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

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

Developmental contributions to macronutrient selection: A randomized controlled trial in adult survivors of malnutrition

Background and objectives: Birthweight differences between kwashiorkor and marasmus suggest that intrauterine factors influence the development of these syndromes of malnutrition and may modulate risk of obesity through dietary intake. We tested the hypotheses that the target protein intake in adulthood is associated with birthweight, and that protein leveraging to maintain this target protein intake would influence energy intake (EI) and body weight in adult survivors of malnutrition.Methodology: Sixty-three adult survivors of marasmus and kwashiorkor could freely compose a diet from foods containing 10, 15 and 25 percentage energy from protein (percentage of energy derived from protein (PEP); Phase 1) for 3 days. Participants were then randomized in Phase 2 (5 days) to diets with PEP fixed at 10%, 15% or 25%.Results: Self-selected PEP was similar in both groups. In the groups combined, selected PEP was 14.7, which differed significantly (P < 0.0001) from the null expectation (16.7%) of no selection. Self-selected PEP was inversely related to birthweight, the effect disappearing after adjusting for sex and current body weight. In Phase 2, PEP correlated inversely with EI (P = 0.002) and weight change from Phase 1 to 2 (P = 0.002). Protein intake increased with increasing PEP, but to a lesser extent than energy increased with decreasing PEP.Conclusions and implications: Macronutrient intakes were not independently related to birthweight or diagnosis. In a free-choice situation (Phase 1), subjects selected a dietary PEP significantly lower than random. Lower PEP diets induce increased energy and decreased protein intake, and are associated with weight gain

Faster rehabilitation weight gain is associated with liver fat in adult survivors of childhood severe acute malnutrition

Background Nutritional rehabilitation during severe acute malnutrition (SAM) aims to quickly restore a healthy body weight, but rapid weight gain has been associated with later cardiovascular risk. We hypothesized that faster weight gain during SAM rehabilitation and post-hospitalization is associated with liver fat in adult survivors. Method Jamaican adult survivors of childhood SAM underwent abdominal CT scan to estimate liver fat as mean liver attenuation (MLA) and liver spleen ratio (L/S). Birth weight (BW) and anthropometry measured during, and post-hospitalization were abstracted from admission records. Results We studied 42 marasmus survivors (MRs) and 40 kwashiorkor survivors (KWs). MRs had a lower mean BW (SD) 2.5 (0.8) vs 3.0 (0.7) kg; p=0.01) and were more wasted (p<0.001) and stunted (p=0.03) than KWs on admission to hospital. MRs and KWs had similar rates of rehabilitation weight gain, which was inversely associated with MLA among all survivors of SM (r=-0.246, p=0.029), but only in MRs when assessed by diagnosis (r= -0.449, p=0.004). The association between rehabilitation weight gain and adult liver fat in MRs was not altered by BW, admission wasting or stunting. In KWs, post-hospitalization height gain was inversely associated with MLA (difference = -0.64, 95%CI: -0.64 to -0.13; p=0.006). Conclusions Faster rehabilitation weight gain is associated with liver fat in adult survivors of childhood severe acute malnutrition. The finding that BW did not influence these outcomes may reflect the timing of the nutritional insult in utero. Target weight gain during nutritional rehabilitation may need to be lowered to optimize long-term outcomes in these children

Diet and kwashiorkor: a prospective study from rural DR Congo

The etiology of kwashiorkor remains enigmatic and longitudinal studies examining potential causes of kwashiorkor are scarce. Using historical, longitudinal study data from the rural area of Bwamanda, Democratic Republic of Congo, we investigated the potential causal association between diet and the development of kwashiorkor in 5 657 preschool children followed 3-monthly during 15 months. We compared dietary risk factors for kwashiorkor with those of marasmus. Kwashiorkor was diagnosed as pitting oedema of the ankles; marasmus as abnormal visibility of skeletal structures and palpable wasting of the gluteus muscle. A 24-h recall was administered 3-monthly to record the consumption of the 41 locally most frequent food items. We specified Hanley–Miettinen smooth-in-time risk models containing potential causal factors, including food items, special meals prepared for the child, breastfeeding, disease status, nutritional status, birth rank, age, season and number of meals. Bayesian Information Criteria identified the most plausible causal model of why some children developed kwashiorkor. In a descriptive analysis of the diet at the last dietary assessment prior to development of kwashiorkor, the diet of children who developed kwashiorkor was characterized by low consumption of sweet potatoes, papaya and “other vegetables” [0.0% , 2.3% (95% CI [0.4, 12.1]) and 2.3% (95% CI [0.4, 12.1])] in comparison with children who did not develop kwashiorkor [6.8% (95% CI [6.4, 7.2]), 15.5% (95% CI [15, 16.1]) and 15.1% (95% CI [14.6, 15.7])] or children who developed marasmus [4.5% (95% CI [2.6, 7.5]) 11.8% (95% CI [8.5, 16.0]) and 17.6% (95% CI [13.7, 22.5])]. Sweet potatoes and papayas have high β-carotene content and so may some of “the other vegetables”. We found that a risk model containing an age function, length/height-for age Z-score, consumption of sweet potatoes, papaya or other vegetables, duration of this consumption and its interaction term, was the most plausible model. Among children aged 10–42 months, the risk of developing kwashiorkor increased with longer non-consumption of these foods. The analysis was repeated with only children who developed marasmus as the reference series, yielding similar results. Our study supports that β-carotene may play an important role in the protection against kwashiorkor development

Effects of Protein Deficiency on Perinatal and Postnatal Health Outcomes

There are a variety of environmental insults that can occur during pregnancy which cause low birth weight and poor fetal health outcomes. One such insult is maternal malnutrition, which can be further narrowed down to a low protein diet during gestation. Studies show that perinatal protein deficiencies can impair proper organ growth and development, leading to long-term metabolic dysfunction. Understanding the molecular mechanisms that underlie how this deficiency leads to adverse developmental outcomes is essential for establishing better therapeuticstrategies that may alleviate or prevent diseases in later life. This chapter reviews how perinatal protein restriction in humans and animals leads to metabolic disease, and it identifies the mechanisms that have been elucidated, to date. These include alterations in transcriptional and epigenetic mechanisms, as well as indirect means such as endoplasmic reticulum (ER) stress and oxidative stress. Furthermore, nutritional and pharmaceutical interventions are highlighted to illustrate that the plasticity of the underdeveloped organs during perinatal life can be exploited to prevent onset of long-term metabolic disease

EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA); Scientific Opinion on Dietary reference values for water

This Opinion of the EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA) deals with the setting of dietary reference values for water for specific age groups. Adequate Intakes (AI) have been defined derived from a combination of observed intakes in population groups with desirable osmolarity values of urine and desirable water volumes per energy unit consumed. The reference values for total water intake include water from drinking water, beverages of all kind, and from food moisture and only apply to conditions of moderate environmental temperature and moderate physical activity levels (PAL 1.6). AIs for infants in the first half of the first year of life are estimated to be 100-190 mL/kg per day. For infants 6-12 months of age a total water intake of 800-1000 mL/day is considered adequate. For the second year of life an adequate total water intake of 1100-1200 mL/day is defined by interpolation, as intake data are not available. AIs of water for children are estimated to be 1300 mL/day for boys and girls 2-3 years of age; 1600 mL/day for boys and girls 4-8 years of age; 2100 mL/day for boys 9-13 years of age; 1900 mL/day for girls 9-13 years of age. Adolescents of 14 years and older are considered as adults with respect to adequate water intake. Available data for adults permit the definition of AIs as 2.0 L/day (P 95 3.1 L) for females and 2.5 L/day (P95 4.0 L) for males. The same AIs as for adults are defined for the elderly. For pregnant women the same water intake as in non-pregnant women plus an increase in proportion to the increase in energy intake (300 mL/day) is proposed. For lactating women adequate water intakes of about 700 mL/day above the AIs of non-lactating women of the same age are derive