nutrition public health.pdf

7/25/2019 nutrition public health.pdf

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Food and nutrition

Prakash S. Shetty

Introduction to food and nutritionFood and the nutrients in it, habitually consumed by individuals,are important determinants o the health o populations worldwide.Nutrition and health interactions are complex and their determi-nants include: the social, economic, and cultural issues related tomaking the right ood choices; purchasing and eating the correcttypes o ood in appropriate quantities; as well as the dai ly humanactivity and behaviour related to ood. Just as the acquisition o

the knowledge o microbiology inuenced our understanding oinectious diseases which in turn led to preventive measures orthe population, so the historical advances in nutrition have led to amore coherent understanding o the patterns o and the preventiono diet-related diseases o public health importance.

Environmental determinants o variations in disease ratesinclude ood and nutrition as one o the primary determinants. Inthe developing world, numerous nutrient deciency diseases per-sist and now coexist with the increasing incidence o diet-relatedchronic diseases. Developing societies now bear the double bur-den o malnutrition with the emergence o the so-cal led diseaseso affluence amidst persisting undernutrition in their populations.Changes in the rates and patterns o nutritional disease and theircontribution to premature death within a population depend largelyon the environmental actors, which include changes in social andeconomic conditions, the implementation o immunization pro-grammes, improvements in womens social and educational statuswithin the society, and changes in agriculture and ood systemsand in the availability o ood. Tese changes have been inuencedin recent times by globalization and the increasing global trade andthe remarkable advances and changes in agricultural practices andthe ood systems that affect individual diets and liestyles. Nationalpolicies that seek to promote economic activity and internationaltrade to boost oreign exchange earnings ignore the impact o thesemeasures on the health o the populations. Economic developmentis normally accompanied by improvements in the quantity andquality o a nations ood supply and improvements in the immedi-

ate environment and living standards o the community. Benecialenvironmental inuences operate through changes in the provi-sion o and access to hygienic and nutritious ood; the availabilityo potable water, clean housing, and sanitary surroundings; andlack o exposure to environmental toxins. Tese changes contrib-ute to a ood and nutrition-mediated improvement in the bodysresistance to inections and better health. Te mutual interdepend-ence o the immune and nutritional status o the population prob-ably explains at least some o the gains in public health in Britainin the last century (McKeown 1976).

Te quantitative and qualitative changes in our ood patternsthat lead to such dramatic changes in lie expectancy also result inthe problems o diet-related chronic diseases. Diet-related chronicdiseases occur typically in middle and later adult lie and can, byincreasing the incidence o premature mortality, undermine thegains in lie expectancy. More importantly they lead to morbidityand the resultant disabil ity-adjusted lie years (DALYs) lost as wellas contributing to economic losses and reducing the quality olie. Tese diet-related chronic diseases are traditionally regardedas maniestations o overconsumption and sel-indulgence in anaffluent society. In practice, some o these chronic diseases may becompounded by relatively decient intakes o some nutrients, thusemphasizing the need or a diversied and balanced daily diet orgood health.

Nutrition has re-emerged as being undamental to publichealth. Nutritional issues were seen in industrialized, developedsocieties as relating to deciency diseases, which were conqueredin the early part o the twentieth century while continuing to per-sist in the relatively poor, developing countries. Now, ood andnutrition are recognized as one o the principal environmentaldeterminants o a wide range o diseases o public health impor-tance globally. Tese diseases reect the cumulative impact o a

variety o pathophysiological processes over a lietime and theinteractions are ofen seen as reecting individual genetic sus-ceptibility, but the different disease patterns o groups living ondifferent diets being maniestly a societal reection o the impacto dietary actors. Te display o nutrientgene interactions is evi-dent, or example, in obesity, alcoholism, cardiovascular disease,type 2 diabetes mellitus, many gastrointestinal disorders, neuraltube deects, and the most prevalent cancers. Molecular epide-miology unravels the basis or genetic susceptibility to some othese disorders while the gene inducers or repressors ofen proveto be o dietary or environmental origin. Societal eatures, whichdetermine human behaviour and economic well-being as well asclimate, tradition, and culture, all affect ood consumption pat-terns and dietary practices. Tese are eatures which need to be

considered in public health rather than simply the epidemiologi-cal or aetiological aspects o diet-related diseases.

Tis chapter seeks to take a global view o ood and nutritionas determinants o public health. Tis is particularly import-ant because deciency diseases are widespread in several partso the world and yet coexist in the same country with chronicdiet-related diseases in adults. Vitamin deciencies, both clinicaland subclinical, continue to maniest in poor communities as wellas in apparently healthy populations. Treat o hunger and star-

vation and severe dietar y inadequacy resulting in malnutrition


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ofen emerges during conict and other emergencies. Tis chapteris structured in such a way that it deals with both sides o the malnutrition in humans as relevant to public health.

Food and nutrition securityTe pre-eminent determinant o hunger (household ood inse-curity) is poverty in societies. Te recognition that poverty andhunger go hand in hand is maniest in the United Nations (UN)Millennium Development Goals (MDGs), which speciy targets orthe reduction o both global poverty and hunger by the year 2015(MDG 1). Improving household ood security is one o the objec-tives o all democratic societies and constitutes an important ele-ment o the human right to adequate ood. Food securityis denedas the access by all people at all times to the ood they need oran active and healthy lie. Te inclusion o the term householdensures that the dietary needs o all the members o the house-hold are met throughout the year. According to the UN Food andAgricultural Organization (FAO) ood insecurity is thus, a situa-tion that exists when people lack secure access to sufficient amountso sae and nutritious ood or normal growth and development

and an active and healthy lie (FAO 2000). Food insecurity may becaused by the unavailability o ood, insufficient purchasing power,inappropriate distribution, or inadequate use o ood at the house-hold level. Hence current denitions o ood security emphasizethe availability, accessibility, stability, and utilization o ood.

Te achievement o household ood security requires an ade-quate supply o ood to all members o the household, ensuringstability o supply all year round, and the access, both physicaland economic, which underlines the importance o the entitle-ment to produce and procure ood. Food insecurity may be aresult o the unavailability o ood, inadequate purchasing power,or inappropriate utilization o ood at the household or individuallevel. Tus, ood security at the household level is a complex phe-nomenon attributable to a range o actors that vary in importance

across regions, countries, and social groups, as well as over time(Shetty 2006). It is described in terms o the availability and sta-bility o good quality, sae, and nutritious ood supplies, and theaccess to, and utilization o, this ood. All these criteria must bemet or the consumption o a healthy diet and the achievement onutritional well-being.

Availability relates to the adequacy o a varied and nutritiousood supply and is inuenced principally by actors that pro-mote agricultural production and trade. Factors that inuencethis include policies and incentives, access to natural resources,and the availability o agricultural inputs, skills, and technolo-gies including biotechnology. Stability o the level and types ooods available or consumption is subject to seasonality and by

the sustainability o production and arming systems in practice.Tese in turn depend on the efficiency o market systems, includ-ing pricing mechanisms and inrastructure such as transport andwarehousing, which inuences the storage, distribution, and owo ood. While reduction o ood losses through improvements inood storage and processing also affects stability, the nature o thearming system adopted and its effect on the environment and onsustainabil ity is also a key determinant o the stability o ood sup-plies in the medium to long term.

Access that a community, household, or individual has to ood isa reection o the ability to either grow and retain the ood grown

or consumption, to purchase the ood rom the market, or toacquire it by a combination o strategies that are described as rep-resenting entitlements to ood (Sen 1981). Tis system dependson a range o actors such as: access to resources such as land,water, agricultural inputs, and improved technologies; the natureo the ood marketing system and the inrastructure to supportit; purchasing power and ood prices; and consumer perceptions,

behaviour, and preerences. Utilization is more concerned withthe biological availability o the ood afer it has been ingested.While age, body size, and physical activity levels are importantdeterminants, the absence o disease and parasitic inestationsalso inuence the utilization o nutrients by the body. As a con-sequence, the biological utilization o ood is largely inuencedby environmental actors such as clean water and good sanitation.

Te necessity to include nutrition into ood security evolvedover time as nutrition security in principle is more than oodsecurity (Shetty 2009). Te nutrition ocus adds physiologicalrequirements or different nutrients and the determinants o theirbioavailability and bioutilization as well as aspects o caring prac-tices and health services and healthy environments that inuenceit. Nutrition securitycan be dened as adequate nutritional status

in terms o protein, energy, vitamins, and minerals or all house-hold members at all times (Quisumbing et al. 1995, p. 12). Whilethis denition illustrates the consideration o the need or ood toensure optimal supply o nutrients in the diet, i.e. physiologicalneeds, other denitions o nutrition security ocus on the vulner-able individual and their needs related to non-ood actors. Whilepointing out the need or a paradigm shif in policy ormulationrom attention to ood security at the aggregate level to nutri-tion security at the level o each individual, Swaminathan (2008)denes nutrition security as , physical, economic and social accessto balanced diet, sae drinking water, environmental hygiene,primary health care and primary education. Tis denition onutrition security involves both ood and non-ood actors andconsequently ood and nutrition security integrates both concep-tual rameworks. Te recognition that ood, which includes water,is a substance that people eat and drink to achieve an adequatenutritional status, i.e. maintain lie and physical, cognitive, andsocial development, and that it has to meet physiological require-ments in terms o quantity, quality, and saety and be sociallyand culturally acceptable, inuenced and amended the denitionurther. Accordingly, ood and nutrition securityis achieved, iadequate ood (quantity, quality, saety, socio-cultural acceptabil-ity) is available and accessible or and satisactorily utilized by allindividuals at al l times to achieve good nutrition or a healthy andhappy lie (Weingartner 2005, p. 5).

Undernutrition in children and adultsTe causes o undernutrition are multidimensional and its deter-minants include both ood- and non-ood-related actors suchas socioeconomic, cultural, and environmental deprivations.Although establishing a relationship between these variables, andthe indicators o undernutrition do not necessari ly imply causality,they demonstrate that in addition to ood availability many social,cultural, health, and environmental actors inuence its preva-lence. People aced with inadequacy o ood are generally poor,but not all the poor are undernourished. Even in households thatare ood secure, some members may be undernourished. Income


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uctuations, seasonal disparities in ood availability, demandor high levels o physical activity, and proximity and access tomarketing acilities may singly or in combination inuence thenutritional status o an individual or a household. ransition romsubsistence arming to commercial agriculture and cash cropsmay help improve nutrition in the long run; however, over theshort term they may have negative impacts unless accompanied

by improvements in access to health services, environmental sani-tation, and other social investments. Rapid urbanization and rura lto urban migration may lead to nutritional deprivation and altercultural attitudes in ood preerences and practices, and womenstime constraints including that available or child-rearing prac-tices, and thus inuence the health o the vulnerable in societies.Inadequate housing and over-crowding, poor sanitation, and lacko access to a protected water supply, through links with inectiousdiseases, are potent environmental actors that inuence biologi-cal ood utilization and nutrition. Inadequate access to ood, lim-ited access to healthcare, and clean environments and insufficientaccess to educational opportunities are in turn determined by theeconomic and institutional structures as well as the political andideological superstructures within society. Tus the presence o

undernutrition is not only causally related to ood insecurity atthe household or individual level, but is also determined by otherhealth-related actors such as access to sae water, good sanita-tion, healthcare, and appropriate care practices and ensuring airintra-household ood distribution.

Poor nutritional status o populations affects physical growth,cognitive development, intelligence, behaviour, and learningabilities o children and adolescents. It impacts on their physi-cal and work perormance and has been linked to impaired eco-nomic work productivity during adulthood. Inadequate nutritionpredisposes them to inections and contributes to the negativedownward spiral o malnutrition and inection. Good nutritionalstatus, on the other hand, promotes optimal growth and develop-ment o children and adolescents. It contributes to better physio-logical work perormance, enhances adult economic productivity,increases levels o socially desirable activities, and promotes bettermaternal birth outcomes. Good nutrition o a population mani-ested in the nutritional status o the individual in the communitycontributes to an upward positive spiral and reects the improve-ment in the resources and human capital o society.

Low birth weight

Intrauterine growth retardation (IUGR) resulting in low birthweights constitutes a major public health problem in develop-ing countries. A World Health Organization (WHO) echnicalReport (WHO 1995) recommended that the 10th percentile o asex-specic, birth weight-or-gestational-age distribution be des-

ignated or the classication o small-or-gestational-age (SGA)inants. While it is difficult to establish with certainty whether thereduced birth weight is the result o in uterogrowth restriction;in developing-country populations the high incidence o SGAinants is largely the result o IUGR.

Te denition o IUGR is an inant born at term (>37 weeks ogestation) with a low birth weight (


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Children throughout the world when well ed and ree o inec-tion tend to grow at similar rates irrespective o their ethnic orracial origin, and healthy children everywhere can, when edappropriately, be expected to grow on average along the 50thcentile o a reerence populations weight and height or age. Byexpressing both height and weight as standard deviations orZ-scores rom the median reerence value or the childs age, the

normal range will correspond to the 3rd and 97th centile, (i.e. 2SDs or 2 Z-scores). By expressing data in this way, it is possibleto express the weight and height data or al l children across a wideage range in similar Z-score units and thereby produce a readilyunderstandable comparison o the extent o growth retardation atdifferent ages and in different countries.

A decit in height is reerred to as stunting whereas a decitin weight-or-height is considered as wasting. Tese two meas-ures are subsumed in the designation o a child s ailure to grow interms o weight-or-age when the decit is termed underweight.Wasting can occur on a short-term basis in response to illnesswith anorexia or malabsorption or because the child goes hungryor several weeks. Changes in weight-or-height thereore reectthe impact o short-term changes in nutritional status. Growth in

height, however, is much more a cumulative index o long-termhealth because growth in length or height stops when a childdevelops an inection and the subsequent growth may be slowduring the recovery period. Children normally grow in spurtsand intermittently. Energy intake is not a crucial determinanto height and the energy cost o growth and weight gain is only25 per cent o total energy intake once the child is 1 year o age.Impairment o growth in height occurs in many communities atthe time o weaning and up to about 2 years o age. Once the chil-dren have ailed to maintain their proper growth trajectory orstature they tend to remain on the lower centiles and track at thislow level or many years.

While the MDGs targeted underweight in children, morerecently the emphasis has shifed rom underweight to stunting.Te damage caused by lack o good nutrition in the rst 5 yearso lie is largely irreversible and stunted children achieve less inschool, are paid less when they enter the workorce, and are atgreater risk o becoming overweight and developing chronic dis-eases later in lie. Tere is now a better appreciation o the crucialimportance o nutrition during the critical 1000-day period cov-ering pregnancy and the rst 2 years o a childs lie, that stuntingreects deciencies during this period and that health and nutri-tion interventions need to ocus on this crucial period.

Global estimates o the main orms o child undernutrition aresummarized in able 2.7.1. Comparisons rom earlier estimatesindicate that the prevalence o underweight and stunting remainhigh despite substantial progress (Black et al. 2013). In most parts

o Arica the numbers o underweight and stunting increased dur-ing this period while the dramatic progress in Asia is outweighedby the persisting high prevalence and numbers o childrenaffected. Stunting is a serious problem reecting poor nutritionand requent inections during the early growth period. Stuntingin South Asia seems also to be related to the high incidence inLBW in this region.

Underweight in children is being used as an indicator or moni-toring progress towards the MDGs. Overall current analyses dem-onstrate some progress in reducing child undernutritionbutprogress is uneven and in some countries has even deteriorated.

o achieve the MDGs more concerted effort is needed, especiallyin those regions with stagnating or increasing trends in childundernutrition. Well-nourished children have a better chanceo surviving and growing into healthy adults. Improving childnutrition requires attention to all three components, i.e. accessto adequate and sae ood, reedom rom illness, and appropriatecare. Ensuring optimal child health and growth can contributeto a healthy adult population and accelerate economic growth ocountries.

Adult undernutrition

Undernutrition among adults has been neglected and this mayhave proound signicance or the economic growth o develop-ing countries. One simple measure o adult nutritional status isthe body mass index(BMI), (i.e. body weight in kilograms dividedby the square o the height in metres); the most suitable indexor both under- and overnutrition in adults (Shetty and James1994). Adults with a BMI less than 18.5 are considered chronic-

ally undernourished while those with a BMI greater than 25.0or greater than 30.0 are overweight or obese respectively (WHO2000); the same BMI cut-offs apply to both males and emales.Undernourished adults show impairment o physical well-beingand exercise capacity and susceptibility to illness and the ability tosustain economic productivity. Hence, it is important to examineadult undernutrition.

Anthropometric measures o adult undernutrition provideobjective estimates o the prevalence o undernutrition worldwide.In practice, children and adults may adapt to a shortage o oodby reducing their physical activity without changing their body

able 2.7.1 Current estimates and progress since 1990 in theprevalence and numbers of child undernutrition globally and indeveloping countries of Africa, Asia, and Latin America

Underweight Stunting

1990 2011 1990 2011

Global

Prevalence (%) 26.5 15.7 33.5 25.7

Numbers (106) 163.4 100.7 206.5 164.8

Africa

Prevalence (%) 23.6 17.7 36.9 35.6

Numbers (106) 25.3 27.9 39.6 56.3

Asia

Prevalence (%) 35.1 19.3 41.1 26.8

Numbers (106) 131.9 69.1 154.6 95.8

Latin America

Prevalence (%) 8.7 3.4 18.3 13.4

Numbers (106) 4.8 1.8 10.0 7.1

Prevalence expressed as percentage below 2 SD of WHO International reference value.

Global estimates are predominantly developing countries in the three regions. Latin

America includes the Caribbean.

Source: data from Te Lancet,Volume 382, Issue 9890, Black RE et al., Maternal and child

undernutrition and overweight in low-income and middle-income countries, pp. 427

451, Copyright 2013 Elsevier Ltd. All rights reserved.


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weight. Tus, measures o the prevalence o low weight-or-heightprovide only a limited index o ood insecurity as physical activityis undamental and desirable or physiological well-being and orlimiting the development o chronic disease while promoting soci-eties to prosper through physically demanding economic activity.

For many years the FAO has attempted to assess the globalprevalence o ood insecurity by relating complex measures o

ood supply and its variable distribution between householdswith estimates o the populations energy needs. Te numberso undernourished estimated most recently by FAO are 870 mil-lion o which 850 million are in developing countries (FAO 2012).Since reducing by hal the proportion o the ood insecure by2015 is one o the targets set in MDG 1, monitoring progress isessential. While there has been progress in this direction since the1990s, most o the progress has been achieved beore 2007/2008,and since then progress has stalled. While the prospect o meetingthe MDG 1 target is good, progress has been variable with someregions showing a worsening o the situation. Reliable global esti-mates o adult undernutrition based on BMI are not availablesince nutritional surveys rarely include adult men and the issue oadult undernutrition has also largely been ignored. With aware-

ness o the increasing problem o overweight and obesity, moreinormation based on anthropometric surveys o adults is beinggenerated which will provide global data on adult undernutrition.

Te basic causes o undernutrition are clearly political andsocioeconomic. Agricultural revolutions such as the green revo-lution have increased ood availability and helped meet the oodneeds o the population. Agricultural productivity has increasedworldwide and developing countries are increasingly producingmore ood even when expressed on a per capita basis. Food pricesor most commodities, particularly or cereals, had also allen totheir lowest until the ood price crisis in 2007/2008. However, pov-erty is ofen the basis o a ailure to have access to ood even whenood is available in plenty; and is aggravated by the rise in oodprices. Accelerated ood production will alleviate hunger only tothe extent that the resources used in the process reduce povertymore than they would i used in other ways. Tus ood entitle-ment decline is a more important orce in sustaining poverty andundernutrition than a decline in the availability o ood in devel-oping societies.

Micronutrient malnutritionMicronutrient malnutrition, also reerred to as hidden hunger, iscaused by lack o adequate micronutrients (vitamins and miner-als) in the habitual diet. Diets decient in micronutrients are char-acterized by high intakes o staple ood and cereal crops, but lowconsumption o oods rich in bioavailable micronutrients such as

ruits, vegetables, and animal and marine products, i.e. the lack oa diversied diet. Micronutrient deciencies are important roma public health perspective as they affect several billion peopleworldwide (able 2.7.2) and can impair cognitive development andlower resistance to disease in children and adults. Tey increasethe risk to both mothers and inants during childbirth and impairthe physical ability and economic productivity o men. Te costs othese deciencies in terms o lives lost and reduced quality o lieare enormous, not to mention the economic costs to society.

Strategies to combat micronutrient deciencies in communitieshave included: (1) supplementationo specic nutrients to meet

the immediate decits; (2)orticationo staple ood items in thedaily dietanother successul strategy that has been adopted todeal with specic nutrient deciencies like iodine; (3) ood-basedapproaches which include promoting kitchen gardens to enableamilies to produce and consume a diversied diet and improvethe nutrition o householdspromoted to reduce vitamin A de-ciency in developing countries; (4) a potential strategy that isshowing signs o great promise is to improve the nutrient qualityo commonly consumed staples by agricultural biotechnologyaprocess reerred to as bioortication. Te micronutrient decien-cies that will be addressed in this chapter include only the signi-cant ones rom a public health viewpoint.

Iron deficiency and anaemia

Iron deciency is probably the most common nutritional de-ciency disorder in the world and it is estimated that globally about1.62 billion people suffer rom anaemia (de Benoist et al. 2008).Hence anaemia and iron deciency are major public health prob-lems with adverse consequences especially or women o repro-ductive age and or young children. Te predominant cause o irondeciency is nutritional, the diet ailing to provide or the bodysrequirements o iron. Intestinal helminthic inestations exac-erbate iron deciency by loss o blood rom the gut and malariaalso contributes to anaemia in tropical countries. A low intake oiron and/or its poor absorption then ails to meet the enhanced

demands or iron and anaemia results. Low intakes o olic acidand vitamin B12also contribute to anaemia.

Te consequences o iron deciency are numerous as ironplays a central role in the transport o oxygen in the body andis also essential in many enzyme systems. Iron deciency leadsto changes in behaviour, such as attention, memory, and learn-ing in inants and children, and negatively inuences the normaldeence systems against inection. -lymphocyte unction, phago-cytosis, and the killing o bacteria by neutrophilic leucocytes areaffected. In pregnant women, iron deciency contributes to mater-nal morbidity and mortality, and increases risk o etal morbidity,

able 2.7.2 Estimated global impact of micronutrient malnutrition

Micronutrient

malnutrition

Estimated impact

Vitamin

A deficiency

140 million preschool children affected with VAD1

Contributes to 1.15 million deaths in children every year2

4.4 million children suffer from xerophthalmia1

6.2 million women suffer from xerophthalmia1

Iron deficiency 2.0 billion women (96 million of them pregnant)2

67,500 maternal deaths per year from severe anaemia2

Iodine deficiency 1.98 billion at risk with insufficient or low iodine intakes3

15.8% of population worldwide have goitre3

17.6 million infants born mentally impaired every year2

Folate deficiency Responsible for 200,000 severe birth defects every year2

Source: data from 1Standing Committee on Nutrition, Fifth report on the world nutrition

situation: Nutrition for improved development,World Health Organization, Geneva,

Switzerland, Copyright 2004; 2UNICEF/Micronutrient Initiative, Vitamin and Mineral

deficiency: A World progress reportUNICEF/Micronutrient, Canada, Copyright 2004;

and 3World Health Organization, Iodine status worldwide,World Health Organization,

Geneva, Switzerland, Copyright 2004.


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mortalitym, and LBWs (Viteri 1997). Iron deciency results in areduction in physical working capacity and productivity o adultsboth in agricultural and industrial work situations. Tese unc-tional impairments are economically important as it is estimatedthat median value o productivity losses is about 0.9 per cent grossdomestic product (GDP) and the economic impact o iron de-ciency can vary rom 2 per cent GDP in the case o Honduras to

7.9 per cent in Bangladesh (Horton and Ross 2003).Iron deciency disorders encompass a range o body iron deple-tion states. Te least severe is diminished iron storesdiagnosed bydecreased serum erritin levels and not usually associated withadverse physiological consequences. Te intermediate, iron de-ciency without anaemia on the other hand, is severe enough toaffect production o haemoglobin without haemoglobin levelsalling below clinical criteria indicative o anaemia and charac-terized by decreased transerrin saturation levels and increasederythrocyte protoporphyrin. Te severe orm with clinical mani-estation is iron deciency anaemia(IDA).

IDA is a serious problem worldwide and the dominant causein all cases is nutritional iron deciency (able 2.7.3). Te high-est prevalence gures or IDA are seen in developing countries.

Global estimates are 18.1 per cent or children under 5 years and19.2 per cent among pregnant women (Black et al. 2013). Even indeveloped countries the prevalence o IDA is signicant. Basedon the estimates o IDA as a risk actor or mortality, the totalattributed global burden is estimated at 841,000 deaths and over35 mill ion DALYs (Stoltzus et al. 2004).

In Arica, Asia, and South America, the availability o iron indiets has been deteriorating and IDA continues to be a serious pub-lic health problem. Te availability o iron in the diet or absorp-tion is affected by both the orm o iron and the nature o oodsconcurrently ingested. Iron exists in the diet in two orms: (1) ashaem iron, ound only in animal source oods, readily absorbableand not inuenced by other dietary constituents; and (2) as inor-ganic iron, not readily available and strongly inuenced by oodsingested at the same time. Both animal oods and ascorbic acidpromote the absorption o inorganic iron. Diets which are primar-ily cereal- and legume-based may contain much iron but, in theabsence o co-actors such as ascorbic acid or presence o phytates,

they provide only low levels o bioavailable iron. Concern aboutiron deciency is an important reason or recommending the con-sumption o some animal source oods as well as oods with ascor-bic acid or populations who rely predominantly on a cereal-baseddiet.

Te strategies to combat iron deciency include: (1) iron supple-mentation; (2) ironorticationo certain oods; (3) dietary modi-

cationto improve the bioavailability o dietary iron by modiyingthe composition o meals; and (4)parasitic disease control. Iron andolate supplementation or pregnant women are currently widelyimplemented in several countries; and many countries have a uni-

versal preventive supplementation programme during pregnancy.Iron supplementation o preschool- or school-aged chi ldren is alsocarried out in several countries. Fortication o oods with ironis a preventive measure or improving and sustaining adequateiron nutrition over a longer term. Many countries like Canadaand the United States have ortied oods with iron and studiesin developing countries have demonstrated the effectiveness oiron ortication o oods and salt provided these programmesare based on careul planning and ollow well-established guide-lines (Viteri 1997). Improvement in the supply, consumption,

and the bioavailability o iron in ood is an important strategyto improve iron status o populations. Food-based approachessuch as diversication and modication o the diet and theinclusion o animal source oods have been tried successully toimprove iron intakes. Te bioavailability o iron is inuenced bythe composition o the meal and ood preparation methods. Teconsumption o ascorbate-rich oods enhances iron absorptionwhile limiting the content o phytate will improve iron bioavail-ability. All o these barriers can be addressed by diversicationand modication o the diets at the household or communitylevel. Sustainable and successul strategies include the promo-tion o homestead gardening, small livestock production, andinvestment in community level technologies or preservationand storage o seasonal ruits and vegetables that are rich inmicronutrients like iron (Tompson and Amoroso 2011). Teintroduction o bioortied cereal crops with higher content ominerals like iron and zinc is also undergoing trials to addressthis huge public health problem.

able 2.7.3 Numbers of people (in millions) affected with iron deficiency anaemia based on blood haemoglobinconcentration in different regions of the world

Children Women (1549 years) Men (1559 years) Elderly

Preschool

(millions)

School age

(millions)

Pregnant

(millions)

Non-pregnant

(millions)

(millions) (millions)

Global 293.1 305 56.4 468.4 260 164Africa 83.5 17.2 69.9

Americas 23.1 3.9 39.0

South East Asia 115.3 18.1 182.0

Europe 11.1 2.6 40.8

East Mediterranean 0.8 7.1 39.8

Western Pacific 27.4 7.6 97.0

Source: data from Bruno de Benoist et al. (eds), Worldwide prevalence of Anaemia 19932005: WHO global database on anaemia, World Health

Organization, Geneva, Switzerland, Copyright 2008.


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Malaria and intestinal parasites are important contributorsto IDA in endemic areas. In populations where hookworm isprevalent, effective treatment o this inection has reduced IDAin school-age children (Stoltzus et al. 1997). Tus strategies thataddress iron nutrition whether ood based, or by supplementa-tion or ortication, must be integrated with programmes such asmalaria prophylaxis, helminth control, environmental health, and

control o other micronutrient deciencies to maximize effective-ness (WHO/UNICEF/UNU 2001).

Iodine deficiency disorders

Te term iodine deciency disorder (IDD) reers to a complex oeffects arising rom decient intakes o iodine. Te mountainousareas o the world are likely to be iodine decient because rainleaches iodine rom the rocks and soils. Severely decient areas arethe Himalayas, the Andes, the European Alps, and the vast moun-tainous regions o China. It also occurs in ooded river valleyso Eastern India, Bangladesh, and Burma. Te Great Lake basinso North America are also iodine decient. Excessive intakes ogoitrogens in ood (excessive consumption o cassavaor brassicagroup o vegetables) and water, as well as the deciency o certain

trace elements in the soil or ood chain (e.g. selenium) may inter-ere with iodine uptake and metabolism and can cause or ampliythe effects o iodine deciency.

Te prevalence o maniest IDD in the orm o goitre variesglobally and at present is conned to developing countries, largelybecause public health initiatives such as mandated or permittediodization o salt have been in orce in the developed world. Iodinedeciency and goitre is still prevalent in Central and EasternEurope. According to recent estimates, goitre prevalence in devel-oping countries is 15.8 per cent (WHO 2004). However, this guremasks the enormous numbers who are at risk o IDD based on uri-nary iodine status that reects the insufficiency o iodine intake inthe diet (able 2.7.4). Iodine deciency is a lso responsible or over

200,000 severe birth deects worldwide while also contributingto lower the intellectual capacity by as much as 1015 percentagepoints (UNICEF and Micronutrient Initiative 2004).

IDD in humans is due to deciency o iodine in the diet. Bothwater and oods are sources o iodine with marine sh being therichest source o iodine. Milk and meat are rich sources o iodine andruits, legumes, vegetables, and reshwater sh are also importantsources. Goitrogens in the diet are o secondary importance asaetiological actors in IDD. It has been shown that staple oodsconsumed largely by poor rural populations, such as cassava,maize, sweet potatoes, and lima beans contain cyanogenic glu-cosides which release a goitrogen thiocyanate. Cassava is nowimplicated as an important contributor to the endemic goitre andcretinism in non-mountainous Zaire and in Sarawak in Malaysia.

Selenium deciency in the soil can result in maniestations o IDDin the presence o modest iodine deciency and is considered rel-evant in several regions o China.

Iodine is readily absorbed rom the diet and is essential or thesynthesis o thyroid hormones which are essential or normalgrowth and development. Failure to synthesize sufficient triiodo-thyronine as a result o iodine deciency may be a actor in thestillbirths that occur as a part o the spectrum o IDD. Tyroidhormone deciency leads to severe retardation o growth andmaturation o all organs and the brain is particularly suscepti-ble to damage during the etal and early postnatal periods. Te

spectrum o IDDs in humans, rom the etus to the adult, has beenoutlined by Hetzel (1987).

Te public health initiatives or correcting iodine deciencyinclude the ollowing: iodization o salt has been the mostavoured method and has greatly reduced the prevalence o IDDsin Switzerland, the United States, and New Zealand. Since its rstsuccessul introduction in the 1920s in Switzerland (Brgi et al.1990) successul programmes have been reported in Central andSouth America, in Europe, and in Asia. However, several devel-oping countries have encountered problems with salt iodiza-tion programmes because it is difficult to produce and maintainenough high-quality iodized salt or large populations such asin India and Bangladesh. Te costs o iodized salt and its avail-ability and distribution to remote regions can also be a problemand may be compounded by cultural prejudices about the use oiodized salt and the loss o iodine with cooking i salt is not added

afer cooking. Iodized oilinjections have been used to prevent goi-tre and cretinism in New Guinea (Pharoah and Connolly 1987).Iodized oil is suitable or mass programmes and can be carriedout alongside mass immunization programmes. Tese methodshave been successul in China, Indonesia, and Nepal. Te majorproblems with iodized oil are the cost, the initial discomort, andthe likely potential risk o the transmission o hepatitis B andHIV. Te need or trained personnel to inject iodized oil can be aurther disadvantage. Iodized oil by mouth may be an alternativeand oral iodized oil has been shown to be as effective in a sin-gle oral dose as an intramuscular injection (Phillips et al. 1988).

able 2.7.4 Proportion of population and number of individuals withinsufficient iodine intake in school-age children (612 years) and thegeneral population and total goitre prevalence in the same UN regions

UN region Insufficient iodine intake (urinary

iodine


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2.7

Although the effects o oral iodized oil seem to last or only hal aslong as a similar dose o injected iodized oil, oral iodized oil doesnot suffer rom the disadvantages o iodized oil injections andso is a preerred method or use in remote areas. IDDs are excel-lent examples o nutritional deciency disorders o public healthimportance which can readily be addressed i mass communityprogrammes are undertaken.

Zinc deficiency

Zinc deciency is the result o inadequate intake or absorption ozinc rom the diet. Excess losses o zinc during episodes o diar-rhoea also contribute to deciency. Te composition o the dietcan inuence zinc bioavailability as high levels o phytates in thediet may result in poor absorption while animal source oodsincrease availability. Based on inadequate intakes in the diet it hasbeen estimated that globally 31.3 per cent o the population haveinadequacy o zinc in the diet (Cauleld and Black 2004) whilezinc deciency has been estimated globally at 17.3 per cent (Blacket al. 2013).

Worldwide, zinc deciency is responsible or approximately16 per cent o lower respiratory tract inections, 18 per cent o

malaria, and 10 per cent o diarrhoeal disease and 1.4 per cent(0.8 million) o deaths worldwide. Attributable DALYs werehigher, with zinc deciency accounting or about 2.9 per cent oworldwide loss o healthy lie years. Dietary diversication andthe addition o animal source oods in the diet have helped reducezinc deciency and agricultural technologies such as addition ozinc enriched ertilizer to the soil (Gibson et al. 2007) and the useo bioortied crops with higher zinc and iron content have alsobeen successul ly tried to reduce the burden o zinc deciency as apublic health problem.

Vitamin A deficiency

Vitamin A deciency (VAD) is a major public health problem in

many developing countries. VAD leads to night blindness andxerosis o the conjunctiva and cornea and disrupts the integrityo their surace and causes corneal clouding and ulceration andmay lead to blindness in children. Xerophthalmia continues to bea major cause o childhood blindness despite the intensive preven-tion programmes worldwide. Te parts o the world most seriouslyaffected include South and South East Asia, and many countries inArica, Central America, and the Near East. Extrapolations romthe best available data suggest that 140 million preschool childrenand more than 7 million pregnant women suffer rom VAD everyyear (Standing Committee on Nutrition 2004). Tis report alsostates that another 4.4 million children and 6.2 million womensuffer rom xerophthalmia. Nearly hal the cases o VAD andxerophthalmia occur in South and South East Asia.

VAD maniests as night blindness and it is estimated that glob-ally 5.17 million preschool age children and 9.75 mil lion pregnantwomen suffer rom night blindnessthe highest prevalence inpregnant women in Arica and South and South East Asia (WHO2009). Global estimates are 0.9 per cent or preschool childrenand 7.8 per cent or pregnant women (Black et al. 2013). Based onlow serum retinol levels the estimates globally are much higher at190 million preschool children and 19.1 million pregnant womenwith Arica and South and South East Asia having the highestprevalence. Global estimates are 33.3 per cent or preschoolersand 15.3 per cent or pregnant women (Black et al. 2013). About

2040 million suffer rom subclinical deciency o vitaminA which has serious consequences or child survival since VADdecreases resistance to inections and increases risk o mortalityand estimates suggest this to be between 1.2 to 3.0 million chil-dren. VAD may also be associated with increased maternal mor-bidity and mortality.

Vitamin A belongs to a class o compounds called retinoids.

Pro-vitamin A carotenoids, chiey -carotene, is also included.Preormed vitamin A is chiey ound in dairy products, egg yolk,in some atty sh, and in the livers o arm animals and sh.Carotenes are generally abundant in yellow ruits (papayas, man-goes, apricots, peaches) and vegetables (carrots). Absorption o

vitamin A is about 80 per cent complete in the presence o an ade-quate at intake, while the absorption o carotenoids is highly bilesalt dependent. Vitamin A (retinol and retinoic acid) plays a veryimportant role in the body in cellular development and differen-tiation. Retinol also has a vital role in normal vision, particularlyby the rods in the retina. Tus, one o the earliest maniestationso VAD is night blindness.

Tere is now increasing evidence that vitamin A supplements indecient populations can reduce morbidity, mortality, and blind-

ness although there is emerging evidence that this is not always thecase (Awasti et al. 2013). Xerophthalmia has become less prevalentin hyperendemic areas in recent years and intervention strategieswith periodic megadose vitamin A supplementation may havecontributed to this. It is now the practice to provide vitamin sup-plements with immunization programmes in many countries withthe aim o providing at least one dose o vitamin A per year or allchildren aged 6 months to 5 years. Te ortication o dietary itemswhich are universally consumed, e.g. sugar in Central America(Arroyave et al. 1981) and monosodium glutamate in Indonesia(Muhilal et a l. 1988), have also had a avourable impact on the vita-min A status o the population. riple ortication (iodine, iron,and vitamin A) o salt using microcapsules has been shown to beeffective (Zimmerman et al. 2004). Following on the success osugar ortication in Central America it has been successully triedin Zambia and South Arica and the Philippines have successullyimplemented ortication o cereals (wheat and maize our) with

vitamin A (UNICEF and Micronutrient Initiative 2004).Te problems with ood ortication are essentially logistical

and technological and many developing countries are beginningthe process o ortiying staple oods and condiments, includ-ing margarine, cooking oil, and soya sauce, with vitamins (andminerals). Food intakes rom different regions o the world showlimited vitamin A availability, and the problem is exacerbated bywithholding vegetables and ruits rom children and pregnant andlactating women or cultural reasons in some parts o the world.Nutrition education is the only approach when VAD develops

despite ruit and vegetable sources o the vitamin being in plenti-ul supply. Tese oods are not incorporated into the diets o youngchildren and mothers, due either to lack o knowledge or culturalbiases. Nutrition education together with practical advice andhelp with growing cheap, nutritious vegetables in home kitchengardens may help eradicate VAD. Horticultural approaches areeffective and potentially sustainable in improving vitamin A sta-tus and micronutrient status generally. Economic developmentand poverty reduction programmes are likely to improve socio-economic status and may indirectly contribute to reducing theproblem o VAD.


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SECION 2 188

Folate deficiency

Folate enables cell division and tissue growth. Adequate olate inthe diet helps prevent malormations that affect the neural tubeand spinal cord such as anencephaly and spina bida as well asbirth deects like clef lip and palate. Without adequate olate inthe diet, two in every 1000 pregnancies may end up with a seri-ous birth deect. Folate deciency is also associated with increased

risk o preterm delivery and LBW (Scholl and Johnson 2000) andmay also contribute to anaemia, especially in pregnant and lac-tating mothers (Dugdale 2001). It may thus contribute indirectlyto increased maternal illness and mortality. With the increasingawareness o the role o olate in reducing the risk o heart diseaseand stroke, a case is being made or olate ortication o our, astrategy already adopted in the United States and Canada.

Addressing the challenge of micronutrientmalnutrition

It is important to acknowledge the contribution o severalnon-government organizations (NGOs), many o them spe-cialized in addressing specic micronutrient deciencies (e.g.

International Council or the Control o Iodine DeciencyDisorders (ICCIDD) with the objective o the sustainable elimina-tion o IDD) while many others such as Micronutrient Initiativetackle al l major micronutrient deciencies o public health signi-cance and the important role they play in addressing the problemo hidden hunger worldwide. Tey closely work in partnershipwith governments, aid agencies, and with the UN agencies and thecommunity to urther this laudable objective.

Tis section has hitherto dealt with only some o the moreimportant nutritionally determined deciency disorders o publichealth importance. It is important to know that segments o popu-lations in the world suffer rom other nutritional disorders such asthe deciency o uoride, zinc, selenium, B group vitamins, andascorbic acid. Some o these seem to occur during seasonal de-

ciencies in their availability and accompany amine and conictsituations when they are seen in reugee camps. In all regions othe world there are still populations affected by one or more othese deciencies despite the signicant advances that have beenmade in controlling nutritional deciency disorders. In someregions o the world, largely the result o increasing populationsize, the numbers o undernourished are increasing even i thepopulation prevalence is declining. In many there is a shif in theseverity o the deciency diseases with decreasing numbers withsevere deciency and increasing numbers with mild-to-moderatedeciencies. For a majority o these countries there is still the needto pursue vigorous policies and targeted action to combat the vari-ous nutritional deciency disorders as a part o the comprehensive

health-oriented national ood and nutrition policies.

Consequences of undernutritionand micronutrient deficienciesAn issue that that deserves attention is to ask the question: human-itarian considerations apart, does widespread undernutrition andmicronutrient malnutrition matter? And is there a case or invest-ing in better nutrition? According to UNICEF, approximately halthe economic growth achieved by developed countries o WesternEurope since 1790 until 1980 can be attributed to better nutrition

and improved health and sanitation (UNICEF 1997). Te socialand economic costs, apart rom costs to the individual due to poornutrition, are huge. Improving nutrition o communities reduceshealthcare costs. More than hal o child mortality in developingcountries is attributable to underweight and the increased risk oinectious diseases. Underweight is the leading risk actor in theglobal burden o disease, and among developing countries with

high mortality it contributes to nearly 15 per cent o the attrib-utable DALYs (WHO 2002). Preventing LBW and stunting alsoreduces childhood mortality and morbidity. Te intimate linksbetween undernutrition in early lie, including LBW and theincreasing risk o chronic disease in later adult lie, are well estab-lished. Diagnosis and treatment o chronic diseases like heartdisease, diabetes, and cancer are expensive and will distort thelimited public health budgets o developing countries.

Undernourished children become smaller adults and demonstratelower physiological perormance and reduced physical and workcapacity. Employment prospects and productivity o short-staturedand undernourished individuals are impaired (Spurr 1987). It short-ens productive lives and increases absence due to illness; impactingin turn on economic productivity o countries. Micronutrient de-

ciencies such as iron deciency impair physical capacity and workproductivity and contribute to economic losses.

Poor nutrition impairs cognitive development and learn-ing in undernourished children in developing societies.Grantham-McGregor (1995) has demonstrated that children whoare stunted and live in deprived circumstances have major decitsin intellectual and cognitive development and social behaviour.Childrens scholastic ability in their teens can be strongly inu-enced by interventions in the second and third year o lie. Iodinedeciency and the syndrome o cretinism is another example othe role o nutrition in brain development and unction. Evenpostnatal iodine deciency can lead to slowing o mental process-ing that results in permanent impairment o mental developmentbecause o the need or adequate nutrition during critical periodso brain development. Similarly, Pollitt (1991a, 1991b) has demon-strated that iron deciency anaemia can permanently handicapchildren at a crucial time in their development even though irondeciency per se is not enough to produce demonstrable clinicaldeciency. Grantham-McGregors (1995) studies show that oodthat stimulates longitudinal bone growth also stimulates braindevelopment, thus implying a more generic demand or a range onutrients i mental unction is to improve. All o these have signi-icant relevance to the act that childrens education is the corner-stone to social and economic development o nations and is nowan important component o the MDGs (MDG 2). Te benets osustained mental and physical development rom childhood intoadult lie ensure that healthy adults with the physical capacity to

maintain high work outputs and with the intellectual ability toexibly adapt to new technologies in this rapidly globalizing worldwill be a national asset. Te importance o ood and nutrition inthe development o human capital in developing societies cannever be underestimated.

Strategies to address the problemof undernutrition in developing societiesReduction o poverty and hunger are high up among MDGs sinceachieving MDG 1halving poverty and hunger by 2015is central


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2.7

to achieving the other health-related MDGs. Economic growthand development should reduce the burden o undernutrition, butthe reduction is slow and many people continue to suffer need-lessly. Tere is thus a need or well-conceived policies or sustain-able economic growth and social development that will benet thepoor and the undernourished. Given the complexity o actors thatdetermine malnutrition o all orms, it is important that appropri-

ate ood and agricultural policies are developed to ensure house-hold ood security and that nutritional objectives are incorporatedinto development policies and programmes at national and locallevels in developing countries. Te deleterious consequences orapid growth and development need to be guarded against andpolicies need to be in place to prevent one problem o malnutritionreplacing another in these societies.

Te pre-eminent determinant o household ood insecurityis poverty in societies. Several policy measures undertaken bygovernments in developing countries are aimed at ensuringood supply and household ood security. Good governance anddemocracy and well-targeted aid and the implementation o poli-cies and relevant programmes will reduce the burden o hungerand undernutrition in developing countries. Te adoption o the

MDGs by the worlds leaders at the Millennium Summit o theUN and the declaration to ree all men, women, and childrenrom the abject and dehumanizing conditions o extreme pov-erty contributed a sense o urgency to address issues o nutritionand public health. Several programmes to address the problem onutrition worldwide have been initiated; signicant among themhas been the Scaling Up Nutrition (or SUN) Initiative. Te SUNmovement is built through the engagement o nations affected byundernutrition and is a country-led movement that brings organi-zations together across sectors to support national plans to scaleup nutrition and ocuses attention on the 1000-day window oopportunity or impact. Te SUN movement promotes the imple-mentation o evidence-based nutrition interventions, as well asintegrating nutrition goals into broader efforts in critical sectorssuch as health, social protection, development, and agriculture.Te latter has resulted in the recent ocus on agricultural strate-gies to sustainably reduce undernutrition just as this approach inthe past addressed the challenge o ood insecurity.

Diet, nutrition, and chronicnon-communicable diseaseshe evidence relating ood and nutrition to chronicnon-communicable diseases (NCDs) such as cardiovascu-lar disease, type 2 diabetes mellitus, and cancers comes rompopulation-based epidemiological investigations and trials.Descriptive population-based epidemiological investigations

yield valuable data that lead to important hypotheses, but can-not be used alone to establish the causal links between diet anddisease. Te most consistent correlation between diet and chronicdiseases has emerged rom comparisons o populations or seg-ments o population with substantially different dietary habits.Epidemiological studies, such as cohort studies and casecontrolstudies, that compare inormation rom groups o individualswithin a population usually provide more accurate estimates oassociations. Examining population-based epidemiological datarelating diet to disease recognizes that every population consistso individuals who vary in their susceptibility to each disease and

part o this difference in susceptibil ity is genetic. As the diet withina population changes in the direction that measures the risk o thespecic disease, an increasing proportion o individuals, particu-larly those most susceptible to the risk, develop the disease. As aresult o this interindividual variability in the interaction o dietwith an individuals genetic make-up and the individuals suscep-tibility to disease, some dietdisease relationships are difficult to

identiy within a single population. In experimental clinical stud-ies and randomized and controlled trials, long exposures may berequired or the effect o diet as a risk actor to be maniest. Strictinclusion criteria or participants need to be adhered to, to showthe effect with small numbers in a reasonable length o time. Tesein turn may restrict the study to homogenous samples and thuslimit the applicabil ity o results to the population at large. Despitethese limitations, when careully designed studies show consist-ent ndings o an association between specic dietary actorsand a chronic disease, they generally indicate a cause and effectrelationship.

Diet and cardiovascular diseases

Te commonest cardiovascular diseases that are diet-related arecoronary heart disease (CHD) and hypertension.

Coronary heart disease

CHD emerged as a burgeoning public health problem in Europeand North America afer the Second World War and by the end othe 1950s had become the single major cause o adult death. Terates o CHD showed marked international differences with over-all rates being higher among men than women. Mortality rateswere sevenold higher in some Eastern European countries whilethreeold differences were evident between Scotland and Spain orPortugal. Migration can contribute to either an increase, as in thecase o Japanese moving to the United States, or decrease whenFinns move to Swedenmigrants tending to approach the ratesin their host countries. In the case o migrants rom South Asia tothe United Kingdom, however, the rates exceed the hosts imply-ing some genetic susceptibility increasing risk in the host environ-ment. Te nearly veold difference in CHD rates among differentcountries and the intrapopulation variations in rates, by socioeco-nomic class, ethnicity, and geographical location, have revealedthe dietary basis o CHD. Te marked changes in CHD rates inmigrant populations that moved across a geographical gradient inCHD risk provided evidence o the environmental nature o thecausative actor.

Several prospective population studies have documented therelationship between habitual diets and the risk o CHD. Teselongitudinal studies have shown that several oods in the diet likewholegrain cereals, sh, ruits and vegetables, nuts, and moderate

intakes o red wine are protective and reduce risk o CHD whileothers such as dietary saturated at, trans atty acids, and increasedconsumption o coffee may increase the risk o CHD. On the basiso the evidence, the WHO Expert Committee on Prevention oCHD (WHO 1982) concluded that the relationship o lipids in thediet and blood met the criteria or an epidemiological associationto be termed causal. Tese data were backed by other evidencerom intervention trials and animal experiments demonstratingthe effects o diet on coronary artery atherosclerosis.

Tis relationship between dietary actors and CHD was sup-ported by the results o the Seven Country Study (Keys 1980). Te


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SECION 2 190

saturated at intakevaried between 3 per cent total energy in Japanand 22 per cent in Finland while the 15-year CHD incidence rates

varied between 144 per 10,000 in Japan and 1202 per 10,000 inFinland. Te annual incidence o CHD among 4059-year-oldmen initially ree o CHD was 15 per 100,000 in Japan and 198per 100,000 in Finland. Evidence rom 16 well-dened cohorts inseven countries and its correlation to the 10-year incidence rate o

CHD deaths provided urther support or this causal association.Te strongest correlation was noted between CHD and percentageo energy derived rom saturated at, while total at was not signi-cantly correlated with CHD.

In the Seven Country Study, the serum total cholesterolvalueswere 165 mg/dL in Japan and 270 mg/dL in Finland, and the vari-ation in serum total cholesterol levels between populations couldlargely be explained by differences in saturated at intake. Te risko CHD seemed to rise progressively within the same populationwith increases in plasma total cholesterol. Observational studiessuggest that one population with an average total cholesterol level10 per cent lower than another will have one-third less CHD anda 30 per cent difference in total cholesterol predicts a ourold di-erence in CHD (WHO 1990). Te Seven Country Study showed a

strong positive relationship between saturated at intake and totalcholesterol level; populations with an average saturated at intakebetween 3 per cent and 10 per cent o the energy intake were char-acterized by serum total cholesterol levels below 200 mg/dL and bylow mortality rates rom CHD. As saturated at intakes increasedto greater than 10 per cent o energy intake a marked and progres-sive increase in CHD mortality was noticed. Saturated ats raisetotal and low-density lipoprotein(LDL) cholesterol; and o theseatty acids myristic and palmitic acids abundant in diets rich indairy and meat products have the greatest effects (able 2.7.5).

Several prospective studies have shown an inverse relationbetween high-density lipoprotein (HDL) cholesterol and CHDincidence. However, HDL cholesterol levels are inuenced by sev-eral non-dietary actors and HDL levels do not explain differencesin CHD mortality between populations. HDL levels are increasedby alcohol, weight loss, and by physical activity. Populations whohave high intakes o mono-unsaturated atty acids (rom oliveoil) or have diets rich in n-3 polyunsaturates o marine origin(like Eskimos) also have low CHD rates. Both mono-unsaturatedand n-3 and n-6 polyunsaturated atty acids (PUFAs) lowerplasma total and LDL cholesterol; PUFAs are more effective thanmonounsaturates (Kris-Etherton 1999; Mori and Beilin 2001).Tere is good evidence that some isomers o atty acids, such astrans atty acids, increase the incidence o CHD by increasing LDLcholesterol levels and decreasing the HDL levels, by intereringwith essential atty acid metabolism and by enhancing the concen-trations o the lipoprotein Lp(a) which, in genetically susceptible

people, seems to be an additional risk actor through mechanismswhich include an antiplasminogen effect to limit brinolysis.

Other dietary components, or example, dietary bre or com-plex carbohydrates, seem to inuence serum cholesterol levels andthe incidence o CHD. Populations consuming diets rich in plantoods high in complex carbohydrates have lower rates o CHD;

vegetarians have a 30 per cent lower rate o CHD mortality thannon-vegetarians and their serum cholesterol levels are signicantlylower than that o lacto-ovo-vegetarians and non-vegetarians.

Alcoholconsumption also reduces the incidence o CHD. A num-ber o observational studies suggest that l ight-to-moderate drinkers

have a slightly lower risk o CHD than abstainers. However, therelationship between alcohol intake and CHD is complicated bychanges in blood pressure and also the nature o the alcoholicdrink. Te presence o phenolic compounds in red wine may con-tribute to the benets o drinking red wine as compared to alcoholconsumption per se in reducing the risk.

Te risk o CHD in individuals is dominated by three majoractors: (1) high serum total cholesterol, (2) high blood pressure,and (3) cigarette smoking (WHO 1982). Tere is also a synergismbetween risk actors, with the Japanese notable or their high smok-ing rates and hypertension but very low cholesterol levels: smok-ing and hypertension are particularly harmul to individuals with

high cholesterol levels. Body weight changes induced by diet andlevels o physical activity, are strongly related to changes in serumtotal cholesterol, blood pressure, and obesity. Obesity in turn, par-ticularly when associated with high waist circumerence or waist/hip ratio, is strongly related to diabetes mellitus, both o which arerisk actors or CHD.

Hypertension and stroke

Te risk o CHD and that o cerebrovascular disease present-ing clinically as stroke, increases progressively throughoutthe observed range o blood pressure, in a number o different

able 2.7.5 Summary of strength of evidence of dietary and lifestylefactors and risk of developing cardiovascular disease

Evidence Decreased risk No relationship Increased risk

Convincing Regular physical

activity

Vitamin E

supplements

Myristic and

palmitic acids

Linoleic acid rans fatty acids

Fish and fish oils1 High sodium

intake

Vegetables and

fruits

Overweight

Potassium High alcohol

intake4

Alcohol intake (low

to moderate)2

Probable Linolenic acid Stearic acid Dietary cholesterol

Oleic acid Unfiltered boiled

coffee

NSP3

Wholegrain cereals

Nuts (unsalted)

Plant sterols/stanols

Folate

Notes:1Eicosapentaenoic acid and docosapentaenoic acid.2For CHD risk.3NSP, non-starch polysaccharide.4For risk of stroke.

Adapted with permission from World Health Organization/FAO, Diet, nutrition and

the prevention of chronic diseases, WHO echnical Report Series 916, World Health

Organization, Geneva, Switzerland, Copyright 2003, available from http://whqlibdoc.

who.int/trs/who_trs_916.pdf.


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2.7

countries (MacMohan et al. 1990). From the combined data itappears that there is a veold difference in CHD and a tenoldrisk o stroke over a range o diastolic blood pressure o only40 mmHg. Analysis indicates that a sustained difference o only7.5 mmHg in diastolic pressure coners a 28 per cent difference inrisk o CHD and a 44 per cent difference in risk o stroke.

Nutritional determinants o hypertension are contributory and

are causally linked to stroke. Obesity and alcohol intake are relatedto hypertension since weight reduction and restricting alcoholintake can lower blood pressures. Te dietary actors that areimplicated (in addition to alcohol and caffeine intakes) are exces-sive sodium and saturated at intake and low potassium and cal-cium intake. Te Intersalt Study (1988) compared blood pressuremeasurements with 24-hour urinary sodium excretion in 10,000individuals aged 2059 years in 32 countries and showed thatpopulations with very low sodium excretion and intakes had lowmedian blood pressures, a low prevalence o hypertension, and noincrease in blood pressure with age. Although sodium intake wasrelated to blood pressure levels and also inuenced the extent towhich blood pressures increased with age, the overall associationbetween sodium, median blood pressure, and the prevalence o

hypertension was less than signicant. A number o explanationshave been put orward to explain why studies such as the IntersaltStudy underestimate the relationship between dietary sodium andblood pressure. Tese include among others: unreliability o assess-ing dietary intake o sodium accurately, genetic variability, and thecontribution o other actors such as obesity or alcohol intake.

Reviews based on meta-analysis correlated blood pressurerecordings in individuals with measurements o their 24-hoursodium intake (Law et al. 1991); an association increasing withage and the initial blood pressure. Te results o intervention trialso sodium restrict ion support this relationship. Aggregation o theresults o 68 cross-over trials and ten randomized control trialso dietary salt reduction have shown that moderate dietary saltreduction over a ew weeks lowers systolic and diastolic pressurein those individuals with high blood pressure (Law et al. 1991). Itwas estimated that such reductions in salt intake by populationwould reduce the incidence o stroke by 26 per cent and that oCHD by 15 per cent in Western countries. Reduction o salt in pro-cessed ood would lower blood pressure even urther and wouldprevent as many as 70,000 deaths per year in the UK. Results otherapeutic trials o drug therapy also support the act that theincidence o stroke can be reduced i blood pressure is lowered,although the benecial effect o lowering the incidence o CHD islower than expected. A recent Cochrane review o 34 clinical trials(He et al. 2013) showed that a modest reduction in salt intake or4 or more weeks causes signicant and important alls in bloodpressure in both hypertensive and normotensive individuals, irre-

spective o sex and ethnic group. Te review supports the viewthat a long-term reduction in population salt intake will lowerpopulation blood pressure and thereby reduce cardiovascular dis-ease. Te observed signicant association between the reductionin 24-hour urinary sodium and the all in systolic pressure indi-cates that larger reductions in salt intake will lead to larger alls insystolic blood pressure. Te current recommendation is to reducesalt intake to 56 g/day and this will have a major effect on bloodpressure. Tis review indicates that urther reductions to 3 g/daywill have a greater effect and should become the long-term targetor population salt intake.

Te other dietary component that has been investigated by theIntersalt Study (1988) is potassium. Urinary potassium excretion,an assumed indicator o intake, was negatively related to bloodpressure as was the urinary sodium/potassium concentrationratio. It has also been observed that potassium supplementationreduces blood pressure in both normotensive and hypertensivesubjects (Cappucio and MacGregor 1991). A recent systematic

review o 22 randomized control trials (Aburto et al. 2013) sup-ports the view that increased potassium intake reduces bloodpressure in people with hypertension and has no adverse effecton blood lipid or catecholamine concentrations, or renal unction.Te higher potassium intake was associated with a 24 per centlower risk o stroke. Tese results suggest that increased potas-sium intake is potentially benecial to most people or the preven-tion and control o elevated blood pressure and stroke.

Some, but not all, cross-sectional and intervention studiessuggest a benecial effect o calcium intake on blood pressure.Epidemiological studies also consistently suggest lower bloodpressures among vegetarians independent o age and body weight.Tese studies may also support the role o other dietary compo-nents because vegetarian diets rich in complex carbohydrates are

also rich in potassium and other minerals.Nutritional intervention is likely to reduce the occurrence o

hypertension and the complications o stroke and CHD in thecommunity, demonstrated in Finland where the average bloodpressure has allen by nearly 10 mmHg and the prevalence ohypertension is only a quarter o what it was prior to the inter-

vention. Along with the alls in average cholesterol levels, CHDand stroke rates in Finland have allen dramatically as the pop-ulations diet was transormed to change its at content and tomore than double the average vegetable and ruit intakes. Tedecline in CHD and stroke rates was predominantly dependenton the all in cholesterol and blood pressure levels respectivelyand these changes occurred despite increasing obesity rates(Puska et al. 1995).

A summary o the strength o evidence (convincing and prob-able) on diet and liestyle actors and risk o developing cardiovas-cular diseases (CHD and stroke) based on the recent Joint WHO/FAO Expert Consultation is provided in able 2.7.5 (WHO/FAO2003). Tere is now general agreement on the population strategiesthat need to be adopted to reduce both the requency and extento the risk actors o cardiovascular disease based on this report.Te nutritional approach including increasing physical activity isaimed at reducing obesity, lowering blood pressure, lowering totaland LDL cholesterol and increasing HDL cholesterol, and lower-ing sodium intakes. Current recommendations take into consid-eration both the entire spectrum o cardiovascular risks includingeffects on thrombosis as well as providing a holistic approach to

recommending a healthy diet that will reduce all chronic NCDsincluding cancers. Tese recommendations include lowering totalat intake to between 30 to 35 per cent o total calories, restrictingsaturated at intake to a maximum o 10 per cent o total calories,and increasing contribution rom monounsaturated and polyun-saturated atty acids (n-3 and n-6 PUFAs) and to increase intakes ocomplex carbohydrates or dietary bre. ranslated into ood com-ponents this would mean reducing in particular intake rom ani-mal at, hydrogenated and hardened vegetable oils, and increasingthe consumption o cereals, vegetables, and ruits. Dietary adviceappears to be effective in bringing about modest benecial changes


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in diet and cardiovascular risk actors over approximately a year(Rees et al. 2013).

Diet nutrition and cancers

It is now widely accepted that one-third o human cancerscould relate directly to some dietary component (Doll and Peto1981) and it is probable that diet plays an important role in inu-

encing the permissive role o carcinogens on the development omany cancers. Tus up to 80 per cent o all cancers may have a linkwith nutrition.

Evidence that diet is a determinant o cancer risk comes romseveral sources. Tese include correlation between ood consump-tion data and the incidence o cancers in the population. Studieson the changing rates o cancer in populations as they migraterom a region or country o one dietary culture to another havecontributed to many important hypotheses. Casecontrol studieso the dietary habits o individuals with and without a cancer andprospective studies as well as intervention trials have providedevidence or the effects o diet on cancer. Only those human can-cers where the role o diet or a nutrient is reasonably well estab-lished (summarized in able 2.7.6) are discussed here.

Cancers o the gastrointestinal tract may be inuenced by thediet. Te intake o alcohol appears to be an independent riskactor or oral, laryngeal, and pharyngeal cancers as well as oroesophagus, liver, and breast cancers. Consumption o saltedsh (Cantonese style), preserved, and ermented oods contain-ing nitrosamines as weaning oods or rom early childhood mayintroduce a substantial risk o nasopharyngeal cancer. Stomachcancer is also associated with diets comprising large amounts osalted and salty oods and low levels o resh ruit and vegetableswhich may contain nutrients that possibly inhibit the ormation onitrosamines. Non-starchy vegetables, allium vegetables (onion,garlic, etc.), and ruits probably decrease risk o stomach cancer.

Cancers o the colon and rectumare the third commonest orm

o cancer and the incidence rates are high in Western Europe andNorth America while they are low in sub-Saharan Arica (Boyleet al. 1985). International comparisons indicate that diets low indietary bre and high in animal at and animal protein increasethe risk o colon cancer. Te epidemiological data relating dietarybre to colorectal cancer generally support the existence o aninverse relationship between the intake o oods rich in dietarybre and colon cancer risk and meta-analysis indicates a 10 percent decreased risk per 10 g bre per day. Diets rich in bre arealso rich sources o antioxidant vitamins and minerals withpotential cancer inhibiting properties. Vegetarian diets seem toprovide a protective effect rom the risk o colon cancer. Tere isnow convincing evidence that red meat and processed meat in thediet increases the risk o colon and colorectal cancers while physi-

cal activity decreases risk. Alcohol intake in men and women aswell as obesity and abdominal atness increase risk o this cancer(World Cancer Research Fund and American Institute or CancerResearch 2007; Vargas and Tompson 2012).

Primary liver cancers have been correlated with mycotoxin(aatoxin) contamination o oodstuffs.

Te primary causal actor or lung cancer, a leading cause odeath among men, is cigarette smoking. Several studies haveshown an interactive effect between cigarette smoking and low re-quency o intake o green and yellow vegetables rich in -carotene.In prospective studies, the requency o the consumption o oods

rich in -carotene has been inversely associated with lung cancerrisk. However, high intakes o -carotene as supplements increaserisk signicantly; and so does arsenic in drinking water.

Breast canceris a common cause o death among women bothin the United States and in the United Kingdom. Te most con-

vincing evidence is that lactation protects against risk o breastcancer in both pre- and postmenopausal women. Physical activityprobably also decreases risk while increases in body atness afermenopause increases risk. While other nutritional actors suchas greater birth weight, attained adult stature, and weight gainincrease risk, consumption o alcoholic drinks also convincingly

increases risk o breast cancer both pre- and post-menopause.Dietary actors are important in the causation o cancers o

many sites and dietary modications may reduce cancer risk.In general diets high in plant oods, especially vegetables andruits, are strongly associated with a lower incidence o a widerange o cancers. Such diets tend to be low in saturated at, highin complex carbohydrate and bre, and rich in several anti-oxidant vitamins. Sustained and consistent intake o alcohol,physical inactivity, and obesity and body atness are also associ-ated with several cancers. On the basis o the evidence, a recentreport (World Cancer Research Fund and American Institute

able 2.7.6 Associations between nutritional factors and somecommon cancers

Cancer Decreasing risk of cancer Increasing risk of cancer

Breast Lactation

Physical activity

Alcohol

Obesity

Colorectal Physical activity

NSP1/dietary fibre

Milk, calcium

Processed red meat

Alcohol

Obesity

Endometrium, and

kidney

Physical activity Obesity

Liver Aflatoxin

Alcohol

Lung Fruits

Physical activity

High-dose supplements of

-carotene

Mouth, larynx,

pharynx

Vegetables and f ruit s Alcohol

Nasopharynx Salted fish2

Oesophagus Fruits and vegetables Alcohol

Obesity

Pancreas Folate rich foods Obesity

Prostate Lycopene and selenium

rich foods

High calcium diets

Stomach Fruits and vegetables High salt intake

Notes:

Both convincing and probable evidence for decreasing and increasing risk combined.1NSP, non starch polysaccharide/dietary fibre2Specifically Cantonese style salted fish

Source: data from World Cancer Research Fund / American Institute for Cancer Research,

Food, Nutrition, Physical Activity, and the Prevention of Cancer: a Global Perspective,

American Institute for Cancer Research, Washington, USA, Copyright 2007 World

Cancer Research Fund International All rights reserved.


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2.7

or Cancer Research 2007) makes the ollowing recommenda-tions: (1) be within the normal range o body weight or heightand be physically active; (2) eat mostly oods o plant originand limit intake o red meat and avoid processed meat; (3) limitconsumption o energy dense oods and avoid sugary drinks;(4) limit alcohol intake; (5) limit consumption o salt, and avoidmouldy ood; (6) mothers must be encouraged and supported to

breasteed their children.

Diet, lifestyles, and obesity

Obesity is one o the most important public health problems andthe prevalence o obesity is increasing worldwide. In developingcountries undergoing rapid economic growth, relatively affluentand urbanized communities are showing an increasing preva-lence o obesity among adults and children.

Overweight and obesity is normally assumed to indicate anexcess o body at. Like adult undernutrition, BMI is used as anindicator o choice or obesity and able 2.7.7 outlines the diag-nostic criteria or overweight and obesity in inants and children,adolescents and adults (WHO 1995, 2000). Recent recommenda-tions are that a BMI o between 18.5 and 24.9 in adults be con-

sidered appropriate weight-or-height; BMI between 25 and 29.9be indicative o overweight and possibly a pre-obese state; whileobesity is diagnosed at a BMI greater than 30.0.

Te main health risk o obesity is premature death due to heartdisease and hypertension and other chronic diseases. In the pres-ence o other risk actors (both dietary and non-dietary), obesityincreases the risk o CHD, hypertension, and stroke. In women,obesity seems to be one o the best predictors o cardiovasculardisease. Longitudinal studies have demonstrated that weight gain,both in men and women, is signicantly related to increases in

cardiovascular risk actors. Weight gain was strongly associatedwith increased blood pressure, elevated plasma cholesterol andtriglycerides, and hyperglycaemia. Te distribution o at in thebody in obesity may also contribute to increased risk; high waisthip ratios (i.e. at predominantly in abdomen and not subcutane-ous) increase the risk o heart disease and type 2 diabetes. Tecoexistence o diabetes is also an important contributor to mor-

bidity and mortality in obese individuals. Obesity also carriesincreased risk o gall bladder stones, breast and uterine cancer inemales, and possibly o prostate and renal cancer in males, as wellas osteoarthritis o weight-bearing joints and obstructive sleepapnoea. While obesity contributes to social problems such as lowsel-esteem and reduced employability it is also associated withincreasing mortality both in smokers and non-smokers.

Several environmental actors, both dietary and liestyle related,contribute to increased obesity. Social and environmental actorsthat either increase energy intake and/or reduce physical activityare o primary interest. Changes in the environment that affect thelevels o physical activity and changes both in the ood consumedand in the patterns o eating behaviour may contribute to increaseenergy intakes beyond ones requirement, thus causing obesity.

Increased intake o dietary at as energy-dense ood may result inpoor regulation o appetite and ood intake while bre-rich com-plex carbohydrates tend to bulk the meal and limit intakes.

International comparisons reveal that obesity increases as the atpercentage o calories in the diet increases (Lissner and Heitmann1995). A recent systematic review indicates that increased intakeo sugars was associated with increase in body weight whileiso-energetic exchange o dietary sugars with other carbohydratesshowed no change in body weight (Morenga et al. 2013). Patternso eating, particularly snacking between meals, may contribute toincreased intakes. However, evidence supports the view that mucho the energy imbalance in modern societies is largely the result odramatic reductions in physical activity levels (both occupationaland leisure time) when ood availability is more than adequate.

ackling overweight and obesity that is approaching epidemicproportions worldwide is o crucial importance since it is asso-ciated with several co-morbidities and the consequent increasedhealthcare costs . It has been estimated that the direct costs o obe-sity or healthcare in the United States in 1995 were US$ 70 billionand those o physical inactivity another US$ 24 billion (Colditz1999). Tese are enormous costs and a huge drain on healthcarebudgets o countries.

Preventive measures to tackle the increasing obesity worldwideare reliant on the strength o evidence related to the actors thatincrease or reduce the risk o weight gain. Te WHO report (WHOand FAO 2003) and a more recent review o the evidence is pro-

vided in able 2.7.8 (World Cancer Research Fund and American

Institute or Cancer Research 2007). Preventive measures haveto start very early and primary prevention may have to be aimedat young children. Tis includes nutrition education o childrenand parents and dealing with problems o school meals, snacking,levels o physical activity, and other related issues. Public healthinitiatives need to address all social and environmental issues thatcontribute to the increasing energy and at intakes and reductionsin physical activity. Since the issues are complex, attempts have tobe made to interact with a wide range o stakeholders and addressissues relevant to work sites, schools, supermarkets, and dealwith marketing, advertising, and promoting activity, etc., and

able 2.7.7 Diagnostic criteria for overweight and obesity in infants

and children, adolescents and adults

Infants and children

(all ages)

Weight-for-height >+ 2 Z scores

Adolescents

Overweight BMI-for-age >85th percentile

Obese BMI-for-age >85th percentile of BMI plus

riceps-for-age >90th percentile of SKF

Subscapular-for-age >90th percentile of SSSKF

Adults

Normal weight range BMI 18.524.9

Overweight orpre-obese

BMI 25.029.9

ObeseGrade I

Grade II

Grade III

BMI

BMI

BMI

30.035.9

35.039.9

> 40.0

SSSKF, supraspinal skinfold thickness; SKF, triceps skinfold thickness.

Adapted with permission from World Health Organization, Physical status: the use

and interpretation of anthropometry,WHO echnical Report Series 854, World Health

Organization, Geneva, Switzerland, Copyright 1995 and World Health Organization,

Obesity: preventing and managing the global epidemic, World Health Organization,

Geneva, Switzerland, Copyright 2000.


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not merely expect the health sector to provide solutions. A recenthigh-level exercise in the UK is a good example o such an inte-grated approach to the problem (Foresight 2007).

ype 2 diabetes mellitus

ype 2 diabetes mellitus (ormerly non-insulin dependent dia-betes mellitus) is a chronic metabolic disorder which occurs inadulthood and is strongly associated with an increased risk oCHD. ype 2 diabetes mellitus has to be distinguished rom type1 diabetes mellitus (ormerly insulin dependent diabetes mellitus)and rom gestational diabetes o pregnancy. Obesity is a majorrisk actor or the occurrence o type 2 diabetes mellitus; the riskbeing related both to the duration and the degree o obesity. Teoccurrence o type 2 diabetes mellitus appears to be triggered byenvironmental actors such as sedentary liestyle, dietary actors,stress, urbanization, and socioeconomic actors. Certain ethnic orracial groups seem to have a higher incidence o type 2 diabetesmellitus; these include Pima Indians, Nauruans, and South Asians(i.e. Indians, Pakistanis, and Bangladeshis). ype 2 diabetes melli-tus also seems to occur when the ood ecosystem rapidly changes,or example, urbanization o Au

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