under-reported

which makes comparison with energy output difficult.

– Nevertheless, the rising incidence of obesity implies that energy intakes still exceeds expenditures

External influences on energy intake

• Food Quantity and Quality– Changes that play a part include:

• Increased consumption of convenience, ready prepared or “fast” food, which has a higher energy density than typical traditional diets, resulting in “passive over consumption” of energy;

• A trend to larger portion sizes becoming the norm, which also inadvertently increases food intake;

• People eating a rising proportion of their meals away from home, hence the impact of the food industry on food quality on quantity becomes more pertinent to obesity trends.

External influences on energy intake

• Snacking and grazing – A trend away from eating regular meals to a less

structured food intake, typified by consumption of snack and convenience foods and soft drinks through out the day, rather than eating to satiety at greater inter intervals

– Such intakes tend to be high in fat and high glycemic carbohydrates, as well as being generally poor sources of slowly absorbable carbohydrate and micronutrients.

– The body’s appetite control mechanism are undermined in this way.

External influences on energy intake

• Psychological aspect– Attitudes and beliefs have a major impact on food

intake.– For any one individual, food intake could be affected

by:• Mood and mental state• Self image and culturally determined body images• Personality• Socialized attitude to food• External factors such as peer effect advertising and media

influences

External influences on energy output

• Increased mechanization– Technological advances results in less need to use human

muscle power to carry out energy demanding manual tasks– There are now fewer occupations that can be classified as

heavy manual work, and even tasks that where not very physically demanding have been lightened with robots and computer –driven technology.

– Fewer have physically demanding jobs in agriculture, as urbanization proceeds rapidly.

– Transport has become increasingly concentrated on the use of the car, as oppose to walking and use of bicycles.

External influences on energy output

• Leisure activities– Secular trends suggests reduced participation in active leisure

pursuits.– The widespread availability of computers and electronic home

entertainment systems reduces outdoor leisure activities.– Physical activity has for many become an item to schedule

into the day, with a trip to the gym or swimming pool, rather than an intrinsic part of existence, as it was in the past.

– Increased urbanization and road traffic, together with safety fears, make outdoor activity less pleasant and compound the problem

Individual susceptibility

– Not everyone exposed to the same external influences on intake or output will experience weight gain.

– There is a heritable element although this remains difficult to quantify and separate from environmental influences within families.

Individual susceptibility

• Genetics– In some inherited conditions there is a clear link

with obesity; most notable among these are Prader-willi and Bardet-Biedel syndromes.

– For the great majority of cases of obesity, the rapid increase in the incidence within a genetically stable population indicates that external factors play the major role.

Individual susceptibility

• Genetics (continue)– This does not exclude a genetic origin to

susceptibility to obesity, which becomes expressed as a result of external changes

• Ethnicity– There are observed differences in patterns of

weight gain between different ethnic groups, including body fat distribution and levels of adiposity at particular BMI values.

Individual susceptibility

• Vulnerable periods– Research from a number of areas suggests that

there are periods during the life cycle when susceptibility to obesity may be programmed(in the fetus and infant)or be increased(during periods of rapid growth, including pregnancy and lactation).

Individual susceptibility

• Vulnerable periods (continue)– The latter may be linked to changes in levels of

specific hormones. Age and gender are compounding factors, with patterns of weight gain in adult life differing between men and women

Obesity

• Consequences– Cardiovascular diseases– Diabetes

Consequences of overweight in childrenImmediate concern Long-term concerns

Physical problems reduce ability to participate in peer activities

Likelihood of remaining overweight/obese, increased risk of associated health and social problems

Social isolation, bullying, difficulty in forming peer relationships

Relationship difficulties with partners

Psychological consequences, including low self –esteem, underachievement, mental health problems

Unemployment

Early onset of medical problems including type 2 diabetes, respiratory problems, sleep apnoea, hypertension, orthopedic problems

Reduced life expectancy

Preventing/managing excess weight gain

– Reduce energy intake:• Food with high satiety value • Regular meals• Reduce snacks/drinks with “empty calories”• Involvement with food selection and preparation

– Increasing energy output• Encourage movement• Reduce sedentary pastimes• Involve family in activity