REVIEWER

1.
Hunger and Malnutrition in the Philippines Danilo Villa B. Agcopra, Nutrition Officer IV National Nutrition
Council-Department of Health Philippines
2. NNC Governing Board DOH - Chair DSWD DILG DOST Vice-Chair DBM DA DepEd DTI NEDA DOLE
League of Corporate Foundations Rural Improvement Clubs of the Phil Union of Local Authorities of the Phil 2
3. 17 Regional Offices NNC Secretariat Office of the Executive Director Executive Director Deputy Executive
Directors Nutrition Policy & Planning Division Nutrition Surveil-lance Division Adminis-trative Division
Finance Division Nutrition Information & Education Division
4. NNC Mandates • Formulate national nutrition policies and strategies • Coordinate the national food and nutrition
program • Coordinate funds for nutrition • Call on any government instrumentality for assistance
5. NNC Mandates (additional) • EO 616 (April 2007) created the Anti-Hunger Task Force • Oversee
implementation of Accelerated Hunger-Mitigation Program • Ensure that hunger-mitigation measures are in place
• Report to the President
6. NNC Other assignments • RA 8172 - Formulate policies and coordinate salt iodization program • RA 8976 –
Determine need for continued mandatory fortification; which nutrients, which food vehicles
7. NNC Other assignments • DA SO98 S1999 - Focal agency for FIVIMS (Food Insecurity and Vulnerability
Information and Mapping Systems) • NEDA Social Development Council Cabinet Level Resolution 1 S2003 -
Lead agency to ensure achievement of MDG goals and target on hunger and malnutrition
8. Organizational Structure
9. Outline • Hunger • Malnutrition • Underweight, stunting, wasting • Micronutrient deficiencies • Overnutrition •
Actions to address hunger and malnutrition
10. MDG 1 • Reduce by half by 2015 • Prevalence of underweight-for age among under-fives • Percent of
households with inadequate energy intake Eradicate extreme poverty and hunger 10
11. Hunger . . . a serious, persistent problem A condition in which people do not get enough food to provide nutrients
for fully productive, active and healthy lives If prolonged and severe, can lead to malnutrition
12. Hunger • Proportion of Filipino households with per capita intake below 100% dietary energy requirement, 1993-
2008 Source : FNRI-National Nutrition Surveys
13. Quarterly surveys on hunger QUESTION: “In the last 3 months, did it happen even once that your family
experienced hunger and did not have anything to eat? If yes, did it happen only once? (moderate) a few times?
(moderate) often or always? (severe)”
14. Hunger
16. Undernutrition (underweight, stunting, wasting) --serious nutritional problems
17. Underweight • Trends in percent of underweight-for-age children 0-59 months old compared with MDG target
Source : FNRI-National Nutrition Surveys
18. Stunting- short for age, indicate long-term food deprivation and frequent infections Wasting– food deprivation or
infection in immediate past
19. High level of stunting & wasting among children under 5 years old Source : FNRI-National Nutrition Surveys
20. Source : FNRI- 2008 National Nutrition Survey
21. High level of stunting & underweight-for-age among children 6-10 years old Source : FNRI-National Nutrition
Surveys, based on NCHS-IRS
22. Nutritional risk among pregnant and lactating women Source : FNRI-National Nutrition Surveys
23. Undernutrition, number affected Source : FNRI-National Nutrition Surveys 2008 *Using NSO 2008 Projected
Population based on 2000 Census
24. Micronutrient deficiencies --still of public health significance
25. Micronutrient deficiencies • Prevalence of vitamin A deficiency Source : FNRI-National Nutrition Surveys
26. Micronutrient deficiencies • Prevalence of iron deficiency anemia by age and physiologic state Source : FNRI-
National Nutrition Surveys
27. Micronutrient deficiencies • Iodine deficiency based on median urinary iodine excretion (UIE) levels Source :
FNRI-National Nutrition Surveys
28. Overnutrition is increasing and at a high level among adults (about 20%)
29. Actions to address hunger and malnutrition PNP 1974-1977 PNP 1978-1982 FNP 1984-1987 PFNP 1987-1992
PPAN 1993-1998 The Medium-term Philippine Plan of Action for Nutrition 2011-2016 PPAN 1999-2004 PPAN
2005-2010
30. Philippine Plan of Action for Nutrition, 2011-2016 Philippine Development Plan, 2011-2016 Health, Nutrition
and Population Social Protection Basic Education Housing Peace and security Asset reform Chapter 9: Social
Development Theme: “Enhancing Peace and Security for Development”
31. MDG 1 • Reduce by half by 2015 • Prevalence of underweight-for age among under-fives • Percent of
households with inadequate energy intake Eradicate extreme poverty and hunger 31
32. Goal and targets • To contribute to • improving quality of human resource base of country • reducing child and
maternal mortality. • Reduce malnutrition to levels below public health significance
33. Strategies • Focus on the first 1,000 days of life or -9 (pregnancy) to 24 months • Support for pregnant and
lactating mothers for desirable infant and young child feeding practices • Capacity building on IYCF counseling •
Peer counseling • RA 10028 and EO 51 or the Milk Code • Human milk bank
34. Strategies • Integration of nutrition services in ante- and post-natal care services • Adoption and implementation
of community management of acute malnutrition (CMAM) guidelines • Nutrition services for school children
(nutrition education, water and sanitation, and personal hygiene)
35. Strategies • Micronutrient supplementation – vitamin A, iron, and iodine • Food fortification - Mandatory for
staples (rice, sugar, flour, cooking oil, and salt)
36. Strategies • Home, school and community-based food production - fruit and vegetable or kitchen gardening,
raising of small-sized animals, fish production (fish cages, inland fishing or pond) • Improve local food supply
and physical and economic access to food
37. Strategies • Prevention and management of infections – deworming, provision of potable water and sanitation
facilities • Promotion of good nutrition and healthy lifestyle behaviors – family, school, community using multi-
media
38. Sustaining Strategies to Address Hunger “Food for Thought: What do the numbers tell us about hunger and what
do we do about it?”
39. Causality MALNUTRITION Low supply of food Low demand for food HUNGER
40. HUNGER MITIGATION MEASURES SUPPLY Increase food production Enhance efficiency of logistics &
food delivery Provision of farm inputs, e.g. improved seeds (OPV vegetables and rice), small animals, post-
harvest facilities such as flat-bed dryers Construction of small-water impounding projects, diversion dams and
other rain-water harvesting and storage facilities Construction and maintenance of RORO systems and farm-to-
market roads Provision of rice subsidy Establishment of trading posts
41. HUNGER MITIGATION MEASURES DEMAND Manage population Put more money in poor people’s pockets
Promote good nutrition Promotion of responsible parenthood including to access to family planning services
Microfinancing Skills training and development for increased employability Employment opportunities in
construction & maintenance of rural infrastructure and facilities, e.g. farm-to-market roads, irrigation canals,
national and provincial road systems Promotion of exclusive breastfeeding and appropriate complementary
feeding Promotion of positive nutrition behavior e.g. reduce plate waste, increase consumption of vegetables
42. Program Highlights • Focused hunger-mitigation measures and services in priority areas
43. A bit of history —Target areas Food Insecurity and Vulnerability Information and Mapping Systems (FIVIMS)
Very, very vulnerable Provinces (VVV) Very vulnerable (VV) Vulnerable (V) Priority provinces based on the
2003 Family Income and Expenditure Survey (FIES) Priority 1 provinces (P1) Priority 2 provinces (P2) Priority
3 provinces (P3)
44. What did being a priority province mean • More resources to P1 provinces • More counterpart funding expected
from P2 and P3 provinces
45. Program Highlights • Gave a hunger-mitigation perspective to some programs, e.g. irrigation, farm-to-market
roads, ports construction and improvement
46. Program Highlights • Reached out to hungry and poor with key services • Small animal raising and fisheries-
related activities; coconut intercropping and salt fertilization; restoration and rehabilitation of irrigation facilities
• Construction/rehabilitation of ports; distribution of flat-bed dryers • Employment generation
47. Program Highlights • Developed new programs to increase food supply and reduce prices • Food for School
Program • TindahanNatin • ProgramangGulayan (home, school and community gardening) • Barangay Food
Terminal or Barangay Bagsakan
48. Program Highlights • Increased investments in nutrition promotion from almost nothing to about Php 400 M
annually • Increased investments in promoting responsible parenthood
49. Learnings • Importance of the following • Data for targeting and on impact • Participative planning • Location-
specific intervention
50. Learnings • Support from the top-most leadership (EO 616, 29-member Anti-Hunger Task Force; regular agenda
item in Cabinet meetings) • Closely working with local government units to facilitate complementation with local
initiatives
51. Sustaining Hunger-Mitigation Strategies
52. Scale Up • Investment in agriculture and fisheries for increased productivity and income • Provide inputs to
artisanal farmers and fisherfolk e.g., outboard motor, hybrid fingerlings, repair of irrigation facilities
53. Scale Up • Home, school and community-based food production (vegetables, small animals, fish) for improved
nutrition and increased income
54. Scale Up • Shift from emergency to more permanent employment • Availment of microfinance • Educate poor on
how to avail of assistance and other skills (financial management, entrepreneurship) • Explore more creative
mechanisms for credit delivery
55. Scale Up • Capacity-building for rural development • Off-farm and in-between seasons employment (product
development, packaging and marketing) • At least one member of the poor household is trained • LGUs to create
links with industries and markets
56. Scale Up • Promotion of responsible parenthood • Invest on IEC materials • Provide access to selected methods •
Promotion of good nutrition • Invest on quad-media • Ensure that cash assistance or incomes are used wisely
57. Continue • Ensuring adequate supply of rice at price levels the poor can afford, if not downright free distribution
• Rice subsidy through NFA’s TindahanNatin
58. Continue • Establishment of trading posts, “bagsakan”, post-harvest facilities, rural infrastructure (farm-to-market
roads), roll-on, roll-off port facilities, food lanes
59. Introduce • Food-Cash for Work • Half food (ready source of food) • Half cash (for other needs)
60. Introduce • Universal health insurance coverage • Less out of pocket medical expenses = more money to buy
food
61. Conclusion Work versus hunger is not yet done AHMP provides vital learnings • integrated, coherent, multi-
sectoral and multi-level approach • Top-level support and leadership Sustained investments crucial
62. Integrated Action for Hunger Alleviation and Improved Nutrition in Convergence Areas (HAIN)
63. Goal • To contribute to • Reduction of hunger • Improvement in the nutrition situation
64. Objectives • To reduce the prevalence of underweight-for-age among children 0-8 years old • To prevent stunting
among children 6 mos to 2 years old • To improve food intake in participating households
65. Objectives • To increase income opportunities among target households • Improve knowledge and practice of key
health and nutrition concepts and behaviors • Infant and young child feeding (breastfeeding and complementary
feeding) • Consumption of vegetables and eggs • Sanitary and hygienic practices (handwashing, tooth brushing,
use of sanitary toilet facilities)
66. Target Area 600 convergence municipalities of the Cabinet Cluster on Human Development and Poverty
Alleviation
67. Target Groups, blanket approach
68. Target Groups, targeted approach
69. Blanket vs. targeted
70. Complementary components Core components Hot meals for particular groups Rice distribution
71. Core A1. Hot meals • Group • Pregnant women • Infants 6 – 11 months old • Children 12 – 23 months old •
Children 3 – 5 years old in day care centers • Pupils in Kindergarten, and Grades 1-3 in PES • Daily, 5 days a
week for 120 days
72. Core A2. Rice distribution • 50 kg per family per 2 months • Should be iron fortified • Need to determine
appropriate distribution scheme
73. B1. Livelihood • Skills training based on market demand/ requirements • At least one member of the target
family to be trained for a specific skill in demand in the nearby community or factory • Includes provision of seed
money and other assistance for livelihood
74. B2. Health services
75. B3. Home, School, and Community Food Production • Seeds – indigenous and open-pollinated varieties •
Seedlings – indigenous and open-pollinated varieties • Small animals • Fish fingerlings
76. B4. Nutrition education and counselling • Counselling on infant and young child feeding • Training of health
workers on counselling • Training and deployment of peer counsellors • Nutrition classes, e.g. Pabasa sa
Nutrisyon scheme • Nutrition education in day care centers and public elementary schools
77. B5. Infrastructure support • Irrigation • Facilities for water and sanitation • Farm-to-market roads • Foot bridges
and trails • Barangay health stations, nutrition posts, day care centers in all barangays
Presentation on theme: "Philippine Plan of Action for Nutrition (PPAN)"— Presentation transcript:
1 Philippine Plan of Action for Nutrition (PPAN) 2017-2022

Let me now give you an overview of PPAN and I hope you will say, “Ahh the PPAN is consistent with the SUN road
map to 2030”.
2 Addresses nutrition situation

Guide for all who want to be involved in nutrition actionLays out targets, directions, and priority
actionsPNPPNPFNPPFNPPPANPPANPPANThePhilippinePlan ofAction forNutritionPPANThe Philippine Plan of
Action for Nutrition is a companion plan of the Philippine Development Plan. It lays out the targets, directions, and
priority actions to achieve nutrition targets that are in turn based on the nutrition situation.9/22/2018
3 Plan formulation process

Engagement of a team of consultants with funding support from Micronutrient Initiative and UNICEFDesk reviewKey
informant interview/one-on-one consultationsFocus group discussions (national and local)Consultation workshopsNNC
Technical Committee as final vetting bodyPlan formulation involved various methodologies and was both multi-sectoral
and multi-level. It involved two consultation workshops.
4 Nutritional problems to address

Child stunting and wastingDeficiencies in vitamin A, iron, and iodineOverweight and obesityPoor nutritional status of
pregnant and lactating womenPoor infant and young child feedingHunger and food insecurityThe PPAN aims to address
malnutrition in the form of child stunting and wasting, micronutrient deficiencies, overweight and obesity across the
population. It also hopes to address maternal malnutrition, poor infant and young child feeding and hunger and food
insecurity that are contributory to the major forms of malnutrition. I will not discuss the details of these problems in the
interest of time.
5 Maternal and child undernutrition and death

Inadequate dietary intakeDiseaseHousehold food insecurityUnhealthy household environment & poor health
servicesInadequate careIncome poverty: employment, self-employment, dwelling, assets, remittances, pensions,
transfersLack of capital: financial, human, physical, social, naturalSocial, economic, and political contextTo address
malnutrition effectively, one should address its immediate and basic causes as shown in the slide. This is the framework
for undernutrition that has been used globally.Source: Black, Robert E. et al. The Lancet Series on Maternal and Child
Undernutrition
6 PPAN Outcome targetsIn general, consistent with the 2025 Global Targets for Maternal, Infant and Young Child
NutritionLet me now touch on the outcome targets, that is the situation we wish to achieve by 2022.As a rule, the targets
for 2022 are consistent with the 2025 global targets for maternal, infant, and young child nutrition. This means that the
estimated numbers for 2022 are part of a straight line to lead to the desired situation in 2025.
7 Outcome targets Reduce levels of child stunting and wasting Indicator

BaselineTarget, 2022Prevalence (in percent) of stunted children under 5 years old*33.421.4Prevalence (in percent) of
wasted children:- Children under 5 years old*7.1<5- Children 6-10 years old8.4Thus, the targets are as follows: reduce
child stunting to about 21.4%, wasting among children to be less than 5%*Targets are consistent with the 2025 Global
TargetsMaternal, Infant, and Young Child Nutrition
8 Outcome targetsTo reduce micronutrient deficiencies to levels below public health

significanceIndicatorBaselineTarget, 2022Vitamin A deficiencyPrevalence (in percent) of children 6 months to 5 years
old with vitamin A deficiency (low to deficient serum retinol)20.4<15AnemiaPrevalence (in percent) of anemia among
women of reproductive age*11.76.0For micronutrient malnutrition, the intent is to bring the problem down to levels that
are below public health significance for vitamin A, anemia, and*Targets are consistent with the 2025 Global Targets
Maternal, Infant, and Young Child Nutrition
9 Outcome targetsTo reduce micronutrient deficiencies to levels below public health

significanceIndicatorBaselineTarget, 2022Iodine deficiency disordersMedian urinary iodine excretion, ug/L- Children
6-12 years old168≥100- Pregnant women105≥150- Lactating mothers77Percent with urinary iodine concentration <50
mcg/L16.4<20%- Lactating women33.4Iodine deficiency.
10 Outcome targetsNo increase in overweight among children, reduced overweight among adolescents and
adultsIndicatorBaselineTarget, 2022Prevalence (in percent) of overweight- Children under five years old*3.8<3.8-
Children 6 – 10 years old8.6<8.6Adolescents9.2<5Adults31,128.0For overweight, the target is to prevent a further
increase among children years old, a reduction to less than 5% among adolescents and from 31.1% to 28% among
adults.*Targets are consistent with the 2025 Global Targets Maternal, Infant, and Young Child Nutrition
11 Sub-outcome or intermediate outcome targets

Reduce the proportion of nutritionally-at- risk pregnant women from 24.8% in to 20% by 2022 (about 20% reduction
between 2013 and 2022)Reduce the prevalence of low birthweight from 21.4% in 2013 to 16.6% by 2022 (to reach the
2025 Global target of 30% reduction)**Targets are consistent with the 2025 Global Targets Maternal, Infant, and
Young Child NutritionWe also propose suboutcome targets or targets that can lead to the achievement of the main
outcomes. Again, when there are global targets committed to by the Philippines, the targets were based on these
commitments. In some cases, the targets were based on observed changes in the past 20 years or so with an additional
acceleration factor.Outcome objectives include reducing nutritionally at risk pregnant women to 20% by 2022, low
birthweight to 16.6%
12 Sub-outcome or intermediate outcome targets

Increase the prevalence of exclusive breastfeeding among infant 5 mos old from 24.7% in 2015 to 33.3 by 2022Increase
the percentage of children months old meeting the minimum acceptable diet from 18.6% in 2015 to 22.5% by
2022Increase the proportion of households with diets that meet the energy requirements from 31.7% in 2013 to 37.1%
by 2022For EBF, the outcome indicator has been limited to the 5-month old age group for a more sensitive measure of
EBF, and the target is to increase EBF rates to For children meeting the minimum adequate diet, the target is a 22.5%
level by 2022.And the last suboutcome target is to increase the proportion of households with diets that meet the energy
requirements from 31.7% to 37.1%.Note for A/Sec. The target for EBF aims for a 50% increase by For complementary
feeding, the target is an increase by 30%. These are “arbitrary” numbers. For households meeting energy requirements,
the target is to increase the households with adequate calorie intake by 15% by This is more or less, twice the observed
reduction between 1993 and 2003 (period of 20 years), applied to a period of about 17 years.)
13 Strategic Thrusts, 2017-2022 Focus on the first 1000 days of life

Complementation of nutrition-specific and nutrition-sensitive programsIntensified mobilization of local government
unitsReaching geographically isolated and disadvantaged areas (GIDAs) and communities of indigenous
peoplesComplementation of actions of national and local governmentsFor the strategic thrusts for nutrition action are as
follows:Focus on the first 1000 days or the period of pregnancy up to the 23th month of lifeComplementation of
nutrition-specific and nutrition-sensitive programsIntensified LGU mobilizationPriority to GIDAs and communities of
indigenous peoplesComplementatin of actions of national and local governments
14 Priority provincesREGIONPROVINCECARAbra2. ApayaoI3. PangasinanII4. IsabelaIII5. AuroraBataan7.

Bulacan8. Nueva EcijaIV - A9. QuezonIV - B10. Palawan11. MarinduqueV12. Albay13. Camarines Norte14.
Camarines Sur15. Catanduanes16. MasbateVI17. Aklan18. Antique19. IloiloREGIONPROVINCEVII20. Bohol21.
Cebu22. Negros OrientalVIII23. Biliran24. Leyte25. Northern SamarIX26. Zamboanga del Norte27. Zamboanga del
SurX28. Bukidnon29. Lanao del Norte30. Misamis OrientalXI31. Davao del Norte32. Davao del SurXII33. North
Cotabato34. South CotabatoARMM35. Sulu36. Tawi-TawiCARAGA37. Agusan del SurNCR38. CAMANAVAFor the
LGU mobilization strategy, 37 provinces and a district in NCR will be prioritized as convergence areas of national and
local programs. These areas were chosen based on the magnitude of stunting.
15 Nutrition-specific programs Nutrition-sensitive programs

Sustainable Development GoalsPhilippine Development Plan GoalFoundation for inclusive growth, a high-trust society,
and a globally competitive knowledge economyReduced wasting among children under-five years oldReduced stunting
among children under-five years oldReduced micronutrient deficienciesImproved situation in overweight and
obesityReduced nutritionally-at-risk pregnant womenIncreased exclusive breastfeedingImproved food intakeReduced
low birthweightImproved complementary feedingNutrition-specific programsNutrition-sensitive programsTo achieve
target outcomes, a mix of nutrition-specific and nutrition-sensitive programs will be implemented together with those
that will create an enabling environment. I will discuss these in more detail in a while.Please note that there is a set of
what we call nutrition-supportive programsNutrition-supportive programsEnabling programs
16 Nutrition supportive programs, examples

ImmunizationFood and agricultural systems, programs and projects that impact on food supplySocial protection
programs like the conditional cash transfer, health insurancethat include immunization, food and agriculture systems
programs and projects that impact on food supply, conditional cash transfer, and health insurance. These programs are
not included in PPAN because these programs were not designed to contribute directly to nutritional outcomes.
17 Nutrition-specific programs – Address immediate causes of malnutrition

Program/ProjectAgency involvedInfant and Young Child FeedingHealth systems supportDOH, LGUsCommunity-based
health and nutrition supportDOH, NGOs, LGUs, Development Partners (DPs)Maternity Protection and Improving
Capacities of Workplaces on BreastfeedingDOLE, Employers, Employees’ Unions, NGOs, LGUs, DPsEstablishment of
breastfeeding places in non-health establishmentsAll agencies, NGOs, LGUs, DPs, CSCEnforcement of the Milk
CodeLet me now go to nutrition-specific programs or programs that address the immediate causes of malnutrition
specifically inadequate food and poor nutrient quality, poor maternal and child caring practices.The first program is on
infant and young child feeding that has 5 projects or program components that aim to ensure that all environments
support the mother for optimum infant and young child feeding.
18 Nutrition-specific programs – Address immediate causes of malnutrition,

Program/ProjectAgency involvedIntegrated Management of Acute MalnutritionDOH, NGOs, LGUs, DPNational
Dietary Supplementation ProgramPregnant womenDOH, NGOs, LGUs, DPsChildren, 6-23 months oldChildren 24 – 59
months oldDSWD, NGOs, LGUs, DPsSchool-age childrenDepEd, NGOs, LGUs, DPsFood plant for producing food
supplementsFNRI, LGUs, SUCs, NGOsThe second program is on the management of acute malnutrition.The third
program is the National Dietary Supplementation Program that targets pregnant women, children 6-23 months old in
food-insecure households, children 3 to under-five years old, and school–age children. Supplementary feeding programs
that target pregnant women and children 6-23 months old are new and will be implemented progressively. Also for ,
there will be a more conscious effort to link the food plants set up by partners of FNRI with supplementary feeding
programs.

Program/ProjectAgency involvedNational Nutrition Promotion Program for Behavior ChangeIn schoolsDepEd, NGOs,
LGUs, DPsIn communitiesDOH, DSWD, NGOs, LGUs, DPsIn workplaceDOH, DOLE, NGOs, LGUs, DPsResource
centerNNC (coordinator)There will be a nutrition promotion program that will aim for behavior change and will tap into
various channels, specifically schools, communities, and the workplace. A resource center will also be set up with the
NNC as coordinator. This program component will aim to integrate all related efforts to a coordinated effort for
promoting desired actions along the Nutritional Guidelines for Filipinos.
Program/ProjectAgency involvedMicronutrient supplementation (vitamin A, iron-folic acid, multiple micronutrient
powder, zinc)In health unitDOH, NGOs, LGUsIn schoolsDepEd, NGOs, LGUsCommunication supportThe distribution
of vitamin A capsules, iron-folic acid tablets, and micronutrient powder, and zinc through the health and school systems
will continue under the Micronutrient Supplementation Program. The program will also include communication support.

Program/ProjectAgency involvedMandatory food fortification (technology development, capacity building, regulation
and monitoring, promotion)Rice fortification with ironDOH, DSWD, DepED, NGOs, LGUs, industryFlour fortification
with iron and vitamin ACooking oil fortification with vitamin ASugar fortification with vitamin ASalt
iodizationMandatory food fortification of staples and salt will continue, and technology development, capacity building,
regulation and promotion will be pursued and strengthened.

Program/ProjectAgency involvedNutrition in emergenciesCapacity building for mainstreaming nutrition protection in
emergenciesDOH, DSWD, National/Local DRRMC, NGOs, LGUs, DPsOverweight and Obesity Management and
Prevention ProgramHealthy Food EnvironmentPromotion of Healthy LifestyleWeight Management InterventionDOH,
DSWD, DOLE, NGOs, LGUs, industry, CSC, DPsUnder the Nutrition in Emergencies Program, nutrition protection in
emergencies and disasters will be strengthened and through a purposive effort of capacity building for a nutrition
response in emergencies.There will also be a program on the management and prevention of overweight and obesity.
23 Nutrition-sensitive programs – Address underlying causes of malnutrition

Projects in development sectors that were tweaked to produce nutritional outcomesTargeting households with
undernourished children, or pregnant women or children 0-23 months old for employmentTargeting areas with high
levels of malnutritionChannel or platform for delivering nutrition-specific interventionsComplementing these nutrition-
specific interventions are nutrition-sensitive projects. These are development projects that were tweaked to produce
nutritional outcomes. Tweaking can be done by targeting households with undernourished children or nutritionally-
vulnerable groups, or targeting areas with high levels of malnutrition, or being a channel for delivering nutrition-specific
interventions.
24 Nutrition-sensitive program – Address underlying causes of malnutrition

Farm-to-market roads and child nutrition, DATarget Actions to Reduce Poverty and Generate Economic Transformation
(TARGET) and child nutrition, DACoconut Rehabilitation Program, PCAGulayan sa Paaralan, BPI, DepEdDiskwento
caravans in depressed areas, DTIFamily development sessions for child and family nutrition, DSWDMainstreaming
nutrition in sustainable livelihood, DSWDPublic works infra and child nutrition, DPWHAdolescent Health and
Nutrition Development, DOHSALINTUBIG and other water, sanitation and hygiene, DOH, DILGFor PPAN , we have
initially identified specific programs that will be tweaked to contribute more directly to nutritional outcomes. These are
as listed in this slide. Additional programs or projects can be identified along the way.
25 Enabling programs Mobilization of LGUs for nutritional outcomes

Enabling policy and legal framework for LGU mobilizationDevelopment of continuing opportunities for LGU
excellence in nutrition programmingMobilization of RICs and other community- based organizations for nutrition
actionThree (3) enabling programs will be implemented to support the operationalization of the PPAN.These include the
Mobilization of LGUs for nutritional outcomes. Thus, selected LGUs will be handheld to formulate, implement,
coordinate, and monitor their responses to their nutrition situation. Other LGUs will be tapped to be hubs of learning or
inspiration of other LGUs. This strategy will be employed to ensure that nutrition programs are budgeted and is well
within the local development plans of LGUs.
26 Enabling programs Policy development for food and nutrition

Securing policy support for nutrition along the priority nutrition legislative measuresPublic advocacyStrengthened
management support to PPANSecuring vital nutrition infrastructure and resource requirementsStrengthened
coordination, monitoring, evaluation and management of PPANPolicy development on the other hand is expected to
strengthen the creation of an enabling environment for the implementation of nutrition programs both at the national and
local levels.The strategy to strengthen the management support to PPAN, covers two projects namely, Project 1:
Securing Vital Nutrition Infrastructure and Resource Requirements for PPAN; Project 2: Strengthening coordinating,
monitoring, evaluation and management of PPAN across NNC including member agencies and NNC Secretariat.
27 Implementation mechanism
National PPAN Implementation Plan,Agencies will commit what chunk of the targets they will “bite”Those involved
will outline the things that should be done to implement the programTo establish accountabilitiesShould be basis of
agency budget proposalsFor annual updatingHow will the PPAN be implemented? A National PPAN Implementation
Plan for will be formulated. At this stage, agencies will commit what chunk of the targets they will bite. Those involved
will also outline the things that should be done to implement the program. The intent is to establish accountabilities.
And we hope the civil society alliance organized today will participate in this process.It is hoped that the
implementation plan will be the basis of preparing agency budgets and forward estimates.The implementation plan will
be updated annually.
Regional Plan of Action for Nutrition,What agencies at the regional level will doThose involved will outline the things
that should be done to implement the programTo establish accountabilitiesShould be basis of agency budget
proposalsFor annual updatingA similar plan will be done at the regional level.
Local nutrition action plansManagement will involveOrganization of technical working groups at the national level to
tackle technical details of each programThe NNC Technical Committee will provide the venue for ensuring cohesive
action across the different programsCrucial to the implementation mechanism is the role of the Local Government Units
(LGUs) particularly in ensuring that local nutrition committees are functional, a local nutrition action plan is regularly
formulated, updated and provided funds.Managing the PPAN will involve the organization of TWGs at the national
level to tackle technical details of the program, while the NNC Technical Committee will continue to provide the venue
for ensuring cohesiveness of program implementation across different partners and stakeholders.
Monitoring system to be set upReporting by national agencies on physical and financial accomplishments–
semestralAssessment of LGUs according to key parametersA monitoring system will be set up that will include
reporting on physical and financial accomplishments. This will be complemented by a system for assessing the
performance of LGUs along nutrition program management.
31 Nutrition-specific programs Nutrition-sensitive programs

Sustainable Development GoalsPhilippine Development Plan GoalFoundation for inclusive growth, a high-trust society,
and a globally competitive knowledge economyReduced wasting among children under-five years oldReduced stunting
among children under-five years oldReduced micronutrient deficienciesImproved situation in overweight and
obesityReduced nutritionally-at-risk pregnant womenIncreased exclusive breastfeedingImproved food intakeReduced
low birthweightImproved complementary feedingNutrition-specific programsNutrition-sensitive programsIn closing the
discussion, let me project once again the overall framework for PPANSome of the elements of PPAN are not new.
Many are continued initiatives. However, what will be endeavored is a better convergence of services at the community
and household levels.Nutrition-supportive programsEnabling programs
32 NATIONAL NUTRITION COUNCIL

Thank You!NATIONAL NUTRITION COUNCILChino Roces Ave Extension, Taguig CityOfficial website:FB
Pages:Youtube acct:us at:telephone no. (02) or fax noWe have once again started a nrw journey for nutrition. I am
confident that all here present will join us in this journey. Thank you and mabuhay!
33 Nutrition problems to address

The PPAN for , like its predecessor plans aims to address prevailing nutrition problems.
34 StuntingStunting or being short for age is most prevalent form of undernutrition; and we have a VERY slow
declinethat includes various forms of undernutrition specifically, stunting or being short-for-age,Child on the right is a
“picture” of a stunted child
35 WastingThe other form of child undernutrition is wasting or being extremely thinHigh risk of dyingwasting or
extreme thinness,
36 deficiencies in vitamin A, iron, and iodine, as well as overall hunger and food insecurity
37 Overweight and obesity
Then on the other end of the pendulum, we do have overweight and obesity specially among adults.
38 Undernutrition among children under five years old

Two key points should be noted in this slide. The level of stunting at 33.4% is considered high based on the WHO
assessment criteria for severity of the problem. The level for wasting is considered poor also by WHO standards.The
other key point is on how undernutrition has remained at about the same level since 2005, with an increase in stunting
between 2013 and 2015.Source. National Nutrition Surveys. Food and Nutrition Research Institute, DOST
39 Trends in the prevalence of stunting from birth up to 3 years of age

A look at stunting prevalence rate by single age group by month would show that stunting prevalence among one-year
old children is almost double the prevalence rate among infants. Thus, there is a need to focus actions on preventing
stunting early in life.
40 Overweight by age/population group

Even as we have undernutrition among children, overweight and obesity are also concerns across various age groups,
with the problem more serious among adults.Source. National Nutrition Surveys. Food and Nutrition Research Institute,
DOST
41 Trends in the prevalence of nutritionally at-risk pregnant and lactating women, 1998-2015
Part of child undernutrition could be traced to poor maternal nutrition. And based on the national nutrition surveys of
FNRI-DOST, undernutrition among pregnant women while showing a downtrend from 1998, has stayed at about the
same level since On the other hand, undernutrition among lactating women showed an increasing trend since
2011.Source. National Nutrition Surveys. Food and Nutrition Research Institute, DOST
42 A look at nutritionally at-risk pregnant women by various socio-demographic characteristics would show that
undernutrition is higher among adolescent pregnant women; among those with low level of education, are not working
and belonging to the lowest wealth quintile.
43 Percent low birthweight

YearPercent low birthweight19989.6200313.0200819.6201321.4Source: National Demographic and Health
SurveyWhile low birthweight can be due to many reasons, poor maternal health and nutrition during pregnancy is one
important cause, resulting to slow growth of the fetus in the womb. The results of the National Demographic and Health
Surveys have not been encouraging as the percentage of low birthweight has been increasing progressively since This
gives us the signal to increase focus on the nutrition of women.
44 Service targets Program Service target

Infant and Young Child Feeding Program90% of pregnant women receive counseling support on nutrition90% of
mothers with infants 0-5 mos old receive counseling support on EBF90% of mothers with infants 6-11 mos old receive
counseling support on complementary feedingFor the service targets or how much of the needy population should be
reached, we have set a 90% target for most of the services, except for those for management and prevention of
overweight and obesity. The 90% was based on a simulation study by a group of researches that showed covering 90%
of the nutritionally needy population could lead to reduced mortality and stunting.Thus, for the IYCF program, pregnant
women, and mothers with children 0-23 months old will be reached.

Philippine Integrated Management of Acute Malnutrition90% of severe acute malnutrition (SAM) cases are treated90%
of near-SAM cases are treatedNational Dietary Supplementation Program90% of poor pregnant women who are
nutritionally-at-risk receive food supplementation90% of children 6-23 mos old from poor families receive food
supplementationFor the PIMAM Program the target is treatment of 90% of severe acute malnutrition or SAM cases, and
90% of near-SAM cases/The new projects under the National Dietary Supplementation Program will target pregnant
women and children 6-23 months old who come from poor and food insecure households.

National Dietary Supplementation Program100% of children in day care centers receive food
supplementationSupplementary feeding expanded to children enrolled in the Supervised Neighborhood Play100% of
severe acute malnutrition cases of school children receive appropriate food supplementation100% of children in day
care centers are targeted for supplementary feeding as are 100% of severe acute malnutrition cases

National Nutrition Promotion Program for Social and Behavior Change90% of pregnant women, mothers with infants 0-
23 months old and acutely malnourished children receive nutrition information through counseling and nutrition
classesMulti-media nutrition campaign on key desired behaviors implementedMicronutrient Supplementation90% of
target population receive vitamin A capsules, iron-folic acid supplements, iodized oil capsules and zincThe National
Nutrition Promotion Program targets at least 90% of those in the first 1000 days.
48 Service targets Program Service target Nutrition in Emergencies

Nutrition-related services delivered to affected population in disaster situationsOverweight and Obesity Management
and Prevention Program50% of preschool children, school children, and adults covered by healthy eating environment
and promotion of healthy lifestyle50% coverage of preschool children, school children, and adults on weight
management interventionsFor the overweight and obesity management and prevention program, about 50% of target
population are covered by Healthy Eating Environment, the promotion of healthy lifestyle, and of adult management
interventions.
The Food and Drug Administration (FDA) of the Philippines, formerly the Bureau of Food and Drugs (BFAD /ˈbiːfæd/;
1982–2009), is a health regulatory agency under the Department of Health created on 1963 by Republic Act No. 3720,
amended on 1987 by Executive Order 175 otherwise known as the “Food, Drugs and Devices, and Cosmetics Act”, and
subsequently reorganized by Republic Act No. 9711 otherwise known as “The Food and Drug Administration Act of
2009”. The agency is responsible for licensing, monitoring, and regulation of cosmetics, drugs, foods, household
hazardous products, medical devices[2] and electromagnetic radiation emitting devices, pesticides, tobacco and related
products, and vaccines for safety, efficacy, and quality in the Republic of the Philippines.
Department of Health (DOH) Secretary Francisco Duque Sr. created a subcommittee on Food and Drugs in 1961–62 to
initiate an administration bill to Congress to enact a law that would ensure the safety, purity and quality of foods, drugs
and cosmetics being made available to the public. The Subcommittee on Food and Drug was chaired by the then
Undersecretary for Special Health Services, Dr. Rodolfo Caños, with members Dr. Trinidad Pesigan, Director of the
Bureau of Research and Laboratories, Mr. Emilio Espinosa of the Bureau of Health Services, Ms. Amor Cita M. Pallera,
Pharmacy Adviser, Office of the Secretary of Health, also as Secretary and Liaison to Congress. Thus, on June 22, 1963,
Republic Act No. 3720 was passed into law known as the “Food, Drug and Cosmetic Act”.
To carry out the provisions of R.A. 3720, the Food and Drug Administration (FDA) was created with offices and
laboratories constructed in the DOH San Lazaro Compound, Sta. Cruz, Manila at a cost of about Php 2.5M. The Food
and Drug Administration became operational with the appointment of its first FDA Administrator, Ms. Luzonica M.
Pesigan on May 25, 1966, to Dec. 7, 1977 with Mr. Emilio Espinosa as Deputy Director. By Virtue of R.A. 3720, the
powers, functions and duties of the Division of Food and Drug Testing of the Bureau of Research and Laboratories and
the Board of Food Inspection, all personnel together with all their equipment, supplies, records, files and balance of
appropriations were transferred to the FDA.
With the Integrated Reorganization Plan of 1973, the Narcotic Drugs Division, Bureau of Internal Revenue, Department
of Finance was Transferred to the Food and Drug Administration headed by Ms. Conception M. Fernandez who retired
in 1975 with Ms. Rita V. Caoile as the next chief of the same. Mrs. Catalina C. Sanchez took over as the next chief of
the Narcotic Drugs Division in 1976.
On December 2, 1982, Executive Order No. 851 by Section 4, under the Minister of Health Hon. Jesus M. Azurin, The
FDA was abolished and created the Bureau of Food and Drugs (BFAD). Mrs. Catalina C. Sanchez was appointed the
first Director of the BFAD on Feb. 20, 1984 and took her oath on Feb. 28, 1984.
In 1987, the Bureau moved to its new site in Alabang, Muntinlupa, and acquired new facilities including state-of-the-art
analytical instruments and a modern experimental animal laboratory with the $12M grant from the Government of Japan
through the Japan International Cooperation Agency (JICA). This new BFAD in Alabang became operational on April
30, 1987.
In 1987, R.A. 3720 was amended by Executive Order 175 to the new title “Foods, Drugs, and Devices and Cosmetics
Act”.
It was also on the same occasion of the inauguration of this new BFAD facility that Pres. Corazon C. Aquino declared
publicly the Philippine National Drug Policy (PNDP) together with its four pillars, i.e., Quality Assurance, Rational Use
of Drugs, Self-Reliance, and Tailored Procurement. Based on the issuance of E.O. Nos. 174 and 175 amendments to
R.A. 5921 “The Pharmacy Law” and R.A. 3720 “Food, Drug, and Cosmetic Act” respectively, the Philippine National
Drug Policy was organized. Executive Order No. 851 was superseded by E.O. No. 119 s. 1987 under Hon. Alfredo R.
A. Bengzon, Sec. of Health, that again reorganized the BFAD on the basis of Administrative Order (A.O.) No. 30 s.
1987, Provisions to Implement the Reorganization of the Department of Health.
Executive Order No. 102 dated May 24, 1999 was signed and redirected the functions and operations of the Department
of Health, with then Hon. Alberto G. Romualdez, Sec. of Health, wherein BFAD was expanded with an added Division,
the Policy, Planning, and Advocacy Division. The joining of the National Drug Policy workforce with that of BFAD in
Alabang, further strengthened the Bureau to meet new challenges in serving the interests of the Filipino people
consistent with the Philippine National Drug Policy and the National Health Policy.
Republic Act No. 9711, an act strengthening and rationalizing the regulatory capacity of the Bureau of Food and Drugs
by establishing adequate testing laboratories and field offices, upgrading its equipment, augmenting its human resources
complement, giving authority to retain its income, renaming it the Food and Drug Administration (FDA), amending
certain sections of Republic Act No. 3720, was signed by President on August 18, 2009.
1. Nutrition= digestion, metabolism, circulation and elimination Nutritional Status= refers to the state of one’s nutrition
Wellness= state of good health with optimal body function (requires good nutrition Nutrition plays a large role in
determining: Height Weight Strength Skeletal and muscle development Physical agility Resistance to disease
Appetite Posture Complexion Mental ability Emotional and psychological health Nutrition and Diet Therapy
2. Immediate effects of good nutrition includes: • Healthy appearance • Good attitude • Proper sleep and bowel habits •
High energy level • Enthusiasm • Freedom from anxiety
3. Good Nutrition may delay or prevent the following: • Hypertension • Atherosclerosis • Osteoporosis: prevented by
good nutrition • Malnutrition • Obesity • Anemia If your neighbor tells you her MD has placed her on a high protein
diet with iron supplements based on her diet which of the above illness is her medical problem?
4. Essential Nutrients • Composed of chemical elements found in food. • Used by the body to perform body functions •
Nutrients in foods replace those used by the body • Essential nutrients are divided into six groups.
5. Carbohydrates Cellulose = indigestible carbohydrate, provides bulk (bran, whole-grain cereal, fibrous fruits, &
veggies • Major source of human energy • Starches or sugars • Easily digested, grow well in most climates, keep
well without refrigeration • Main sources: bread, cereals, pasta, crackers, potatoes, corn peas, fruits, sugars and
syrups
6. Fats Aid in absorption of fat-soluble vitamins • Lipids • Concentrated form of energy • Help maintain body
temperature by providing insulation • Help cushion organs and bones • Provide flavor to meals
7. Fats Continued • Main sources: butter, margarine, oils, creams, fatty meats, cheeses, and egg yolk • Classified as
saturated or poly unsaturated Excess cholesterol is believed to contribute to atherosclerosis Cholesterol: fatty
substance found in body cells and animal fats – eggs, meat, shellfish, butter cream, cheese, milk, organ meats
8. Proteins • Build and repair body tissue • Provide heat and energy • Help makes antibodies • Make up to 22 amino
acids (9are essential) • Main sources complete protein: meat, fish, milk, cheese, eggs, • Incomplete proteins: cereal,
soybeans, dry beans, peas and peanuts
9. Vitamins • Organic compounds that are essential to life • Regulate body functions • Repair body tissues • Only a
small amount required –well balanced diet provides required vitamins • Excess or deficiency can cause poor health •
Water soluble or fat soluble Someone who eats fat free diet could become deficient in fat-soluble vitamins
10. Minerals • Inorganic (nonliving) elements found in all body tissues • Regulate body functions • Build and repair
body tissues • they include: calcium, phosphorus, sodium, potassium, iron, iodine, fluorine and others.
11. Water • Found in all body tissues • Essential for digestion • Makes up most of blood plasma • Helps body tissues
absorb nutrient • Helps move waste material through body Average person should drink 6-8 glasses of water a day.
12. Utilization of Nutrients • Digestion- breaks down the foods we eat by 1. Mechanical or chemical 2. Peristalsis •
Absorption – process of taking in nutrients by the body 1. Most absorption occurs in the small intestine 2. Water,
salts and some vitamins in large intestine
13. Metabolism – use of nutrients by the body 1. Basal Metabolic rate (BMR) Measuring Food Energy 1. Calorie- the
amount of heat produced during metabolism 2. Most people use an average of 3,500 calories/day 3. To lose wt. a
person must take in fewer calories then are burned 4. To gain weight, a person must take in more calories than the
body uses. Utilization.
14. Therapeutic Diets • http://www.dietsite.com/dt/diets/hearthealthy/lowsalt.asp • Regular Liquid Soft • Diabetic Low
Calorie • High Calorie Low Cholesterol • Fat-restricted Sodium-restricted • Protein Bland Low-residue
1. Malnutrition • Malnutrition results from imbalance between the body's needs and the intake of nutrients, which can
lead to syndromes of deficiency. Condition related to malnutrition • Over nutrition: Consumption of excessive food
or nutrient, as occurs in obesity, megadoses of vitamins leading to toxicity. • Under nutrition: inadequate ingestion of
nutrients as in PEM (Protein Energy Malnutrition), Vit. Deficiencies
2. Malnutrition • Malnutrition may be caused by endogenous factors, such as faulty metabolism, or exogenous factors,
such as inadequate dietary intake • it may be classified as primary resulting from inadequate or excessive intake of
one or more essential nutrients “or secondary” resulting from altered body functions such as malabsorption
syndrome.
3. Risk factors associated with malnutrition • Low education • Poverty • Mental/physical disabilities • Old age •
Alcoholism • Drug addiction • Food fadism (no food) • Institutionalization “prisons”
4. Secondary malnutrition. Risk factors predisposing to S. M. • 1- Failure to meet the excess nutritional need during,
fast growing period, lactation, pregnancy and physical stress • 2- Problem involving ingestion, digestion, absorption
and metabolism, pathological conditions as in • Anorexia loss of appetite, nausea and vomiting, fever, poor dentition.
• Gastrectomy, cholicystitis (inflammation of gallbladder) or pancreatic insufficiency • Achlorhydria (low gastric
acid production), liver and gall bladder diseases, diarrhea, colitis (inflammation of the colon), malabsorption.
5. Excessive loss of nutrients via execration as an high sweating or polyuria (large production of urine). • Excessive
loss of nutrients via hemorrhage (blood loss), diarrhea and parasites • Abnormal metabolism as in DM, liver failure,
alcoholism and in some leukemia’s • prolonged usage of antibiotics which destroys the natural flora causing vits.
Deficiency (B and K)
6. Prevention • 1- Adequate and well-balanced diet emphasizing the deficient nutrient(s) • 2- Alleviating the patho.
cause and provide supplement if necessary.
7. Dietary Recommendations • All dietary recommendations should be considered within the framework of a
nutritionally balanced diet. The goal for each and every patient is healthy eating primarily achieved by consumption
of a combination of low fat, high fiber foods, and exercise.
8. Monounsaturated fat 10-15% Saturated fat<10% Protein15% Carbohydrate 50-60% Polyunsaturated fat <10%
9. PROTEIN • RDA: for a healthy adult is 0.8-1.0 gm/kg IBW/d. • Children require 1-2 gm/kg/d
10. Protein • Excess • High ptn. Intake is wasteful “economically” • High ptn. Intake is a burden for diseased liver or
kidney. • High Ca loss in urine • Sources of animal ptn. Are sources of saturated fat too, which will lead to
undesirable levels of fat intake if ptn. Intake is high.
11. GOUT
12. Purines-rich foods predispose to gout. • Gout is a condition of abnormal purine metabolism in which individuals has
reduced ability to execrate uric acid and may also produce it in excessive amounts. It builds up in the blood and
eventually is deposited in the joints.
16. Causes • The cause of gout is an inflammation in your joint resulting from an accumulation of urate crystals. Uric
acid is a waste product formed from the breakdown of purines. • These are substances found naturally in your body
as well as in certain foods, especially organ meats — such as liver, brains, kidney and sweetbreads — and anchovies,
herring, asparagus and mushrooms.
17. Prevention & Self-care • Maintain a healthy weight • Avoid excessive amounts of animal protein • Avoid alcohol •
Drink plenty of liquids
18. Protein deficiency • Occur when individual dose not eat enough ptn. foods of low biological value, or obtain
insufficient calories
19. Protein energy malnutrition • Kwashiorkor, and marasmus, are major health problems for infants and young children
in Africa, or after the infant is weaned • Kwashiorkor: Lack of protein in diet over period of time (first-second child),
affects older children • Marasmus: Severe Nutritional def in general, and affect infants and very young children
20. Prevention of kwashiorkor, and marasmus • 1- Provide adequate nourishment of vulnerable group • 2-provide ptn-
rich foods or supplementation • 3- Control problems associated with K and M • 4- Nutrition education for care-
givers
21. Deficiency 1. Kwashiorkor • Loss of pigmentation of the hair • The children have dry scaling, pale skin • A
protuberant abdomen • Fail to grow normally • Swelling ( edema )
22. 2. Marasmus • caused by an inadequate intake of both protein and calories.
23. FAT A- Excess: lead to • Obesity and related problem • Excess intake of fat-soluble vitamins B- Deficiency: lead to
• 1- Lack of essential fatty acids and fat-soluble vitamins • 2- Weight loss • 3-Inefficient utilization of Protein and
CHO
24. Monounsaturated Fatty Acids • Appear to lower LDL (“bad”) cholesterol and help raise levels of HDL (“good”)
cholesterol. • Food sources: olives, olive oil, avocados, peanuts oil and canola oil.
25. SOURCES of MONO-UNSATURATED FATS Canola oil Olive oil
26. Polyunsaturated Fatty Acids • Fats that seem to lower total cholesterol levels. • Food sources: many vegetable oils,
such as corn oil, soybean oil and safflower oil, sunflower oil.
27. VEGETABLE SOURCES OF POLYUNSATURATED FATTY ACIDS Corn oil Safflower oil Sunflower oil
28. Polyunsaturated Fatty Acids (ESSENTIAL FA) Linoleic sunflower, soybean Linolenic fatty fish, shell fish
29. High fat diets are linked to… • Heart Disease • Obesity • Cardiovascular Related Problems
30. Lowering Fat and Cholesterol in the Diet • Exercise • Replace saturated fats with unsaturated fats in the diet •
Choose lean cuts of meat • Steam, boil or bake foods instead of cooking them in oil or fat • (See the last page of your
handout for more tips)
31. CARBOHYDRATES A- Excess: lead to • Obesity and related problem B- Deficiency : lead to 1- Abnormal energy
metabolism 2- Weight loss 3-Inefficient utilization of Protein and Fat
1. Malnutrition and obesity
2. What is malnutrition? World Health Organization definition: The term is used to refer to a number of diseases,
each with a specific cause related to one or more nutrients (for example, protein, iodine or iron) and each
characterized by cellular imbalance between the supply of nutrients and energy on the one hand, and the body's
demand for them to ensure growth, maintenance, and specific functions, on the other.
3. HUMAN NUTRITION • Obesity & under-nutrition are the 2 ends of the spectrum of malnutrition. • A healthy
diet provides a balanced nutrients that satisfy the metabolic needs of the body without excess or shortage. •
Dietary requirements of children vary according to age, sex & development.
4. Macro andmicro nutrients • Macro-nutrients • Protein (amino acids) • Energy (carbohydrates) • Fat (fatty acids) •
Micro-nutrients • Water soluble vitamins (assist in energy-release of carbohydrates and red blood cell formation)
• Fat soluble vitamins (development & metabolism) • Minerals
5. Malnutrition: definition • Malnutrition : chronic state of nutrition due to insufficient food intake (caloric and / or
protein) specific for infants and small child. • Along with major deficits of nutrients occur also deficiencies in
vitamins and minerals (deficiency anemia, rickets, avitaminoses). • Depression of cellular immunity caused by
malnutrition favors increased susceptibility to infection, which worsens the initial deficit, the infection is often
the one that causes death. • Half of the states of malnutrition : first 6 months of life, overlapping maximum period
of CNS development (neuronal proliferation - to a maximum of 18 months).
6. Types of malnutrition • Severe Protein-Energy Malnutrition (>3 S.D.) • Kwashiorkor (low protein) • Marasmus
(low calories) • Mild/moderate undernutrition (>2 S.D.) • Stunting • Underweight • Wasting • Micro-nutrient
deficiency • Iodine • Iron • Vitamin A • Vitamin D
7. OVERVIEW OF MALNUTRITION • The majority of world’s children live in developing countries • Lack of
food & clean water, poor sanitation, infection & social unrest lead to LBW & PEM • Malnutrition is implicated
in >50% of deaths of children <5years (5 million/yr).
8. OVERVIEW OF MALNUTRITION • WHO estimated that 32% of children in developing countries are
underweight (182 million). • 78% of these children live in South-east Asia & 15% in Sub-Saharian Africa. • The
reciprocal interaction between PEM & infection is the major cause of death & morbidity in young children.
9. EPIDEMIOLOGY • The term protein energy malnutrition has been adopted by WHO in 1976. • Highly prevalent
in developing countries among children <5 years; severe forms 1-10% & underweight 20-40%. • All children
with PEM have micronutrient deficiency.
10. Classification/Terminololgy The term malnutrition (Anglo-Saxon School) or dystrophy (French School) define
the states of malnutrition through food intake deficiency- qualitatively and/or quantitatively. • Protein energy
malnutrition (PEM); • Protein malnutrition (PM).
11. Classification/Terminololgy WHO proposes 2terms (referring to states of severe malnutrition) • Marasmus -
severe PEM; • Kwashiorkor - severe PM. These terms are unsatisfactory for practice - do not include light and
intermediate states of malnutrition→new terminology. WHO - classification of malnutrition • Primary
malnutrition • Secondary malnutrition.
12. Primary Malnutrition :ETIOLOGY Primary malnutrition • correctfood intake; • negativ prognosis due to
disturbed growth that can not be influenced therapeutically (frequent association with mental deficiency); •
commonly associated with: fetal malnutrition, low birth weight and small height sometimes. The causes of
primary malnutrition: • organics (severe malformations: renal, digestive, cardiac) • genetically conditioned
diseases (chromosomal, metabolic) • fetal infections (toxoplasmosis, syphilis, cytomegalovirus).
13. Etiology of Primary Malnutrition • Failure of lactation. • Improper weaning practices • Poverty • Food taboos • 2
or more children under 5 years of age in same household • Death of mother • Incompetent/ ignorant mother. •
Lack of family planning
14. SECONDARY MALNUTRITION Secondary malnutrition (exogenous): • deficiency due to dietary intake
qualitatively or quantitatively, • prognosis is generally good by correcting the cause and food intake , • usually no
mental deficits.
15. SECONDARY MALNUTRITION Classification of secondary malnutrition (WHO): I. Moderate malnutrition: -
mild (grade I dystrophy, hypotrophy, "poor child"); - medium (grade II dystrophy); II. Severe malnutrition (grade
III dystrophy): - energy-protein malnutrition (PEM) :marasmus, atrepsia; - protein malnutrition (PM) • acute
form (kwashiorkor); • chronic form (marasmickwashiorkor ).
16. Etiology of secondary malnutrition A)Dietary deficiency • quantitatively: native hipogalactia; late diversification
over 6 months of age; improper dilution of milk, restrictive diets, taboos related to food, family, religious, ethnic;
• quality: carbohydrate deficiency ( cow’s milk distrofy ), protein deficiency (edematous dystrophy by excess
flour, using vegetable protein low biological value), lipid deficiency ( regimes without lipids) • lead to imbalance
by decreasing caloric intake.
17. Etiology of secondary malnutrition B) infections:entericinfection;bronchopneumonia, otomastoidite, chronic
urinary tract infection, bacterial or parasitic diarrhea, syphilis, tuberculosis- poor appetite, digestive losses,
increased catabolism. c) psychosocial events:maternal deprivation, neglect of physiological rhythm of
alimentation, lack of hygiene, pollution, cold, hospitalism;
18. Etiology of secondary malnutrition D) psychosomatic disorders : - anorexia , • organic disease (hypertrophic
pyloric stenosis, congenital malformations that cause repeated vomiting, cystic fibrosis, celiac disease, congenital
intolerance to disaccharides, labio-maxillo-palatine cleft) , • infantile cerebral palsy with impaired swallowing,
pharyngeal incoordination.
19. Etiology of secondary malnutrition Chronicillnessesthatcommonly are associatedwithnutritionaldeficiencies
include thefollowing: • Cysticfibrosis • Chronic renal failure • Childhoodmalignancies • Congenital heartdisease •
Neuromuscular diseases • Chronicinflammatoryboweldiseases
20. Etiology of secondary malnutrition • In addition, thefollowingconditions place children at significantrisk for
thedevelopment of nutritionaldeficiencies: • Prematurity • Developmentaldelay • In uterotoxinexposure (ie, fetal
alcoholexposure) • Childrenwith multiple foodallergiespresent a special nutritionalchallengebecause of severe
dietaryrestrictions. Patientswith active allergicsymptomsmayhaveincreasedcaloricandproteinneeds.
21. Protein-energy malnutrition pathogenesis In severe forms when nutritional deficit exceeds a certain limit, the
consequences are severe: • regression of all metabolic activities (decreased basal metabolism, decreased
intracellular water, decreasing opportunities to retain water and salt); • low digestive tolerance (decreased activity
of disaccharideses, pancreatic secretion, bile acids); • loss of defense to infection. Very low digestive tolerance
and dietary intake can not maintenance energy needs lead to autophagic processes (the metabolism of starvation).
22. Protein-energy malnutrition pathogenesis Severe lack of calorie and protein → hypoglycemia, decreased serum
amino acids in pancreatic reaction → → hipoinsulinism (main endocrine changes in starvation) → decrease
peripheral insulin and the appearance adaptive responses: • mobilization of fatty acids from adipose tissue
(lipolysis) to the liver to be an energy source; • decrease in muscle glucose utilization and incorporation of amino
acids that are directed to the liver, where they are used for protein synthesis and neoglucogeneză (the exhausted
body fat); • hepatic protein synthesis is achieved by sacrificing muscle proteins.
23. Protein-energy malnutrition pathogenesis Infection - is the vicious circle in severe malnutrition, worsening
starvation and being the main cause of death by: • loss of appetite; • digestive losses (diarrhea); • increased
catabolism (febrile illness); • disorders of intermediary metabolism by reducing metabolic efficiency of nutrients;
• increased urinary nitrogen loss, K, Mg, Zn, P, vitamin A, C, B2.
24. Pathogenesis of protein malnutrition The acute form (typical Kwashiorkor) • occurs after 6-8 months; •
diversification normal calorie but devoid of protein; • deposits of fat are consumed, stature is normal and causes
severe loss of protein (proteins from the liver, muscle, pancreatic proteins, serum albumins deficiency) and loss
of intracellular K (preservation mitosis), hepatic fatty infiltration if infection occurs - marked reduction albumin
(hepatic synthesis deficient) → fluid retention (decrease in colloid osmotic pressure capillary) → edema.
25. Pathogenesis of protein malnutrition Chronic form (MarasmicKwashiorkor) - secondary selective protein intake
deficiency is characterized by: - sufficient caloric intake; - normal secretion of insulin: • favors lipogenesis (fatty
acids are not available in place of amino acid oxidation - fatty tissue is preserved); • reduced level of plasma
amino acids by three mechanisms: • reduce the release of amino acids from muscle; • stimulates the passage of
serum amino acids in muscle; • favors the the incorporation of amino acids into the muscle.
26. MARASMUS/KWASHIORKOR • Marasmus represents an adaptive response to starvation, whereas
kwashiorkor represents a maladaptive response to starvation • In Marasmus the body utilizes all fat stores before
using muscles.
27. Assessment of NutritionStatus • Clinical • Anthropometric • Dietary • Laboratory
28. Investigations for PEM • Full blood counts, inflammatory markers; • Blood glucose profile, lipidic profile • Iron,
vitamin levels; • Microbiology: septic screening,stool & urine for parasites & germs; • Electrolytes, Ca, Ph &
Mg; • Serum proteins, protein electrophoresis; • immunological status: cellular immunity - decreased T cell,
interferon, IDR lack of response to tuberculin; humoral immunity - low IgA (secretoryIgA), IgM - high, low IgG.
• Decrease complement C3; • Exclude HIV & malabsorption.
29. Investigations for PEM In essence: • decrease serum albumins → edema; • decrease apoproteins (lipoproteins
carrier); • storage of fat in the liver (fatty infiltration); Clinical outcomes: oedema, hepatomegaly (fatty liver),
changes in hair growth and skin (areas of hypo-or hyperpigmentation, fissures), diarrhea (villous atrophy),
predisposition to infection (humoral and cellular immunity disturbed).
30. Anthropometric assessment of malnutrition anthropometric criteria : • percentiles method (normal 10-90). •
standard derivations method (normal + / - 2 SD). • ponderal index (PI) PI = actual weight of the child / ideal
weight (W of child of the same age located on the 50th percentile of the growth curve). After the PI values :
3degrees of PEM(Gomez) • degree I (PI = 0.89 to 0.76); • degree II (PI = 0.75 to 0.60); • degree III ( PI = 0.60).
PI = 0.90- underweight or child at risk of malnutrition.
31. Anthropometric assessment of malnutrition The protein malnutrition are two degrees: • degree I PI = 0.8-0.6 -
KWASHIORKOR; • degree II PI= 0.6 – MARASMIC KWASHIORKOR Nutritional index (NI) - index diets. •
NI= actual weight / weight appropriate waist. After this indicator there are 3 degrees of malnutrition: • grade I
(NI= 0.89 to 0.81); • grade II (NI= 0.80 to 0.71); • grade III (NI= 0.70). Head circumference (HC) - highlights the
true growth in the first two years. Midarm circumference (measured at the ½ distance between the acromion and
olecranon) pathological - under 13 cm - available in children over 2 years.
32. Assessment of malnutrition- functional criteria Appreciation of the digestive tolerance: • paradoxical reaction to
hunger (disproportionate weight loss); • food paradoxical reaction (weight loss to increased food intake,
sometimes diarrhea); • sensitivity to fasts - by spacing meals: hypoglycaemia, especially nocturnal → apnea,
sudden death. • immunological reactivity : - increased responsiveness to infection; - reactivity collapsed (serious
infection without fever, leukocytosis, sometimes opportunistic).
33. Assessment of malnutrition Neuropsychological development: • Archaic reflexes; • Muscle tone; • Posture; •
Mobility; • Development of language; • Affection. They are affected differently depending on the severity of
malnutrition .
34. Clinical features in marasmus • Marked muscle wasting and loss of subcutaneous fat; • Monkey facies; • Skin
becomes loose and hangs in folds; • Abdomen protuberant due to hypotonic muscles; • Temperature is usually
sub-normal; • Child is alert.
35. Clinical features of kwashiorkor • Generalized edema more marked in lower extremeties, muscle wasting; •
Growth retardation; • Psychomotor changes; • Apathy and irritability; • Fine and discolouredhair; • Anemia; •
Usually flaky paint dermatitis; • Enlarged liver due to fatty changes.
36. Complications of PEM • Hypoglycemia • Hypothermia • Hypokalemia • Hyponatremia • Heart failure •
Dehydration & shock • Infections (bacterial, viral & thrush)
37. TREATMENT: Prevention of Malnutrition • Primary Prevention • Health Education to mothers about good
nutrition and food hygiene • Immunization of children. • Growth monitoring on Growth Charts specially of all
children under 3 years of age • Secondary Prevention • Mass Screening of high risk populations, using simple
tools like Weight for age . • Tertiary Prevention • Good Nutritional Care, supplementary feedings and
rehabilitation, counselling of mothers.
38. TREATMENT: Prevention of Malnutrition • Natural nutrition - first 4-6 months; • Artificial nutrition - milk type,
dilution, enrichment rice mucilage; - Compliance with immunization schedule, the correct treatment of
infections; - Inadequate conditions and social environment.
39. TREATMENT OBJECTIVES: • accurate assessment of the form and degree of malnutrition; • pointing out the
main deficiencies (protein, fat, carbohydrates, fluid and electrolyte minerals and vitamins), immune status and the
possibility of co-infection; • finding the cause which produced malnutrition; • recovery plan individualized for
the nutritional deficiency as quickly as possible.
40. TREATMENT General principles: The recovery of PEM (II and III degree) : I. The initial phase •Correction of
water & electrolyte imbalance; • Treatment of infectious complications. II. Repair phase • Dietary therapy; •
Correction of deficiencies (anemia, rickets, hypovitaminosis, etc). III. Convalescence phase • Restoration of body
composition; • Enhancing healing. Optimal objective is to resume growth after 2-3 weeks of starting the diet and
clinical recovery in 6-8 weeks.
41. TREATMENT I)Parenteralnutrition for 2-3 days →enteral nutrition with flow probe using hyperproteic and
hypercaloric solutions ; II) Early initiation of oral nutrition : hypoallergenic preparations rich in proteins and
calories, low osmolarity:Alfare, PeptiJunior, Pregestimil, Nutramigen, Pregomin or amino acid formulas, such as
Neocate . • Keep in parallel parenteral intake of carbohydrates, amino acids, lipids. • Simultaneously treating
infections, hypoproteinemia, anemia, multivitamins deficiencies . • This variant is also little used because it
requires specials dietetics and carefully monitorization of nutritional therapy .
42. TREATMENT III) after fluid replacement and electrolyte - digestive tolerance : • with carrot soup or rice
mucilage (in various concentrations ) in a dose of 150-200 ml / kg ( not exceeding 1000 ml / day) • carbohydrates
were obtained from glucose 5%, 7 %, 10 % and chicken mixed proteins ( hypoallergenic, 100g , 17g protein). •
after normalization of the stools ( 7 days) :oil gradually (3-4 ml / day ) and after 10 days from the beginning of
enteral diet →hypoallergenic preparation can be inserted (!preparations lactose free- can induce cow's milk
protein intolerance ) . • week 4 :sugar (restoring lactose tolerance is difficult , 3-4 months); • flour products
containing gluten will not enter until full recovery; • increases in protein - calorie intake by parenteral
administration of carbohydrates , amino acids and proteins; • treat the infection , iron or vitamin deficiencies .
43. TREATMENT Malnutrition has its weight age. • correct food intake : 8-10% protein, 54-50% fat, 50-60%
carbohydrates: 1 g lipid- 9 kcal; 1 g protein - 4.1 kcal; 1 g carbohydrate - 4.1 kcal. • complete metabolism of 1 g
of protein are required 35-40 kcal. • a protein intake ˃5 g / kg / day is dangerous, resulting hyperammonemia,
increased blood urea nitrogen ; • Increasing K intake to 4-5 mEq / l .
44. TREATMENT Recovery of PEM degree II(advenced) and III (Suskie) contains: • calorie - 175 kcal / kg / day; •
protein - 4 g / kg / day; • lipid - 9.59 g / kg / day; • carbohydrate - 18.3 g / kg / day. • Research and treating
infection with antibiotics (ideally etiologic) is mandatory. • In severe malnutrition ↓ IgG: iv administration of
gamma globulin • protein malnutrition (low albuminandproteinemia ): human albumin administered iv (1 g / kg /
day). • basal energy needs - 70 kcal / kg / day.
45. TREATMENT Mild forms of MPC • Treat at home by correcting the diet (food ration for age - increasing protein
intake to 0.5-1 g / kg / day→ 20 to 30 kcal / kg / day). • correction of the causes: maternal
hipogalactia,hypocaloriec diet with incorrect mixed or artificial nutrition, extending over six months natural
nutrition with delayed/incorrect diversification. • Quick recovery in 1-2 weeks.
46. TREATMENT PEM (severe forms degree II-III , III) • Treat only in hospital. • The first 24 hours - fluid
replacement and electrolyte and acid-base fluid resuscitation. • The following 48-72 hours (sometimes more)
partial or total parenteral nutrition, reaching 80-90 kcal / kg / day.
47. TREATMENT • the rate of protein :4-5 g / kg / day (increasing protein is progressively 1-1.5 g / kg / day,
reaching in 4-5 days at this rate) • 180-160 kcal / kg to 180-200 kcal / kg / day • from day 3-4 start exploratory
digestive maintaining iv administration sugars, amino acids ; • Diet exploratory :rice mucilage 3%, 5%, 8%;
carrot soup 300 ‰ or 500 ‰, • sweetener - glucose 5%, 7%, 10% (even 15%). • 7-8 lunches, from 30-50 ml
ground in 2-3 days, if tolerance is good - 140-150 kcal / kg.
48. TREATMENT Criteria to follow: • normalization of the stools ; • growth rate - slow resume after 2-3 weeks to
restore digestive tolerance and achieve optimum value caloric and protein intake (early treatment can decrease
the growth rate - restore electrolyte balance, after the disappearance of edema). • avoid prolonged fasts - risk of
hypoglycaemia. • immune recovery 25-30 days after initiation of dietary therapy. • histochemical normalization
of intestinal mucosa after 3-4 months.
49. OBESITY Obesity-chronicdisorder of thenutrition in infants,
childrenandadolescentscharacterizedbytheaccumulation of fat in adiposetissueandothertissuesandorgans as a
result of energyimbalance. The prevalence of thediseaseis on therise: accordingto WHO 22 millionchildrenunder
5 years are obese, theprevalencebecoming triple in thepast 30 yearsandovercomingtheprevalence of malnutrition.
For childrenwhohave an overweight or obeseparent, therisk of becomingobeseadultsishigherthan in normal
weightchildren. Ifbothparents are obese, a child'srisk of becomingobeseis 80%. 80% of
obeseadolescentsbecomeobeseadults.
50. OBESITY Obesityis a plurifactorial disease, favorablefactorsbeing: • prenatal factors: maternal caloric intake,
maternal diabetes, dismaturity, smallsizeandsmallheadcircumference at birth; • perinatalfactors: cold climate at
birth. • post-natal factors: theintensity of theincrease in body fatbytheage of 1 year, artificial feedingfrombirth,
adolescenceweight.
51. OBESITY - pathophysiological mechanisms and clinical features The major disturbances encountered in obesity
are insulin and glucose homeostasis, dyslipidemia and hypercortisolemia. clinical picturea) Characteristic
anthropometric data of obesity are: -excessive weight according to height, excessive weight in relation to the
ideal weight for age; -normal-sized or even increased height compared to the average age; -increased upper-arm
circumference comparing to age values; -subcutaneous fat thickness increased compared to normal age; -sexual
maturation and somatic maturation(bone age) normal or accelerated. b) somatic appearance: generalized
symmetrically increased fat deposits, breast enlargement and distension of the abdomen.
52. OBESITY : Symptoms -psychological problems: bad image of oneself, feelings of inferiority and rejection from
the same aged children community, depression, frustration, tendency to antisocial behavior, difficult family
relationships and social immaturity, increased dependence to the family. -mechanical overload-related symptoms
represented by the excess weight: cardio-circulatory inadequacy, fatigue, polipnea and dyspnea on moderate
effort, lower limb orthostatic edema, joint pain. -skin changes: intertrigo, skin folds irritation, itching, abcesses,
acne. -nonspecific disorders: headache, vertigo, dizziness, fatigue, flatulence, constipation, difficult digestion,
menstrual disorders in adolescents.
53. OBESITY: LABORATORY DATA • carbohydrate metabolism: over 50% of obese children have impaired
glucose tolerance. • lipid metabolism: hypercholesterolemia, hypertriglyceridemia, elevated levels of LDL and
apolipoprotein B, decreased HDL and apolipoprotein AI. • protein metabolism: moderate increase in serum
protein, the α2-and β-globulins. • hormonal profile: elevated levels of insulin and cortisol; thyroid function is
generally normal. • fluid and electrolyte balance : sodium retention and potassium excretion are
elevated;aldosteroneexcretion is significantly increased.
54. OBESITY: Positive diagnosis - clinical appearance ; -anthropometric data : body mass index(BMI), size of skin
fold. WHO recommendations : - overweight : BMI ˃1 SD or between 95-99 percentile; - obesity:BMI ˃2 SD or
above the 99th percentile ; - by the age of 2years , overweight : reporting the actual weight to ideal weight for
height , age and sex. The correct definition of obesity in children is given by the content of body fat mass
measured by bioelectric impedance . Up to age 16 years:obesity→fat mass ˃20 % reference values for age and
sex ; Over 16 years :obesity →fat mass ˃25 % of body weight in boysand ˃32 % for girls.
55. OBESITY: DIFFERENTIAL DIAGNOSIS In case of suspected genetic or endocrine obesity, differential
diagnosis should be done with: • Laurence-Moon- Bardet-Biedl syndrome, • Prader-Willi syndrome, • Albright
(pseudohypoparathyroidism), • Cushing's syndrome, • Stein-Leventhal syndrome(or Policystic ovarian syndrome)
• Frolichsyndrome( or AdiposogenitalDistrophy) • Mauriac syndrome(complication of diabet mellitus type I) •
Von Gierkeglycogenosis (storage disease).
56. OBESITY: TREATMENT Treatment protocol includes: - dietary treatment, - physical activity program, -
behavioral therapy, - drug therapy, -surgery, - treatment of complications, - family nutrition education. Dietary
treatment remains a therapeutic basis.
57. OBESITY: TREATMENT a)Dietary treatment during growth and development needs to ensure their normal
ongoing, so that can not be overcome certain minimum amounts of caloric intake and dietary protein: -110
calories / kg / day in infants <6 months; - 90 calories / kg / day in infants 6-12 months; - 60 calories / kg / day of
ideal weight under 12 years; - 850 Calories / day in teenager during the weightloss period,1000 calories / day
after the initial period of minimum one month.
58. OBESITY: TREATMENT In most obese children good results are obtained by decreasing initial caloric intake
with 30%. Nutritional content of the diet: • 20% proteins, • 40% carbohydrates, • 40% fats, • 5-6 meals / day,
with the following distribution of calories: 20% at breakfast, 30% at lunch, 20% at dinner and two snacks by 15%
in 5 meals / day version and by 10% in snacks in the 6 meals / day version. Diet is suitable for inducing a weight
loss of 0.5-2 kg / week. In obese infants, the treatment goal is not to reduce weight, but slowing down the rate of
weight gain in relation to increasing waistline.
59. OBESITY: TREATMENT b) physical activity: important role in weight loss programs (discrepancy between
caloric intake and physical energy expenditure). Activitaty will be chosen according to the personality,
preferences and abilities of the child. c) behavioral therapy: to correct the habits that caused weight excess and
promote a healthy lifestyle. d) drug treatment: minor role. e) surgery: surgical techniques recommended for adult
are not appropriate for child.
60. OBESITY:EVOLUTION AND PROGNOSIS Prophylaxis should start from prenatal period by identifying
parents with increased familial risk for obesity. Factors that may influence the evolution and prognosis of
obesity are: -etiology of obesity: endocrine obesity is refractory to dietary therapy versus exogenous obesity; -
severity: more severe degrees respond poorly to therapy and have higher risk of complications; -during evolution:
as the disease is aging, eating habits are harder to be influenced by therapeutic measures; -age: critical periods in
the development of obesity are infancy, preschool and adolescent; -the response to dietary treatment.
61. OBESITY: EVOLUTION AND PROGNOSIS Slimming regime favorable results are: • acquiring a feeling of
well being, • lowering blood pressure, • improving heart function, • reducing the number of apneas / hour,
increase blood oxygen saturation and lung capacity, • decreased basal hyperglycemia and hyperinsulinemia and
reduced postprandial insulin resistance, relieving joints symptoms.
62. OBESITY: COMPLICATIONS Complications of obesity: • orthopedic complications: genuvalgum, flat feet,
Blount disease, coxavara, epiphysitis of femoral head, aseptic necrosis of the femoral head, hyperlordosis, leg
pain after prolonged standing. • metabolic complications: dyslipidemia, hyperinsulinemia, insulin resistance, type
II diabetes, hyperuricemia (rare).
63. OBESITY: COMPLICATIONS • hormonal complications: hiperandrogenemy, menstrual cycle disorders,
hypercortisolismreagent. • respiratory complications: hypoventilation syndrome, obstructive apnea during sleep,
asthma. The extreme manifestation of alveolar hypoventilation is Pickwick syndrome. • cardiovascular
complications:hypertension, right ventricular hypertrophy, coronary atherosclerosis or generalized
atherosclerosis.
64. OBESITY: COMPLICATIONS • digestive complications: hepatic steatosis, cholelithiasis, cholecystitis. •
psychological complications: neuro-cognitive deficits, feelings of inferiority, family conflict, social isolation,
school problems, truancy, emotional and mental immaturity. • endocrine complications: polycystic ovary disease.
• skin complications: fungal and bacterial skin infections, trophic disorders of the lower limbs, nail dysplasia.
MALNUTRITION and DISABILITY Dr Ingrid Bucens, Vientiane, May 2011.
2. E emerging global priority More difficult to measure 23% screen positive for ‘significant disability’ 39% ‘not
fulfilling developmental potential’ 33% (mod) stunted
3. Layout of talk • MN – definitions, prevalence, consequences • Links between malnutrition and disability •
Interventions for prevention and treatment of malnutrition related disability • Programmatic issues.
4. Malnutrition – Classifications • Macronutrient (‘Protein-energy’) vs micronutrient • Degree - mild/moderate/severe •
How far anthropometric measures deviate from normal • Rapidity of onset and duration • Acute (wasting +/–
oedema) • Chronic (stunting) • Timing of onset / age group affected • In-utero • Childhood • Adult (life-long)
5. Recognising Childhood Malnutrition MACRONUTRIENT (protein - energy) deficiency
6. Recognising Malnutrition in Mothers and Babies • MOTHERS • LOW BMI • < 18.5kg/m2 • MUAC • <20-25cm •
SHORT • Height < 145cm • Chronic undernutrition. • BABIES • LBW (< 2.5kg) • ‘Mixed bag’ - Preterm + SGA •
SGA (IUGR + others)
7. Recognising MICRONUTRIENT deficiencies • IRON • Anaemia • Mucous membranes, nail changes • FOLIC
ACID • Anaemia • IODINE • Endemic regions (mountains, non-iodinised salt) • Goitre • ZINC • Skin rash +
persistent diarrhoea (acrodermatitisenteropathica) • VITAMIN A • Night blindness (not so easy to recognise in
children)
8. Prevalence • 33% stunting • Some regions ~ 50% • 10% wasting • S Asia ~ 16% • Kwashiorkor less common •
Severe wasting 3.5% • 10-19% mothers low BMI • 11% babies IUGR • 45% children <5 yrs have anaemia ~ half
due to iron deficiency HUGE NUMBERS OF MOTHERS, BABIES AND CHILDREN AFFECTED BY
MALNUTRITION IN LOW AND MIDDLE INCOME COUNTRIES.
9. CONSEQUENCES of Malnutrition • Individual (death, disease, disability) • DEATH • INFECTIONS • +/- death /
disability • GROWTH FAILURE • ADULT HEALTH OUTCOMES • ‘Barker’ • DISABILITIES • Families /
Generations • Growth • Reproductive health • Maternal complications and death • Small size at birth , disability
outcomes • Educational / Economic • Societal • Economic • Burden of treatment • Loss of productivity • DALYS
10. SIZE OF THE BURDENGlobal deaths and disease burden measured in DALYS, in children < 5 yrs, attributed to
nutritional status measures in 2004 21.2 21.4 Lancet (2008) Maternal and Child Undernutrition Series, 1st paper.
11. THE LINKS TO DISABILITY • Common risk factors / root causes • Psychosocial • Biological • Disability is a
cause of MN. • MN is a cause of disability. • Overlap of intervention strategies.
12. Link 1:- Common multiple risks • The common milieu of MN and disability • WHO ‘The Critical Link’ • Common
mechanisms (CARING) are important for healthy physical growth and psychological development. • Children in low
resource contexts (POVERTY) are often exposed to multiple, cumulative risks which compromise caring – and
therefore compromise both growth and development.
13. The link between poverty and disability, +/- via Malnutrition. MALNUTRITION • Low (maternal) education •
Overcrowding • Poor sanitation • Poor health practices:- breastfeeding, diet , reproductive health (FP), care-seeking,
toxins (alcohol) • Infections / diseases • Maternal stress • (‘Poor parenting’) • Weak health services • etc POVERTY
Insufficient food DISABILITY • Other • Trauma • Genetic • Metabolic • Asphyxia • etc
14. Many of the ‘causes’ / risks are common
15. LINK 2Disability is a direct cause of MN. • Children with disability often develop MN • Babies suck poorly –
breastfeeding failure • Less actively seek food (motor, sensory, cognitive) • Neglected by ‘carers’ • Rejected by
society • Develop secondary illnesses which in turn cause MN (TB)
16. LINK 3Malnutrition is a cause of disability ?How much disability from MN is directly due to MN and how much is
due to the co-existing risks? • MN directly causes disability • Stunting • Wasting • Micronutrient deficiencies •
Iodine • Vit A • Folic acid • Iron • MN indirectly causes disability • IUGR • Maternal MN DISABILITY POVERTY
Risks – milieu of poverty other
17. Vitamin A deficiency and DISABILITY • May cause irreversible blindness. • Vit A related blindness is a VERY
common cause of blindness in low resource countries.
18. Iron deficiency and DISABILITY • Children who are not otherwise malnourished but who have iron deficiency and
iron deficiency anaemia have impaired cognitive development and behaviour when compared to non-iron deficient
children. • They score lower on cognitive, motor and behavioural tests. • Association is less consistent or less strong
for iron deficiency without anaemia.
19. Folic Acid and Disability • Spina bifida (neural tube defect, myelomeningocoele) +/- hydrocephalus • Vit B12
20. IODINE deficiency and disability • Iodine is needed for thyroid hormone, essential for brain development. •
Irreversible severe intellectual disability (and stunting) in offspring of deficient mothers. • Lesser but significant
cognitive impairment in children in iodine deficient areas. • Iodine deficiency is endemic in mountain populations
without iodinised salt. Congenital hypothyroidism
21. SEVERE ACUTE MALNUTRITION and DISABILITY • Children hospitalised with SAM (+/-oedema) consistently
have developmental and behavioural abnormalities. • Cognitive scores lower • Motor lower • Behaviour markedly
abnormal • No specific deficits.
22. With rehabilitation behaviour virtually returns to normal; other developmental deficits persist. • Children
/adolescents who were earlier hospitalised for acute MN show persistent deficits in cognition, school function
including behaviour – attention - social interaction. • How much of the deficit is due to associated stunting and the
social milieu at home?
23. Stunting and DISABILITY • Strong evidence for association between early childhood stunting and significant
cognitive impairment (moderate to large effect). • Concurrent and longterm association, through to adulthood. •
Young child height correlates to cognition at 40y! • Poorer development, lower IQ, poorer school performance even
after controlling for confounders (social milieu). No specific deficit. • Younger children also have emotional and
behavioural, attentional problems and relationships at school. • Individual and population level.
24. IUGR and disability • Some studies found cognitive deficits in infancy for IUGR babies vs normally nourished
newborns. • Review of IUGR studies, controlling for confounding (preterms, other neonatal problems eg asphyxia,
causes of IUGR, home environment, quality of NBC) concluded that, provided no secondary asphyxia, there is little
effect of IUGR on developmental outcome.
25. Maternal malnutrition and DISABILITY • No direct link between maternal malnutrition and disability however •
Maternal malnutrition is a cause of IUGR which may lead to stunting. • Maternal malnutrition increases the risk of
maternal death (delivery complications) • ‘Motherless children don’t do well’ (malnutrition and disability). Orphan
studies.
26. LINK 4Interventions for MN + disability. MN • Interventions for root causes will reduce MN and disability of all
causes. • Interventions which prevent MN will prevent disability due to MN. • Interventions which treat MN
reducereversible disability due to MN. • Interventions for disability may also improve growth. • Combined
interventions are most effective. DISABILITY POVERTY MILIEU OF POVERTY At risk kids OTHER
27. Nutrition interventions • PREVENTIVE • Supplementation • Micronutrient • Macronutrient (food / milk) • Health
education • Breastfeeding • Complementary • Sanitation / hygiene • Disease prevention • HIV, IPT, zinc, BCG •
STIMULATION • Root cause strategies • Poverty alleviation • Food security • Family planning • ‘CURATIVE’ •
Treatment of acute severe MN (in/outpatient) • Supplementation for catch up growth for IUGR and stunting •
Micronutrients • Vit A, iron, folic acid • Iodine, zinc • Health education • STIMULATION
28. Prevention strategies for Micronutrient deficiency/disability. Micronutrient deficiencies cause severe and often
irreversible disability. Effective prevention strategies exist for at risk populations. • Vit A • Regular supplements to
children. • Iron supplementation (fortification) • Prevents iron deficiency and anaemia. • Improves developmental
outcomes. • Is recommended for young children except in malaria endemic areas. • Deworming
29. Folic acid supplementation pre-conception in all contexts prevents folate deficiency and related disability. • Iodine •
Antenatal supplements (oil or inject) begun before T2 reduces stillbirths, prevents congenital hypothyroidism and
improves childhood cognitive outcomes even for subclinical deficiency. • Childhood supplementation (oil) may
improve cognition but results mixed. Supplementation at school recommended for girls. • Universal salt iodinisation
is a very effective strategy.
30. Treatment for micronutrient deficiencies/disability. • Except for iron for school aged children with IDA, these
strategies are less effective. • Iron • May not fully reverse the developmental disability in infants /preschool children
with IDA. • In school age deficits are reversible. • Iodine – lesser grades of disability may be improved if treatment
started early. • Vitamin A – only early eye changes are reversible. • Folic acid disability is not reversible.
31. Preventing IUGR and childhood MN • IUGR can be reduced with • Antenatal supplementation interventions •
Childhood MN can be prevented • Antenatal interventions • Interventions in infancy / very early childhood • These
interventions, in turn, reduce maternal malnutrition • Via prevention of childhood stunting
32. Preventive interventions. • Foodto pregnant / lactating women / infants • Food is more effective than individual
micronutrients. • Improves birthweight. • Improves infant growth and prevents stunting • Improves developmental
outcomes in infancy and the benefit may be sustained • Stimulationinterventions pregnancy / postnatally • Improve
developmental outcomes • May improve growth
33. Food + stimulation • May improve growth better than food alone • Has a greater effect on cognition than either
intervention alone. These interventions have most effect if interventions begin in pregnancy or at birth and continue
through 2-3 years. More effective in populations at risk of malnutrition including maternal MN and IUGR.
34. Treatment interventions The developmental disability of MN is partly reversible. • FOOD • Reverses weight loss of
wasting • Stunting is more difficult to reverse; may improve if food supplementation before 3 years. • Concurrent
benefits on motor and cognitive development. May be sustained, especially if begun < 2 yrs, but evidence limited. •
Effect on development is not as strong as with preventive interventions.
35. STIMULATION • Benefits development • FOOD + STIMULATION • May improve growth better than food alone.
• Significantly improves cognitive development in wasting and stunting. • Do not reach level of normally nourished •
Effect on development is sustained • Best results on growth and cognition if begin < 2yrs.
36. SUPPLEMENTATION + STIMULATION for stunting Stunted children have long term deficits in cognition. Deficit
improved by stimulation +supplementation, but not to normal. Walker SP, Chang SM, Gratham-McGregor SM.
Effects of early childhood psychosocial stimulation and nutritional supplementation on cognition and education in
growth-stunted Jamaican children: prospective cohort study. Lancet 2005; 366: 1804-07.
37. ‘Developmental intervention’ for children with MN is more effective if begun < 2yrs. L3 ….
38. Developmental interventions • Benefits • Lots of evidence of effectiveness in improving developmental outcomes,
school readiness and educational outcomes. • Effective in developing world settings • May improve nutritional status
• Interventions are most effective if • Target populations / groups most likely to benefit (MN) • Input is intensive -
targets both children and carers • Begun antenatally and continued for at least 3 years • Good quality • Delivered
together with nutritional intervention!
39. The mutual reinforcement of nutritional and developmental interventions. • Developmental interventions hope to •
Improve the way mothers CARE for their children • includes caring for feeding, hygiene, health seeking • become
more responsive to children’s needs • Nutrition interventions make children stronger • child can benefit more from
his environment • can elicit more care
40. Key messages. • MN and disability are both highly prevalent and co-exist in poor populations. • Both may be the
result of the risks that co-exist in poverty and each may cause or aggravate the other. • Early growth impacts
cognitive development • Effects of MN and malnutrition induced disability (educational failure) are perpetuated
through generations, for biological and environmental reasons. • The economic consequences of this are very
significant and government, including non-health sectors, need to be aware of this.
41. Interventions for each affect the other. The most effective interventions for both MN and disability are those which
include both a nutritional and developmental component. • Preventive interventions are more effective than
treatment because some malnutrition induced disability is irreversible. • Interventions are most effective if begun
during pregnancy or the first two years (most intensive periods of both growth and development) and if they target
at-risk populations.
42. Considerations for programming • Examine existing MNCH systems and services from a life cycle approach •
Review what is being done that affects MN and / or disability • Are there any key intervention gaps? • Consider if
your health system can improve efficiency or can feasibly increase interventions • Combine interventions that target
similar ages and are to be delivered by same HW • Select priorities based on local epidemiology (Iodine, bed nets) •
Beware high cost and complex interventions • Phase in changes and target risk groups • Multi-sectoral collaboration
(education, root causes)
43. EG. Preventing malnutrition + disability
44. Most important messages of all. • Preventing malnutrition (in its various forms) is a priority for reducing the burden
of disability in low resource contexts.
45. A WELL BALANCED DIET AND A STIMULATING ENVIRONMENT ARE GOOD FOR CHILDREN!
1. MALNUTRITION
2. WHAT IS MALNUTRITION? Malnutrition is: • poor nutrition due to an insufficient, poorly balanced diet,
faulty digestion or poor utilization of foods. (This can result in the inability to absorb foods.) • Malnutrition is not
only insufficient intake of nutrients. It can occur when an individual is getting excessive nutrients as well.
3. WHAT CAUSES MALNUTRITION? Human beings need a wide variety of nutrients to supply essential energy.
Do you know what nutrients we need? • protein • vitamins • minerals If any one of these nutrients is deficient in a
person's diet, he/she may suffer from malnutrition
4. WHAT CAUSES MALNUTRITION?(continued) Malnutrition also occurs when there is an imbalance of energy
and protein in an individual’s diet. The body may become unable to absorb the nutrients it requires to function
properly. *For example, if a child is suffering from energy and protein malnutrition, they will most likely have
deficiencies in iron, calcium, and other vitamins and minerals.
5. WHO IS AFFECTED BY MALNUTRITION? • Individuals who are dependent on others for their nourishment.
(infants, children, the elderly, prisoners) • Mentally disabled or ill because they are not aware of what to eat. •
People who are suffering from tuberculosis, eating disorders, HIV/AIDS, cancer, or who have undergone surgical
procedures are susceptible to interferences with appetite or food uptake which can lead to malnutrition.
6. BUT DO YOU KNOW THE NUMBER ONE FACTOR THAT CAUSES MALNUTRITION? POVERTY!
8. POVERTY… • Nearly 3 billion people in the world are living on less than $1 a day. They have little access to
their basic needs, including adequate nutrition to help their bodies stay in balance. Poverty may also prevent
individuals from accessing education, which can lead to misinformation about adequate nutrition.
9. Effects of malnutrition Nutritional deficiencies can contribute to various diseases which can be found
everywhere, but most often go without cures/treatment in Less Developed Countries (LDCs).
10. Kwashiokor/Marasmus • Kwashiokor, which means “disease of the displaced child” in the Ga language of Ghana
is a protein deficiency which results is characterized by inability to gain weight, diarrhea, lethargy and a swollen
belly. Kwashiokor can lead to comatose as well as death. • Similarly, Marasmus is a disease resulting from
protein deficiency which affects chidlren early in life (typically in the 1st year) slowing growth, decreasing
weight and hindering proper development. • Nutrition supplements, rehydration and education all can all serve to
cure and prevent these diseases.
12. Beriberi • Beriberi is a thiamine (vitamin B1) deficiency which is common in South East Asia where many diets
consist solely of white rice. • Beriberi affects the proper functioning of the nervous system as well as the
circulatory system and heart. • Pregnancy, breast feeding mothers and those who are ill with fever may have a
heightened dependency on thiamine and may develop a deficiency. • Thiamine is best acquired through foods
such as pork, beef and whole grain (unrefined) breads and grains.
14. Pellagra • Pellagra ”rough skin” is a niacin (or Tryptophan) deficiency which often results in the “3 Ds”; diarrhea,
demetia and dermatitis. • The large scale consumption of corn has resulted in many cases of pellagra because
corn is poorly absorbed in the body. The best sources of Niacin are broccoli, eggs, dates, beef, salmon, seeds and
peanuts.
16. Scurvy • Scurvy is a disease which is born of Vitamin C deficiency. It is characterized by bleeding around hair
follicles, anemia and gingivitis. • Scurvy may occur in those who consume large amounts of junk foods, smokers
(as smoking depletes Vitamin C) and those who don’t have proper access to sources of vitamin C. Namely, the
poor.
18. Rickets • Vitamin D deficiencies may result in “Rickets” which is a lack of proper calcium characterized by
poorly developed and deformed bones. • Vitamin D can be best found in beef products (especially cows milk) but
is very low in breast milk. Thus, women in developing countries are contributing to this disease if their babies
sole source of nourishment is breast milk.
1. Geriatric Malnutrition Richard Allan Bettis, Fourth-Year Pharm.D. Candidate Preceptor: Dr. Ali Rahimi
University of Georgia College of Pharmacy
2. Background • A frequent and common condition in the elderly associated with: • Increased morbidity • Increased
mortality • Increased hospitalizations • Reduced quality of life
3. Frequency • Occurs in 5-10% of older patients residing in nursing homes or long-term care facilities • Occurs in
up to 50% of older patients when discharged from the hospital • Most reversible or treatable causes of
undernutrition are frequently overlooked by physicians
4. Background • Undernutrition or malnutrition can be a result of two likely scenarios: • Protein energy wasting
characterized primarily by weight loss • Individual nutrient deficiencies characterized by a lack of single nutrients
and seen more commonly in older persons
5. The Body & Energy • Total energy expenditure based upon an individual’s basal metabolic rate (or BMR) •
Energy required for physical activity and creating fuel reserves after feeding • Dependent upon age, weight,
gender, and activity level
6. Energy & Aging • BMR decreases with age regardless of constant body weight • Result of muscle tissue
replacement by less metabolically active adipose tissue
7. Energy & Nutrients • Protein, carbohydrates, and fat account for a percentage of total calories to meet nutritional
needs
8. Energy & Nutrients • Energy yield varies between different types of foods
9. Energy & Proteins • More energy from protein is highly encouraged and supported
10. The Body & Energy • Metabolic fuels in excess of energy expenditure results in obesity • A lack of metabolic
fuel to supply energy expenditure results in emaciation, wasting, marasmus, kwashiorkor • Bothsituations are
associated with increased mortality
11. Nutrient Deficiency • A lack of single nutrients resulting in less common disease states • Very rarely seen in
developed countries except occasionally in older persons
12. Weight Loss & Mortality • When older patients lose weight they have a doubling in their risks for death • Even if
the patient is overweight! • Weight loss increases likelihood of: • Hip fractures • Institutionalization • Downward
spiral of negative events • Weight loss is the best sign of treatable undernutrition
13. Caregiver Perceptions • Weight loss is the best sign of treatable undernutrition or malnutrition
14. Nutritional Status • There is no gold standard for diagnosis of malnutrition • There are several quick assessment
tools
15. Nutritional Assessment Tools • Mini-Nutritional Assessment (MNA) • Most established screening tool for older
adults • Difficult to distinguish between patients at risk for malnutrition and frailty • Notapplicable if patients are
non-communicable
16. Nutritional Assessment Tools • Simplified Nutritional Assessment Questionnaire (SNAQ) • High sensitivity and
specificty to detect weight loss over next 6 months • Malnutrition Universal Screening Tool (MUST) • Uses BMI,
weight loss, and an acute disease effect score • Predictor of mortality and length of stay in hospital
17. Simplified Nutritional Assessment Questionnaire (SNAQ)
18. Nutritional Assessment Tools • Nutritional Risk Screening (NRS) • Proposed universal screening tool for
malnutrition in hospitalized patients • Assesses BMI, weight loss, appetite, and severity of disease • Applicable to
more types of patients
19. Nutritional Markers • Serum protein assays • Albumin, prealbumins, retinol binding proteins • Not specific to
detect malnutrition or changes in nutritional status • Reductions in these proteins are better indicators of illness
20. Nitrogen Balance • Normally at equilibrium • Intake = output • No change in total body content of protein •
Positive nitrogen balance • Growing children, pregnancy, recovery from protein loss • Excretion of nitrogenous
compounds is less than intake • Net retention of nitrogen is in the body as protein
21. Nitrogen Balance • Nitrogen balance studies show consuming more than 14% of energy source from protein is
more than enough to increase muscle protein synthesis
22. Amino Acids • Essential • Cannot be synthesized in the body • If any of these are lacking, then nitrogen balance
will not be possible • Histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and
valine • Non-essential • Can be synthesized from the body or from essential amino acids • Not necessary for
nitrogen balance
23. Weight Loss Complications • Severe weight loss leads to protein malnutrition and a downward spiral of adverse
effects • Loss of weight also leads to loss of: • Fat • Muscle • Bone • Albumin
24. Weight Loss Cause • A lack of metabolic fuel to supply energy expenditure results in weight loss, emaciation,
and wasting
25. Weight Loss Causes • Six major causes of weight loss in older patients: • Anorexia • Cachexia • Sarcopenia •
Malabsorption • Hypermetabolism • Dehydration The “Triple Threat”
26. “Anorexia of Aging” • Anorexia is an independent predictor of mortality • Reduction in food intake as
individual’s age • Males – 30% • Females – 20% • Causes of anorexia in older patients are multifactorial •
Physiological • Psychological • Drug or disease induced
27. “Anorexia of Aging” • Causes of anorexia in older patients are multifactorial • Physiological • Psychological •
Depressed or cognitively impaired patients • Disease or drug induced • Decreased appetite due to acute disease or
medication effects
28. “Anorexia of Aging” • Physiological changes • Decreasein taste and olfaction resulting in decreased enjoyment
of food • Decreasein gastric emptying resulting in early satiation signals • Changesin gut hormones involved in
(satiety or feelings of fullness)
29. Gut Hormones
30. “Anorexia of Aging” • Gut hormone changes and contribution to anorexia • Increasein cholecystokinin (CKK)
release and sensitivity resulting in greater satiating effects • Increasein leptin levels resulting in increased satiety
after meals • Reducedsensitivity to ghrelin associated with reductions in hunger sensation
31. “Anorexia of Aging” Anorexia is multifactoral
32. Causes of Weight Loss • Six major causes of weight loss in elderly: • Anorexia • Cachexia • Sarcopenia •
33. Cachexia • Severe wasting disorder characterized by loss of both fat and muscle • Caused by effects from the
overproduction of pro-inflammatory cytokinesresulting from a variety of illnesses • Marked by changes in other
markers: • Increases C-reactive protein • Decreases serum albumin • Causes anemia
34. Cytokine Overproduction • Usually overlapped with anorexia and sarcopenia in older individuals • Increases
resting metabolic rate resulting in higher metabolic demands • Decreases both gastric emptying and intestinal
motility
35. Causes of Weight Loss • Six major causes of weight loss in older patients: • Anorexia • Cachexia • Sarcopenia •
36. Sarcopenia • In Greek, translates literally to “poverty of flesh” • Characterized by muscle atrophy and a loss of
muscle functionality • Associated with aging and prevented by exercise
37. The “Triple Threat”
Malabsorption • Hypermetabolism • Dehydration
39. Malabsorption • Most commonly caused by celiac disease and pancreatic insufficiency in older patients • Serum
levels of vitamin A and beta-carotene used to diagnose fat malabsorption • Screenings for various
immunoglobins and antibodies used to diagnose celiac disease
41. Hypermetabolism • When energy demand exceeds nutrient intake • Most commonly caused by hyperthyroidism
and pheochromocytoma in older patients
42. Hypermetabolism • Apathetic hyperthyroidism • Weight loss • Atrial fibrillation • Proximal muscle weakness •
Blepharoptosis (not exophthalmos) • Pheochromocytoma • Adrenal gland tumor • Consider if hypertensive and
losing weight
44. Dehydration • Reduced total body water • Normal daily fluid requirement is 30ml/kg body mass
45. “Anorexia of Aging” • Causes of anorexia in older patients are multifactorial • Physiological • Psychological •
Drug or disease induced
46. “Anorexia of Aging” • Psychological manifestations • Reactive depression • Change in living conditions • Food
refusal behaviors • All are not uncommon and can lead to weight loss and malnutrition
47. Depression • Most common cause of treatable anorexia in community and institutional settings • Late-life
depression is significantly underdiagnosed in older persons • Corticotropin-releasing hormone (an anorexogenic)
is elevated in patients with depression
48. Relocation • Change in living conditions evokes psychological anorexic responses • Late-onset paranoia • Fear of
poisoning • Indirect self-destructive behavior (ISDB) • An unconscious method of suicide • May be due to trauma
of relocation
49. Food Refusal Behaviors • Most prevalent in cognitively impaired • Common in demented elderly patients due to
agnosia or dyspraxia • Difficulty interpreting sensory data and not recognizing an object as food • Difficulty with
motor movements and unable to open mouth despite intentions to • Common refusal behaviors in intermediate-
stage Alzheimer’s patients would be: • Distraction from eating • Verbal refusal to eat
50. Food Refusal Behaviors • Deliberate refusal • Indirect self-destructive behavior (ISDB) • Reflexive withdrawal
behavior • Dislike of a certain food • Protest against certain caregiver • It is crucial to distinguish between refusal
to eat and lack of ability to eat • Patients with dysphagia may refuse food
51. Indirect self-destructive behavior (ISDB) ‘‘The grandfather, 81, one day removed his false teeth and announced
that he was no longer going to eat or drink. Three weeks later, to the day, he died.”
52. Management Nutrition Refusals
53. Energy Wasting & Weight Loss • The basics: • Provide adequate food supplementation • Early on: • Food variety
• High calorie food • Calorie supplements • Focus on: • Diagnosing causes • Treating treatable causes
54. “Anorexia of Aging” • Common causes of pathological and treatable anorexia in the elderly: • Depression •
Medications • Therapeutic diets • Cancer • Uncontrolled pain
55. Treatable Causes
56. Management • Calorie supplementation decreases mortality and hospital lengths of stay • Cachexia shown to be
responsive to protein calorie supplementation • Increase in 6-minute walks • Decreased hospitalizations
57. When? • Oral calorie supplements between meals • Avoid supplementing calories during meals • Reduction in
food intake • No net increase in total caloric ingestion
58. How? • Environmental considerations • Improve food taste • Avoid therapeutic diets with limited justification •
Allow extra time to eat during mealtimes • Spend time feeding impaired patients • Other aesthetic considerations
• Behavioral modifications • Improve quality of relationships between patient and feeder • Use touch or verbal
cueing
59. What Else? • Orexigenic medications available to stimulate appetite • Megestrol acetate • Dronabinol •
Testosterone
60. Megestrol Acetate • Orexigenic agent with mechanisms to increase food intake and cause weight gain •
Progestational agent • Corticosteroid activity • Mild testosterone-like activity • More effective in women than
men • Reduces cytokine activity
61. Megestrol Acetate • Side effects • Deep vein thrombosis • Severe constipation in older patients • Fluid retention •
Not recommended for sedentary patients • Not recommended for use >3 months at one time • Synergistic effects
when combined with olanzapine
62. Dronabinol • Orexigenic agent and extract of tetrahydrocannabinol (THC) with mechanisms to produce small
increases in appetite and weight gain • Used in palliative care settings: • Reduces nausea • Increases enjoyment of
both food and life
63. Other Agents • Testosterone • Produces weight gain • Decreases hospitalizations in frail older patients • Used in
combination with caloric supplementation • Agents with roles in cachexia treatment • Low dose steriods (5mg
prednisone daily) • Selective androgen receptor modulators (ostarine) • ActivinIIR decoy antibodies • Myostatin
antibodies
64. Medications • Medications can cause weight loss by: • Affecting food intake • Diminishing appetite • Causing
nausea, vomiting, or GI irritation • Altering taste and smell • Induce depression • Should consider using a
minimum effective dose or discontinuing medications opposing weight gain or caloric supplementation
65. Medications • Some medications may cause anorexia • Theophylline • Digoxin • Neuroleptics • SSRIs
66. Nutritional Rehabilitation • Specialized nutrition regarded as a last resort • Parenteral feeding • Enteral feeding •
Overused in the U.S. especially in patients with dementia • No evidence of a reduction in mortality or
improvements of quality of life
67. Specialized Nutrition • Only small fraction of malnourished patients will benefit from specialized nutritional
support (or SNS) • In elderly or chronically ill patients the decision to specialty feed is based upon whether or not
quality of life will be extended • Multiple considerations before decision to implement SNS
68. Algorithm Will quality of life be extended?
69. Specialized Nutrition • Enteralor “tube feeding” • Tube placed into the gut to deliver liquid formulations which
contain all essential nutrients • Parenteral or “intravenous feeding” • Infusion of nutrient solutions directly into
the bloodstream via peripherally located or centrally located vein • Both associated with risk and discomfort •
Both difficult to stop once started
70. Specialized Nutrition Risk • Safest route is to avoid SNS • Closely monitor and ensure adequate oral food intake •
Adding oral liquid supplement • Using an appetite stimulant in eligible patients
71. Enteral Feeding • Preferred route – “If the gut works, then use it” • Maintains gut functionality • Less risk for
infection • Intestinal tolerance limited by gastric retention or diarrhea • Often required in patients with: •
Anorexia • Impaired swallowing or dysphagia • Bowel disease
72. Parenteral Feeding • Less preferred route • Greater risk for infection • Higher chance of inducing hyperglycemia •
Often required in patients with: • Prolonged ileus or obstruction • Severe hemorrhagic pancreatitis
73. Electrolytes & Specific Nutrients
74. Trace Metals
75. Ethics & Controversy • Food refusals • Distinguishing between competent and demented patients • Identifying
reversible symptoms such as unmanaged pain or depression • Caregiver decision to force feed patients
76. Ethics & Legality • Enteral and parenteral feeds • Ordinary care or other medical treatment? • A patient has the
right to refuse? • Supportive care while starving?
77. Management • Undernutrition or malnutrition can be a result of two likely scenarios: • Individual nutrient
deficiencies characterized by a lack of single nutrients and seen more commonly in older persons • Protein energy
wasting characterized primarily by weight loss
78. Nutrient Deficiencies • The basics: • Replace the target nutrient • Prevention is key • Important deficiencies in
older patients: • Vitamin D • Iron • Folate • B-12 • Zinc
79. Vitamin D Deficiency • Associated with fractures, muscle loss, falls, and increased mortality • 25-hydroxy
vitamin D levels are gradually reduced as part of the aging process • Levels are <30ng/mL in many older patients
• Replacement of 800-1000 IU daily is appropriate for most older patients
80. Iron Deficiency • Most commonly associated with iron deficient anemia • Characterized by low iron and ferritin
levels • Once daily oral replacement for 6 weeks is appropriate for most older patients • Reticulocyte count after
1 week of therapy • Parenteral products may be necessary if no increase in reticulocytes (likely due to
malabsorption)
81. Folate & B12 Deficiencies • Most commonly associated with • Both deficiencies characterized by elevated
homocysteine levels • Methymalonic acid specific for B12 deficiency • Oral or injectable replacement is
appropriate for most older patients • Vitamin B12 1000 IU orally every day or 1000IU weekly injections x
4weeks
82. Zinc Deficiency • Most commonly associated with: • Diabetics • Cancer patients • Individuals receiving diuretics
• Role of replacement is uncertain
83. Recommended Intakes
84. Vitamin D Supplementation
1. Micronutrient malnutrition Why talking about micronutrient malnutrition?

3. Micronutrients • Affect a variety of health and disease outcomes: • Child growth and development • Maternal
health • Malnutrition and vulnerability to infectious diseases • Estimates of micronutrient malnutrition vary from
20% of the world population (or more than one billion persons) • Dietary deficiencies represents an enormous
problem of “hidden hunger”
4. Agenda • Series of lectures • Week #1: Vitamin A and D • Week #2: Iron, Iodine and Zinc deficiencies • Week
#3: Obesity and the other spectrum of malnutrition
6. Vitamin A
7. Overview • Third most common deficiency in the world • Affects an estimated • 125-130 million preschool age
children • And 7 million pregnant women in low-income countries • Prevalent cases of pre school xerophthalmia
are believed to number about 5 million • 10% can be considered potentially blinding
8. Leading cause of preventable pediatric blindness in developing world Underlying cause of at least 650,000 early
childhood deaths due to diarrhea, measles, malaria and other infectious disease Maternal deficiency may increase
risk of maternal morbidity and mortality
9. NEITHER HUMANS or ANIMALS can synthesize or survive without Vitamin A
10. Epidemiology Public Health problem in approx 78 countries • Most widespread across South and Southeast Asia
and Sahelian and Sub-Saharan Africa (where food supplies lack preformed vitamin A) • Clusters within counties
due to common exposures to poor diet and inadequate care, malnutrition
11. Epidemiology • Age • Corneal xerophthalmia- 2-3y/o • Acute onset of corneal disease may follow recent
weaning from breast milk, or s/p illnesses • Gender • Male > Girls • Socioeconomics • Inversely correlates with
Vit A deficiency
13. Sources of Vitamin A • Retinol (preformed Vit A): animal products, liver • Beta-carotenes: Provitamin A
(converted to Vit A in intestines) • Plant source of retinol from which mammals make 2/3 of their Vit A •
Carotenoids: yellow, red fruits/vegetables
14. Vitamin A • Essential in regulating numerous key biologic processes in the body • Morphogenesis • Growth •
Nutrition • Vision • Reproduction • Immunity • Cellular differentiation and proliferation
15. Vitamin A deficiency disordersVADDs
16. Main cause of deficiency: Insufficient intake Increase requirements during growth, pregnancy and lactation,
infection Change from breast feeding to inadequate complimentary feeding Socio-cultural and economics factors
(intra household distribution and gender preferences)
17. Clinical features
18. Xerophthalmia • Three clinical stages: • Retinal dysfunction causing night blindness • Conjunctiva and corneal
xerosis • Corneal ulceration and necrosis
19. Night blindness Earliest manifestation Most prevalent stage of xerophthalmia Failure in rod photoreceptors cells
in the retina Responsive to Vitamin A supplementation
20. Ask about night blindness A positive history of night blindness is associated with low-to-deficient serum retinol
concentrations in preschool aged children and pregnant women Can serve as an indicator of individual and
community risk of Vitamin A deficiency
21. Conjuctival xerosis withBitot’s spots Xerosis of the conjunctiva Appears as dry, non-wettable, rough or granular
surface (best seen on oblique illumination with hand light) Histological: transformation of normal columnar
epithelium with abundant goblet cells to stratified, squamous epithelium that lacks goblet cells.
23. Bitot’s spots: gray-yellow patches of keratinized cells and saprophytic bacilli that aggregate on temporal limbus
(lesions are bubbly, foamy or cheesy like)
24. Corneal xerosis Corneal xerosis (“drying”) presents as superficial punctuate erosions that lend a hazy, non-
wettable, irregular appearance to the cornea Usually both eyes Severe xerosis, cornea becomes edematous with
dry granular appearance (“peel of an orange”) Vitamin A successfully treats corneal xerosis
26. Corneal Ulceration Appearance: Round or oval, shallow or deep, sharply demarcated and often peripheral to the
visual axis Only one eye Vit A will heal lesion leaving a stromal scar or leukoma
28. Corneal Necrosis Keratomalacia (“corneal melting or softening”) Initially opaque localized lesions that can cover
and blind the cornea Treatment with Vit A leaves a densely scarred cornea
29. Conjunctival xerosis and localized corneal necrosis in a severely malnourished 2-year-old Indonesian boy. Same
eye 2 months after Vitamin A therapy
31. Poor Growth Experimental Vitamin A depletion in animals causes a deceleration in weight gain to a “plateau” as
hepatic retinol reserves becomes exhausted Corneal xerophthalmia is associated with severe linear growth
stunting and acute wasting malnutrition Recovery from xerophthalmia has been associated with gain in weight
32. Infection Predisposes individuals to severe infection Higher mortality rates in children and pregnant women Vit
A maintains epithelial barrier function and regulates cellular and antibody-mediated immunity
33. Treatment • Children with any stages of xerophthalmia • High potency Vit A at presentation, the next day and 1-4
weeks later (WHO recommendations) • Children at high risk Vit A deficiency: measles, diarrhea, respiratory
diseases, severe malnutrition • High dose supplementation: single dose if no supplement in 1-4 mo
34. Replacement • q4-6 months • Infants 50K IU PO • Infants 6-12mo: 100K IU PO • Mothers: 200K IU PO w/in 8
wks delivery (WHO recommendation) • Pregnant or women of reproductive age: small doses 10K IU/d or 25K
IU wkly
35. Prevention Dietary diversification Fortification Supplementation
36. Dietary diversification Increase intake from available and accessible foods Nutrition education Social marketing
Community garden programs Measures to improve food security
37. Fortification • Taking advantages of existing consumption patterns of fortifiable foods to carry Vitamin A into
the diets • Examples: • Vitamin A fortification of sugar in Guatemala • Vitamin A fortified monosodium
glutamate in Southeast Asia
38. Supplementation • Encompassing community based efforts to provide Vit A supplements to high-risk groups •
Preschool-aged children • Mothers within 6-8weeks after childbirth • UNICEF procures and distributes over 400
million Vit A supplements to nearly 80 countries • Integrating vitamin A delivery with immunization services
during each of three routine contacts in the first 6 months of life
41. Nutritional Rickets and Vitamin D deficiency
43. Overview Resurgence in the prevalence of Rickets In developing countries, not only associated with effects on
bone growth and mineral homeostasis but also with infant and child mortality when accompanying lower-
respiratory tract infections
44. Definition Disease of the growing bones from a failure or delay in the calcification of newly formed cartilage at
the growth plates of long bones and failure of mineralization of newly formed osteoid (osteomalacia) Bones no
longer able to maintain normal shapes
45. Causes of Rickets • Calciopenic rickets • Phosphopenic rickets • Primary defect of mineralization * Nutritional
Rickets is a form of calciopenic rickets and is classically associated with Vitamin D deficiency
46. Effects of Vitamin D deficiency • Active Rickets • Impaired Calcium homeostasis • Consequent to impaired
dietary calcium absorption or inadequate intake • Vit D (or more specifically 1,25-(OH)2D) controls the
absorption of Calcium • ↓serum Ca → induce ↑ PTH secretion → osteoclasts ↑ resorb bone → demineralization
of bone & cartilage at sites of rapid growth & remodeling
47. Effects of Vitamin D deficiency • Predisposition to lower respiratory tract infections by • Effects on immune
system • Muscle weakness and hypotonia • Effects of rickets and osteomalacia on rigidity and support provided
by the ribs during respiration
48. Effects of Vitamin D deficiency • During pregnancy and early infancy • Poor maternal weight gain • Higher
incidence of maternal hypocalcaemia, poor neonatal bone mineralization and fractures, and reduced longitudinal
growth • Increase risk of DM type 1, multiple sclerosis and bipolar disorder
49. Sources of Vitamin D • Diet • Fortified food products • Fish oils, egg yolks, mushrooms • Animal products (fatty
parts, liver) • Vit D in diet: cholecalciferol or ergocalficerol
50. Via skin synthesis under the influence of UV-B radiation
51. Factors influencing Vitamin D deficiency • Decrease amount of UV-B reaching the earth • Season of the year •
time of the day • pollution, clouds • distance form equator
52. Factors influencing Vitamin D deficiency • Human factors • Amount of skin exposure (cloth coverage, social and
religious customs) • Duration of exposure • Sunscreens • Degree of melanin concentration
53. Factors influencing Vit D deficiency • In young children • Before children start to walk- decrease sun exposure •
Breast-fed – very little Vit D in breast milk • Low dietary Calcium intake (ex. Consumption of polish rice) •
Genetic causes • Malabsorption (repeated GI infections) • Chronic renal, liver disease
54. Clinical Features • Results of the widening and splaying of the growth plates and resultant deformities of the
metaphyses of the long bones • Widening of wrist, knees and ankles • Palpable and enlarged costochondral
junctions (rickety rosary) • Deformities of the long bones
55. Age dependant • Early • Craniotabes, head asymmetry, frontal bossing, delayed closing anterior fontanelle •
Delayed tooth eruption, abnormal formation enamel, cavities • Rachitic rosary
56. Late • Pigeon chest irregularity, Harrison groove • Classic limb abnormalities • Genu varum, genu valgum •
Fraying, widening, cupping metaphysis long bones, fxs • Lordosis, kyphosis, scoliosis • Narrow pelvis:
obstructed labor
59. Other clinical manifestations Hypotonia and myopathies resulting in delayed motor milestones (muscle
weakness) Hypocalcemia manifestations like apneic attacks and convulsions in infants
60. Diagnosis • Clinically: presence of bony deformities • Radiological examination of growth plates • Biochemically
• hypocalcemia • hypophosphatemia • elevated alkaline phosphatase • elevated PTH • Confirmation of low
25(OH)D concentrations
61. Treatment • Vitamin D supplements (Oral Vitamin D2 or D3) • 5,000 to 15,000 IU/day for 4-8 weeks • Single
large dose when compliance problematic?? • Adequate UV radiation • Vitamin D + Calcium supplementation
(50mg/kg for several months) • Calcium supplementation alone
62. Prevention In US and Canada- fortification of all dairy milk formulas with Vit D (400 IU/quart) American
Academy of Pediatrics recommends supplementation with 200 IU/day to all breast-fed and children not drinking
at least 500ml of cow’s milk
63. Prevention Large doses of Vitamin D supplementation every 3 months??? Add ground fish bones to pourish????
Education about sunlight and animal food ingestion
1. Thiamine An Essential Micronutrient

2. Thiamine, also known as thiamin or vitamin B1, is a vitamin found in food, and manufactured as a dietary
supplement and medication. Thiamine is an essential micronutrient that plays a key role in energy metabolism. It
is not endogenously synthesized in the body and the richest food sources of thiamine are whole grains, yeasts,
meats, legumes, and nuts.
3. In developing countries, thiamine deficiency remains a widespread concern. Thiamine deficiency may develop by
ingesting diets which areeither contaminated with thiamine-metabolizing enzymes (e.g., thiaminase) or that
underwent thiamine inactivation by heat or sulfur dioxide. Heavy consumption of tannin-containing or food rich
in caffeine, theobromine, and theophylline (such as those present in coffee, chocolate, and tea, respectively) can
inactivate thiamine, thereby compromising the thiamine status.
4. Thiamine is present in the body as free thiamine, as well as in several phosphorylated forms: thiamine
monophosphate (TMP), thiamine diphosphate (TDP), and thiamine triphosphate (TTP) . Although thiamine
deficiency is fairly uncommon in developed countries, various factors or conditions, such as alcoholism or
advanced age, can increase the risk. Thiamine deficiency can present itself in various ways, and symptoms are
often nonspecific, which makes it difficult to identify. Fortunately, a thiamine deficiency is usually easy to
reverse with supplementation.
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impurities and stable isotopes atvery competitive prices. Thiamine Hydrochloride
6. Details of reference standards Thiamine Hydrochloride and its impurities are tabulated below:
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Hydrochloride each come with a comprehensive Certificate of Analysis detailing the characterisation process for
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your peace of mind.
2. - an essential trace element
3. Basics
4. What is selenium? • discoverer: Berzelius (1817) • occurrence in the earth‘s crust: 0.05 ppm • nonmetal (chalcogen)
• close chemical relationship with sulphur • fields of application: semi-conductor technology/photo technique,
medicine • essential trace element for humans and animals, possibly for plants as well
5. Close chemical relationship
6. Important inorganic selenium compounds Na2SeO3• 5 H2O Sodium selenite = an inorganic salt of selenium so-
called sodium salt of selenous acid (as pentahydrate)
7. Selenium intake Selenium Selenium Selenium Selenium
8. Selenium intake in Europe SCF (2000): Opinion of the scientific committee on food on the tolerable intake level of
selenium. SCF/CS/NUT/UPPLEV/25 final
9. Selenium intake in Europe Rayman MP (2000): The importance of selenium to human health. Lancet Vol 356, 233-
241
10. Occurrence of selenium inorganic 1. in traces in sulfides: iron pyrites FeS2 chalcopyrites CuFeS2 zinc blende ZnS 2.
in rare minerals 3. technical: lead chamber slurry (1817 Berzelius) 4. drinking water (selenite, selenate; e.g. < 2 µg/l)
organic 1. protein-bound: vegetable: predominantly as SeMet animal: predominantly as SeCys
11. Daily kidney? Vegetableca. (µg): brussels sprouts 1 boletus 184 Bread, bakery products rye bread 3 pasta
(containing eggs) 20 Grain rye 1 wheat bran 2 oat flakes 10 Meat, fish ca. (µg): liver (beef) 21 filet (beef) 35 trout 25
herring 43 kidney (beef) 112 Milk, eggs, milk products cow‘s milk 1 Camembert, 45% F.i.d.m. 3 Fruit banana 1
grape 2 (circa data on selenium in µg/100g) Elmadfa, Muskat, Fritzsche, (2004/05): Die große GU-
Nährwertkalorientabelle, Neuausgabe
12. Selenium supply in Germany Medium daily selenium intake: 30 µg/day 41 µg/day  suboptimal supply: Ø 0.67
µg/kg body weight VERA-study: Selenium serum concentrations 83 µg/l 82 µg/l max. activity GPX: 95 µg/l lowest
cancer incidence: > 121 µg/l  optimum intake: 1.5 µg/kg body weight Source: DAZ Nr. 11, 2005
13. Recommendations of the DGE (German Society for Nutrition) Age Selenium µg/day infants 0 to 4 months 5 - 15 4
to 12 months 7 - 30 children 1 to 4 years 10 - 40 4 to 7 years 15 - 45 7 to 10 years 20 - 50 10 to 15 years 25 - 60
Source: Deutsche Gesellschaft für Ernährung e. V.: "Selen - Schätzwerte für eine angemessene Zufuhr“ , 2000.
14. Recommendations of the DGE (German Society for Nutrition) Age Selenium µg/day adolescents 15 to 65 years 30 -
70 + adults pregnancy 30 - 70lactation 30 - 70 Source: Deutsche Gesellschaft für Ernährung e. V.: "Selen -
Schätzwerte für eine angemessene Zufuhr“ , 2000.
15. Toxicology 1200 µg selenium / day LOAEL “Lowest observed adverse effect level” 850 µg selenium / day NOAEL
“No observable adverse effect level” 300 µg selenium / day UL “Tolerable upper intake level” Source: SCF, (2000):
Opinion of the scientific committee on food on the tolerable intake level of selenium. SCF/CS/NUT/UPPLEV/25
Final
16. Safe total daily intake Safe total daily intake according to age groups “Tolerable upper intake level” Age group UL
(Tolerable upper intake level) 1 - 3 years60µg selenium / day 4 - 6 years90µg selenium / day 7 - 12 years130µg
selenium / day 13 - 14 years200µg selenium / day 15 - 17 years250µg selenium / day adults 300µg selenium / day
Source: SCF, (2000): Opinion of the scientific committee on food on the tolerable intake level of selenium.
SCF/CS/NUT/UPPLEV/25 Final
17. Selenium metabolism Modified according to: Windisch, Gabler, Kirchgeßner, (1997): Umwelttoxikologie (VO
910.305) Systemkomponente “Tier”: Selen WS (2004/05)
18. How does selenium reach the protein? Modified according to: Windisch, Gabler, Kirchgeßner, (1997):
Umwelttoxikologie (VO 910.305) Systemkomponente “Tier”: Selen WS (2004/05)
19. Distribution of selenium in the body Selenium content of human organs and body fluids: Source: Biesalski HK,
Köhrle J, Schümann K, (2002): Vitamine, Spurenelemente und Mineralstoffe. Prävention und Therapie mit
Mikronährstoffen. Georg Thieme Verlag, Stuttgart
20. Selenium deficiency situations Possible reasons of an absolute or relative selenium deficiency • reduced selenium
supply • disturbed selenium intake • increased selenium losses • increased selenium demand • increased endogenous
strain with radicals and peroxides • increased exogenous strain with noxa
21. Reduced selenium supply • nutritional conditions and habits - extremely unbalanced nutrition - vegetarians - vegans
• parenteral nutrition • diets
22. Disturbed selenium intake • gastro-intestinal diseases • maldigestion, malabsorption, celiac disease
23. Increased selenium demand • pregnancy • lactation • high physical strain or stress • elder persons • immune
deficiency
24. Increased selenium demand • chronical destructive diseases, above all tumour diseases • rheumatism-related diseases
(arthritis, arthroses) • cardiovascular diseases (coronary heart disease, cardiomyopathy, atherosclerosis) •
inflammatory diseases of the gastro-intestinal tract (pancreatitis, Crohn‘s disease, ulcerative colitis)
25. Increased exogenous strain with noxa • workplace • heavy metals (e.g. amalgam) • chemotherapy • radiotherapy •
alcohol, nicotine
26. Diagnosis of the selenium status • The determination from the whole bloodhas been proven for the measurement of
the selenium level. • Hair isn‘t that suitable as examination material as it‘s not actively involved inthe metabolism. •
Special laboratories measure theselenium content as a matter of routine and relatively low-priced.
27. Selenium status Recommendations for laboratory analysis (Germany) Serum: Short-term parameter deficient < 65
μg/l = < 0.81 μmol/l normal 50 - 120 μg/l = 0.81 - 1.25 μmol/l optimal 101 - 135 μg/l = 1.26 - 1.71 μmol/l Whole
blood: Long-term parameter deficient < 85 μg/l = < 1.06 μmol/l normal 60 - 120 μg/l = 1.06 - 1.50 μmol/l optimal
121 - 162 μg/l = 1.51 - 2.05 μmol/l Source: Gröber U, (2003): Selen. OM. Z. f. Orthomolekulare Medizin 4, 25-26
28. State of selenoprotein research 1973 - 2002 Selenoproteins with known enzymatic function: glutathione peroxidase
thioredoxin reductase deiodase 2003 Selenogenome: human: 25 genes rodent: 24 genes drosophila: 4 genes C.
elegans: 1 gene 2005 Selenoproteome: 30 - 70 forms Modified according to: Schomburg L, Schweizer U, Köhrle J,
(2005): Selen und Selenoproteine. Humboldt Spektrum 3, 12-18
29. Selenium-containing proteins in humans Enzymes glutathione peroxidase thioredoxin reductase deiodase
selenophosphate synthetase 2 Selenium-binding selenoprotein Pprotein Proteins with still selenoprotein W
unexplained function several other selenoproteins Selenoproteins: Proteins, specifically containing selenocysteine
30. Selenium-containing proteins in humans muscle proteins globin other tissue proteins Proteins, containing non-
specifically integrated selenium
31. Glutathione peroxidase • 1973 identified as selenoprotein • contains 4 Se-atoms, bound as selenocysteine in the
active centre • can be found everywhere in the organism • catalytic activity: reduction of peroxides
32. Origin and effect of radicals UV-radiation elimination of foreign substances inflammations (phago-cytosis, PG-
synthesis) metabolic processes O2-transport (Hb) reper-fusion X-rays damage of cell membraneDNA damage
protein cross-linkingcell destruction
33. Glutathione peroxidase Peroxide detoxification by glutathione peroxidase GSH = reduced glutathione GSSG =
oxidised glutathione E = enzyme
34. Glutathione peroxidases Function protect the organism from the toxicity of endogenous and exogenous peroxides
35. Glutathione peroxidases Selenium deficiencydecrease in enzyme activity oxidative destruction of biomolecules,
cells and tissues involved in numerous human diseases and disorders where radicals have either a primary or
secondary role, such as e.g. • atherosclerosis • cardiomyopathy • amyotrophic lateral sclerosis • rheumatism •
infertility • cancer
36. Deiodases Function activation (T4 to T3) and deactivation (T4 to rT3) of thethyroid hormones provide appropriate
levels of thyroid hormonesessential for growth, differentiation and metabolism
37. Deiodases Selenium deficiencydecrease in enzyme activity suboptimal (type-I and type-II-5’-deiodases) or
supraoptimal levels of active T3 (type-III-5-deiodase) plays a role in various diseases, such as e.g. • Hashimoto‘s
thyroiditis • H2O2-dependent destruction of thyroid due tocontinuous stimulation by TSH • disorders in fetal brain
development
38. Thioredoxin reductases play a decisive role in regulation of transcription (transcription factors NF-κB and AP-1) are
involved in DNA biosynthesis regulate the cellular redox status, have a bearing onthe redox status of GSH
(glutathione) modulate folding (and consequently the function) of proteins have a large substrate range (Trx, H2O2,
dehydro-ascorbate, proteins) Function
39. Thioredoxin reductases dysregulation of proliferation and differentiation of cells: is supposed to be part of the
malignant transformation of cells is considered to be a lethal factorin theearly embryonic stage Selenium
deficiencydecrease in enzyme activity total knockout of the enzyme
40. and cancer Tumour prevention
41. Selenium is effective on two levels 1. indirectly via incorporation into specific selenoproteins e.g. GPx 2. directly
through built-up selenium metabolites e.g. methylselenol
42. Chemopreventive effect of selenium Fig. modified according to: Combs GF Jr, (1999): Chemopreventive
mechanisms of selenium. Medizinische Klinik (Munich) 94 (Suppl. III), 18-24
43. Selenium has a tumour-preventive property Tumour-preventive effect verified in large studies • Qidong-study:
Primary hepatic cancer(China 1985-1989, primary hepatic cancer, placebo-controlled, 20,847 probands) • Linxian-
study: Esophageal cancer(China 1986-1991, esophageal cancer, 29,584 probands) • Clark-study
44. Selenium has a tumour-preventive property Clark-study Effects of selenium supplementation for cancer prevention
in patients with carcinoma of the skin. A randomized controlled trial. Nutritional Prevention of Cancer Study Group.
Clark LC, Combs GF Jr, et. al., (1996): JAMA 276 (24), 1957-1963 Design: multicentre, randomised, double-blind,
placebo-controlled Probands: 1,312 Test centres: USA, low selenium regions 1983 - 1996 Period of surveillance: 4.5
years Medication: 200 µg selenium/day
45. Selenium has a tumour-preventive property Results of the Clark-study Reduced incidence for secondary carcinoma
in skin cancer patients by selenium supplementation
46. and cancer Kinds of cancer
47. Cancer figures in Germany Estimated number of cancer incidences in Germany 2002 Man Woman 18,850 11,200
5,500 7,800 6,050 900 oral cavity and throat Hodgkin‘s disease urinary bladder pancreas leukemia stomach 7,100
2,600 6,600 4,750 8,250 850 55,150 mammary gland 11,350 uterine corpus 6,500 cervix 9,950 ovary 32,550 lung
12,450 48,650 prostate 4,350 testes 35,600 large bowel and rectum 35,800 5,850 Non-Hodgkin‘s lymphoma 6,250
218,250* total *Figures without non-melanotic skin cancer 206,000* Source: Gesellschaft der epidemiologischen
Krebsregister e.V. in Zusammenarbeit mit dem Robert-Koch-Institut. 5. überarbeitete, aktualisierte Ausgabe
Saarbrücken, 2006
48. Prostate carcinoma • important role as chemopreventive agent • correlation between selenium deficiency and
increased incidence to contract prostate cancer • inhibition of the growth in vitro by blocking the cell cycle, the DNA
synthesis and induction of apoptosis Reduction of prostate carcinoma incidence by preventive selenium
administration!
49. Mammary carcinoma • tumour-protective characteristics in vivo • low selenium concentrations in the blood incase of
mammary carcinoma patients • secondary lymphedema: - adjuvant therapy with selenium - better transportation of
the lymphs - binding of radicals in the congested tissue - positive influence of immunocompetent cells - avoidance of
appearance of erysipelas
50. Ovarian carcinoma • second most frequent malignant disease of the female sexual organs • increase with rising age •
9,950 incidences per year • 1.7% risk to contract ovarian carcinomain one‘s life
51. Bronchogenic carcinoma • selenium supplementation protects from lung carcinoma risk • low plasma selenium
levels increase lung carcinoma risk
52. Colorectal carcinoma • selenium deficiency correlates with the risk to contract bowel cancer • higher plasma
selenium levels are associated significantly with a lower risk of bowel cancer • induction of selenoprotein P andthus,
cell protection • reduction of the risk of recurrence ofa colorectal adenoma
53. Dosage recommendations
54. and cancer Chemotherapy
55. Selenium and chemotherapy PRO selenium +reduction of side effects +resensitization of cells resistant to cytostatics
+chemoprotective effect +cytostatic efficacy is not influenced +improvement of the quality of life
56. Lowered selenium levels in tumour patients healthy patient tumour patient = selenium concentration in blood •
mostly before the tumour is diagnosed • oxidative stress is reinforced by the chemotherapy  increased radical strain
57. Chemotherapy side effects • Cytostatic action approaches and effects: • inhibition of replication and transcription •
induction of the apoptosis • antimetabolite effect • inhibition of the development of the mitotic spindle • inhibition of
the cell division • formation of radicals chemotherapy as exogenous source of free radicals
58. Possible side effects of a chemotherapy • nausea, vomiting, loss of appetite • diarrhea, constipation • loss of hair •
tiredness, exhaustion • increase in infections • chronic organ damages
59. Reduction of side effects oxidative stress healthy body cell sodium selenite • side effects • quality of life
60. No reduction of the cytostatic efficacy Example etoposide and bronchogenic carcinoma cells Source: Schroeder CP,
Goeldner EM, Schulze-Forster K, Eickhoff CA, Holtermann P, Heidecke H, (2004): Effect of Selenite combined
with chemotherapeutic agents on the proliferation of human carcinoma cell lines. Biological Trace Element Research
99 (1-3), 17-25
61. Increase in anti-tumour efficacy of cytostatics Example 5-Fluorouracil (5-FU)-sensitive colon carcinoma cells
Source: Schroeder CP, Goeldner EM, Schulze-Forster K, Eickhoff CA, Holtermann P, Heidecke H, (2004): Effect of
Selenite combined with chemotherapeutic agents on the proliferation of human carcinoma cell lines. Biological
Trace Element Research 99 (1-3), 17-25
62. Selective effect of selenium + Na-Selenite Processes in the tumour cell • high GSH-concentration intracellularly • a
lot of GSH leads to sensitivity for selenium • administration of selenium results in formation of GS-Se-GS •
consequence 1. tumour cell becomes impoverished in GSH 2. multidrug resistance is prevented 3. cells, resistant to
cytostatics, are resensitized 4. high concentrations of GS-Se-GS induce apoptosis
63. Selective effect of selenium + Na-Selenite Processes in the normal cell • normal GSH-concentration intracellularly •
normal selenium sensitivity • no increased formation of GS-Se-GS • consequence 1. no impoverishment in GSH 2.
selenium is available for selenium-dependent enzyme systems 3. the antioxidative defence works 4. increased
resistance to cytostatics 5. no induction of apoptosis
64. Advantages of a selective sodium selenite therapy + reduction of the side effects + better compliance, fewer
abruptions of the therapy + improvement of the quality of life + inhibition of inflammatory processes + lower
susceptibility to infections + good tolerability
65. Dosage recommendations days(s) before the first chemotherapy: duration 1 - 2 days 900 µg selenium/day directly
successive treatment day(s): duration 1 up to max. 5 days 900 µg selenium/day from 6th day of treatment 300 µg
selenium/day treatment-free days: duration variable 300 µg selenium/day Chemotherapy
66. and cancer Radiotherapy
67. Selenium and radiotherapy PRO selenium +stabilisation of the immune system +reduction of side effects
+radioprotective effect +improvement of the quality of life
68. Radiotherapy and possible consequences
69. Possible side effects of a radiotherapy • damages to mucous membranes, inflammations • damaging the blood count •
dysfunctions of the organs in the radiation area, such as diarrhea (intestines), micturition difficulties (bladder),
breathlessness (lung), difficulties in swallowing (throat) • permanent damages to organs in the radiation area • skin
damages • exhaustion, tiredness
70. Redox status Tumour patient lowered selenium concentration in blood and serum reduced glutathione peroxidase
activity • limited redox capacity • balance between oxidation and antioxidation is disturbed reduction of the ability to
detoxify free radicals
71. Advantages of a selective sodium selenite therapy + in general fewer side effects + fewer severe infections + better
quality of life + improvement of the radiation-induced lymphedema + accelerated hematopoetic regeneration + good
tolerability
72. Dosage recommendations day(s) before the first radiotherapy: duration 1 - 2 days 900 µg selenium/day directly
successive treatment day(s): duration variable 300 µg selenium/day treatment-free days: duration variable 300 µg
selenium/day Radiotherapy
73. and thyroid
74. Position of the thyroid epiglottis hyoid bone larynx thyroid cartilage thyroid trachea Source: Forum Schilddrüse
e.V.60596 Frankfurt/Main
75. The thyroid, our organ with the highest content of selenium • essential for the function of the thyroid • has a key role
in the metabolisation of iodine • protects the thyroid from destruction by peroxides/radicals • has an antioxidative
und anti-inflammatory effect • is supplied only inadequately with nutrition
76. Autoimmune diseases of the thyroid Graves‘ disease A form of hyperthyroidism appearing spontaneously.The body
forms antibodies, specifically directed to the thyroid, which stimulate the thyroid for an increased production of
thyroid hormones. Frequently, the disease is combined with protruding eyes or other symptoms of the thyroid-
associated ophthalmopathy. Thyroid-associated ophthalmopathy (TAO) Most frequent accompanying symptom to
Graves‘ disease. From the clinical point of view, the appearance of hyperthyroidism and TAO often is closely
coupled. The orbital inflammatory process results in a swelling of the orbital connective and muscle tissue leading to
mechanical complications in the orbits localized by bones (proptosis). Hashimoto‘s thyroiditis
77. What is Hashimoto’s thyroiditis? Dr. Hakaru Hashimoto (1881-1934) Hashimoto‘s thyroiditis = Chronic
autoimmune thyroiditis (AIT) Disease starts from the immune system - immigration of lymphocytes into the thyroid
Immune system attacks the thyroid- shrinkage (= destruction and loss of glandular cells) - replacement of glandular
cells by connective tissue AIT mostly chronic
78. Hashimoto‘s thyroiditis The chameleon among the thyroid diseases The Hashimoto‘s thyroiditis cannot be regarded
as pure thyroid disease but as dysfunction of the immune balance with consequences for many organ systems and
bodily functions. For this reason, it is associated with numerous possibly hardly tangible symptoms. Typical
complaints of a hypothyroidism, hyperthyroidism and of the autoimmune disease can appear.
79. Hashimoto‘s thyroiditis The chameleon among the thyroid diseases • symptom-free to poor in symptoms • at the
beginning, even hyperfunction is possible • is gradually replaced by a hypofunction • fluctuating hormone values,
fluctuating TPO-Abvalues possible • complex disaease
80. Frequency • up to 10% of the population • women circa 10x more often • in every age • more frequently in selenium
deficiency regions • more often in case of high iodine supply
81. Consequence: Hypothyroidism hormone level decreasing hormone production Hypothyroidismformation of
insufficient thyroid hormones slowdown of the metabolism  increase in weight  weak performance
82. Symptoms in case of thyroid hormone deficiency • Women • menstrual cycle disturbances • infertility • Men • loss of
libido • impotency • Toddlers • growth retardation • backward intellectual development Physical symptoms
83. Symptoms in case of thyroid hormone deficiency Psychic symptoms  general slowdown  tiredness  difficulty in
concentrating  weak memory  listlessness  depressed mood
84. Clinical studies Selenium and Hashimoto‘s thyroiditis Design: placebo-controlled, randomised Duration: 3 months
Patient collective: 70 female patients, TPO-Ab(antibodies against thyroidal peroxidase) > 350 IU/ml Medication: all
hormone substitution (LT4) 36 patients 200 µg Se/day 34 patients placebo Main objective criteria: change of the
concentration of TPO-antibodies (TPO-Ab = antibodies against thyroidal peroxidase) Secondary end point:
subjective quality of life Source: Gärtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW, (2002): Selenium
supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J
Clin Endocrinol Metab 87 (4), 1687-1691
85. Clinical studies course of the TPO-Ab under selenium substitution change of the general well-being Results: Source:
Gärtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW, (2002): Selenium supplementation in patients with
autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J Clin Endocrinol Metab 87 (4),
1687-1691
86. Clinical studies Follow-up study Design: cross-over follow-up Duration: 6 months Patient collective: 47 female
patients (average age 41) Medication: 13 patients (previously already verum): 200 µg selenium/day 14 patients
(previously placebo): 200 µg selenium/day 11 patients (previously already placebo): placebo 9 patients (previously
selenium): placebo Source: Gärtner R, Gasnier BC, (2003): Selenium in the treatment of autoimmune thyroiditis.
Biofactors 19 (3-4), 165-170
87. Clinical studies course of TPO-Ab under selenium substitution left column = start follow-up right column = end
follow-up after 6 months Results follow-up study: Source: Gärtner R, Gasnier BC, (2003): Selenium in the treatment
of autoimmune thyroiditis. Biofactors 19 (3-4), 165-170
88. Conclusion of both studies • selenium supplementation over a total of 9 months results in a significant decrease in
TPO-Ab • discontinuation of selenium after 3 months results in a significant reincrease in TPO-Ab • remarkable
improvement of the quality of life due to selenium supplementation • very good tolerability, especially with long-
term intake of selenium over months
89. Treatment – Hashimoto’s thyroiditis Triiodothyronine (T3) substitution - according to the demand - of the lacking
hormone quantity selenium therapy with sodium selenite
90. Dosage recommendations children 50 µg selenium/day adolescents 150 µg selenium/day adults 200 - 300 µg
selenium/day Hashimoto‘s thyroiditis
91. and rheumatism
92. Rheumatism One name for many manifestations • inflammatory joint and spine diseases(e.g. chronic polyarthritis,
Bechterew‘s disease, psoriasis arthritis) • degenerative joint and spine diseases (e.g. arthrosis of the knee, hip,
shoulder and finger joints or the spine) • non-articular rheumatism (e.g. fibromyalgia) • metabolic disorders with
rheumatic complaints
93. Rheumatoid arthritis presented antigen T-cell scavenger cell substances supporting inflammation Development of a
joint inflammation
94. Rheumatoid arthritis Development of a joint inflammation 1. • immune system discovers foreign substance
(antigen/virus) • scavenger cells take up the antigen and present parts on the surface • T-cells recognise foreign
substance, search further foreign substances in blood and tissue • T-cells react to endogenous tissue properties in
thesynovial membrane 2.
95. Rheumatoid arthritis Development of a joint inflammation 3. • wrongly programmed T-cells release messengers
(among others IL-2, IFN) • thus, activation of further T-cells and scavenger cells (and other immune cells / tissue
and cartilage cells) 4. • this way, scavenger cells receive the inflammation
96. Arachidonic acid metabolism food (animal fats) arachidonic acid messengers supporting inflammation development
(= support + strengthening) of rheumatism
97. Inflammation metabolism has an anti-inflammatory potential • modulation of the prostaglandin and leukotriene
synthesis • restriction of the production of inflammatory cytokines • inhibition of the pro-inflammatory transcription
factor NF-k(kappa)B • detoxification of peroxides
98. Risk factor: Selenium deficiency Selenium status in patients suffering from rheumatic diseases Selenium status
(μmol/l; mean value ± SD) of patients with rheumatism and healthy people (* JRA = juvenile rheumatoid arthritis)
Modified according to: Sill-Steffens R, (2003): Bedeutung und Einsatzmöglichkeiten von Selen bei Rheuma. OM. Z.
f. Orthomolekulare Medizin 4, 4-6
99. Risk factor: Selenium deficiency Result • people suffering from rheumatism show lowered selenium levels • in case
of chronically increased inflammatory activity, there are high strains with free radicals, which are involved
decisively in the destruction of the joints • low selenium levels correlate with a higher disease activity • reduced
glutathione peroxidase activities lead to increased oxidative stress and thus, to a strengthening of inflammatory
processes
100. Advantages of a selective sodium selenite therapy + balances selenium deficits + ideal glutathione peroxidase
activities + decrease in the inflammation or disease activity + pain reduction, less morning stiffness, decline of joint
swellings + saving of NSAIDs, reduction of the corticoid demand
101. Dosage recommendations rheumatoid arthritis over 3 months 200 µg selenium/day acute attacks initially 900
µg selenium/daythen 300 µg selenium/day maintenance therapy 200 µg selenium/day Rheumatic diseases
102. and immune system
103. Selenium and immune system The well-coordinated immune system responds particularly sensitively to a
selenium deficiency!  antiviral defence  antimicrobial defence  better defence performance  lower susceptibility
to infections
104. Influence of the immune system – tumour diseases Prospective study Natural cytotoxic activity of peripheral-
blood lymphocytes and cancer incidence: an 11-year follow-up study of a general population. Imai K, Matsuyama S,
Miyake S, Suga K, Nakachi K, (2000): Lancet 356, 1795-1799 Duration of study: 11 years Patient collective: 3,625
patients 211 patients with cancer disease Measurement: cytotoxicity of the peripheral lymphocytes • connection
between activity of the immune system and development of cancer • risk of a cancer disease is lower in case of
higher cytotoxicity of the lymphocytes
105. NK cells Definition Natural killer cells are populations of lymphocytes, which can be activated to cause a
significant cytotoxic activity and high concentrations of cytokines and chemokines. Their function is among others
to destroy malignant cells.
106. NK cells Important immune parameter in oncology • A low NK cell activity is a risk factor for the
development of tumours. • The survival rate correlates with the intensity of the NK cell activity.Tumor patients with
a high NK cell activity show a significantly longer survival time without developing metastases than patients with a
low NK cell activity. • As part of the unspecific immune defence, the NK cells bind to the target cells and initiate
their lysis.If the target cell possesses apoptosis receptors, the conse-quence will be the release of the programmed
cell death (apoptosis).
107. Selenium increases the NK cell activity Practice study Improvement of the immunocompetence of tumour
patients Erpenbach K, (2003): Practice study, unpublished Patient collective: 70 chronically sick patients
Medication: Cefasel® 300 µg daily Measurement: NK cell activity • initial situation: clearly lowered values or basal
NK activities in tumour patients • NK cell activity was increased significantly by 300 µg selenium significant
improvement of the immunocompetence
108. Selenium increases the NK cell activity rise in the selenium level (standard value: 74-139 µg/l) correlates with
an increase in the NK cell activity (desired value > 25%) Source: Erpenbach K, (2003): Improvement of the
immunocompetence of tumour patients. Practice study, unpublished
109. Selenium and its effect on the immune system • increases the activity and quantity of NK cells • modulates the
proliferation of lymphocytes • raises the efficiency of the phagocytosis • stimulates the synthesis of g-interferon •
increases the antibody synthesis
110. Dosage recommendations adults 100 - 200 µg selenium/day Immune system
111. Pharmacology Pharmacological properties • antioxidative • immune-modulating • chemopreventive •
influence on the metabolism of the tumour cell • support of DNA repair mechanisms • support of the apoptosis •
anti-inflammatory • cardioprotective • detoxifying in case of heavy metal strain
Presentation on theme: "Chapter 40 Medical Nutrition Therapy for Cancer Prevention, Treatment, and Recovery."—
Presentation transcript:
1 Chapter 40Medical Nutrition Therapy for Cancer Prevention, Treatment, and Recovery
2 CancerWhen cells divide and reproduce abnormally and have the potential to spread throughout the body, crowding
out normal cells and tissuesOne third of the cancer deaths in the United States each year can be attributed to nutrition
and other lifestyle factors.
3 Cancer—CauseAlgorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.
4 Cancer—Pathophysiology
Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.
5 Cancer—Medical and Nutritional Management

6 Prevention Factors Energy balance and exercise Fat Protein Fiber

Fruits and vegetablesChemoprevention
7 Prevention Factors—cont’d
AlcoholCoffee and teaArtificial sweetenersNitrates, nitrites, and nitrosaminesMethod of food preparation
8 Fruits and VegetablesAppear to have a protective effect against cancerThought to be due to the phytoestrogen and
phytochemical content of the plant- based diet
9 FatResearch, although controversial, has shown evidence that high-fat diets are linked to an increased risk of cancer
of the breast, colon, lung, and prostate
10 American Cancer Society’s Dietary Recommendations for Cancer Prevention

1. Eat a variety of healthful foods, with an emphasis on plant sources.2. Adopt a physically active lifestyle.3. Achieve
and maintain a healthy body weight throughout life.4. Limit consumption of alcoholic beverages.
11 Metabolic agents and cytokine blockers Prokinetic drugs

Pharmacological Agents for Anorexia-Cachexia Syndrome and Weight Loss ManagementAppetite stimulantsMetabolic
agents and cytokine blockersProkinetic drugsAnabolic agents
12 Factors That Affect Appetite

Reference: American Institute for Cancer Research: Food, nutrition, and the prevention of cancer: a global perspective,
Washington, DC, 1997, AICR.
13 Nutritional Implications of Cancer Therapy
Chemotherapy—Taste abnormalities, diarrhea, constipationRadiation therapy—Fatigue, loss of appetite, skin
changesSurgery—Fatigue, pain, loss of appetiteImmunotherapy—Flulike symptoms, decreased food intake
14 Nutritional Implications of Cancer Therapy—cont’d

Bone marrow transplant—Nausea, vomiting, diarrhea, mucositis, xerostomia, dysgeusiaSevere oral muscositisGraft
versus host disease (GVHD)Veno-occlusive disease (VOD)
15 Marrow Transplantation—Cause
16 Marrow Transplantation—Pathophysiology
17 Marrow Transplantation— Medical and Nutritional Management

18 Severe Oral Mucositis Following Marrow Transplantation
19 Guidelines for Oral Feeding During Antitumor Therapy
20 Guidelines for Oral Feeding During Antitumor Therapy —cont’d
21 Commonly Used Complementary and Alternative Therapies

Macrobiotic dietVegetarian dietGerson therapyKelley/Gonzales regimenJuice therapiesShark
cartilageDHEAEnzymesOxymedicineCoenzyme Q10
22 Commonly Used Complementary and Alternative Therapies—cont’d

Black cohoshEchinaceaFlaxseedGingerIscadorMilk thistlePC-SPECSSaw palmettoSoy and soy foodsTeas
23 Nutrition in the Etiology of Cancer

Epidemiologic research has evaluated the role of diet in the etiology of cancer in different population groups.Diets
contain inhibitors and enhancers of carcinogenesis.Laboratory studies have served as models to test the effect of food
and nutrition on cancer development.

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1.

1 Philippine Plan of Action for Nutrition (PPAN) 2017-2022

2 Addresses nutrition situation

3 Plan formulation process

4 Nutritional problems to address

5 Maternal and child undernutrition and death

7 Outcome targets Reduce levels of child stunting and wasting Indicator

8 Outcome targetsTo reduce micronutrient deficiencies to levels below public health

9 Outcome targetsTo reduce micronutrient deficiencies to levels below public health

11 Sub-outcome or intermediate outcome targets

12 Sub-outcome or intermediate outcome targets

13 Strategic Thrusts, 2017-2022 Focus on the first 1000 days of life

14 Priority provincesREGIONPROVINCECARAbra2. ApayaoI3. PangasinanII4. IsabelaIII5. AuroraBataan7.

15 Nutrition-specific programs Nutrition-sensitive programs

16 Nutrition supportive programs, examples

17 Nutrition-specific programs – Address immediate causes of malnutrition

18 Nutrition-specific programs – Address immediate causes of malnutrition,

19 Nutrition-specific programs – Address immediate causes of malnutrition

21 Nutrition-specific programs – Address immediate causes of malnutrition

22 Nutrition-specific programs – Address immediate causes of malnutrition

23 Nutrition-sensitive programs – Address underlying causes of malnutrition

24 Nutrition-sensitive program – Address underlying causes of malnutrition

25 Enabling programs Mobilization of LGUs for nutritional outcomes

26 Enabling programs Policy development for food and nutrition

31 Nutrition-specific programs Nutrition-sensitive programs

32 NATIONAL NUTRITION COUNCIL

33 Nutrition problems to address

38 Undernutrition among children under five years old

39 Trends in the prevalence of stunting from birth up to 3 years of age

40 Overweight by age/population group

43 Percent low birthweight

44 Service targets Program Service target

45 Service targets Program Service target

46 Service targets Program Service target

47 Service targets Program Service target

48 Service targets Program Service target Nutrition in Emergencies

MALNUTRITION and DISABILITY Dr Ingrid Bucens, Vientiane, May 2011.

1. Micronutrient malnutrition Why talking about micronutrient malnutrition?

1. Thiamine An Essential Micronutrient

5 Cancer—Medical and Nutritional Management

6 Prevention Factors Energy balance and exercise Fat Protein Fiber

10 American Cancer Society’s Dietary Recommendations for Cancer Prevention

11 Metabolic agents and cytokine blockers Prokinetic drugs

12 Factors That Affect Appetite

14 Nutritional Implications of Cancer Therapy—cont’d

17 Marrow Transplantation— Medical and Nutritional Management

18 Severe Oral Mucositis Following Marrow Transplantation

19 Guidelines for Oral Feeding During Antitumor Therapy

20 Guidelines for Oral Feeding During Antitumor Therapy —cont’d

21 Commonly Used Complementary and Alternative Therapies

22 Commonly Used Complementary and Alternative Therapies—cont’d

23 Nutrition in the Etiology of Cancer

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