Obesity II: Establishing causal links between chemical exposures and obesity

Jerrold J Heindel; Sarah Howard; Keren Agay-Shay; Juan P Arrebola; Karine Audouze; Patrick J Babin; Robert Barouki; Amita Bansal; Etienne Blanc; Matthew C Cave; Saurabh Chatterjee; Nicolas Chevalier; Mahua Choudhury; David Collier; Lisa Connolly; Xavier Coumoul; Gabriella Garruti; Michael Gilbertson; Lori A Hoepner; Alison C Holloway; George Howell; Christopher Kassotis; Mathew K Kay; Min Ji Kim; Dominique Lagadic-Gossmann; Sophie Langouet; Antoine Legrand; Zhuorui Li; Helene Le Mentec; Lars Lind; P Monica Lind; Robert H Lustig; Corinne Martin-Chouly; Vesna Munic Kos; Normand Podechard; Troy A Roepke; Robert M Sargis; Anne Starling; Craig R Tomlinson; Charbel Touma; Jan Vondracek; Frederick Vom Saal; Bruce Blumberg

doi:10.1016/j.bcp.2022.115015

Obesity II: Establishing causal links between chemical exposures and obesity

Jerrold J Heindel, Sarah Howard, Keren Agay-Shay, Juan P Arrebola, Karine Audouze, Patrick J Babin, Robert Barouki, Amita Bansal, Etienne Blanc, Matthew C Cave, Saurabh Chatterjee, Nicolas Chevalier, Mahua Choudhury, David Collier, Lisa Connolly, Xavier Coumoul, Gabriella Garruti, Michael Gilbertson, Lori A Hoepner, Alison C HollowayGeorge Howell, Christopher Kassotis, Mathew K Kay, Min Ji Kim, Dominique Lagadic-Gossmann, Sophie Langouet, Antoine Legrand, Zhuorui Li, Helene Le Mentec, Lars Lind, P Monica Lind, Robert H Lustig, Corinne Martin-Chouly, Vesna Munic Kos, Normand Podechard, Troy A Roepke, Robert M Sargis, Anne Starling, Craig R Tomlinson, Charbel Touma, Jan Vondracek, Frederick Vom Saal, Bruce Blumberg

Research output: Contribution to journal › Article › peer-review

127 Citations (Scopus)

Abstract

Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity.

Original language	English
Article number	115015
Journal	Biochemical Pharmacology
Volume	199
Early online date	05 Apr 2022
DOIs	https://doi.org/10.1016/j.bcp.2022.115015
Publication status	Published - May 2022

Bibliographical note

Funding Information:
Jan Vondracek, Czech Science Foundation #21–00533s, Institute of Biophysics of the Czech Academy of Science, RVO-68081707, European Union Horizon 2020 Research and Innovation Program, Oberon #825712.

Publisher Copyright:
© 2022 Elsevier Inc.

Keywords

Adipocyte differentiation
Endocrine disruptor
Obesity
Obesogen
Weight gain

ASJC Scopus subject areas

General Biochemistry,Genetics and Molecular Biology
General Medicine
General Agricultural and Biological Sciences
Pharmacology, Toxicology and Pharmaceutics(all)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.bcp.2022.115015Licence: Unspecified

Cite this

Heindel, J. J., Howard, S., Agay-Shay, K., Arrebola, J. P., Audouze, K., Babin, P. J., Barouki, R., Bansal, A., Blanc, E., Cave, M. C., Chatterjee, S., Chevalier, N., Choudhury, M., Collier, D., Connolly, L., Coumoul, X., Garruti, G., Gilbertson, M., Hoepner, L. A., ... Blumberg, B. (2022). Obesity II: Establishing causal links between chemical exposures and obesity. Biochemical Pharmacology, 199, Article 115015. https://doi.org/10.1016/j.bcp.2022.115015

@article{281afd4b45b2451ca7b9706d73c026ea,

title = "Obesity II: Establishing causal links between chemical exposures and obesity",

abstract = "Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity. ",

keywords = "Adipocyte differentiation, Endocrine disruptor, Obesity, Obesogen, Weight gain",

author = "Heindel, {Jerrold J} and Sarah Howard and Keren Agay-Shay and Arrebola, {Juan P} and Karine Audouze and Babin, {Patrick J} and Robert Barouki and Amita Bansal and Etienne Blanc and Cave, {Matthew C} and Saurabh Chatterjee and Nicolas Chevalier and Mahua Choudhury and David Collier and Lisa Connolly and Xavier Coumoul and Gabriella Garruti and Michael Gilbertson and Hoepner, {Lori A} and Holloway, {Alison C} and George Howell and Christopher Kassotis and Kay, {Mathew K} and {Ji Kim}, Min and Dominique Lagadic-Gossmann and Sophie Langouet and Antoine Legrand and Zhuorui Li and {Le Mentec}, Helene and Lars Lind and {Monica Lind}, P and Lustig, {Robert H} and Corinne Martin-Chouly and {Munic Kos}, Vesna and Normand Podechard and Roepke, {Troy A} and Sargis, {Robert M} and Anne Starling and Tomlinson, {Craig R} and Charbel Touma and Jan Vondracek and {Vom Saal}, Frederick and Bruce Blumberg",

note = "Funding Information: Jan Vondracek, Czech Science Foundation #21–00533s, Institute of Biophysics of the Czech Academy of Science, RVO-68081707, European Union Horizon 2020 Research and Innovation Program, Oberon #825712. Publisher Copyright: {\textcopyright} 2022 Elsevier Inc.",

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language = "English",

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Heindel, JJ, Howard, S, Agay-Shay, K, Arrebola, JP, Audouze, K, Babin, PJ, Barouki, R, Bansal, A, Blanc, E, Cave, MC, Chatterjee, S, Chevalier, N, Choudhury, M, Collier, D, Connolly, L, Coumoul, X, Garruti, G, Gilbertson, M, Hoepner, LA, Holloway, AC, Howell, G, Kassotis, C, Kay, MK, Ji Kim, M, Lagadic-Gossmann, D, Langouet, S, Legrand, A, Li, Z, Le Mentec, H, Lind, L, Monica Lind, P, Lustig, RH, Martin-Chouly, C, Munic Kos, V, Podechard, N, Roepke, TA, Sargis, RM, Starling, A, Tomlinson, CR, Touma, C, Vondracek, J, Vom Saal, F & Blumberg, B 2022, 'Obesity II: Establishing causal links between chemical exposures and obesity', Biochemical Pharmacology, vol. 199, 115015. https://doi.org/10.1016/j.bcp.2022.115015

TY - JOUR

T1 - Obesity II: Establishing causal links between chemical exposures and obesity

AU - Heindel, Jerrold J

AU - Howard, Sarah

AU - Agay-Shay, Keren

AU - Arrebola, Juan P

AU - Audouze, Karine

AU - Babin, Patrick J

AU - Barouki, Robert

AU - Bansal, Amita

AU - Blanc, Etienne

AU - Cave, Matthew C

AU - Chatterjee, Saurabh

AU - Chevalier, Nicolas

AU - Choudhury, Mahua

AU - Collier, David

AU - Connolly, Lisa

AU - Coumoul, Xavier

AU - Garruti, Gabriella

AU - Gilbertson, Michael

AU - Hoepner, Lori A

AU - Holloway, Alison C

AU - Howell, George

AU - Kassotis, Christopher

AU - Kay, Mathew K

AU - Ji Kim, Min

AU - Lagadic-Gossmann, Dominique

AU - Langouet, Sophie

AU - Legrand, Antoine

AU - Li, Zhuorui

AU - Le Mentec, Helene

AU - Lind, Lars

AU - Monica Lind, P

AU - Lustig, Robert H

AU - Martin-Chouly, Corinne

AU - Munic Kos, Vesna

AU - Podechard, Normand

AU - Roepke, Troy A

AU - Sargis, Robert M

AU - Starling, Anne

AU - Tomlinson, Craig R

AU - Touma, Charbel

AU - Vondracek, Jan

AU - Vom Saal, Frederick

AU - Blumberg, Bruce

N1 - Funding Information: Jan Vondracek, Czech Science Foundation #21–00533s, Institute of Biophysics of the Czech Academy of Science, RVO-68081707, European Union Horizon 2020 Research and Innovation Program, Oberon #825712. Publisher Copyright: © 2022 Elsevier Inc.

PY - 2022/5

Y1 - 2022/5

N2 - Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity.

AB - Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity.

KW - Adipocyte differentiation

KW - Endocrine disruptor

KW - Obesity

KW - Obesogen

KW - Weight gain

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DO - 10.1016/j.bcp.2022.115015

M3 - Article

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SN - 0006-2952

VL - 199

JO - Biochemical Pharmacology

JF - Biochemical Pharmacology

M1 - 115015

ER -

Obesity II: Establishing causal links between chemical exposures and obesity

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

R6548GFS: PROTECTion against Endocrine Disruptors; Detection, mixtures, health effects, risk assessment and communication

Corrigendum to “Obesity II: Establishing causal links between chemical exposures and obesity” [Biochem. Pharmacol. 199 (2022) 115015] (Biochemical Pharmacology (2022) 199, (S0006295222001095), (10.1016/j.bcp.2022.115015))

Cite this

Obesity II: Establishing causal links between chemical exposures and obesity

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Projects

R6548GFS: PROTECTion against Endocrine Disruptors; Detection, mixtures, health effects, risk assessment and communication

Research output

Corrigendum to “Obesity II: Establishing causal links between chemical exposures and obesity” [Biochem. Pharmacol. 199 (2022) 115015] (Biochemical Pharmacology (2022) 199, (S0006295222001095), (10.1016/j.bcp.2022.115015))

Cite this