Animals and 6-Month-Old Infants Are Getting Fatter … Which Mean that It’s Something In the Environment

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.

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 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).


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 (

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.

. 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.

. 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.

. 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 [12,13], 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 and figure 1). 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 and figure 1.

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:

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]. 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’ ( According to a recent review by German [16], ‘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]. 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]. 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 [19,20] 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], 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].


Category: Think Tank

Please use the comments to demonstrate your own ignorance, unfamiliarity with empirical data and lack of respect for scientific knowledge. Be sure to create straw men and argue against things I have neither said nor implied. If you could repeat previously discredited memes or steer the conversation into irrelevant, off topic discussions, it would be appreciated. Lastly, kindly forgo all civility in your discourse . . . you are, after all, anonymous.

11 Responses to “Why Are Animals Getting Fatter, Too?”

  1. Jojo says:

    Hey BR – It’s not clear at all that this article contents came from Washington’s Blog, especially when we see “By Barry Ritholtz” up top. Suggest you make this clearer and provide a direct link back to the source, which is:

  2. bear_in_mind says:

    American legislators and corporations could remove BPA (bisphenol A) from the production of food products within three months, but there has been an utter lack of conviction to enforce this common sense measure. Profit margins have been a bigger priority than human (and animal) health.

    The National Institute of Environmental Health Sciences (NIEHS) at the National Institutes of Health (NIH)
    Since You Asked – Bisphenol A (BPA)

    What is BPA, and what are the concerns about BPA?
    The Mayo Clinic

  3. Marcus says:

    All these animals are caged except feral rats. They all eat food prepared by humans which means they eat trans fat (especially the rats). Trans fat is formed by “hydrogenation”, the process of bubbling hydrogen gas through edible oils while in contact with a platinum gauze (a wire mesh made of a noble metal). This catalyzes the oil to switch from a digestible form to a stable form. In simple language, hydrogenation changes cooking oil from something your body can easily metabolize, into a form that can sit on the shelf for years without spoiling and ruining the oil or product made from the oil.

    Metabolism is compromised when you eat trans fat and weight increases. Fry in virgin olive oil if you want to avoid hydrogenation.

  4. scharfy says:


    Is the fat animals theory in any way related to the military controlling the weather, or super nano-thermite found at ground zero, or the cover-up at Fukishima?

    Keep digging, you are so close.

    (BR, you should make sure GW puts his initials on top of the garbage he posts. BTW, does he pay alot of $$$ for posting privileges here? be honest… just saying his stuff is trash and you have a good blog except for him and mauldin..)

  5. bda_guy says:

    I was critical of the last post and am similarly skeptical of this post.

    First, babies. While babies may not “binge” the same way that adults do, their parents are the ones regulating the type of food that the babies eat. If the parents are not eating a healthy diet, it’s likely the same that the babies are being fed food that is less nutritious and heavily calorie-laden. In addition, if the parents do not have a problem being overweight, they’re less likely to intervene or modify the diet of their children. I live in a place where I’ve seen parents give their overweight 7-10 year old kids daily ice cream treats and then justify their kids weight by saying that they haven’t lost their baby fat!

    As for most of the animal examples provided, all but two of the samples are from laboratories where humans can directly influence the type and amount of food that the animals eat. As a part of these studies, there should be a review of the diets provided to the animals and how they have changed over time.

    Regarding domestic dogs and cats, owners once again are a major factor in what type of and how much food is provided. The type of pre-packaged food for cats and dogs these days is arguably more healthy now than it was 30 years ago. However, quantity provided probably has varied. And once again, if the owner doesn’t have a problem being overweight, they probably won’t have an issue with their pet being overweight either. And what owner doesn’t let their dog eat table scraps and other food that falls on the floor by their toddler!

    Finally, as for feral rats, a major source of their food are the trash bins of the people they live around. If people are throwing away larger amounts of high-calorie food, it’s likely the rats are also much better fed than they’ve ever been before.

    While I’m as concerned as anyone about the hormone-changing chemicals being introduced into the food cycle that very well could affect people’s weight, I still believe that the vast majority of the society’s weight issues are caused by the increased abundance of high-calorie, low nutrition foods along with society’s changing acceptance of what is a normal, healthy weight. This extends to animals since the foods that we introduce into the food chain affect the whole food chain including the animals that are closest to us in proximity.

  6. super_trooper says:

    Most of your examples are related to animals in captivity. There is a correlation between overweight owners and overweight pets. The fatter you are the more likely you are to give the animal more food and exercise them less. Ask your vet next time your dog needs a check-up. Many pet food manufacturers target this specific phenomenon.

  7. hank panky says:

    I know you’ve talked a lot about this but this whole idea is still theory. The idea that there are environmental chemicals with hormonal possibilites for producing fatsos needs to be thoroughly examined but watch out for your own tendency toward confirmation bias.

    All of these animals live in unnatural circumstances and most are fed by human beings and protected from Darwinian imperatives. I don’t know of any natural populations of animals where obesity is a common phenomenon.

    As for Western societies and obesity the China Study expounds the relationship well and shows that natural diets are not likely to make fatsos.

    Fetal humans eat what mama gives them and if that’s mama cass then baby’s gonna have a problem. In the developmental period of life (fetal months and early childhood) if you get too much fat, protein and calories, you are going to grow a lot of fat cells and they never go away. They will scream to be filled for the rest of your life.

  8. inessence says:

    Goddamn, get your ass off of the couch, put the dog on a leash, and walk around the block a few times. The problem is not food or its processing, it is the increasing perpetual nature of Americans to plop their ginormous fannies in front of the television.

  9. Greg0658 says:

    if the systems could survive? (probably not possible for more than 30mintes)
    what do you think a total shutdown of all man made electro magenetic processes would feel like?
    I wonder if our heads would explode?

    Fuch that gd language – not pc anymore – I’d use the ‘k’ but that would probably get moderated – F’ing FCC

  10. readerOfTeaLeaves says:

    BR, thanks for keeping this in the public eye.

    My required reading this week includes:
    Obesogens: An Environmental Link to Obesity

    A parent may feed a child wonderfully, but if the foods have been stored in certain kinds of plastic containers, if baby crawls on a carpet treated with certain chemicals and is surrounded by certain kinds of building materials and fabrics, baby is likely absorbing chemicals that alter the genetic functions of genes that control baby’s metabolism. Multiply by millions of babies, and you just might end up with an obesity epidemic, all over the globe.

    And fat cells (adipose), once activated, function like little chemical signaling systems: they get chatty with one another. Think of them as little chemical cheerleaders and agitators, often located around the abdomen (“make me fatter! make more of meeeee!”). No matter how well you eat, if your genes have been highjacked by ‘obesogens’, those fat cells continue to multiply.

    But it gets worse than simply being overweight.
    There are some smart, diligent people tracking down linkages between metabolic and cognitive functions: IOW, as metabolism is impacted, so (eventually) is cognition. Check back when baby is in about the fifth grade, and if baby’s brain is *not* getting all the nutrients necessary to make his-her synapses snappy, then color me unsurprised.

    Meanwhile, billions are spent to ‘treat’ (ha!) diabetes, rather than putting money into prevention.

    The clinical methods for reversing the metabolic processes involved in pre-diabetes for patients developing Type II exist, but they require coaching and ongoing care that don’t jibe with existing healthCo financial models. IOW, there is likely to be a lot of profit in diabetes treatment, until the system collapses under the weight of the demands — and people realize that prevention would be far more affordable over the long term.

    It turns out that it’s not just about what we eat, when, nor how much we exercise. It’s far more complicated than that, and a new category of chemicals now starting to be referred to as ‘obesogens’ seem to be implicated in obesity.

    Meanwhile, eat organics when possible, keep food in glass rather than most kinds of plastics, be careful about the materials in your home furnishings, and notice when you start to hear a new word entering the mainstream conversation: “Obesogens”.

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