Nestlé Nutrition Institute Workshop Series
Pediatric Program Volume 63
Emerging Societies -
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© 2008, Nestec Ltd., Vevey, Switzerland
Nestlé Nutrition Institute Workshop Series
Pediatric Program Volume 63
Emerging Societies –
New Delhi, March 30–April 3, 2008
Satish C. Kalhan
Andrew M. Prentice
Chittaranjan S. Yajnik
1 Global Changes in Diet and Activity Patterns as
Drivers of the Nutrition Transition
Barry M. Popkin
5 Regional Case Studies – India
K. Srinath Reddy
9 Regional Case Studies – China
11 Regional Case Studies – Africa
Andrew M. Prentice
13 Evolutionary Origins and the Impact of a
Rapid Nutrition Transition
Andrew M. Prentice
15 Prenatal Origins of Undernutrition
17 Postnatal Origins of Undernutrition
20 Malnutrition, Long-Term Health and the Effect of
Ana Lydia Sawaya
23 Epigenetic Inheritance and the Environment
Suyinn Chong, Alyson Ashe, Nathan Oates, Marnie Blewitt,
Nicola Vickaryous and Emma Whitelaw
25 Methionine in Development, Protein Restriction, and in
Fatty Liver Disease
Satish C. Kalhan
27 Adiposity and Comorbidities: Favorable Impact of
29 Obesity, Inflammation, and Macrophages
Vidya Subramanian and Anthony W. Ferrante, Jr.
33 Obesity, Hepatic Metabolism and Disease
John M. Edmison, Satish C. Kalhan and Arthur J. McCullough
36 The Imperative of Preventive Measures Addressing
Chittaranjan S. Yajnik
39 New Approaches to Optimizing Early Diets
41 Prevention of Low Birthweight
Dewan S. Alam
44 Community-Based Approaches to Address Childhood
Undernutrition and Obesity in Developing Countries
47 List of Speakers
Three Nestlé Nutrition Institute Workshops have addressed the
topics of obesity and malnutrition; namely the 49th NNW in 2001 on
‘Obesity in Childhood and Adolescence’, and ‘The Malnourished Child’
and ‘Linear Growth Retardation in Less Developing Countries’ in the
1980s. Since then, the problems of malnutrition and obesity and their
associated health issues have worsened. The WHO estimates that 22
million children under 5 years of age are overweight at present. In
the USA the number of overweight children has doubled since 1980.
Despite an overall decrease in the prevalence of stunting in developing
countries since 1980, childhood malnutrition remains at a disturbingly
high level and as such a major public health problem. The coexistence
of these two major public health concerns lead us to organize the 63rd
Nestle Nutrition Institute Workshop entitled ‘Emerging Societies –
Coexistence of Childhood Malnutrition and Obesity’.
The coexistence of undernutrition (low birthweight, poor growth)
alongside overnutrition (mainly obesity) is a phenomenon afflict-
ing many countries as their economies develop and food availability
increases. This phenomenon, otherwise known as the ‘nutrition tran-
sition’, is becoming increasingly prevalent in many emerging nations.
To date, community-based interventions are the most widely used
approaches to counteract malnutrition. However, evidence is grow-
ing that interventions targeting the improvement in maternal nutrition
and health may deliver the most promising results for improving child
nutrition. The nutrition transition now poses the challenge of how to
balance short-term benefits versus long-term risks of increased meta-
bolic diseases. India was cited as an example to demonstrate the mag-
nitude of potential long-term consequences, with a 300% increase in
the prevalence of diabetes amounting to an estimated 80 million cases
by 2025. The contribution not only of nutritional factors, but also
genetic background and epigenetic factors, to these outcomes were
addressed. In this context, hypotheses such as the thrifty gene hypoth-
esis were discussed as potential mechanisms to explain the increased
susceptibility to obesity in emerging nations.
Considerable research still lies ahead in order to address the ques-
tion of which population segments and at what stage(s) of their life-
cycle should be targeted in order to have the most impactful results.
We are deeply indebted to the three chairpersons of this work-
shop: Prof. Satish Kalhan from the Case Western Reserve University in
Cleveland; Prof. Andrew Prentice from the London School of Hygiene,
and Prof. Chittaranjan Yajnik from the King Edward Memorial Hospi-
tal in Pune, experts recognized worldwide in their respective fields in
nutrition research. Our warm thanks go also to Dr. Natalia Wagemans
and her team for their excellent logistic support of the workshop and
for enabling the participants to enjoy the wonderful Indian culture.
Dr. Petra Klassen, PhD
Chairman Scientific Advisor
Nestlé Nutrition Institute Nestlé Nutrition Institute
Vevey, Switzerland Vevey, Switzeralnd
Prof. Ferdinand Haschke, MD, PhD
Global Changes in Diet and Activity
Patterns as Drivers of the Nutrition
Barry M. Popkin
The Nutrition Transition
The nutrition transition covers the shifts in the way we eat and
move and subsequent effects on our body composition over man’s
history . In the 20th century, in most poor and all middle and high
income countries, the populations were dominated by the emergence
of nutrition-related non-communicable diseases (NR-NCDs).
The Dietary Drivers: More Fats,
More Added Caloric Sweeteners,
More Animal-Source Foods
Edible oil has been a major source of dietary change in the lower
and middle income countries in the last several decades. The recent
shift in the pattern of the nutrition transition in developing countries
typically begins with major increases in the domestic production and
imports of oilseeds and vegetable oils, rather than meat and milk.
The global availability of soybean, sunflower, rapeseed, and palm oil
has approximately tripled between 1961 and 1990 and continued to
increase since then, though at a slightly reduced global pace. See table
1 for the dietary and physical activity pattern data for China.
Caloric sweeteners in 2000 were consumed on a daily basis of
306 kcal/capita across the globe. Figures that underestimate the con-
sumption based on much higher quality diet data. The shift to caloric
beverages as the source of calories is particularly important because
they do not sate us and there is an emerging consensus that calories
from beverages are a potential source of energy imbalance globally.
This is true whether the calories come from high fat, high protein or
high carbohydrate beverages.
Animal source foods (ASF): The revolution in ASF refers to the
increase in demand and production of meat, poultry, fish, and milk in low-
income developing countries. Most of the world’s growth in production
and consumption of these foods comes from the developing countries.
Underlying Eating Behaviors
We have begun to see rapid shifts in the way people eat in terms
of location, methods of cooking, and frequency of intake . Frying
is rapidly displacing more healthful cooking methods, snacking and
away-from-home consumption are up significantly.
Physical Activity Dynamics: Changes in the
Technology of Work and Movement and
Declines in physical activity are particularly profound across
market work, but significant changes also have been shown in work
at home, leisure, and transportation – each affecting significantly
increases in obesity.
Market work: The proportion of individuals working in energy
expenditure-intensive jobs such as farming, mining, and forestry is
Table 1. Dietary and physical activity trends of Chinese adults aged
Plant oils, g/day 014.8 030.9
All calories per capita from edible oil, % 004.9 012.4
Beef and pork, g/day 052.1 070.6
Poultry, g/day 004.4 009.3
Fish + other aquatic products, g/day 014.4 018.3
Eggs, g/day 009.4 025.1
Dairy, g/day 001.6 011.6
Total animal source foods 102.4 140.5
Adults in light level occupations, % 024.7 040.0
Households with color TV, % 020.5 095.7
Households with washing machine, % 036.8 072.8
Households with refrigerator, % 013.3 052.7
Source: China Health and Nutrition Survey.
way down while manufacturing has increased slightly, but the major
shift is toward lower activity service sector jobs. Equally important
has been a major shift in the activity of each occupation .
Work at home: Time in food preparation has declined over the
past half century from about 2 h/day to less than a 0.5 h in the US and
variable amounts elsewhere. Time-saving home technologies affect
cooking, cleaning, and shopping time .
Transport shifts from active to passive: In most countries the
proportion of individuals walking to work or shopping and other activ-
ities has declined drastically .
Leisure is a major global focus for obesity control but is it earned:
There is little leisure time in most of our low and middle income devel-
oping countries and a key issue will be how to expand this in a health-
ful manner. For children, studying, computers, TV viewing and gaming
are all important. For adults TV viewing is becoming more important,
but its impact is poorly documented.
Figure 1 shows shifts in METS of physical activity changes for
Chinese men. The changes in urban and rural areas are comparable.
1 Popkin BM: Global nutrition dynamics: the world is shifting rapidly toward a
diet linked with noncommunicable diseases. Am J Clin Nutr 2006;84:289–298.
2 Wang Z, Zhai F, Du S, Popkin BM: Dynamic shifts in Chinese eating behaviors.
Asia Pacific J Clin Nutr, in press.
1991 1993 1997 1997 2000 2004 2006
Fig. 1. Shift in MET hours per week by activity among Chinese men (18–
55 years old).
3 Monda KL, Zhai F, Popkin BM: Longitudinal relationships between occupa-
tional and domestic physical activity patterns and overweight status in China.
Eur J Clin Nutr 2007 Jul 18 [Epub ahead of print].
4 Bell AC, Ge K, Popkin BM: The road to obesity or the path to prevention:
motorized transportation and obesity in China. Obes Res 2002;10:277–283.
Regional Case Studies – India
K. Srinath Reddy
As a proportion of all deaths in India by the year 2020, cardiovas-
cular disease (CVD) will be the largest cause of disability and death
. At the present stage of India’s health transition, chronic diseases
contribute to an estimated 53% of deaths and 44% of disability-adjusted
life-years lost. India also has the highest number of people with diabe-
tes in the world, with an estimated 19.3 million in 1995 and projected
57.2 million in 2025. On the basis of recent surveys, the Indian Coun-
cil of Medical Research estimates the prevalence of diabetes in adults
to be 3.8% in rural areas and 11.8% in urban areas. The prevalence of
hypertension has been reported to range between 20 and 40% in urban
adults and 12 and 17% among rural adults. The number of people with
hypertension is expected to increase from 118.2 million in 2000 to
213.5 million in 2025, with nearly equal numbers of men and women.
Over the coming decade, until 2015, CVD and diabetes will contribute
to a cumulative loss of USD 237 billion for the Indian economy. Much
of this enormous burden is already evident in urban as well as semi-
urban and slum dwellings across India, where increasing lifespan and
rapid acquisition of adverse lifestyles related to demographic transi-
tion are contributing to the rising prevalence of CVDs and its risk fac-
tors such as obesity, hypertension, and type 2 diabetes. The underlying
determinants lie in socio-behavioral factors such as smoking, physical
inactivity, improper diet and stress .
Unhealthy diets and physical inactivity are two of the main risk fac-
tors for increased blood pressure, increased blood glucose, abnormal
blood lipids, overweight/obesity, and for the major chronic diseases
such as CVDs, cancer, and diabetes . Globally it is estimated that
approximately 2.7 million deaths are attributable to low fruit and veg-
etable intake while 1.9 million deaths are attributable to physical inac-
tivity. A large majority of these deaths occurs in low and middle income
countries. The changes in diet and physical activity have resulted
largely from epidemiological transition that is underway in most low
income countries including India. The main driving forces of these
epidemiological shifts are a globalized world, rapid and uneven urban-
ization, demographic shifts and inter- and intra-country migrations – all
of which result in alterations in dietary practices (a shift from high fiber,
vegetable and fruit-rich diets to diets rich in saturated fats, trans fats
and high salt-containing processed foods) and a decrease in physical
activity (due to availability of mass transport systems and mechaniza-
tion of daily activities). While these changes are global, India has sev-
eral unique features. The transitions in India are uneven with several
states in India still battling the ill effects of under nutrition and infec-
tious diseases, while in other states with better indices of development,
chronic diseases including diabetes are emerging as major areas of con-
cern. Regional differences and urban-rural differences in the occurrence
of CVD is the hallmark. There is marked heterogeneity in total energy
intake in both rural and urban areas. Assam, Gujarat, Kerala, Maharash-
tra and Tamil Nadu have the lowest rural average caloric intake as com-
pared to mean intakes in Punjab or Haryana (tables 1, 2).
Figures 1 and 2 show comparisons between the rural and urban
averages per capita fat and protein intakes, respectively.
All these differences result in a differing prevalence of CVD and
its risk factors. For example even among industrial workers and their
Table 1. Change in average calorie consumption by states – rural (kcal/
capita and day)
1972–1973 1983 1993–1994 1999–2000
Andhra Pradesh 2,103 2,204 1,052 2,021
Assam 2,074 2,055 1,983 1,915
Bihar 2,225 2,189 2,115 2,121
Gujarat 2,142 2,113 1,994 1,986
Haryana 3,215 2,554 2,491 2,455
Karnataka 2,202 2,260 2,073 2,028
Kerala 1,550 1,884 1,955 1,982
Madhya Pradaan 2,423 2,323 2,164 2,062
Maharashtra 1,895 2,144 1,938 2,012
Orissa 1,995 2,103 2,199 2,119
Punjab 3,493 2,577 2,418 2,381
Rajasthan 2,730 2,433 2,470 2,425
Tamil Nadu 1,955 1,861 1,884 1,826
Uttar Pradesh 2,575 2,399 2,307 2,327
West Bengal 1,921 2,027 2,211 2,095
Source: Chandrashekhar and Ghosh .
families who are economically better off than the general community,
there are wide-ranging differences in CVD risk factors. In industries
located predominantly in urban localities, CVD risk factor levels are
high as compared to those in peri-urban locations . However local
Table 2. Change in average calorie consumption by states – urban (kcal/
capita and day)
1972–1973 1983 1993–1994 1999–2000
Andhra Pradesh 2,143 2,009 1,992 2,052
Assam 2,135 2,043 2,108 2,174
Bihar 2,157 2,131 2,088 2,171
Gujarat 2,172 2,000 2,027 2,058
Haryana 2,404 2,242 2,140 2,172
Karnataka 1,925 2,124 2,025 2,045
Kerala 1,723 2,048 1,966 1,995
Madhya Pradesh 2,229 2,137 2,082 2,132
Maharashtra 1,971 2,028 1,989 2,039
Orissa 2,275 2,219 2,251 2,298
Punjab 2,783 2,100 2,089 2,197
Rajasthan 2,357 2,255 2,184 2,335
Tamil Nadu 1,841 2,140 1,922 2,030
Uttar Pradesh 2,161 2,043 2,114 2,131
West Bengal 2,080 2,048 2,131 2,134
Source: Chandrashekar and Ghosh .
1983 1993–1994 1999–2000
Fig. 1. Average all-India per capita fat consumption (g/day). Source:
dietary practices may alter the prevalence. For example, tea garden
workers of Assam receive extra salt as compensation for the putative
loss of sodium due to their outdoor work. This has resulted in high
prevalence of high blood pressure though other CVD risk factors
are similar to other industrial populations which are predominantly
located in peri-urban areas.
Therefore while studying nutrition and physical activity shifts in
India, the marked heterogeneity and secular changes in dietary and
physical activity practices should be taken into account. This princi-
ple should also apply to strategies, policies and nutrition and physical
activity guidelines so that they take regional differences into account.
1 Lopez AD, Mathers CD, Ezzati M, et al (eds): Global Burden of Risk Factors.
Washington, Oxford University Press/World Bank, 2006.
2 Reddy KS, Shah B, Varghese C, Ramadoss A: Responding to the threat of
chronic diseases in India. Lancet 2005;366:1744–1749.
3 WHO 2007
4 Reddy KS, Prabhakaran D, Jeemon P, et al: Educational status and cardiovas-
cular risk profile in Indians. Proc Natl Acad Sci USA 2007;104:16263–16268.
5 Chandrashekhar CP, Ghosh J: The calorie consumption puzzle. The Hindu,
Feb 11, 2003.
6 FAO 2003.
1983 1993–1994 1999–2000
Fig. 2. Average all-India per capita protein consumption (g/day). Source:
Regional Case Studies – China
The status of childhood malnutrition and obesity in China is
reviewed according to the 2002 National Nutritional and Health Survey
in China [1–3] and data from a national survey on the health and physi-
cal fitness of Chinese students in 2005 . Between 1979 and 2008 a
rapid change in economic development has been seen in China, and
characteristic of this transition period is the significant increase in the
prevalence of chronic non-communicable diseases. Compared with
the results in 1992, the body weight and height of preschool children
in urban and rural areas were significantly improved; the prevalence of
malnutrition (underweight and stunting) in urban and rural areas was
significantly reduced; the national average prevalence of overweight
and obesity for the children under 6 years was 3.4 and 2.0%, respec-
tively, as estimated by the Chinese and WHO standards (fig. 1, 2) [1, 5];
a deficiency in micronutrients, including calcium, zinc, vitamin A, vita-
min B1 and B2, is rather common in the preschool and school children.
The current data show that the growth and development of Chinese
Fig. 1. The prevalence of overweight and obesity in children and adoles-
cents (%). OW = Overweight; Ob = obesity; C = using the Chinese standard;
W = using the WHO standard.
children is far from ideal. We are now facing double challenges: malnu-
trition and the increase in overweight and obesity in children.
1 Wang LD: The General Report in the Nutritional and Health Status of the
Chinese Population – 2002 National Nutrition and Health Survey. Beijing,
People’s Medical Publishing House, 2005.
2 Zhai FY, Yang XG: The status of dietary and nutrient intakes of the Chinese
population – 2002 National Nutrition and Health Survey. Beijing, People’s
Medical Publishing House, 2006.
3 Yang XG, Zhai FY: The body mass and nutrition status of the Chinese popula-
tion – 2002 National Nutrition and Health Survey. Beijing, People’s Medical
Publishing House, 2006.
4 Ji CY, Sun JL: Analyses of the epidemiological status of overweight and
obesity in Chinese students and the prevalence. J Peking Univ Health Sci
5 Chen CM, He W, Fu ZY, et al: Ten-Year Tracking Nutritional Status in China.
Beijing, People’s Medical Publishing House, 2004.
Fig. 2. The prevalence of overweight and obesity in children and adoles-
cents estimated by the Chinese standard in different areas. OW = Overweight;
Ob = obesity.
Regional Case Studies – Africa
Andrew M. Prentice
Africa is the final continent to be affected by the nutrition transi-
tion and, like others that have passed through this phase previously,
is characterized by the paradoxical coexistence of malnutrition and
obesity. This is vividly apparent by a visit to almost any major hospital
in urban Africa where children’s wards are struggling to rehabilitate
severely malnourished children whilst neighboring adult wards are
dealing with amputations of diabetic feet and other consequences of
In sub-Saharan Africa, progress towards meeting one of the key
indicators of the first Millennium Development Goals – the proportion
of underweight children – is slow and in several countries is in reverse.
Current projections indicate that Africa will not meet its target by 2015.
Africa is still the home of the most acute nutritional emergencies with
unacceptably high levels of severe-acute malnutrition in many regions
of conflict and in countries failed by their political leaders.
Proportions of the adult population with a body mass index of
<18.5 (set as the definition of chronic energy deficiency) are sub-
stantial, but less than in many South Asian countries, and are a lesser
concern. Adult height is also greater than in many Asian countries. In
mothers the larger adult stature than in the Indian sub-continent is
accompanied by larger mean birthweights and a lower proportion of
low birthweight babies. This may be significant in terms of the rate at
which Africa can emerge from the nutrition transition. It is arguable
that Africa will suffer a lesser burden of chronic disease than Asia in
which the ‘Developmental Origins of Health and Disease’ thesis pre-
dicts a major future burden of chronic disease based upon the mis-
match between the fetal and adult nutritional environment.
Yet obesity rates in Africa are escalating fast. The increase is espe-
cially rapid in urban areas, though the trends are by no means confined
to Africa’s cities. There are several features of the obesity epidemic
in Africa that mirror those in other emerging nations: it penetrates
the richer nations first (in Africa these tend to be in North Africa); it
penetrates urban areas first with a strong urban-rural gradient, but this
diminishes with time; initially it affects the wealthy, but later there is
a demographic switch and obesity becomes a condition more associ-
ated with poverty (as in Western nations), and it shares many of the
same drivers related to the increasing affordability of highly refined
oils and carbohydrates, and a move away from subsistence farmwork
and towards sedentary lifestyles.
Africa also has some characteristics of the obesity epidemic that
stand out from other regions as follows. (1) Africa is probably the only
region in which obesity (especially among women) is viewed cultur-
ally as a positive and desirable trait. This leads to major gender dif-
ferences in obesity rates in many countries, and fuels a syndrome of
intentional weight gain in young women. (2) Most of Africa has very
low rates of obesity in children. To date African obesity is mostly an
adult syndrome. (3) Africans seem genetically prone to higher rates
of diabetes and hypertension in association with obesity than Cauca-
sians, but seem to be relatively protected from dyslipidemias. (4) The
case-specific deaths and disabilities from diabetes and hypertension
in Africa are very high due to the paucity of health services and the
strain that the ‘double burden’ of disease places on health systems. (5)
Recent data suggest that some non-African races may have evolved
recently to select genetic traits that offer them some protection from
obesity and diabetes, but that these traits have not been under positive
selection in Africans.
Evolutionary Origins and the Impact
of a Rapid Nutrition Transition
Andrew M. Prentice
There are many obvious and plausible reasons (and some less
obvious ones) that may account for the rapid increase in obesity rates
in developing and emerging nations. Changes in diet and activity pat-
terns brought about by the economic transition have been previously
discussed in this symposium by Popkin. In later papers we will explore
the possibility that undernutrition in fetal and early life can reset the
metabolic phenotype in ways that make people especially vulnerable
to the influences of an obesogenic environment if they escape from the
frugality of a subsistence living.
This paper seeks to answer whether people from developing
countries may have a genetic predisposition to obesity and its most
common clinical outcome, type 2 diabetes mellitus (T2DM).
The concept of ‘thrifty genes’, first proposed by Neel  in the
1960s, has been prominent amongst the various theories proposed to
explain the sudden rise in global obesity levels in the late 20th cen-
tury. The basic premise of the thrifty gene hypothesis is that an ability
to rapidly deposit energy as body fat in times of plenty would have
assisted individuals to survive periods of starvation, and hence would
have been under positive natural selection. Many of the earlier propo-
nents of the theory used it to explain why certain populations had very
high levels of obesity and diabetes. For instance, it was suggested that
modern Polynesian Islanders are the product of a small founder group
that had survived starvation during the long sea journeys across the
Pacific as the islands were first colonized.
Contemporary interpretations of the thrifty gene story  propose
that: (a) almost all ancient populations have been frequently subjected
to selective pressure by famine, especially since the dawn of agricul-
ture, and hence thriftiness is likely to affect all racial groups in some
form; (b) that transmission is unlikely to have been strongly selected
by mortality within famines (viability selection) and is much more
likely to have been due to fertility selection mediated through the
powerful effects of regular annual hungry seasons, or episodic starva-
tion, on female fecundity, and (c) that the concept of thriftiness (which
is generally interpreted in relation to saving of energy) should also
encompass an element of the ‘greedy gene’ since disregulated appetite
control systems are the most common cause of the genetically based
human obesity syndromes so far identified.
It must be stressed that the thrifty gene concept lacks any experi-
mental validation to date and that there are no data to suggest that
racial and ethnic groups currently undergoing the nutrition transition
(e.g. native Africans and Asians) have a particular genetic predisposi-
tion to obesity. However the latest findings in relation to the FTO gene
(the first of the multigenic contributors to human obesity to be iden-
tified with certainty) strongly suggest that the variant that promotes
leanness is only carried by Caucasians. This may be in line with Dia-
mond’s  suggestion that Caucasians have been selected to have a
lower susceptibility to T2DM, though the likely origins of such putative
selection remain a mystery.
Exciting times lie ahead with respect to understanding whether
or not evolution has endowed any of us with particular susceptibil-
ity to obesity. New statistical methods for comparing genome-wide
scans between different ethnic/racial groups are starting to pinpoint
those genes that show evidence of recent differential selection. These
will soon assist in interpreting whether past famines and food scarcity
have created specially vulnerable populations.
Whether such knowledge would ever influence the public health
messages and government initiatives required to combat obesity
remains a moot point. We already have strong evidence that urban
populations in developing countries do exhibit high levels of obesity,
and this fact alone should drive the public health agenda.
1 Neel JV: Diabetes mellitus: a ‘thrifty’ genotype rendered detrimental by ‘prog-
ress’. Am J Hum Genet 1962;14:353–362.
2 Prentice AM, Rayco-Solon P, Moore SE: Insights from the developing world:
thrifty genotypes and thrifty phenotypes. Proc Nutr Soc 2005;64:153–161.
3 Diamond J: The double puzzle of diabetes. Nature 2003;423:599–602.
Prenatal Origins of Undernutrition
Childhood undernutrition including stunting and wasting contin-
ues to be high in many regions of the developing world. Overall, 178
million children under 5 years of age throughout the developing world
are estimated to be stunted and 19 million are severely wasted. Birth-
weight, a common proxy measure of intrauterine growth, is commonly
low in the same regions of the world where childhood undernutrition
exists. Low birthweight (<2.5 kg) caused either by preterm birth or
intrauterine growth restriction affects immediate survival and func-
tion and is a determinant of later life risk of chronic diseases including
type 2 diabetes and cardiovascular diseases. Birth size is influenced
by numerous prenatal factors including maternal nutritional, environ-
mental and lifestyle exposures during pregnancy and infection. Mater-
nal pre-pregnancy weight and height are independently and directly
associated with birthweight and are also known to modify the effects
of pregnancy weight gain and interventions during pregnancy on birth-
weight and perinatal mortality. Few studies have examined nutritional
interventions beginning in the pre-periconceptional phase for out-
comes such as gestational duration and birthweight. Maternal diet dur-
ing pregnancy, specifically of micronutrient-rich foods such as milk,
and fruits and vegetables, may also enhance birth outcomes. Other
prenatal factors commonly known to impact birthweight in develop-
ing countries include maternal age, parity, sex, and birth interval. In
many settings early marriage and pregnancy are a norm resulting in
a substantial proportion of pregnancies occurring during adolescence
when competition for nutrients for growth of the mother and the fetus
is high, especially in environments where food availability is low. Life-
style factors such as physical activity and maternal stress, as well as
environmental toxicants have variable influences on birth outcomes.
Tobacco and other substance use can reduce gestational duration and
be deleterious to fetal growth. Infections, specifically ascending repro-
ductive tract infections, malaria and, increasingly, HIV can cause pre-
term and intrauterine growth restriction (IUGR) in many settings. Few
studies have examined the contribution of birthweight and prenatal
maternal nutritional status to childhood stunting and wasting. Studies
have generally found adjusted odds ratios for low birthweight rang-
ing between 2 and 5. In other words, after adjusting for determinants
of childhood undernutrition including feeding practices and morbid-
ity, being born low birthweight continues to carry a two- to fivefold
increased risk of stunting in many developing country settings. Even
fewer studies have examined birth length or maternal nutritional status
as risk factors. More research is needed to determine the proportion of
childhood undernutrition attributable to IUGR in different settings in
order to better target interventions to appropriate life stages for com-
bating childhood undernutrition.
Postnatal Origins of Undernutrition
Emerging countries are undergoing a rapid nutrition transition.
Non-communicable diseases are the leading causes of death, but
underweight together with iron, zinc and vitamin A deficiencies are
still among the 15 biggest killers. Undernutrition impairs physical
growth, increases morbidity and mortality, impairs cognitive develop-
ment, reduces economic productivity, and, later, increases the risk of
chronic diseases and impacts on offspring birthweight. In this chapter I
review how inadequate nutrition, infection, and inappropriate mother–
child interactions are the main drivers of undernutrition in childhood.
Underlying socioeconomic, environmental and genetic factors are also
explored. Some perspectives on how urbanization and globalization
may affect undernutrition are discussed.
Globally, length starts to falter immediately after birth while
weight starts faltering around 3–6 months, suggesting very different eti-
ologies . Breast milk provides enough energy and protein for growth
during the first 6 months. In deficient populations, infants’ micronutri-
ent stores at birth and intakes through breast milk may not suffice to
cover the needs for optimal linear growth. Among the 2–5 months age
group, early introduction of complementary foods affects both weight
and length growth by reducing the quality and quantity of the diet, and
increasing infection incidence. Beyond 6 months of age, complemen-
tary foods fail to provide enough energy and other nutrients to meet
the increasing needs for growth and activity. Poor energy intakes are
associated with wasting while micronutrient imbalances affect linear
growth. Iron and zinc have been consistently identified as ‘problem
nutrients’ in the 6–23 months age group worldwide .
Infections are strongly associated with growth faltering. Diarrheal
diseases show the strongest association with short-term weight defi-
cit. Other acute and chronic infections impact differently on growth.
Effects are greater in high prevalence settings as well as in nutrition-
ally compromised children . The severity, duration, frequency, and
type of infection are key factors mediating the effect on growth by
increasing nutrient requirements, losses, and impairing intakes and
Care provided to children, defined by maternal endogenous fac-
tors and societal determinants, affects growth . Maternal influences
include education, health status, and self-confidence. Between mater-
nal and societal determinants are maternal workload, time availability,
and maternal autonomy and control of resources. The level of social
support received by mothers also impacts on care quality.
Factors at the national level explain most of the undernutrition
variability between countries, including lower energy availability,
lower female literacy rates, lower gross domestic product, or lower
vaccination coverage . Other factors consistently correlated with
undernutrition include access to safe water, healthcare, sanitation,
but also parity, birth spacing, birth order, and marital status. Maternal
size at birth has been shown to influence birth size in their offspring,
suggesting a transgenerational effect of undernutrition . Weight and
length show marked seasonal variations in agro-pastoral communi-
ties. Weight variations have been correlated with the timing of low-
est food availability and periods of highest diarrhea incidence in many
3 6 9 12 15 18 21 24 27 30 33
Z score (NCHS)
36 39 42 45 48 51 54 57 60
Weight for length
Weight for age
Length for age
Fig. 1. Worldwide timing of growth faltering. Mean anthropometric z
scores by age relative to the NCHS reference (0–59 months) in 39 nationally
representative surveys conducted in Latin America, Asia, and Africa from 1987
to 1997. Reproduced with permission from Shrimpton et al. .
In 2008 the proportion of the urban population will equal the rural
population. In developing countries more than 30% of the urbanized
live in shanty towns, meaning higher transmission rates of infections
due to a lack of water, poor housing conditions, overcrowding, poor
hygiene, and environmental pollution. Urbanization also affects behav-
ior. For instance the duration of breastfeeding is lower in urban than
rural settings. Although trade globalization has meant greater food
availability, it has also increased the vulnerability to global price fluc-
tuations. Nowadays a booming demand for oil and food commodities
from emerging countries drives global prices up. How it will affect the
poorest countries is unknown, but they surely are ill equipped to face a
global competition for dwindling resources.
The burden of child undernutrition remains so great that there is a
renewed moral urgency to find integrated solutions to tackle the prob-
lem. Over- and undernutrition are now seen as different manifestations
of a global phenomenon. Since they are linked, fighting undernutrition
should impact positively on both outcomes.
1 Shrimpton R, Victora CG, de Onis M, et al: Worldwide timing of growth falter-
ing: implications for nutritional interventions. Pediatrics 2001;107:e75.
2 Dewey K, Brown K: Update on technical issues concerning complementary
feeding of young children in developing countries and implications for inter-
vention programs. Food Nutr Bull 2003;24:5–28.
3 Bhan MK, Bahl R, Bhandari N: Infection: How important are its effects on
child nutrition and growth?; in Martorell R, Haschke F (eds): Nutrition and
Growth. Nestlé Nutr Workshop Ser Pediatr Program. Philadelphia, Lippincott
Williams & Wilkins, 2001, vol 47, pp 197–221.
4 Engle PL, Menon P, Haddad LJ: Care and Nutrition: Concepts and
Measurements. Washington, IFPRI, 1997.
5 Frongillo EA, de Onis M, Hanson KMP: Socioeconomic and demographic fac-
tors are associated with worldwide patterns of stunting and wasting of chil-
dren. J Nutr 1997;127:2302–2309.
6 Ramakrishnan U, Martorell R, Shroeder DG, et al: Role of intergenerational
effects on linear growth. J Nutr 1999;129(suppl):544S–549S.
Malnutrition, Long-Term Health and
the Effect of Nutritional Recovery
Ana Lydia Sawaya
Worldwide malnutrition is responsible for 50% of deaths in child-
hood. The prevailing type of malnutrition is stunting, which stands
out as an indicator not only of malnutrition, but also of poverty. The
causes for stunting are: insufficient nutrition of the mother; intrauter-
ine malnutrition; lack of breastfeeding until the child is 6 months old;
late introduction of complementary foods; inadequate quantity and
quality of complementary foods, and nutrient absorption impaired by
infections and intestinal parasitic diseases. The data on malnourished
children being treated at a center for recovery from malnutrition in
São Paulo, Brazil (CREN), showed that over 70% were born with low
or insufficient weight. CREN is a center that offers treatment to slum
children with mild to severe malnutrition. Pediatricians, nutrition-
ists, social workers and psychologists participate in the treatment.
The pediatrician monitors the clinical status, laboratory findings and
anthropometric progress of each child. The nutritionist follows the
child’s diet and corrects the problems identified during treatment.
Laboratory tests (blood and stools) are done in each semester. The
children also receive Fe and vitamin (A, B, C and D) supplements in
prophylactic doses. The children are either treated in an outpatient
clinic or in a day-hospital. The children treated in the day-hospital are
more severely malnourished. Data from CREN showed that, among
the moderately malnourished children under treatment, about 80% had
at least one infectious episode in the previous month and, among the
severely malnourished ones, that prevalence rose to about 90%. The
difference in the severity of malnutrition referred mainly to the rate of
infections. 60% of these children also had parasites. Another very com-
mon occurrence was anemia, which was verified in 62% of them.
It was estimated that 51.7 million people lived in slums in Bra-
zil in 2003. This population is growing faster than the urban one. This
condition is associated with poor sanitation, bad food habits, lower
birthweight and stunting. Longitudinal and cross-sectional studies in
stunted adolescents have shown the high susceptibility to gain cen-
tral fat, lower fat oxidation and lower resting and postprandial energy
expenditure. In addition, higher blood pressure, higher plasma uric
acid and impaired flow-mediated vascular dilation were all associated
with a higher level of hypertension in low birthweight and stunted
children. Stunted boys and girls also showed lower insulin production
by pancreatic ␤ cells. All these factors are linked with a higher risk
of chronic diseases later in life. Among stunted adults alterations in
plasma lipids, glucose and insulin were also present.
Combining all these findings we can say that insufficient con-
sumption during growth causes stress in the organism, leading to an
increase in the cortisol-to-insulin ratio. As is well known, malnutrition
is a powerful stress stimulator and causes an increase in the cortisol
levels and its catabolic action, to direct energy as glucose to brain.
Besides, food deficiency reduces the anabolic action of tissue synthe-
sis that depends on insulin, causing wasting. That hormonal balance
leads to a reduction in the hormone responsible for growth, insulin-
like growth factor-1 (IGF-1). The high cortisol-to-insulin ratio and low
IGF-1 also reduce muscle mass gain and linear growth, besides increas-
ing the waist-to-hip ratio and reducing body fat oxidation. If a child in
that condition starts to ingest a ‘modern’ diet and presents physical
inactivity due to urban living conditions, an excessive fat gain will take
f Energy intake
during growth ⫹
F Fat gain
Fig. 1. Association between short stature, obesity, hypertension and
place, which can result in an association between stunting, obesity,
hypertension and diabetes (fig. 1).
Recent studies in children who had an adequate nutritional recov-
ery with linear catch-up growth, after treatment in the nutritional
rehabilitation center, CREN, showed that the alterations in body com-
position, bone density and insulin production (found in non-treated
stunted children) were no longer apparent.
Epigenetic Inheritance and the
Suyinn Chong, Alyson Ashe, Nathan Oates,
Marnie Blewitt, Nicola Vickaryous and
Hypothesized as a possible interface between the genetic and
environmental factors that give rise to phenotype, the field of epigenet-
ics is being heralded as the explanation for hitherto poorly understood
instances of non-Mendelian inheritance. There exists a small group
of genes, known as metastable epialleles, which are sensitive to envi-
ronmental influences, such as diet, and undergo molecular changes
that remain for the life of the individual. These modifications are
called epigenetic and in some cases they survive across generations,
that is, through meiosis. This is termed transgenerational epigenetic
inheritance. These findings have led to the temptation to infer similar
processes in humans. Although it seems clear that the lifestyle of one
generation can significantly influence the health of the next generation
in humans, in the absence of supporting molecular data, it is hard to
justify the idea that this is the result of transgenerational epigenetic
inheritance in the light of other, more plausible explanations. What is
required first is to identify genes that are sensitive to the epigenetic
state, that is, metastable epialleles, in humans. Methods are emerg-
ing by which we can do this. In light of the paucity of evidence, when
extrapolating results seen in mice to humans, we should proceed with
Fig. 1. Chromatin proteins and epigenetic modifications attached to the
Methionine in Development, Protein
Restriction, and in Fatty Liver
Satish C. Kalhan
The coexistence of intrauterine and neonatal malnutrition, and
the development of obesity and type 2 diabetes in adults, has been con-
firmed in a number of studies in humans and animal models. Although
the exact mechanism of such imprinting has not been understood, data
from animal studies suggesting hypermethylation of the genomic DNA
suggest that epigenetic changes may be responsible for such pattern-
ing . Since DNA methylation is affected by the availability of the
methyl groups, derangements in one carbon (methyl) metabolism and
of methionine induced by nutritional and environmental perturbations
can impact the expression of certain genes at vital moments during
Methionine, an essential amino acid, plays a critical role in the
one-carbon metabolism in vivo. Methionine is metabolized first by the
ubiquitous transmethylation (‘methionine’) cycle, wherein the methyl
groups from methionine and from folate-dependent one-carbon pool
participate in methyltransferase reactions . The catabolic pathway
of methionine involves the transsulfuration sequence, resulting in the
synthesis of cysteine, which then participates in the formation of gluta-
thione – a major intracellular antioxidant. Metabolism of methionine is
regulated by nutrients, folate, cobalamine, pyridoxine, protein intake,
and by insulin and glucagon.
Methionine metabolism has not been examined in detail during
pregnancy and in the fetus. Data from studies in human pregnancy
show a progressive decline in plasma homocysteine concentration dur-
ing pregnancy and an increase in plasma choline concentration . In
addition, the umbilical arteriovenous concentration gradient suggests
fetal uptake and utilization of homocysteine. Finally, it is significant to
note that hepatic transsulfuration is not active in the human fetus and
appears for the first time after birth. Preliminary data from our studies
in the rat, using the commonly employed model of intrauterine growth
restriction, show that as a result of dietary protein restriction, major
changes in the plasma amino acid pattern are accompanied by down-
regulation of the methionine transsulfuration pathway . Gene-array
studies showed a marked increase in the pathway of serine synthesis.
The impact of these changes on fetal growth and specific epigenetic
changes remains to be determined.
In human adults, obesity and fatty liver disease are also accompa-
nied by changes in methionine metabolism, resulting in a lower plasma
concentration of glutathione and an increase in the plasma concentra-
tion of homocysteine and cysteine. A significant correlation between
insulin resistance and plasma glutathione and cysteine was observed.
A significant association between MTHFR 677CT homozygosity,
which may impact folate metabolism, and non alcoholic fatty liver dis-
ease was observed .
Perturbations in methionine metabolism, as a result of nutrient/
environment interactions early in life or as a result of hepatic dysfunc-
tion in adult life, may play a key role in metabolic patterning during
development and propagation of the disease process in adults.
1 Jones PA, Takai D: The role of DNA methylation in mammalian epigenetics.
2 Stipanuk MH: Sulfur amino acid metabolism: pathways for production and
removal of homocysteine and cysteine. Annu Rev Nutr 2004;24:539–577.
3 Velzing-Aarts FC, Holm PI, Fokkema MR, et al: Plasma choline and betaine
and their relation to plasma homocysteine in normal pregnancy. Am J Clin
4 Kalhan SC, Parimi PS, Hanson RW: Impact of dietary protein restriction on one
carbon metabolism in the rat. Pediatric Academic Societies Annual Meeting,
5 Edmison JM, Dasarathy S, Kalhan SC, McCullough AJ: Severity of non-alco-
holic fatty liver disease is related to MTHFR 677CT homozygosity, lower
glutathione and insulin resistance. Hepatology 2007;46:749A.
Adiposity and Comorbidities:
Favorable Impact of Caloric
The focus of my presentation will be on research involving long-
term calorie restriction (CR) to prevent or delay the incidence of the
metabolic syndrome with age. The current societal environment is
marked by overabundant accessibility of food coupled with a strong
trend to reduced physical activity, both leading to the development of a
constellation of disorders including central obesity, insulin resistance,
dyslipidemia and hypertension (metabolic syndrome).
Prolonged CR has been shown to extend median and maximal
lifespan in a variety of lower species (yeast, worms, fish, rats, and
mice). Mechanisms of this lifespan extension by CR are not fully eluci-
dated, but possibly involve alterations in energy metabolism, oxidative
damage, insulin sensitivity, and functional changes in neuroendocrine
systems. Ongoing studies of CR in humans now makes it possible to
identify changes in ‘biomarkers of aging’ to unravel some of the mech-
anisms of its anti-aging phenomenon.
Analyses from controlled human trials involving long-term CR
will allow investigators to link observed alterations from body com-
position down to changes in molecular pathways and gene expression,
with their possible effects on the metabolic syndrome and aging.
A summary of the physiological and psychological/behavioral
responses to 6 months of CR in humans from the Pennington CAL-
ERIE randomized clinical trial are summarized in table 1.
Physiological responses Psychological/behavioral responses
Abdominal fat (visceral and
Abdominal fat cell size
Intra-hepatic lipid content
Intra-myocellular lipid content
Development of eating disorder
Concern about body size and
Fear of fatness
Diabetes risk factors
Insulin sensitivity (not
Acute insulin response to
MAEDS Depression scale
Beck Depression Inventory II
Cardiovascular disease risk
Subjective feelings of hunger
Eating Inventory, Perceived
Biomarkers of longevity
Core body temperature
Quality of life
24-hour sedentary energy
Metabolic adaptation for 24-hour
Sleeping metabolic rate (SMR)
Metabolic adaptation for SMR
Short-term memory and
Visual perception and memory
Physical activity level (TDEE
adjusted for SMR)
Spontaneous physical activity
Obesity, Inflammation, and
Vidya Subramanian and Anthony W. Ferrante, Jr.
The incidence of obesity has dramatically increased worldwide
and is associated with numerous clinical pathologies. Particularly con-
cerning is the rapid increase in obesity and associated comorbidities
in children. White adipose tissue not only stores excess calories as
energy but is an active endocrine organ that regulates metabolic and
immunological processes in the body. In recent years it has become
clear that obesity is associated with chronic low grade inflammation
that involves activation of inflammatory signaling pathways, increased
production of cytokines and acute-phase proteins. This state of sys-
temic inflammation is thought to be a common denominator for the
development of many metabolic complications of obesity. The inflam-
matory response in obesity seems to originate predominantly from adi-
pose tissue though other organs like liver may also be involved during
progression of the disease. In both obese humans and rodents, adipose
tissue expression and secretion of numerous inflammatory cytokines
and acute phase proteins including tumor necrosis factor-␣ (TNF-␣),
monocyte chemoattractant proteins (MCPs), interleukin-6 (IL-6), and
plasminogen activator inhibitor-1 (PAI-1) are significantly increased
. Studies show that elevated circulating concentrations of proin-
flammatory factors predict the development of insulin resistance and
other metabolic complications of obesity.
Adipose tissue is a heterogeneous organ consisting of adipocytes
and the non-adipocyte stromal vascular cells. Numerous studies have
shown an unexpected role for immune cells, particularly macrophages
within the stromal vascular fraction of adipose tissue in the develop-
ment and progression of systemic inflammation. Gene expression
analyses revealed that most of the proinflammatory factors secreted
by adipose tissue are predominantly expressed by macrophages in the
adipose tissue . Furthermore, in obesity not only is the number of
macrophages increased but the character of macrophages from adipose
tissue of obese subjects is more inflammatory. These macrophages are
Lean adipose tissue
Obese adipose tissue
Fig. 1. Adipose tissue macrophages in obesity-induced inflammation.
a In lean animals the macrophage content is low in adipose tissue. These mac-
rophages express low amounts of inflammatory factors including tumor necro-
sis factor alpha (TNF-␣), interleukin 6 (IL-6), and plasminogen activator
inhibitor-1 (PAI-1) and high levels of anti-inflammatory factors including inter-
leukin-10 (IL-10). b Obesity increases monocyte adhesion and recruitment to
adipose tissue consequently increasing macrophage number in adipose tissue.
The macrophages in obese adipose tissue express increased amounts of
inflammatory factors including TNF-␣, IL-6, and PAI-1 and decreased amounts
of IL-10. The inflammatory molecules act locally in a paracrine fashion to alter
adipocyte function and adipokine production.
bone marrow derived and their number in adipose tissue is strongly
correlated with body weight, body mass index and total body fat .
Macrophages actively recruited during weight gain are phenotypically
different from resident adipose tissue macrophages. Resident mac-
rophages in the adipose tissue of lean individuals produce relatively
low levels of inflammatory molecules including TNF-␣, PAI-1, and
IL-6 (fig. 1a). In contrast, the recruited macrophages in adipose tissue
express high levels of inflammatory molecules that contribute to sys-
temic inflammation and insulin resistance (fig. 1b).
The recruitment of bone marrow-derived circulating monocytes
to adipose tissue is a complex process under the control of various
chemokines, cytokines, and other local factors . In obesity, among
the inflammatory molecules whose expression is increased is the
MCPs family that binds a common receptor C-C chemokine receptor-2
(CCR2). CCR2 is expressed on circulating monocytes, and is important
in many forms of inflammation that involve macrophage accumula-
tion, including bacterial infections, autoimmune diseases and athero-
sclerosis. In obese rodents, the genetic deletion or pharmacological
antagonism of CCR2 decreases macrophage accumulation in adipose
tissue and improves obesity induced inflammation and insulin resis-
tance . In obesity, adipocytes also increase secretion of factors that
enhance the adhesion and transmigration of monocytes into adipose
tissue as well as their survival. Macrophage colony-stimulating factor
(CSF-1), a key factor for the proliferation, differentiation, and survival
of monocytes and macrophages, is significantly increased in obese adi-
pose tissue. Additionally, obesity-induced increase in adipocyte death
secondary to hypertrophy is also thought to play a role in recruiting
macrophages . However, further studies are required to identify the
exact signals that turn on macrophage recruitment and inflammation
in obese adipose tissue.
Macrophage accumulation and adipose tissue inflammation are
dynamic process under the control of multiple mechanisms. Interven-
tions aimed at either reducing macrophage numbers or decreasing their
inflammatory characteristics improve insulin sensitivity and decrease
inflammation. Investigating the role of macrophages in adipose tissue
biology and the mechanisms involved in their recruitment and activa-
tion in obesity will provide useful insights for developing new thera-
peutic options to treat obesity-induced complications.
1 Wellen KE, Hotamisligil GS: Inflammation, stress, and diabetes. J Clin Invest
2 Charo IF, Ransohoff RM: The many roles of chemokines and chemokine
receptors in inflammation. N Engl J Med 2006;354:610–621.
3 Weisberg SP, Hunter D, Huber R, et al: CCR2 modulates inflammatory and
metabolic effects of high-fat feeding. J Clin Invest 2006;116:115–124.
4 Cinti S, Mitchell G, Barbatelli G, et al: Adipocyte death defines macrophage
localization and function in adipose tissue of obese mice and humans. J Lipid
Obesity, Hepatic Metabolism and
John M. Edmison, Satish C. Kalhan and
Arthur J. McCullough
Nonalcoholic steatohepatitis (NASH), the most severe form of
nonalcoholic fatty liver disease (NAFLD), is emerging as a common
and clinically important type of chronic liver disease in industrialized
countries. Rates are rapidly increasing in developing countries as well
. NAFLD and obesity should be regarded as a global health problem
of increasing dimensions (table 1).
The prevalence of NAFLD and its most severe form, NASH, are
estimated to be 30 and 7–8%, respectively, in the Western world 
NASH is a progressive fibrotic disease in which cirrhosis and liver-
related death occur in up to 20 and 12%, respectively, over a 10-year
period . NASH-associated cirrhosis can also decompensate into
subacute liver failure, progress to hepatocellular carcinoma and recur
post-transplantation. In contrast, steatosis alone has a more benign
course [1, 3].
Table 1. Prevalence of obesity (%) in Asia using WHO criteria for
Country Men Women
China 12 14
Japan 24 20
Malaysia 24 18
Philippines 13 15
Taiwan 18 16
Thailand 17 20
Table 2. Unadjusted and age-adjusted prevalence (%) of the metabolic syndrome among US adults aged 艌20 years
nOriginal NCEP/ATP III definition Revised NCEP/ATP III definition
Unadjusted 6,436 1,677 23.1 (0.9) 26.7 (1.5) 15.7 3.6 0.043 28.0 (1.1) 31.9 (1.5) 13.8 3.9 0.041
Age adjusted 6,436 1,677 24.1 (0.8) 27.0 (1.5) 12.1 2.9 0.088 29.2 (0.9) 32.3 (1.5) 10.9 3.2 0.072
Unadjusted 3,069 841 22.9 (1.4) 24.1 (2.1) 5.4 1.2 0.625 29.3 (1.6) 30.6 (2.1) 4.2 1.2 0.648
Age adjusted 3,069 841 24.6 (1.4) 25.2 (2.1) 2.2 0.5 0.831 31.4 (1.4) 31.8 (2.2) 1.4 0.4 0.866
20–39 years 1,218 28.3 10.2 (1.7) 10.7 (1.9) 4.4 0.4 0.858 15.7 (2.1) 16.5 (2.5) 4.9 0.8 0.815
40–59 years 841 234 29.3 (2.4) 33.0 (3.8) 12.9 3.8 0.399 36.3 (2.3) 40.3 (4.4) 10.9 4.0 0.426
艌60 years 1,010 324 42.6 (2.4) 39.7 (4.3) ⫺6.8 ⫺2.9 0.560 50.5 (2.3) 46.4 (4.3) ⫺8.2 ⫺4.1 0.404
Unadjusted 3,367 836 23.3 (1.3) 29.3 (2.0) 25.8 6.0 0.016 26.8 (1.4) 33.2 (1.9) 24.0 6.4 0.010
Age adjusted 3,367 836 23.5 (1.1) 29.0 (2.0) 23.5 5.5 0.021 27.0 (1.2) 32.9 (2.0) 21.8 5.9 0.014
20–39 years 1,430 250 9.7 (1.6) 18.0 (2.8) 86.1 8.3 0.013 10.8 (1.7) 19.1 (2.9) 76.7 8.3 0.018
40–59 years 949 281 26.0 (2.3) 30.6 (3.8) 17.8 4.6 0.303 30.5 (2.3) 33.8 (3.8) 10.9 3.3 0.459
艌60 years 988 305 43.9 (2.0) 46.1 (3.7) 5.0 2.2 0.601 50.3 (2.2) 56.0 (4.0) 11.3 5.7 0.214
Data are percent (SE). According to Ford .
There is a strong link between NAFLD/NASH and the metabolic
syndrome and, in particular, obesity. It should be emphasized that
obesity (defined by BMI) differs between Western and Asian societ-
ies, being >30 and >25, respectively. Assessment of central adiposity
is extremely important in ‘lean’ people. Although there are a number
of potential pharmacological therapies being developed, diet and exer-
cise should be the initial options for the management.
Public health initiatives are imperative to halt or reverse the
‘diabesity’ epidemic, which is the underlying cause of NAFLD. A num-
ber of important and unresolved issues must be clarified before the
true epidemiology and natural history of NAFLD/NASH can be fully
understood; this is particularly so in developing countries [4, 5].
1 McCullough AJ: The epidemiology and risk factors of NASH; in Fatty Liver
Disease: NASH and Related Disorders. Oxford, Blackwell, 2005, pp 23–37.
2 Browning JD, Szczepaniak LS, Dobbins R, et al: Prevalence of hepatic steato-
sis in an urban population in the United States: impact of ethnicity. Hepatology
3 Matteoni CA, Younossi ZM, Gramlich T, et al: Nonalcoholic fatty liver dis-
ease: a spectrum of clinical and pathological severity. Gastroenterology
4 Vikram NK, Misra A, Pandey RM, et al: Heterogeneous phenotypes of insu-
lin resistance and its implications for defining metabolic syndrome in Asian
Indian adolescents. Atherosclerosis 2006;186:193–199.
5 Misra A, Misra R, Wijesuriya M, Banerjee D: The metabolic syndrome in
South Asians: continuing escalation and possible solutions. Indian J Med Res
6 Ford ES: The metabolic syndrome and mortality from cardiovascular disease
and all-causes: findings from the National Health and Nutrition Examination
Survey II Mortality Study. Atherosclerosis 2004;173:309–314.
The Imperative of Preventive
Measures Addressing Lifecycle
Chittaranjan S. Yajnik
The epidemiological characteristics of chronic non-communicable
diseases (NCDs) are changing fast. The prevalence has risen to unprec-
edented levels, and the young and the underprivileged are increasingly
affected. The classic view of the etiology of NCDs consists of a genetic
susceptibility which is precipitated by aging and modern lifestyle. In a
virtual absence of any methods to tackle genetic susceptibility, the pre-
ventive approach has so far focused on control of lifestyle factors in
those at high risk (the elderly and those with a positive family history
and elevated risk factors). Thus diet and physical activity modification
have been claimed to ‘prevent diabetes’, while some trials have used
pharmacological agents. Such an approach might help high risk indi-
viduals but is unlikely to curtail the burgeoning epidemic of obesity
and diabetes which is rapidly spreading to the young.
Recent research has suggested that susceptibility to NCDs origi-
nates in early life through non-genetic mechanisms (fetal program-
ming), and tackling these may offer a unique opportunity to curtail this
epidemic. Size at birth and childhood growth characteristics are strong
risk factors for NCDs. Both low and high birthweight and rapid child-
hood growth (including early adiposity rebound) predict adult diabe-
tes and related disorders. Children born small but having grown big
have the highest levels of risk factors (fig. 1). This has led to the new
paradigm of ‘Developmental Origins of Health and Disease’ (DOHaD),
applicable to a number of conditions which make up the modern day
NCD epidemic (diabetes, hypertension, coronary artery disease, can-
cer, etc.). This new paradigm shifts our attention to the intrauterine
and childhood environment, in addition to regulating lifestyle factors in
adults. This philosophy is part of the ‘life course’ model of NCD (fig. 2).
It is easy to appreciate the importance of the intrauterine period in the
life cycle if we remember that over three fourths of cell divisions are
over before we are born, and that a newborn human is almost a min-
There has been intense research in humans and animal models
of the factors which regulate growth and which might contribute to
the DOHaD. The mechanisms involved in fetal programming are only
beginning to be understood. Maternal nutrition and metabolism, and
placental function are all involved. Periconceptional maternal nutri-
tion (for example, vitamin B12 and folate) is an important determinant
of not only neural tube growth but also of body composition and the
metabolic characteristics of the offspring. Thus, there are windows of
opportunity in the early life to improve the health of the individual.
Research has also pointed towards genetic factors which affect growth
Adolescence Adult life
Development of NCD
1 3 42
Fig. 1. Insulin resistance. Source: Bavdekar et al. .
Fig. 2. The WHO life course model suggests that non-communicable dis-
eases have their origins in early life. The risk progressively accumulates
throughout the life course and disease manifests in later life. According to
and disease susceptibility (fetal insulin hypothesis). The focus is likely
to be on the environmental regulation of the expression of such genes
during crucial phases of development (epigenetics). One such mecha-
nism is methylation of regulatory portions of the genome which may
be modified by the availability of methyl groups in the diet (nutritional
programming), so elegantly shown in Agouti mice. Intergenerational
transmission of such epigenetic changes explains some of the observa-
tions on transmission of phenotypes which otherwise could be mis-
taken for ‘genetic’ effects.
Thus, improving the early life environment offers a new and excit-
ing opportunity to control the NCD epidemic by influencing the sus-
ceptibility in a more durable manner than only controlling lifestyle
factors in adult life. The imperative is to address the life cycle rather
than concentrate on the end stages.
1 Barker DJP: Mothers, Babies and Health in Later Life. London, Churchill
2 Yajnik CS: Early life origins of insulin resistance and type 2 diabetes in India
and other Asian countries. J Nutr 2004;134:205–210.
3 Yajnik CS, Deshpande SS, Jackson AA, et al: Vitamin B12 and folate concen-
trations during pregnancy and insulin resistance in the offspring: The Pune
Maternal Nutrition Study. Diabetologia 2008;51:29–38.
4 Eriksson JG, Forsén T, Tuomilehto J, et al: Early adiposity rebound in child-
hood and risk of type 2 diabetes in adult life. Diabetologia 2003;46:190–194.
5 Bavdekar A, Yajnik CS, Fall CH, et al: Insulin resistance syndrome in
8-year-old Indian children: small at birth, big at 8 years, or both? Diabetes
New Approaches to Optimizing Early
The increasing number of surviving extremely preterm infants
with gestational age of 23 weeks and birthweights from 400 g yields a
new challenge to neonatal nutrition. The vast majority of extremely low
birthweight (ELBW; <1,000 g) infants will survive if they are born and
taken care of at a hospital with a tertiary neonatal intensive care unit.
Preterm infants should be given optimal nutrition for brain growth and
development. Nutrition during the vulnerable preterm period, prefer-
ably based on human milk, leads to adequate growth, at least corre-
sponding to the intrauterine growth rate.
In Sweden, an individualized feeding system has been developed
during the last 10–15 years. Most ELBW infants are fed according to the
scheme: (1) mother’s own milk (preferred); (2) banked milk (if mother’s
milk is not available); (3) preterm infant formula (if human milk is not
available), and (4) supplementary parenteral nutrition (starting at birth).
There is a trend to a more ‘aggressive’ nutrition of preterm infants,
i.e. initiating nutrition early after birth including administration of not
only intravenous glucose but also amino acids and lipids immediately
after birth or during the first day of life. Enteral feeding, preferably
with human milk, is also started during the first few hours of life.
There is growing evidence that human milk is superior to infant
formula for all newborn infants including the ELBW infants. Human
milk confers nutritional and non-nutritional advantages, and there is
now a worldwide trend using more human milk for feeding of preterm
infants than infant formula. Outcome data support improved neuro-
logical development with human milk, even if the human milk intake
has been limited to only a few weeks.
Unfortunately, but still in widespread use over the world, is the
misconception that human milk has a predictable and uniform compo-
sition. However, several studies have underlined the enormous varia-
tion in the nutrient composition of human milk, particularly fat and to
a less extent protein. There is a variation between mothers during the
course of lactation, during individual meals and also as a consequence
of varying pumping techniques.
To account for this fact, a system with routine macronutrient anal-
yses of the milk based on an infrared technique is used once a week,
allowing optimal intakes of protein and energy. Analyses are always
performed on 24-hour collections as spot samples cannot be used due
to the enormous meal-to-meal-variation. Also, all banked milk is ana-
lyzed, and the most protein-rich milk is chosen for a newborn ELBW
To further reduce the variation in nutrient intake of ELBW infants,
mother’s own milk is given in chronological order, i.e. in the order
it was pumped. Also, all milk is mixed in 24-hour collections before
being given or frozen. This will substantially reduce the day-to-day and
meal-to-meal-variation in nutrient content, which is likely to increase
the gut tolerance.
After a few weeks when the volumes cannot be further increased,
the milk is fortified when a computerized calculation has shown that
the protein and, secondly, energy intakes need to be further increased.
Parenteral nutrition is discontinued when the enteral intake consti-
tutes 75–80% of the total volume intake. The goal is to reach daily pro-
tein and energy intakes of 3.5–4 g/kg and 110–120 kcal/kg, respectively.
To further assess the metabolic capacity to utilize the protein given,
markers, e.g. serum urea and transthyretin, are evaluated. Growth is
monitored by regular measurements of weight, crown-heel length and
head circumference, preferably by the same person each time, and for-
tification is continued throughout the tube-feeding period until breast-
feeding is initiated before discharge.
1 Ziegler EE: Breast-milk fortification. Acta Paediatr 2001;90:720–723.
2 Heiman H, Schanler RJ: Enteral nutrition for premature infants: the role of
human milk. Semin Fetal Neonatal Med 2007;12:26–34.
3 Michaelsen KF, Skafte L, Badsberg JH, Jørgensen M: Variation in macronutri-
ents in human bank milk: Influencing factors and implications for human milk
banking. J Pediatr Gastroenterol Nutr 1990;11:229–239.
4 Polberger S, Räihä NCR, Juvonen P, et al: Individualized protein fortifica-
tion of human milk for preterm infants: comparison of ultrafiltrated human
milk protein and a bovine whey fortifier. J Pediatr Gastroenterol Nutr
5 Omarsdottir S, Casper C, Åkerman A, et al: Breast milk handling routines for
preterm infants in Sweden: a national cross-sectional study. Breastfeed Med
2008, in press.
Prevention of Low Birthweight
Dewan S. Alam
Globally an estimated 20 million or 15.5% of babies are born with
low birthweight (LBW) defined as less than 2,500 g at birth with wide
variations over different geographic locations . However, over 90%
of all LBW infants are born in developing countries and a half of the
total global burden of LBW infants is distributed in South Central
Asian countries. LBW may result from suboptimal fetal growth rela-
tive to gestational age, called intrauterine growth retardation (IUGR)
or small for gestational age (SGA), or too early delivery called preterm
delivery (<37 weeks of gestation). The distinction of these two entities
has important programmatic implications as the determinants are dif-
ferent and so are the interventions.
LBW infants are at increased risk of mortality, morbidity, impaired
growth and cognitive function, decreased motor and psychomotor
development. In the longer term they are at increased risk of type 2
diabetes, hypertension, and cardiovascular disease . These chronic
diseases are emerging as epidemic in many developing countries. This
high prevalence of non-communicable diseases in developing coun-
tries is consistent with the very high prevalence of LBW. The economic
cost of LBW is also enormous due to its immediate and long-term con-
sequences on health and economic productivity .
Major determinants included low caloric intake during pregnancy
or low gestational weight gain, low prepregnancy weight, short stat-
ure, morbidity and cigarette smoking with different attributable risks
for LBW in developed and developing countries . In some settings,
particularly in African countries where HIV and malaria coexist with
maternal malnutrition HIV status, malaria and intestinal parasitic
infestations are also important determinants. Micronutrient deficien-
cies are also likely to influence birth outcome.
Major interventions aimed to prevent LBW include balanced
energy protein supplementation, micronutrient supplementation, fish
oil, treatment of infection, cessation of smoking, and social inter-
ventions. The summary result of the systematic review of balanced
protein-energy supplementation show a positive effect of supplement
on birthweight (+32 g) and a one-third reduction in LBW but no effect
on gestational age . High protein supplementation during pregnancy
is reported to be harmful.
Intervention with micronutrient supplementation includes either
single or a combination or more recently a mix of 15 micronutrients
recommended by UNICEF and WHO. Among single micronutrient
supplementation trials only calcium and magnesium supplementa-
tion during pregnancy was found to reduce LBW. A recent study in
the United States reported that iron supplementation during preg-
nancy in iron-replete women improved birthweight and reduced the
incidence of LBW . Results of multiple micronutrient supplementa-
tion on birthweight and the incidence of LBW have been mixed. Some
studies showed no additional benefits on birthweight over traditional
iron folate supplementation, and some studies reported the superior
efficacy of multiple micronutrients on birthweight and lowering the
incidence of LBW [7–9]. Noticeably, the positive effect of multiple
micronutrients shown in Nepal worked selectively on normal BMI
women and female infants. One study reported multiple micronutri-
ents to be associated with increased perinatal mortality .
While absolute prevention of LBW is unrealistic, bringing the
incidence to a more acceptable level requires a very comprehensive
approach based on the need and feasibility of combined interventions,
as single interventions often showed either no or very little effect.
There is no single strategy that seems to be universally applicable or
efficacious. While IUGR seem to respond well to intervention, preterm
delivery is more complex and resilient to intervention, and further
investigation on the mechanistic aspect of this problem is required to
identify effective interventions. The global epidemic of diabetes, car-
diovascular diseases and hypertension which is linked to size at birth
can only be effectively prevented with a healthy start to life by prevent-
1 United Nation Children’s Fund and World Health Organization: Low
Birthweight: Country, Regional and Global Estimates. New York, UNICEF,
2 Barker DJ: The fetal origins of diseases of old age. Eur J Clin Nutr 1992;46(suppl
3 Alderman H, Berhman JR: Reducing the incidence of low birth weight in low-
income countries has substantial economic benefits. World Bank Res Observ
4 Kramer MS: Intrauterine growth and gestational duration determinants.
5 Kramer MS: Balanced protein/energy supplementation in pregnancy. Cochrane
Database Syst Rev 2001;3.
6 Cogswell ME, Parvanta I, Ickes L, et al: Iron supplementation during preg-
nancy, anemia, and birth weight: a randomized controlled trial. Am J Clin Nutr
7 Christian P, Khatry SK, Katz J, et al: Effects of alternative maternal micronutri-
ent supplements on low birth weight in rural Nepal: double blind randomised
community trial. BMJ 2003;326:571.
8 Osrin D, Vaidya A, Shrestha Y, et al: Effects of antenatal multiple micronutri-
ent supplementation on birthweight and gestational duration in Nepal: dou-
ble-blind, randomised controlled trial. Lancet 2005;365:955–962.
9 Ramakrishnan U, Gonzalez-Cossio T, Neufeld LM, et al: Multiple micronutri-
ent supplementation during pregnancy does not lead to greater infant birth
size than does iron-only supplementation: a randomized controlled trial in a
semirural community in Mexico. Am J Clin Nutr 2003;77:720–725.
10 Christian P, West KP, Khatry SK, et al: Effects of maternal micronutrient sup-
plementation on fetal loss and infant mortality: a cluster-randomized trial in
Nepal. Am J Clin Nutr 2003;78:1194–1202.
Community-Based Approaches to
Address Childhood Undernutrition
and Obesity in Developing Countries
Community-based approaches have been the mainstay of inter-
ventions to address the problem of child malnutrition in developing
societies. The conceptual frameworks that have underpinned commu-
nity-based approaches to improve child health and nutrition include
the food-care-health triad and the triple A process  and the life cycle
approach to undernutrition . Many programs have been in opera-
tion in several countries for decades and originated largely as social
welfare, food security and poverty eradication programs, although
the evaluation of the evidence of what intervention works and hence
should be central to the community-based program is of more recent
occurrence [3, 4]. Conceptual frameworks were developed to guide
this activity as our understanding of the complex nature of the deter-
minants of undernutrition and its links to the risk of overnutrition and
chronic disease emerged. Alongside this evolution is the accumulation
of the evidence of the types of interventions in the community that are
effective, practical and also sustainable.
Critical evaluation of the evidence base of intervention studies in
developing countries provides key insights [3, 4]. Strategies that aim
to improve maternal nutrition and health appear to be the most sig-
nificant interventions that have the best possible pregnancy outcomes.
An adequate and diversified diet promotes weight gain in pregnancy
and hence food supplements or balanced energy-protein supplementa-
tion may be used to target vulnerable groups such as undernourished
pregnant women and adolescent mothers. Multivitamin supplements
have shown to be effective not only in improving maternal health and
birth outcomes but also have an impact on subsequent infant growth
and health. Promotion of exclusive breastfeeding for early infancy fol-
lowed by optimum complementary feeding in the presence of good
hygienic practices diminishes risk of infections, promotes infant
growth and prevents child undernutrition. The success, effectiveness
and the impact of large scale nutrition interventions, on the other hand,
depend both on the contextual success factors, i.e. the macro-environ-
ment in which the program operates, and the program success factors,
i.e. the components, features and structure of the program itself [4, 5].
In addition the sustainability of the program depends on political will,
availability of resources, both monetary and human, community par-
ticipation and involvement and the level of institutionalization of the
program that takes place over time.
The changing environment in developing societies with rapid
developmental transition and urbanization is probably determining
the changing scenario of child nutrition and is responsible for the
emerging problems of obesity and other metabolic disorders in child-
hood and in later adult life. This dramatic transition in developing
societies is contributing to the double burden of malnutrition where
the existing unfinished agenda of undernutrition is complicated and
overwhelmed by the shift towards the emerging epidemic of obesity
and increasing risk of chronic diseases. Community interventions
hence need to be integrated and joined up to reduce both aspects of
this malnutrition in societies and the interventions have to begin early
in life. Because maternal and child undernutrition is the result of many
factors, multiple sectors and strategies will have to bear on the objec-
tive of eradicating this problem. Community-based approaches can
work if established as broad-ranging, multi-sectored and integrated
food and nutrition programs. With child undernutrition and obesity
and adult chronic disease apparently linked, tackling the double bur-
den of malnutrition is a priority. The evidence that community-based
nutrition interventions can have a positive impact on this emerging
problem needs to be evaluated to enable programs to prioritize and
incorporate those interventions that work in the community. Com-
munity-based approaches have to ensure a minimum package which
addresses the ‘food-health-care’ triad of child malnutrition recogniz-
ing the documented synergies in these approaches. Programs that are
operational and successful need to be evaluated and disseminated
in order to enable countries to generate their own programs tailored
to tackle the changing nutritional problems of the children in their
1 UNICEF: Strategy for Improved Nutrition of Children and Women in
Developing Countries. New York, UNICEF, 1990.
2 Commission on the Nutrition Challenges of the 21st Century: Ending
Malnutrition by 2020:An Agenda for Change in the Millennium. Geneva, UN
Standing Committee on Nutrition, 2000.
3 Bhutta ZA, Darmstadt GL, Hasan BS, Haws RA: Community-based interven-
tions for improving perinatal and neonatal health outcomes in developing
countries: a review of the evidence. Pediatrics 2005;115(suppl):519–617.
4 Allen L, Gillespie S: What Works? A Review of the Efficacy and Effectiveness
of Nutrition Interventions. Geneva, ACC/SCN; Manila, ADB, 2001.
5 FAO: Community-Based Food and Nutrition Programmes – What Makes Them
Successful: A Review and Analysis of Experience. Rome, Food & Agriculture
List of Speakers
Prof. Dewan Shamsul Alam
Public Health Sciences Division
68 Shaheed Tajuddin Ahmed
Mohakhali, Dhaka – 1212
Prof. Parul Christian
Department of International
Program in Human Nutrition
Johns Hopkins Bloomberg
School of Public Health
615 N. Wolfe Street, Rm E2541
Baltimore, MD 21205
Prof. Satish C. Kalhan
Department of Pathobiology
Cleveland Clinic Lerner College
Case Western Reserve University
Cleveland, OH 44195
Prof. Arthur McCullough
Department of Gastroenterology
Cleveland Clinic Lerner College
9500 Euclid Avenue, A-30
Cleveland, OH 44195
Prof. Staffan Polberger
Neonatal Intensive Care Unit
Department of Paediatrics
SE–221 85 Lund
Prof. B.M. Popkin
Interdisciplinary Obesity Center
Department of Nutrition, School
of Public Health
University of North Carolina
Carolina Population Center
123 West Franklin Street
Chapel Hill, NC 27516-3997
Prof. Andrew M. Prentice
MRC International Nutrition
London School of Hygiene and
London WC1E 7HT, UK
Prof. Marc-André Prost
MRC International Nutrition
Nutrition & Public Health
Epidemiology and Population
London School of Hygiene &
London WC1E 7HT
Prof. Eric Ravussin
Pennington Biomedical Research
6400 Perkins Road
Baton Rouge, LA 70808
Prof. K. Srinath Reddy
Public Health Foundation of
PHD House, Second Floor
4/2, Sirifort Institutional Area
August Kranti Marg, New Delhi
Prof. Ana Lydia Sawaya
Department of Physiology
Federal University of São Paulo
Rua Botucatu 862, 2o andar
São Paulo, SP
Prof. Prakash Shetty
Institute of Human Nutrition
University of Southampton
Southampton SO16 6YD
Dr. Vidya Subramanian
Naomi Berrie Diabetes Center
Department of Medicine
1150 St. Nicholas Avenue
New York, NY 10032
Prof. Emma Whitelaw
Division of Population Studies
and Human Genetics
Queensland Institute of Medical
300 Herston Road
Herston, Brisbane 4006
Prof. Chittaranjan S. Yajnik
King Edward Memorial Hospital
Sardar Moodliar Road
Prof. Shi-an Yin
National Institute for Nutrition
and Food Safety
Chinese Center for Disease
Control and Prevention
29 Nan Wei Road, Xuanwu
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NOTA IMPORTANTE: AS GESTANTES E NUTRIZES
PRECISAM SER INFORMADAS QUE O LEITE MATERNO
É O IDEAL PARA O LACTENTE, CONSTITUINDO-SE
A MELHOR NUTRIÇÃO E PROTEÇÃO PARA ESTAS
CRIANÇAS. A MÃE DEVE SER ORIENTADA QUAN-
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NESTE PERÍODO E QUANTO À MANEIRA DE SE
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DEVE SER DESENCORAJADO, POIS PODE TRAZER
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SEIO. ANTES DE SER RECOMENDADO O USO DE
UM SUBSTITUTO DO LEITE MATERNO, DEVEM SER
CONSIDERADAS AS CIRCUNSTÂNCIAS FAMILIARES E
O CUSTO ENVOLVIDO. A MÃE DEVE ESTAR CIENTE
DAS IMPLICAÇÕES ECONÔMICAS E SOCIAIS DO NÃO
ALEITAMENTO AO SEIO – PARA UM RECÉM-NASCIDO
ALIMENTADO EXCLUSIVAMENTE COM MAMADEIRA
SERÁ NECESSÁRIA MAIS DE UMA LATA POR SEMANA.
DEVE-SE LEMBRAR À MÃE QUE O LEITE MATERNO
NÃO É SOMENTE O MELHOR, MAS TAMBÉM O MAIS
ECONÔMICO ALIMENTO PARA O LACTENTE. CASO
VENHA A SER TOMADA A DECISÃO DE INTRODUZIR
A ALIMENTAÇÃO POR MAMADEIRA É IMPORTANTE
QUE SEJAM FORNECIDAS INSTRUÇÕES SOBRE OS
MÉTODOS CORRETOS DE PREPARO COM HIGIENE
RESSALTANDO-SE QUE O USO DE MAMADEIRA E
ÁGUA NÃO FERVIDAS E DILUIÇÃO INCORRETA PO-
DEM CAUSAR DOENÇAS. OMS – CÓDIGO INTERNA-
CIONAL DE COMERCIALIZAÇÃO DE SUBSTITUTOS
DO LEITE MATERNO. WHA 34:22, MAIO DE 1981.
PORTARIA Nº 2.051 – MS, DE 08 DE NOVEMBRO DE
2001, RESOLUÇÃO Nº 222 – ANVISA – MS, DE 05 DE
AGOSTO DE 2002 E LEI 11.265/06 – PRESIDÊNCIA DA
REPÚBLICA, DE 04.01.2006 – REGULAMENTAM A CO-
MERCIALIZAÇÃO DE ALIMENTOS PARA LACTENTES
E CRIANÇAS DE PRIMEIRA INFÂNCIA E TAMBÉM A
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