24 research outputs found

    Accounting for nutrition-related health impacts in food life cycle assessment: insights from an expert workshop

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    \ua9 The Author(s) 2024.Sub-optimal dietary patterns make major contributions to the Global Burden of Disease and are among the most pressing issues affecting human health. Consequently, they are key to consider when assessing the human health and other environmental impacts of foods and diets within life cycle assessments. The UN Environment Life Cycle Initiative convened a task force on nutrition-related human health impacts as part of the Global Life Cycle Impact Assessment Method (GLAM) project. The health impacts of dietary patterns can be expressed in disability-adjusted life years (DALYs), in line with reporting human health impacts of other impact categories within the life cycle impact assessment (LCIA) framework. The task force held a workshop with nutrition experts to receive guidance in its process to develop a consensus-based impact assessment framework for addressing nutrition-related health impacts in LCIA. The workshop aimed to (1) evaluate the general assessment framework, (2) discuss scientific questions for quantifying human health impacts from nutrition for food items and diets, and (3) provide initial guidance for further development. The proposed framework based on the Global Burden of Disease (GBD) risk ratios was regarded as a good starting point to assess the relative health risks of the general population, provided that the dietary context is considered and several limitations, such as incomplete disease coverage, are acknowledged. The experts advised against a potentially misleading use of adult-derived dietary risk factors for children. To improve global coverage of the GLAM framework, it is important to consider a wider range of dietary patterns. The experts also recommended using a metric complementary to DALYs, such as nutrient adequacy, also considering, e.g., vitamin A and iron, to complement the assessment

    Clinical practice: Protein-losing enteropathy in children

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    Protein-losing enteropathy (PLE) is a rare complication of a variety of intestinal disorders characterized by an excessive loss of proteins into the gastrointestinal tract due to impaired integrity of the mucosa. The clinical presentation of patients with PLE is highly variable, depending upon the underlying cause, but mainly consists of edema due to hypoproteinemia. While considering PLE, other causes of hypoproteinemia such as malnutrition, impaired synthesis, or protein loss through other organs like the kidney, liver, or skin, have to be excluded. The disorders causing PLE can be divided into those due to protein loss from intestinal lymphatics, like primary intestinal lymphangiectasia or congenital heart disease and those with protein loss due to an inflamed or abnormal mucosal surface. The diagnosis is confirmed by increased fecal concentrations of alpha-1-antitrypsin. After PLE is diagnosed, the underlying cause should be identified by stool cultures, serologic evaluation, cardiac screening, or radiographic imaging. Treatment of PLE consists of nutrition state maintenance by using a high protein diet with supplement of fat-soluble vitamins. In patients with lymphangiectasia, a low fat with medium chain triglycerides (MCT) diet should be prescribed. Besides dietary adjustments, appropriate treatment for the underlying etiology is necessary and supportive care to avoid complications of edema. PLE is a rare complication of various diseases, mostly gastrointestinal or cardiac conditions that result into loss of proteins in the gastrointestinal tract. Prognosis depends upon the severity and treatment options of the underlying disease

    Adult Body Weight Is Programmed by a Redox-Regulated and Energy-Dependent Process during the Pronuclear Stage in Mouse

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    In mammals fertilization triggers a series of Ca2+ oscillations that not only are essential for events of egg activation but also stimulate oxidative phosphorylation. Little is known, however, about the relationship between quantitative changes in egg metabolism and specific long-term effects in offspring. This study assessed whether post-natal growth is modulated by early transient changes in NAD(P)H and FAD2+ in zygotes. We report that experimentally manipulating the redox potential of fertilized eggs during the pronuclear (PN) stage affects post-natal body weight. Exogenous pyruvate induces NAD(P)H oxidation and stimulates mitochondrial activity with resulting offspring that are persistently and significantly smaller than controls. Exogenous lactate stimulates NAD+ reduction and impairs mitochondrial activity, and produces offspring that are smaller than controls at weaning but catch up after weaning. Cytosolic alkalization increases NAD(P)+ reduction and offspring of normal birth-weight become significantly and persistently larger than controls. These results constitute the first report that post-natal growth rate is ultimately linked to modulation of NAD(P)H and FAD2+ concentration as early as the PN stage
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