written by Sarah Howard
Coordinator of the Diabetes-Obesity Working Group
Two worldwide gatherings of experts have published consensus statements on the role of environmental chemicals in diabetes, obesity, and metabolism:
- Parma Consensus Statement on Metabolic Disruptors, Heindel et al. Environmental Health. 2015 Jun 20;14:54.
- Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic, Lind et al. Environmental Health Perspectives. 2016 May 1;124(5):A81-3.
The Parma Statement was based on a workshop held in Parma, Italy, in May 2014, and the Uppsala Statement was based on a workshop held in Uppsala, Sweden, in October 2015.
Both focus on guiding future scientific research in the field, but also contain recommendations for policy makers, health care providers, and other professionals. Both call for reducing environmental chemical exposures, especially in early life, to help prevent the development of metabolic problems later in life.
The sections below are direct quotes of some of the conclusions and recommendations from the Statements (the full text of both statements are available for free at the links above):
From the Parma Consensus Statement on Metabolic Disruptors
The Parma workshop helped to focus this emerging field by developing an overarching hypothesis for the role of environmental chemicals in the current worldwide epidemics of obesity, diabetes and related metabolic diseases. …The objective is both to indicate the strength of the current data and to provide a roadmap for further studies. A coherent, enhanced research agenda will help identify strategies to prevent metabolic diseases through actions that can be taken by individuals as well as public health agencies. History shows that prevention is always the best strategy. Increased understanding of the importance of the metabolic disruptor hypothesis to the epidemics of obesity and metabolic syndrome offers the potential for these diseases to be mitigated by modifying exposures, thereby creating a healthier environment for future generations.
Existing data lead us to predict that:
- The effects of metabolic disruptors may be difficult to detect at the individual level due to human genomic variability creating a heterogeneous population requiring a genomic and statistical approach.
- Some effects of metabolic disruptors may be transgenerational, requiring a multigenerational approach: a minimum of two generations for paternal line effects and three generations for maternal line effects.
- Effects of metabolic disruptors will likely be dependent on the dose and route of exposure and may exhibit non-monotonic dose responses; this will require dose response studies and a pharmacokinetic approach.
- We should expect effects to be due to multiple chemicals with varying half-lives, metabolism, persistence, tissue accumulation and target sensitivities; complete analysis will require a mixtures approach.
- Certain metabolic disruptors will have specific actions, causing only obesity, diabetes or altered liver function whereas others will affect many aspects of metabolism leading to metabolic syndrome.
- We are underestimating the importance of metabolic disruptors in obesity, diabetes, and metabolic syndrome because current research designs focus on studying one or a small subset of chemicals at a time, during limited windows of sensitivity, in single tissues (including only one adipose tissue) and often only endpoints related to a single disease outcome per study.
- Reducing exposures to environmental chemicals and improving nutrition during development offers the possibility of preventing obesity and metabolic diseases.
- The totality of environmental effects on obesity (drugs, chemicals, stress and nutrition) will likely be greater than the effects of genetic predisposition.”
From the Uppsala Consensus Statement on Environmental Contaminants and the Global Obesity Epidemic
In conclusion, since there are now numerous animal and epidemiological studies indicating that environmental pollutants could contribute to the global obesity epidemic, there is an urgent need to reduce the burden of environmental contaminants so that obesity does not become the normal outlook in the future. The workshop attendees concluded that public health efforts should focus on the importance of early obesity prevention by means of reducing chemical exposures, rather than only treating the established disease. Just as a bad start can last a lifetime and beyond, a good start can last a lifetime as well.
Recommendations for an Action Plan
Based on results discussed at the workshop, the authors suggested several actions that should be taken to restrict the potentially harmful effects of environmental contaminants on metabolism:
- Increase research initiatives and funding to further explore mechanisms associated with chemical obesogen-induced metabolic disruptions, to examine mixtures, and to use exposure levels relevant to those encountered by human populations.
- Educate physicians and other health care professionals regarding the effects of environmental contaminants on metabolism to increase the awareness of this problem, and how they could guide their patients, as well as the general population, to limit their exposure to these contaminants.
- Ensure that knowledge of obesogenic environmental chemicals is incorporated into regulatory and policy making.
- Demand that new chemicals that are to be released onto the market are tested in an appropriate fashion regarding their effects on metabolism.
- Demand that all chemicals included in consumer products are disclosed in order to increase public awareness of their use and to provide individuals with the information they need to avoid exposures.
- Find additional ways to increase public awareness about factors beyond caloric balance that are involved in obesity development, including the role of some environmental contaminants.
- Increase awareness about the potential of these exposures to generate effects in future generations. This action item should also include education on how to avoid exposure to these contaminants.