We’ve extensively documented that toxic chemicals in our food, water and air our causing an epidemic of obesity … even in 6 month old infants [5].
No matter how lazy and gluttonous adults may have become recently, 6-month-olds can’t be lazy … they can’t even walk, let alone go to the gym.
And 6-month-olds can’t “binge” … Gerber doesn’t make corn dogs or milk chocolate truffles with rum.
The same thing is being observed in animals … hardly your stereotypical couch potatoes.
Specifically, the Proceeding of the Royal Society published a scientific paper [6] in 2010 showing that animals – as well as humans – are getting hit with more obesity:
‘Like humans, domestic animals and fish and other wildlife are exposed to contaminants in air, soil, water, and food, and they can suffer acute and chronic health effects from such exposures. Animal sentinel systems—systems in which data on animals exposed to contaminants in the environment are regularly and systematically collected and analyzed—can be used to identify potential health hazards to other animals or humans.’
National Academy of Sciences (1991, p. 1).
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From 24 distinct populations (12 subdivided into separate male and female populations), representing eight species (see §2 for inclusion criteria), over 20 000 animals were studied. Time trends for mean per cent weight change and the odds of obesity (see the electronic supplementary material for definition) were tested for the samples from each population at an age period that corresponded roughly to early-middle adulthood (35 years) in human development (see the electronic supplementary material for calculation) because on a per cent basis, in United States adults, 30–39 years is the decade of human life in which obesity has increased at least as much as any age interval during the last several decades (http://www.cdc.gov/nchs/data/nhanes/overweight.pdf [7]).
The animals came from a variety of different settings and environments, which reduces the possibility that all of the animals were lazy or more gluttonous than normal:
Macaques—Wisconsin. Our sample consisted of 65 (23 males, 42 females) rhesus macaques (Macaca mulatta—Indian origin) from the Wisconsin National Primate Research Center (WNPRC) measured between 1971 and 2006.
Macaques—Oregon. Our sample consisted of 46 (14 males, 32 females) rhesus macaques (Macaca Mulatta—Indian strain) from the Oregon National Primate Research Center (ONRPC), measured between 1981 and 1993.
Macaques—California. Our sample consisted of 77 (30 males, 47 females) rhesus monkeys (Macaca mulatta), primarily of Indian origin from the CNPRC (California National Primate Research Center), measured between 1979 and 1992.Chimpanzees. Our sample consisted of 46 (16 males, 30 females) chimpanzees (Pan troglodytes) that had been born and lived their entire lives at the Yerkes National Primate Research Center (YNPRC). These animals were measured between the years 1985–2005.Vervets. Our sample included a total of 117 (36 males, 81 females) vervet monkeys (Chlorocebus aethiops sabaeus) living in 18 captive social groups at the UCLA-VA Vervet Research Colony, measured between the years 1990 and 2006.Marmosets. Our sample included a total of 143 (65 males, 78 females) common marmosets (Callitrichix jacchus jacchus) from the WNPRC, measured between the years 1991 and 2006.Mice and rats (laboratory). Our sample consisted of animals from 106 rat and 93 mouse studies. There was some variation in sample size between studies. For both rats and mice, the majority of studies had sample sizes of 60 males and 60 females. However, some studies had fewer (i.e. 50, 49, etc.) or more (i.e. 70) animals. In calculating our sample size, we decided to use a conservative estimate of 50 animals per study. Body weights for only untreated control mice and rats used in National Toxicology Programme (NTP) studies between the years of 1982 and 2005 were analysed.Domestic dogs and cats. Our sample of dogs included a total of 2806 (1366 males, 1440 females) animals measured between the years of 1990 and 2002. Our sample of cats included a total of 574 (265 males, 309 females) animals, measured between the years of 1989 to 2001.Feral rats. Our sample consisted of 6115 (2886 males, 3229 females) wild Norway rats (Rattus norvegicus) that were captured in the central alleys of high-density residential neighbourhoods using single-capture live traps, while rural rat populations were sampled from parklands and agricultural areas in areas surrounding the city [12 [8],13 [9]], between the years 1948 and 2006.
The results showed across-the-board increases in obesity:
For per cent weight change, 24 out of 24 time trends were positive (i.e. increasing). The probability of all out of 24 independent trend estimates being in the same direction by chance is 1.2 × 10−7. For the odds of obesity, 23 out of 24 cases were positive (p = 3.0 × 10−6; table 1 [10] and figure 1 [11]). When we combine males and females of each species into a single analysis, we find that in all 12 populations, per cent weight change and odds of obesity time trends were positive (p = 4.9 × 10−5, for 12 out of 12 in the same direction). Given these overwhelmingly significant results at the ensemble or meta-analytical level, we describe the results below for samples from each individual population focusing on the magnitude of the coefficients. Standard errors, confidence intervals and p-values are shown in table 1 [10] and figure 1 [11].
The study concluded that animals are gaining weight, even though they are not subject to the same factors normally blamed for the human obesity epidemic [5]:
Our findings reveal that large and sustained population increases in body weights can occur in mammalian populations, just as they have occurred among human populations, even in the absence of those factors that are typically conceived of as the primary determinants of the human obesity epidemic via their influence on diet (e.g. access to vending machines) and physical activity (e.g. less physical education classes in schools). Though results were not statistically significant in every population (11 out of 24 are statistically significant for per cent increase in weight per decade, and 7 out of 24 are statistically significant for odds of obesity), viewed as an ensemble, the fact that nearly all independent time-trend coefficients were in the positive direction for both weight gain and for the odds of obesity, is overwhelmingly statistically significant.
That large population level changes in body weight distributions of mammalian populations can occur even when those populations are neither under obvious selection by predation nor are living with or among humans has been documented [15 [12]]. The particular upward trend we have observed towards obesity in multiple datasets of non-human animals has been suggested by anecdotal evidence for some time. A 2008 news report indicated that ‘trends in pet insurance are mirroring human healthcare. Obesity… is a growing problem for dogs and cats… (and 2007) saw a 19 per cent increase in claims related to obesity’ (http://www.petfirsthealthcare.com/2008/02/07/petfirst-pet-insurance-to-be-more-popular-in-2008/ [13]). According to a recent review by German [16 [14]], ‘Most investigators agree that, as in humans, the incidence of obesity in the pet population is increasing’. Despite this strong sentiment that obesity rates are increasing in pets (note that the United States Food and Drug Administration recently approved the first drug to treat obesity in dogs; Food and Drug Administration, 2007), we were unable to find previously published data actually showing this increase.
Others reported that 19 per cent of horses in a large cohort were obese, even among largely pasture-fed animals. Although a direct comparison with a similarly sampled earlier cohort was not available, the investigators remarked that the levels were higher than a 5 per cent rate observed in an earlier study [17 [15]]. Similarly, an increase in body weights was observed among rats used in carcinogenicity studies in France between 1979 and 1991, despite similar husbandry conditions [18 [16]]. The authors attributed the increase to the introduction of animals of the same substrain but raised under specific pathogen-free conditions, reinforcing the perspective that the presence of viral or other microbial pathogens [19 [17],20 [18]] may affect body weight in populations either positively or negatively, depending on the pathogen. It is also noteworthy that the obesity epidemic has also occurred among children of six months of age and under [21 [19]], an age group for which explanations involving food marketing, less physical education is schools, and more labour-saving devices seem questionable.
The authors raise numerous possible explanations, including hormone-disrupting chemicals:
One set of putative contributors to the human obesity epidemic is the collection of endocrine-disrupting chemicals (endocrine-disruptors), widely present in the environment [24 [20]].
Exactly.