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  1. Article ; Online: Obesogens: a unifying theory for the global rise in obesity.

    Heindel, Jerrold J / Lustig, Robert H / Howard, Sarah / Corkey, Barbara E

    International journal of obesity (2005)

    2024  Volume 48, Issue 4, Page(s) 449–460

    Abstract: Despite varied treatment, mitigation, and prevention efforts, the global prevalence and severity of obesity continue to worsen. Here we propose a combined model of obesity, a unifying paradigm that links four general models: the energy balance model (EBM) ...

    Abstract Despite varied treatment, mitigation, and prevention efforts, the global prevalence and severity of obesity continue to worsen. Here we propose a combined model of obesity, a unifying paradigm that links four general models: the energy balance model (EBM), based on calories as the driver of weight gain; the carbohydrate-insulin model (CIM), based on insulin as a driver of energy storage; the oxidation-reduction model (REDOX), based on reactive oxygen species (ROS) as a driver of altered metabolic signaling; and the obesogens model (OBS), which proposes that environmental chemicals interfere with hormonal signaling leading to adiposity. We propose a combined OBS/REDOX model in which environmental chemicals (in air, food, food packaging, and household products) generate false autocrine and endocrine metabolic signals, including ROS, that subvert standard regulatory energy mechanisms, increase basal and stimulated insulin secretion, disrupt energy efficiency, and influence appetite and energy expenditure leading to weight gain. This combined model incorporates the data supporting the EBM and CIM models, thus creating one integrated model that covers significant aspects of all the mechanisms potentially contributing to the obesity pandemic. Importantly, the OBS/REDOX model provides a rationale and approach for future preventative efforts based on environmental chemical exposure reduction.
    MeSH term(s) Humans ; Reactive Oxygen Species ; Obesity/epidemiology ; Environmental Exposure ; Weight Gain ; Energy Metabolism ; Insulin
    Chemical Substances Reactive Oxygen Species ; Insulin
    Language English
    Publishing date 2024-01-11
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 752409-2
    ISSN 1476-5497 ; 0307-0565
    ISSN (online) 1476-5497
    ISSN 0307-0565
    DOI 10.1038/s41366-024-01460-3
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  2. Article: History of the Obesogen Field: Looking Back to Look Forward.

    Heindel, Jerrold J

    Frontiers in endocrinology

    2019  Volume 10, Page(s) 14

    Abstract: The Obesogen field developed from two separate scientific research areas, endocrine disruptors and the Developmental Origins of Health and Disease (DOHaD). Endocrine Disrupting Chemicals (EDCs) are exogenous chemicals or mixtures of chemicals that ... ...

    Abstract The Obesogen field developed from two separate scientific research areas, endocrine disruptors and the Developmental Origins of Health and Disease (DOHaD). Endocrine Disrupting Chemicals (EDCs) are exogenous chemicals or mixtures of chemicals that interfere with the action of hormones. Exposure to EDCs during early development (DOHaD) has been shown to increase susceptibility to a variety of diseases including infertility, asthma, breast and prostate cancer, early puberty, susceptibility to infections, heart disease, autoimmune disease, and attention deficit hyperactivity disorder/learning disability. The effects of EDCs on obesity and fat cell development first gained attention around the turn of the twenty-first century. In 2002 Dr. Paula Baillie-Hamilton wrote the first review article focusing on environmental chemicals and obesity. She suggested that the obesity epidemic correlated with the increased production of chemicals after World War II. Baillie-Hamilton identified studies showing that exposures to a variety of chemicals led to weight gain. Shortly after that a commentary on an article showing that nonylphenol would increase fat cell differentiation
    Language English
    Publishing date 2019-01-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2019.00014
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  3. Article ; Online: The developmental basis of disease: Update on environmental exposures and animal models.

    Heindel, Jerrold J

    Basic & clinical pharmacology & toxicology

    2018  Volume 125 Suppl 3, Page(s) 5–13

    Abstract: At the Prenatal Programming and Toxicity (PPTox) Conference I in 2008, I presented an overview of the developmental origins of health and disease field focusing on environmental chemical exposures and disease outcomes. At that time, I noted that the ... ...

    Abstract At the Prenatal Programming and Toxicity (PPTox) Conference I in 2008, I presented an overview of the developmental origins of health and disease field focusing on environmental chemical exposures and disease outcomes. At that time, I noted that the field was getting off the ground with a focus on developmental exposure to a small number of endocrine disrupting chemicals (EDCs) and disease outcomes across the lifespan in animal models. In this update, I note that the DOHaD field has changed significantly over the last decade. There are new windows of susceptibility including preconception, prepuberty, a focus on the mother and not just the offspring, and a significant focus on the new field of epigenetic transgenerational inheritance. New disease focus areas have sprung up including obesity, type 2 diabetes and fatty liver disease, all with a connection to developmental exposures to EDCs. There is also a focus on the study of new EDCs, molecular mechanisms, the development of new biomarkers of exposure and disease outcomes and studies focusing on intervention and prevention studies.
    MeSH term(s) Animals ; Congresses as Topic ; Diabetes Mellitus, Type 2/chemically induced ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/prevention & control ; Disease Models, Animal ; Embryonic Development/drug effects ; Endocrine Disruptors/toxicity ; Environmental Exposure/adverse effects ; Environmental Monitoring/legislation & jurisprudence ; Environmental Monitoring/standards ; Environmental Pollutants/toxicity ; Epigenesis, Genetic/drug effects ; Fatty Liver/chemically induced ; Fatty Liver/prevention & control ; Female ; Fetal Development/drug effects ; Genetic Predisposition to Disease ; Humans ; Inheritance Patterns ; Maternal Exposure/adverse effects ; Obesity/chemically induced ; Obesity/genetics ; Obesity/prevention & control ; Pregnancy ; Prenatal Exposure Delayed Effects/chemically induced ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/prevention & control
    Chemical Substances Endocrine Disruptors ; Environmental Pollutants
    Language English
    Publishing date 2018-09-28
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2134679-3
    ISSN 1742-7843 ; 1742-7835
    ISSN (online) 1742-7843
    ISSN 1742-7835
    DOI 10.1111/bcpt.13118
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  4. Book ; Conference proceedings: Linking environmental agents to autoimmune diseases

    Heindel, Jerrold J.

    monograph based on papers developed from the Workshop on Linking Environmental Agents to Autoimmune Diseases held 1 - 3 September 1998 in Research Triangle Park, North Carolina

    (Environmental health perspectives ; 107, Suppl. 5 ; NIH publication ; 99-218)

    1999  

    Event/congress Workshop on Linking Environmental Agents to Autoimmune Diseases (1998, ResearchTriangleParkNC)
    Author's details ed. by Jerrold J. Heindel
    Series title Environmental health perspectives ; 107, Suppl. 5
    NIH publication ; 99-218
    Collection
    Language English
    Size S. 659 - 820 : Ill., graph. Darst.
    Publisher Public Health Service, US
    Publishing place Research Triangle Park, NC
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT011140595
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    Zs B 1360 -107,Suppl.5- verfügbar in Königswinter Königswinter

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  5. Article ; Online: A special Issue on the environment and Developmental Origins of Health and Diseases.

    Heindel, Jerrold J

    Reproductive toxicology (Elmsford, N.Y.)

    2016  Volume 68, Page(s) 1–2

    MeSH term(s) Animals ; Environment ; Environmental Pollutants/toxicity ; Female ; Gene Expression Regulation, Developmental ; Humans ; Maternal-Fetal Exchange ; Metabolic Diseases ; Pregnancy ; Prenatal Exposure Delayed Effects ; Prenatal Nutritional Physiological Phenomena
    Chemical Substances Environmental Pollutants
    Language English
    Publishing date 2016-11-05
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 639342-1
    ISSN 1873-1708 ; 0890-6238
    ISSN (online) 1873-1708
    ISSN 0890-6238
    DOI 10.1016/j.reprotox.2016.11.003
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  6. Article ; Online: Do Environmental Chemicals Make Us Fat?

    Zoeller, R Thomas / Heindel, Jerrold J

    Endocrinology

    2017  Volume 158, Issue 10, Page(s) 3086–3087

    Language English
    Publishing date 2017-10-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2017-00715
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  7. Book: Female reproductive toxicology

    Heindel, Jerrold J.

    (Methods in toxicology ; 3B)

    1993  

    Author's details ed. by Jerrold J. Heindel
    Series title Methods in toxicology ; 3B
    Collection
    Keywords Ovum ; Reproduction ; Genitalia, Female / chemistry ; Genitalia, Female / cytology ; Toxicology / methods
    Language English
    Size XI, 404 S. : Ill., graph. Darst.
    Publisher Acad. Press
    Publishing place San Diego u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT006371340
    ISBN 0-12-461209-1 ; 0124612105 ; 978-0-12-461209-9 ; 9780124612105
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1994 A 3657 on loan 0 Vormerkungen

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  8. Article ; Online: Environmental Obesogens: Mechanisms and Controversies.

    Heindel, Jerrold J / Blumberg, Bruce

    Annual review of pharmacology and toxicology

    2018  Volume 59, Page(s) 89–106

    Abstract: Obesity is a worldwide pandemic in adults as well as children and adds greatly to health care costs through its association with type 2 diabetes, metabolic syndrome, cardiovascular disease, and cancers. The prevailing medical view of obesity is that it ... ...

    Abstract Obesity is a worldwide pandemic in adults as well as children and adds greatly to health care costs through its association with type 2 diabetes, metabolic syndrome, cardiovascular disease, and cancers. The prevailing medical view of obesity is that it results from a simple imbalance between caloric intake and energy expenditure. However, numerous other factors are important in the etiology of obesity. The obesogen hypothesis proposes that environmental chemicals termed obesogens promote obesity by acting to increase adipocyte commitment, differentiation, and size by altering metabolic set points or altering the hormonal regulation of appetite and satiety. Many obesogens are endocrine disrupting chemicals that interfere with normal endocrine regulation. Endocrine disrupting obesogens are abundant in our environment, used in everyday products from food packaging to fungicides. In this review, we explore the evidence supporting the obesogen hypothesis, as well as the gaps in our knowledge that are currently preventing a complete understanding of the extent to which obesogens contribute to the obesity pandemic.
    MeSH term(s) Animals ; Endocrine Disruptors/adverse effects ; Energy Metabolism/physiology ; Environmental Exposure/adverse effects ; Humans ; Obesity/etiology
    Chemical Substances Endocrine Disruptors
    Language English
    Publishing date 2018-07-25
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 196587-6
    ISSN 1545-4304 ; 0362-1642
    ISSN (online) 1545-4304
    ISSN 0362-1642
    DOI 10.1146/annurev-pharmtox-010818-021304
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  9. Article: Interventions to Address Environmental Metabolism-Disrupting Chemicals: Changing the Narrative to Empower Action to Restore Metabolic Health.

    Sargis, Robert M / Heindel, Jerrold J / Padmanabhan, Vasantha

    Frontiers in endocrinology

    2019  Volume 10, Page(s) 33

    Abstract: Metabolic disease rates have increased dramatically over the last four decades. Classic understanding of metabolic physiology has attributed these global trends to decreased physical activity and caloric excess; however, these traditional risk factors ... ...

    Abstract Metabolic disease rates have increased dramatically over the last four decades. Classic understanding of metabolic physiology has attributed these global trends to decreased physical activity and caloric excess; however, these traditional risk factors insufficiently explain the magnitude and rapidity of metabolic health deterioration. Recently, the novel contribution of environmental metabolism-disrupting chemicals (MDCs) to various metabolic diseases (including obesity, diabetes, and non-alcoholic fatty liver disease) is becoming recognized. As this burgeoning body of evidence has matured, various organic and inorganic pollutants of human and natural origin have emerged as metabolic disease risk factors based on population-level and experimental data. Recognition of these heretofore underappreciated metabolic stressors now mandates that efforts to mitigate the devastating consequences of metabolic disease include dedicated efforts to address environmental drivers of disease risk; however, there have not been adequate recommendations to reduce exposures or to mitigate the effects of exposures on disease outcomes. To address this knowledge gap and advance the clinical translation of MDC science, herein discussed are behaviors that increase exposures to MDCs, interventional studies to reduce those exposures, and small-scale clinical trials to reduce the body burden of MDCs. Also, we discuss evidence from cell-based and animal studies that provide insights into MDC mechanisms of action, the influence of modifiable dietary factors on MDC toxicity, and factors that modulate MDC transplacental carriage as well as their impact on metabolic homeostasis. A particular emphasis of this discussion is on critical developmental windows during which short-term MDC exposure can elicit long-term disruptions in metabolic health with potential inter- and transgenerational effects. While data gaps remain and further studies are needed, the current state of evidence regarding interventions to address MDC exposures illuminates approaches to address environmental drivers of metabolic disease risk. It is now incumbent on clinicians and public health agencies to incorporate this knowledge into comprehensive strategies to address the metabolic disease pandemic.
    Language English
    Publishing date 2019-02-04
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2019.00033
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  10. Article ; Online: European Medicines Agency Conflicts With the European Food Safety Authority (EFSA) on Bisphenol A Regulation.

    Zoeller, R Thomas / Birnbaum, Linda S / Collins, Terrence J / Heindel, Jerrold / Hunt, Patricia A / Iguchi, Taisen / Kortenkamp, Andreas / Myers, John Peterson / Vom Saal, Frederick S / Sonnenschein, Carlos / Soto, Ana M

    Journal of the Endocrine Society

    2023  Volume 7, Issue 9, Page(s) bvad107

    Abstract: The European Food Safety Authority (EFSA) has revised their estimate of the toxicity of bisphenol A (BPA) and, as a result, have recommended reducing the tolerable daily intake (TDI) by 20 000-fold. This would essentially ban the use of BPA in food ... ...

    Abstract The European Food Safety Authority (EFSA) has revised their estimate of the toxicity of bisphenol A (BPA) and, as a result, have recommended reducing the tolerable daily intake (TDI) by 20 000-fold. This would essentially ban the use of BPA in food packaging such as can liners, plastic food containers, and in consumer products. To come to this conclusion, EFSA used a systematic approach according to a pre-established protocol and included all guideline and nonguideline studies in their analysis. They found that Th-17 immune cells increased with very low exposure to BPA and used this endpoint to revise the TDI to be human health protective. A number of regulatory agencies including the European Medicines Agency (EMA) have written formal disagreements with several elements of EFSA's proposal. The European Commission will now decide whether to accept EFSA's recommendation over the objections of EMA. If the Commission accepts EFSA's recommendation, it will be a landmark action using knowledge acquired through independent scientific studies focused on biomarkers of chronic disease to protect human health. The goal of this Perspective is to clearly articulate the monumental nature of this debate and decision and to explain what is at stake. Our perspective is that the weight of evidence clearly supports EFSA's proposal to reduce the TDI by 20 000-fold.
    Language English
    Publishing date 2023-08-12
    Publishing country United States
    Document type Journal Article
    ISSN 2472-1972
    ISSN (online) 2472-1972
    DOI 10.1210/jendso/bvad107
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