scholarly journals The role of infant nutrition in the global epidemic of non-communicable disease

2016 ◽  
Vol 75 (2) ◽  
pp. 162-168 ◽  
Author(s):  
Atul Singhal

Non-communicable diseases (NCD) and atherosclerotic CVD in particular, are the most important health problems of the 21st century. Already in every world region except Africa, NCD account for greater mortality than communicable, maternal, perinatal and nutritional conditions combined. Although modifiable lifestyle factors in adults are the main determinants, substantial evidence now suggests that factors in early life also have a major role in the development of NCD; commonly referred to as the Developmental Origins of Health and Disease hypothesis. Factors in utero, early postnatal life and throughout childhood, have been shown to affect NCD by influencing risk factors for CVD such as obesity, diabetes, hypertension and dyslipidaemia. Infant nutrition (e.g. breastfeeding rather than bottle feeding) and a slower pattern of infant weight gain have been shown to be particularly protective against later risk of obesity and CVD in both low- and high-income countries. The mechanisms involved are poorly understood, but include epigenetic changes; effects on endocrine systems regulating body weight, food intake and fat deposition; and changes in appetite regulation. As a consequence, strategies to optimise early life nutrition could make a major contribution to stemming the current global epidemic of NCD. This review will consider the role of early life factors in the development of NCD, focusing on the impact of infant nutrition/growth on obesity and CVD. The review will highlight the experimental (randomised) evidence where available, briefly summarise the underlying mechanisms involved and consider the implications for public health.

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Cristian Carmeli ◽  
Zoltán Kutalik ◽  
Pashupati P. Mishra ◽  
Eleonora Porcu ◽  
Cyrille Delpierre ◽  
...  

AbstractIndividuals experiencing socioeconomic disadvantage in childhood have a higher rate of inflammation-related diseases decades later. Little is known about the mechanisms linking early life experiences to the functioning of the immune system in adulthood. To address this, we explore the relationship across social-to-biological layers of early life social exposures on levels of adulthood inflammation and the mediating role of gene regulatory mechanisms, epigenetic and transcriptomic profiling from blood, in 2,329 individuals from two European cohort studies. Consistently across both studies, we find transcriptional activity explains a substantive proportion (78% and 26%) of the estimated effect of early life disadvantaged social exposures on levels of adulthood inflammation. Furthermore, we show that mechanisms other than cis DNA methylation may regulate those transcriptional fingerprints. These results further our understanding of social-to-biological transitions by pinpointing the role of gene regulation that cannot fully be explained by differential cis DNA methylation.


2020 ◽  
Author(s):  
Carol Wang ◽  
John Attia ◽  
Stephen Lye ◽  
Wendy Oddy ◽  
Lawrence Beilin ◽  
...  

Abstract Background: It is well established that genetics, environment, and interplay between them play crucial roles in adult disease. We aimed to evaluate the role of genetics, early life nutrition, and interaction between them, on optimal adult health. Methods: As part of a large international consortium (n~154,000), we identified 60 SNPs associated with both birthweight and adult disease. Utilising the Raine Study, we developed a birthweight polygenic score (BW-PGS) based the 60 SNPs and examined relationships between BW-PGS and adulthood cardiovascular risk factors, specifically evaluating interactions with early life nutrition. Findings: Healthy nutrition was beneficial for all individuals; longer duration of any breastfeeding was associated with lower BMI and lower Systolic Blood Pressure in those with higher BW-PGS. Interpretation: Optimal breastfeeding offers the greatest benefit to reduce adult obesity and hypertension in those genetically predisposed to high birthweight. This provides an example of how precision medicine in early life can improve adult health.


2018 ◽  
Vol 9 (5) ◽  
pp. 487-491 ◽  
Author(s):  
S. Tu’akoi ◽  
M. H. Vickers ◽  
K. Tairea ◽  
Y. Y. M. Aung ◽  
N. Tamarua-Herman ◽  
...  

AbstractSmall Island Developing States (SIDS) are island nations that experience specific social, economic and environmental vulnerabilities associated with small populations, isolation and limited resources. Globally, SIDS exhibit exceptionally high rates of non-communicable disease (NCD) risk and incidence. Despite this, there is a lack of context-specific research within SIDS focused on life course approaches to NCD prevention, particularly the impact of the early-life environment on later disease risk as defined by the Developmental Origins of Health and Disease (DOHaD) framework. Given that globalization has contributed to significant nutritional transitions in these populations, the DOHaD paradigm is highly relevant. SIDS in the Pacific region have the highest rates of NCD risk and incidence globally. Transitions from traditional foods grown locally to reliance on importation of Western-style processed foods high in fat and sugar are common. The Cook Islands is one Pacific SIDS that reports this transition, alongside rising overweight/obesity rates, currently 91%/72%, in the adult population. However, research on early-life NCD prevention within this context, as in many low- and middle-income countries, is scarce. Although traditional research emphasizes the need for large sample sizes, this is rarely possible in the smaller SIDS. In these vulnerable, high priority countries, consideration should be given to utilizing ‘small’ sample sizes that encompass a high proportion of the total population. This may enable contextually relevant research, crucial to inform NCD prevention strategies that can contribute to improving health and well-being for these at-risk communities.


2020 ◽  
Author(s):  
Cristian Carmeli ◽  
Zoltán Kutalik ◽  
Pashupati P. Mishra ◽  
Eleonora Porcu ◽  
Cyrille Delpierre ◽  
...  

ABSTRACTIndividuals growing up during childhood in a socioeconomically disadvantaged family experience a higher rate of inflammation-related diseases later in life. Little is known about the mechanisms linking early life experiences to the functioning of the immune system decades later. Here we explore the relationship across social-to-biological layers of early life social exposures on levels of adulthood inflammation (C-reactive protein) and the mediating role of gene regulatory mechanisms, epigenetic and transcriptomic profiling from blood, in 2,329 individuals from two European cohort studies. Consistently across both studies, we find transcriptional activity explains a substantive proportion (up to 78%) of the estimated effect of early life disadvantaged social exposures on levels of adulthood inflammation. Furthermore, we show that mechanisms other than DNA methylation potentially regulate those transcriptional fingerprints. These results further our understanding of social-to-biological transitions by pinpointing the role of pro-inflammatory genes regulation that cannot fully be explained by differential DNA methylation.


2021 ◽  
Vol 12 ◽  
Author(s):  
Anne-Lise Pocheron ◽  
Gwenola Le Dréan ◽  
Helene Billard ◽  
Thomas Moyon ◽  
Anthony Pagniez ◽  
...  

Understanding the link between mother’s obesity and regulation of the child’s appetite is a prerequisite for the design of successful preventive strategies. Beyond the possible contributions of genetic heritage, family culture, and hormonal and metabolic environment during pregnancy, we investigate in the present paper the causal role of the transmission of the maternal microbiotas in obesity as microbiotas differ between lean and obese mothers, maternal microbiotas are the main determinants of a baby’s gut colonization, and the intestinal microbiota resulting from the early colonization could impact the feeding behavior of the offspring with short- and long-term consequences on body weight. We thus investigated the potential role of vertical transfers of maternal microbiotas in programming the eating behavior of the offspring. Selectively bred obese-prone (OP)/obese-resistant (OR) Sprague-Dawley dams were used since differences in the cecal microbiota have been evidenced from males of that strain. Microbiota collected from vagina (at the end of gestation), feces, and milk (at postnatal days 1, 5, 10, and 15) of OP/OR dams were orally inoculated to conventional Fischer F344 recipient pups from birth to 15 days of age to create three groups of pups: F-OP, F-OR, and F-Sham group (that received the vehicle). We first checked microbiotal differences between inoculas. We then assessed the impact of transfer (from birth to adulthood) onto the intestinal microbiota of recipients rats, their growth, and their eating behavior by measuring their caloric intake, their anticipatory food reward responses, their preference for sweet and fat tastes in solutions, and the sensations that extend after food ingestion. Finally, we searched for correlation between microbiota composition and food intake parameters. We found that maternal transfer of microbiota differing in composition led to alterations in pups’ gut microbiota composition that did not last until adulthood but were associated with specific eating behavior characteristics that were predisposing F-OP rats to higher risk of over consuming at subsequent periods of their life. These findings support the view that neonatal gut microbiotal transfer can program eating behavior, even without a significant long-lasting impact on adulthood microbiota composition.


mSystems ◽  
2020 ◽  
Vol 5 (5) ◽  
Author(s):  
K. C. Bauer ◽  
K. E. Huus ◽  
E. M. Brown ◽  
T. Bozorgmehr ◽  
C. Petersen ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) remains a global epidemic, but it is often studied in the context of obesity and aging. Nutritional deficits, however, also trigger hepatic steatosis, influencing health trajectories in undernourished pediatric populations. Here, we report that exposure to specific gut microbes impacts fatty liver pathology in mice fed a protein/fat-deficient diet. We utilize a multiomics approach to (i) characterize NAFLD in the context of early undernutrition and (ii) examine the impact of diet and gut microbes in the pathology and reversal of hepatic steatosis. We provide compelling evidence that an early-life, critical development window facilitates undernutrition-induced fatty liver pathology. Moreover, we demonstrate that sustained dietary intervention largely reverses fatty liver features and microbiome shifts observed during early-life malnutrition.


Author(s):  
Jenny Svanberg

This chapter examines the impact of health inequalities on addiction and how the recommendations of the Marmot Review could influence recovery from addiction. The Marmot Review was tasked with devising strategies to reduce health inequalities in England, and rightly recognised that health equality requires a debate about what kind of society we want to live in. When considering societies as a whole, there is a clearer relationship between poor health outcomes and societal inequality; rich countries with a steep social gradient do worse than poorer, but more equal, countries. The chapter first provides an overview of factors that cause substance use and addiction before discussing the role of early life adversity in addiction and the link between inequality and addiction. More specifically, it explains how unequal societies lead to addiction and goes on to consider how society can support recovery from addiction.


2014 ◽  
Vol 73 (4) ◽  
pp. 457-469 ◽  
Author(s):  
Lotta Nylund ◽  
Reetta Satokari ◽  
Seppo Salminen ◽  
Willem M. de Vos

In the first years after birth, the intestinal microbiota develops rapidly both in diversity and complexity while being relatively stable in healthy adults. Different life-style-related factors as well as medical practices have an influence on the early-life intestinal colonisation. We address the impact of some of these factors on the consecutive microbiota development and later health. An overview is presented of the microbial colonisation steps and the role of the host in that process. Moreover, new early biomarkers are discussed with examples that include the association of microbiota and atopic diseases, the correlation of colic and early development and the impact of the use of antibiotics in early life. Our understanding of the development and function of the intestinal microbiota is constantly improving but the long-term influence of early-life microbiota on later life health deserves careful clinical studies.


2018 ◽  
Vol 101 (4) ◽  
pp. 332-359 ◽  
Author(s):  
Susan Finn ◽  
Eamonn P. Culligan ◽  
William J. Snelling ◽  
Roy D. Sleator

Nutritionally, the first 1,000 days of an infant's life – from conception to two years – has been identified as a highly influential period, during which lasting health can be achieved. Significant evidence links patterns of infant feeding to both short and long-term health outcomes, many of which can be prevented through nutritional modifications. Recommended globally, breastfeeding is recognised as the gold standard of infant nutrition; providing key nutrients to achieve optimal health, growth and development, and conferring immunologic protective effects against disease. Nevertheless, infant formulas are often the sole source of nutrition for many infants during the first stage of life. Producers of infant formula strive to supply high quality, healthy, safe alternatives to breast milk with a comparable balance of nutrients to human milk imitating its composition and functional performance measures. The concept of ‘nutritional programming’, and the theory that exposure to specific conditions, can predispose an individual's health status in later life has become an accepted dictum, and has sparked important nutritional research prospects. This review explores the impact of early life nutrition, specifically, how different feeding methods affect health outcomes.


Genetics ◽  
2009 ◽  
Vol 183 (3) ◽  
pp. 951-964 ◽  
Author(s):  
Annett Eberlein ◽  
Akiko Takasuga ◽  
Kouji Setoguchi ◽  
Ralf Pfuhl ◽  
Krzysztof Flisikowski ◽  
...  

The increasing evidence of fetal developmental effects on postnatal life, the still unknown fetal growth mechanisms impairing offspring generated by somatic nuclear transfer techniques, and the impact on stillbirth and dystocia in conventional reproduction have generated increasing attention toward mammalian fetal growth. We identified a highly significant quantitative trait locus (QTL) affecting fetal growth on bovine chromosome 6 in a specific resource population, which was set up by consistent use of embryo transfer and foster mothers and, thus, enabled dissection of fetal-specific genetic components of fetal growth. Merging our data with results from other cattle populations differing in historical and geographical origin and with comparative data from human whole-genome association mapping suggests that a nonsynonymous polymorphism in the non-SMC condensin I complex, subunit G (NCAPG) gene, NCAPG c.1326T>G, is the potential cause of the identified QTL resulting in divergent bovine fetal growth. NCAPG gene expression data in fetal placentomes with different NCAPG c.1326T>G genotypes, which are in line with recent results about differential NCAPG expression in placentomes from studies on assisted reproduction techniques, indicate that the NCAPG locus may give valuable information on the specific mechanisms regulating fetal growth in mammals.


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