evidence-based blog of Filippo Dibari

Posts Tagged ‘life cycle’

The evolution of human adiposity and obesity: where did it all go wrong?

In Over-nutrition on August 22, 2012 at 7:57 pm

by Jonathan C. K. Wells

Dis. Model. Mech.September 2012, vol. 5; no. 5; pages: 595-607

(download the entire paper)

Abstract

Because obesity is associated with diverse chronic diseases, little attention has been directed to the multiple beneficial functions of adipose tissue.

Adipose tissue not only provides energy for growth, reproduction and immune function, but also secretes and receives diverse signaling molecules that coordinate energy allocation between these functions in response to ecological conditions. Importantly, many relevant ecological cues act on growth and physique, with adiposity responding as a counterbalancing risk management strategy.

The large number of individual alleles associated with adipose tissue illustrates its integration with diverse metabolic pathways. However, phenotypic variation in age, sex, ethnicity and social status is further associated with different strategies for storing and using energy. Adiposity therefore represents a key means of phenotypic flexibility within and across generations, enabling a coherent life-history strategy in the face of ecological stochasticity.

The sensitivity of numerous metabolic pathways to ecological cues makes our species vulnerable to manipulative globalized economic forces. The aim of this article is to understand how human adipose tissue biology interacts with modern environmental pressures to generate excess weight gain and obesity.

The disease component of obesity might lie not in adipose tissue itself, but in its perturbation by our modern industrialized niche.

Efforts to combat obesity could be more effective if they prioritized ‘external’ environmental change rather than attempting to manipulate ‘internal’ biology through pharmaceutical or behavioral means.

Find other posts related to obesity on this blog.

 

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Prenatal factors contribute to the emergence of kwashiorkor or marasmus in severe undernutrition: evidence for the predictive adaptation model

In Under-nutrition on May 9, 2012 at 7:37 am


TE Forrester, AV Badaloo, MS Boyne, C Osmond, D Thompson, C Green, C Taylor-Bryan, A Barnett, S Soares-Wynter, MA Hanson, AS Beedle, and PD Gluckman

PLoS One, January 1, 2012; 7(4): e35907

 

“BACKGROUND: Severe acute malnutrition in childhood manifests as oedematous (kwashiorkor, marasmic kwashiorkor) and non-oedematous (marasmus) syndromes with very different prognoses. Kwashiorkor differs from marasmus in the patterns of protein, amino acid and lipid metabolism when patients are acutely ill as well as after rehabilitation to ideal weight for height. Metabolic patterns among marasmic patients define them as metabolically thrifty, while kwashiorkor patients function as metabolically profligate. Such differences might underlie syndromic presentation and prognosis. However, no fundamental explanation exists for these differences in metabolism, nor clinical pictures, given similar exposures to undernutrition. We hypothesized that different developmental trajectories underlie these clinical-metabolic phenotypes: if so this would be strong evidence in support of predictive adaptation model of developmental plasticity.

“METHODOLOGY/PRINCIPAL FINDINGS: We reviewed the records of all children admitted with severe acute malnutrition to the Tropical Metabolism Research Unit Ward of the University Hospital of the West Indies, Kingston, Jamaica during 1962-1992. We used Wellcome criteria to establish the diagnoses of kwashiorkor (n?=?391), marasmus (n?=?383), and marasmic-kwashiorkor (n?=?375). We recorded participants’ birth weights, as determined from maternal recall at the time of admission. Those who developed kwashiorkor had 333 g (95% confidence interval 217 to 449, p<0.001) higher mean birthweight than those who developed marasmus.

“CONCLUSIONS/SIGNIFICANCE: These data are consistent with a model suggesting that plastic mechanisms operative in utero induce potential marasmics to develop with a metabolic physiology more able to adapt to postnatal undernutrition than those of higher birthweight. Given the different mortality risks of these different syndromes, this observation is supportive of the predictive adaptive response hypothesis and is the first empirical demonstration of the advantageous effects of such a response in humans. The study has implications for understanding pathways to obesity and its cardio-metabolic co-morbidities in poor countries and for famine intervention programs.”

 

Patterns of stunting and wasting: potential explanatory factors.

In Under-nutrition on April 25, 2012 at 6:38 am

R Martorell and MF Young
Adv Nutr, January 1, 2012; 3(2): 227-33.

Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, GA

“We investigated the causes of stunting and wasting using nationally representative data on preschool children from India (2005-2006, N = 41,306) and Guatemala (2008-2009, N = 10,317). We estimated stunting and wasting using the 2006 WHO standard and the 1976 WHO/National Center for Health Statistics (NCHS) reference. India and Guatemala had high levels of stunting; wasting was common in India but rare in Guatemala. Use of the WHO standard (based on breast-fed children) increased the prevalence of stunting in both countries but dramatically changed the pattern of wasting by age in India. In Indian children 0-5 mo of age, wasting more than tripled, from 8% to 30%, leading to the highest prevalence of wasting. Using the NCHS reference, the lowest and highest prevalence among Indian children occurred in children 0-5 and 12-23 mo, respectively. Also, we showed that household wealth and the condition of women were related to both stunting and wasting; review of the literature on wasting failed to identify factors that were not also related to stunting (e.g., seasonality, infections, and intrauterine growth retardation). Possible explanations for high levels of wasting in India include the poor status of women, the “thin-fat” infant phenotype, chronic dietary insufficiency, poor dietary quality, marked seasonality, and poor levels of sanitation. Use of the WHO standard calls for urgent attention to improving prenatal and infant nutrition and uncovers an alarming level of wasting in the young infant in India that use of the NCHS growth reference (based on bottle-fed infants) had masked.”

http://highwire.stanford.edu/cgi/medline/pmid;22516733

Promoting healthy growth: what are the priorities for research and action?

In Under-nutrition on April 25, 2012 at 6:31 am

E Piwoz, S Sundberg, and J Rooke
Adv Nutr, January 1, 2012; 3(2): 234-41.  

“Healthy growth from conception through the first 2 y of life is the foundation for adequate organ formation and function, a strong immune system, physical health, and neurological and cognitive development. Recent studies identified several low-cost interventions to address undernutrition during this age period and noted the lower returns on investment of intervening after this critical period. Although these interventions should be implemented widely, it is recognized that existing nutrition solutions, even if universally applied, would only avert a minority fraction of the estimated death and disability due to undernutrition. This paper reviews some of the knowledge and learning needed to close this “impact gap.” Five areas are prioritized for future research: 1) study healthy growth from a lifecycle perspective, because maternal, fetal, and newborn outcomes are connected; 2) understand why growth faltering begins so early in breast-fed infants in the developing world; 3) apply new tools and technologies to study long-recognized problems such as the interaction between nutrition and infection; 4) explore new hypotheses for understanding nutrient assimilation and use to discover and develop intervention leads; and 5) understand the role of the environment in healthy growth and the potential synergistic benefits of multi-sectoral interventions. Policymakers are urged to invest in nutrition-specific and -sensitive interventions to promote healthy growth from conception through the first 2 y of life because of their immediate and long-term health and development benefits.”

http://highwire.stanford.edu/cgi/medline/pmid;22516734

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