The discovery of a form of chronic, low-grade systemic inflammation (“metaflammation”) linked with obesity, but also associated with several lifestyle-related behaviours not necessarily causing obesity, suggests a re-consideration of obesity as a direct cause of chronic disease and a search for the main drivers—or cause of causes. Factors contributing to this are considered here within an environmental context, leading to the conclusion that humans have an immune reaction to aspects of the modern techno-industrial environment, to which they have not fully adapted. It is suggested that economic growth—beyond a point—leads to increases in chronic diseases and climate change and that obesity is a signal of these problems. This is supported by data from Sweden over 200 years, as well as “natural” experiments in disrupted economies like Cuba and Nauru, which have shown a positive health effect with economic downturns. The effect is reflected both in human health and environmental problems such as climate change, thus pointing to the need for greater cross-disciplinary communication and a concept shift in thinking on prevention if economic growth is to continue to benefit human health and well-being. 1. Introduction Obesity is currently pandemic, as are many of the chronic diseases often associated with this (e.g., type 2 diabetes) [1]. However, attributing the rise in chronic diseases to obesity does little to explain the true aetiology of the problem—the “cause of the causes” [2], which lies in more distal determining factors. This is indicated by recent findings that suggest a more complicated aetiological role for obesity than just a simple weight-disease association. The discovery of a form of low-grade systemic inflammation associated with obesity [3], as well as with other lifestyle and environmental factors (e.g., aspects of nutrition, inactivity, inadequate sleep, stress, depression, excessive alcohol intake, smoking, etc. [4, 5]) only some of which are linked to obesity, suggests that obesity may be just a marker of a type of environment and accompanying human lifestyle, which is mediated by aspects of the modern industrial environment to which humans have had little time to adapt. Furthermore, it has been shown, using the metaphor of inflammation, that this environment, is a driver not just of biological, but of ecological “disease,” manifest in excessive greenhouse gas emissions and potential climate change, as well as obesity and chronic disease [6]. In the current paper, which is proposed as a forum for a broader discussion in prevention, this
References
[1]
J. Proietto, “Obesity and disease: insulin resistance, diabetes, metabolic syndrome and polycystic ovary syndrome,” in Clinical Obesity, P. G. Kopelman, I. D. Caterson, and W. H. Dietz, Eds., Blackwell Publishing, Oxford, UK, 2nd edition, 2005.
[2]
G. Rose, The Strategy of Preventive Medicine, Oxford University Press,, New York, NY, USA, 1992.
[3]
G. S. Hotamisligil, N. S. Shargill, and B. M. Spiegelman, “Adipose expression of tumor necrosis factor-α: direct role in obesity-linked insulin resistance,” Science, vol. 259, no. 5091, pp. 87–91, 1993.
[4]
G. Egger and J. Dixon, “Should obesity be the main game? or do we need an environmental makeover to combat the inflammatory and chronic disease epidemics?” Obesity Reviews, vol. 10, no. 2, pp. 237–249, 2009.
[5]
M. -F. O'Connor and M. R. Irwin, “Links between behavioral factors and inflammation,” Clinical Pharmacology and Therapeutics, vol. 87, no. 4, pp. 479–482, 2010.
[6]
G. Egger, “Dousing our inflammatory environment(s): is personal carbon trading an option for reducing obesity—and climate change?” Obesity Reviews, vol. 9, no. 5, pp. 456–463, 2008.
[7]
G. Egger and B. Swinburn, Planet Obesity: How We Are Eating Ourselves and the Planet to Death, Allen and Unwin, Sydney, Australia, 2010.
[8]
J. C. Riley, Rising Life Expectancy: A Global History, Cambridge University Press, New York, NY, USA, 2001.
[9]
J. Frenk, J. L. Bobadilla, J. Sepulveda, and M. Lopez Cervantes, “Health transition in middle-income countries: new challenges for health care,” Health Policy and Planning, vol. 4, no. 1, pp. 29–39, 1989.
[10]
T. N. Robinson and J. R. Sirard, “Preventing childhood obesity: a solution-oriented research paradigm,” American Journal of Preventive Medicine, vol. 28, no. 2, supplement 2, pp. 194–201, 2005.
[11]
D. Fleming, Energy and the Common Purpose: Descending the Energy Staircase with Tradable Energy Quotas (TEQs), The Lean Economy Connection, London, UK, 2005, http://www.theleaneconomyconnection.net/.
[12]
G. Bray, “Historical framework for the development of ideas about obesity,” in Handbook of Obesity, G. Bray, C. Bouchard, and W. P. T. James, Eds., Marcel Dekker, New York, NY, USA, 1998.
[13]
R. N. Bergman, S. P. Kim, and S. P. Kim, “Why visceral fat is bad: mechanisms of the metabolic syndrome,” Obesity, vol. 14, supplement, pp. 16S–19S, 2006.
[14]
R. Poupon, “Differentiating between benign and non-benign obesity: Look at the liver,” Gastroenterology Clinical and Biology, vol. 34, no. 4-5, pp. 244–245, 2010.
[15]
G. S. Hotamisligil, “Inflammation and metabolic disorders,” Nature, vol. 444, no. 7121, pp. 860–867, 2006.
[16]
H. Tilg and A. R. Moschen, “Inflammatory mechanisms in the regulation of insulin resistance,” Molecular Medicine, vol. 14, no. 3-4, pp. 222–231, 2008.
[17]
P. Libby, “Inflammatory mechanisms: the molecular basis of inflammation and disease,” Nutrition reviews, vol. 65, no. 12, pp. S140–S146, 2007.
[18]
A. Laporte, “Do economic cycles have a permanent effect on population health? Revisiting the Brenner hypothesis,” Health Economics, vol. 13, no. 8, pp. 767–779, 2004.
[19]
C. J. Rhum, “Good times make you sick,” Journal of Health Economics, vol. 22, pp. 637–658, 2003.
[20]
C. J. Ruhm, “Commentary: mortality increases during economic upturns,” International Journal of Epidemiology, vol. 34, no. 6, pp. 1206–1211, 2005.
[21]
B. Harris, “Public health, nutrition, and the decline of mortality: the McKeown thesis revisited,” Social History of Medicine, vol. 17, no. 3, pp. 379–407, 2004.
[22]
J. A. Tapia Granados, “Economic growth, business fluctuations and health progress,” International Journal of Epidemiology, vol. 34, no. 6, pp. 1226–1233, 2005.
[23]
J. A. Salomon and C. J. L. Murray, “The epidemiologic transition revisited: compositional models for causes of death by age and sex,” Population and Development Review, vol. 28, no. 2, pp. 205–228, 2002.
[24]
J. A. Tapia Granados and E. L. Ionides, “The reversal of the relation between economic growth and health progress: Sweden in the 19th and 20th centuries,” Journal of Health Economics, vol. 27, no. 3, pp. 544–563, 2008.
[25]
R. Medzhitov, “Origin and physiological roles of inflammation,” Nature, vol. 454, no. 7203, pp. 428–435, 2008.
[26]
M. Franco, P. Ordu?ez, and P. Ordu?ez, “Impact of energy intake, physical activity, and population-wide weight loss on cardiovascular disease and diabetes mortality in Cuba, 1980–2005,” American Journal of Epidemiology, vol. 166, no. 12, pp. 1374–1380, 2007.
[27]
M. De Courtin, “Personal communication,” 2009.
[28]
A. M. Hodge, G. K. Dowse, G. Koki, B. Mavo, M. P. Alpers, and P. Z. Zimmet, “Modernity and obesity in coastal and Highland Papua New Guinea,” International Journal of Obesity, vol. 19, no. 3, pp. 154–161, 1995.
[29]
J. A. Tapia Granados, “Macroeconomic fluctuations and mortality in Postwar Japan,” Demography, vol. 45, no. 2, pp. 323–343, 2008.
[30]
J. A. Tapia Granados, E. L. Ionides, and O. Carpintero, “Concentrations rather than emissions: a threatening link between world economic growth and atmospheric CO2,” Unpublished.
[31]
G. Egger, “Health, 'Illth,' and economic growth. medicine, environment, and economics at the crossroads,” American Journal of Preventive Medicine, vol. 37, no. 1, pp. 78–83, 2009.
[32]
D. H. Meadows, D. L. Meadows, J. Randers, and W. Behrens, The Limits to Growth, Universe Books, New York, NY, USA, 1972.
[33]
Intergovernmental Panel on Climate Change, “Climate change: synthesis report 2001,” November 2007, http://www.ipcc.ch/publications_and_data/publications_and_data_reports.htm#1.
[34]
Global Commons Institute, Contraction and Convergence. A Global Solution to a Global Problem, GCI, London, UK, 2007, http://www.gci.org.uk/contconv/cc.html.
[35]
S. Roberts, J. Thumim, and Centre for Sustainable Energy, “A rough guide to individual carbon trading: the issues, ideas and the next steps,” Report to DEFRA, November 2007, http://www.ubuntu.com.
[36]
G. Egger, “Personal carbon trading: a potential 'stealth intervention' for obesity reduction?” Medical Journal of Australia, vol. 187, no. 3, pp. 185–187, 2007.
[37]
R. H. Unger and P. E. Scherer, “Gluttony, sloth and the metabolic syndrome: a roadmap to lipotoxicity,” Trends in Endocrinology and Metabolism, vol. 21, no. 6, pp. 345–352, 2010.
[38]
J. S. Mill, Principles of Political Economy, 1848. Electronic Reproduction, e-brary, Palo Alto, Calif, USA, 2003.
[39]
A. A. Bartlett, “What part of arithmetic does not hold in Boulder?” Boulder Daily Camera. In press.
[40]
T. Jackson, Prosperity without Growth, Earthscan, London, UK, 2009.