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Parenteral and Enteral Nutrition in Critical Illness
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Finally, there is the issue of the calories required by the gut to digest enteral nutrition. This is referred to as the thermic effect of food (TEF; also called diet-induced thermogenesis, DIT or specific dynamic action, SDA). In regular eating, this amounts to approximately 15% of the total daily energy expenditure or roughly 300 kcal in an average patient. The amount of energy expended in digesting enteral feedings depends on the complexity of the formula. For example, an elemental feeding would be expected to have a lower thermic effect of food (TEF) than polymeric.
Genetics of Energy Expenditure in Humans
Published in Claude Bouchard, The Genetics of Obesity, 2020
Claude Bouchard, Olivier Dériaz, Louis Pérusse, Angelo Tremblay
The thermic effect of food (TEF) is the integrated increase of energy expenditure after food ingestion. TEF is generally divided into an obligatory component, associated with the energy cost of nutrient storage, and a facultative component that has proven to be very difficult to investigate. To our knowledge, only one study has dealt with the heritability of TEF.3 In that study, energy expenditure was recorded during 4 h after a 1000-kcal carbohydrate meal in 21 pairs of DZ twins and 37 pairs of MZ twins as well as in 31 parent-offspring pairs. Correlations of 0.35, 0.52, and 0.30 in DZ, MZ, and parent-offspring pairs, respectively, were found for TEF. These results suggest a genetic effect of at least 30% and perhaps more for TEF. The biological significance of such a heritability level is highlighted by the fact that the standard deviation of TEF over 4 h in this study reached about 20 kcal, and the 95% confidence intervals were thus ±40 kcal or ±4% of the energy intake.
Ecological Risk Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Most dioxins, furans, and dioxin-like compounds lack individual screening benchmarks. However, the congener-specific dioxin and furan data can be consolidated into a single measure called the toxic equivalence (TEQ) of the sample. The TEQ is calculated by multiplying the concentrations of each congener or congener containing chlorine at the 2,3,7, and 8 positions in a sample by a toxicity equivalence factor (TEF) and summing those products. The TEF normalizes the toxicity of those congeners to the toxicity of the 2,3,7,8-TCDD congener, generally considered to be the most toxic of the dioxin, furan, and dioxin-like compounds. A great deal of effort by internationally known scientists have gone into developing the TEF scheme for dioxin-like chemicals.40,41 In effect, the TEQ indicates the concentration of 2,3,7,8-TCDD that would have the same toxicity as the mixture of dioxins and furans being evaluated. The TEFs used here reference the World Health Organization values for mammals, birds, and fish.42Figure 7.3 shows the structure of some PCDD/Fs.
Bringing together scientific disciplines for collaborative undertakings: a vision for advancing the adverse outcome pathway framework
Published in International Journal of Radiation Biology, 2021
Vinita Chauhan, Ruth C. Wilkins, Danielle Beaton, Magdalini Sachana, Nathalie Delrue, Carole Yauk, Jason O’Brien, Francesco Marchetti, Sabina Halappanavar, Michael Boyd, Daniel Villeneuve, Tara S. Barton-Maclaren, Bette Meek, Catalina Anghel, Crina Heghes, Chris Barber, Edward Perkins, Julie Leblanc, Julie Burtt, Holly Laakso, Dominique Laurier, Ted Lazo, Maurice Whelan, Russell Thomas, Donald Cool
Dr. Daniel Villeneuve, Toxicologist at US EPA discussed how incorporating reference stressors within the AOP framework could aid in the quantitative application. To date most of the evidence supporting AOPs has been qualitative, making it suitable for hazard identification but not for more quantitative aspects of effect characterization in support of risk assessment. A proposed approach to enhance quantitative application of AOPs is to identify ‘prototypical stressors’ for which concentration-response relationships or thresholds have been defined across multiple KEs. Employing many of the same assumptions as the toxic equivalency factor (TEF) approach widely used for the risk assessment of dioxin-like chemicals, response-response relationships that can be generalized across stressors can be derived. These can be used to aid quantitative extrapolation to downstream events along the pathway based on equivalent biological effect levels at one or more KEs along an AOP. While error and uncertainty associated with deviation from the TEF assumptions can be expected, the approach can utilize the more detailed toxicological characterization available for data-rich prototypical chemicals to estimate the likely responses to other stressor acting via the same pathways. Additionally, the approach is conceptually compatible with AOP network analyses, making it well suited for analysis of mixtures and multiple stressors whenever a biological response to the mixture can be measured at one or more KEs.
Levels of PCDDs/PCDFs in waste incineration ash of some Jordanian hospitals using GC/MS
Published in Toxin Reviews, 2021
Sharif Arar, Mahmoud A. Alawi, Nisreen E. Al-Mikhi
For risk assessment purposes due to variation of the PCDDs/Fs with their toxicity and degree of chlorination and occurrence in samples (Environment Australia 1999), the toxic equivalency of a mixture is defined by the sum of the concentrations of individual compounds (Ci) multiplied by their toxicity equivalence factor (TEF) with reference to the most toxic dioxin (2,3,7,8 TCDD) (TEF = 1), and n is the number of congeners with available TEF value (The International Toxicity Equivalency Factor (I-TEF) method of risk assessment) (Kutz et al.1990).
A systematic review on biomonitoring of individuals living near or working at solid waste incinerator plants
Published in Critical Reviews in Toxicology, 2019
Laura Campo, Petra Bechtold, Lucia Borsari, Silvia Fustinoni
PCDD/Fs and PCBs are included in the broad class of persistent organic pollutants (POPs), together with mono and polychlorophenols (MCP and PCP), hexachlorobenzene (HCB) and other chlorobenzenes, polybrominated diphenylethers (PBDE), and dichlorodiphenyldichloroethylene (DDE) (http://chm.pops.int). PCDD/Fs and PCBs contain several congeners (e.g. there are 209 PCBs). Exposure to POPs can be assessed by measuring their levels in blood, in breast milk, and in urine (the last limited to MCP and PCP). Given the complexity of dealing with so many chemicals at once, a simplified approach to assess the toxicity of these mixtures has been developed. This is based on the identification of an indices of relative toxicity (TEF) for each dioxin and dioxin-like PCBs, taking 2,3,7,8-tetrachlorodibenzo p-dioxin as reference; the toxic equivalency of a mixture (TEQ) is calculated as the sum of the concentrations of individual compounds multiplied by their TEF (Van den Berg et al. 2006). The concern regarding POPs has been associated with both their long life and their biomagnification in the environment and to several different toxic effects, among which carcinogenicity. The International Agency for Research on Cancer (IARC) has classified both 2,3,7,8-tetrachlorodibenzo p-dioxin and PCBs as group 1 carcinogens (carcinogenic to human) (IARC 2012, 2016). PCDD/Fs and PCBs were studied in association with SWI exposure in some large population studies in Flanders, France, Spain, Japan, South Korea, and North Taiwan (Kitamura et al. 2001; Tajimi et al. 2005; Chen, Su, and Lee 2006; Huang et al. 2007; Frery et al. 2007a, 2007b; Schroijen et al. 2008; Zubero et al. 2011, 2017; Park et al. 2014), and in several occupational studies (Angerer et al. 1992; Wrbitzky et al. 1996; Kitamura et al. 2000; Hu et al. 2004; Yoshida et al. 2006; Mari et al. 2013).