The Animals are Also Getting Fat

In a remarkable paper Allison et al. (2011) gather data on the weight at mid-life from 12 animal populations covering 8 different species all living in human environments. Dividing the sample into male and female they find that in all 24 cases animal weight has increased over the past several decades.

Cats and dogs, for example, both increased in weight.  Female cats increased in body weight at a rate of 13.6% per decade and males at 5.7% per decade. Female dogs increased in body weight at a rate of 3% per decade and males at a rate of 2.2% per decade.

One ready, although not necessarily correct explanation, is that fat people feed their cats and dogs more and exercise them less. Thus, the authors also looked at animals not directly under human control such as rats.

…For the 1948–2006 time period, male rats trapped in urban
Baltimore experienced a 5.7 per cent increase in body
weight per decade from 1948 to 2006 and a nearly
20 per cent increase in the odds of obesity. Similarly,
female rats trapped in urban Baltimore experienced a
7.22 per cent per decade increase in body weight, along
with a 26 per cent increase in the odds of obesity.

that too has a ready, although not necessarily correct, explanation:

fat mouse… just as human real wealth and food
consumption have increased in the United States, rats
which presumably largely feed on our refuse, may also
be essentially richer.

To counter both of these objections the authors do something very clever, they gather data on the weight of control mice used in many different experiments over decades.

Among mice in control groups in the National Toxicology
Programme (NTP), there was a 11.8 per cent
increase in body weight per decade from 1982 to 2003
in females coupled with a nearly twofold increase in the
odds of obesity. In males there was a 10.5 per cent
increase per decade.

Control mice are typically allowed to feed at will from a controlled diet that has not varied much over the decades, making obvious explanations less plausible. Could mice have gained weight due to better care? Possibly although that is speculative.

More generally, there are specific explanations for the weight gain in each of the animal populations, just as there are for humans. Each explanation looks plausible taken on its own but is it plausible that each population is gaining weight for independent reasons? Could there instead be a unifying explanation for the weight gain in all populations? No one knows what that explanation is: toxins? viruses? epigenetic factors? I am not ready to jump on any of these bandwagons and in some cases the author’s samples are small so I am not yet fully convinced of the underlying facts, nevertheless this is intriguing and important research.

Hat tip: David Berreby writing in Aeon about The Obesity Era.


How has the size of the rat population changed in the period 1948-2006? I would guess that there is much more pest control now than 60 years ago.

Rats may be fatter because so many are being exterminated that the ones who survive face little competition for food.

This doesn't explain the trend for mice in control groups, obviously, but I am skeptical that the two are related.

Even with a constant diet shouldn't subsequent generations of mice turn out to be fitter. Even in an inbred control mice population.

If fitness manifests itself as higher weights why the surprise. Weight gain need not mean obesity; perhaps the mice just grew taller or longer or more muscular or whatever?

The other change from 982 to 2003 may have been in the general standard of care of animal houses (humidity, air circulation etc.). It wouldn't be crazy to even expect that "wellbeing" to manifest as an increase in body weight?

That's the biggest two falllacies of evolution. 1. Expecting changes in a brief period of time and 2. Placing value judgements on the direction if change. What is fittest is determined by the environment, not by our ideas of what us better. It is an objective criteria if whether the trait enhances (or merely survives) the probability of surviving and reproducing. Ex post, most mutations appear optimal because of survivorship bias.

Observed changes in a few generations are likely environmental, not genetic. Some species, eg dogs, however, change much more rapidly.

Thanks, very concise and useful. It's distressing how many conversations include talk of evolution when people really misunderstand the theory, very fundamentally. It's a hard one to get a good hold on.

Yes, I agree with your underlying points; but how brief is a "brief period of time"? If you look at Kettlewell's experiment and the peppered moth story, the color change in moths happened over the period of a decade I think.

British Moths have one generation per year, lab mice about two generations per year. Is it impossible that average fitness improved, especially under strong artificial selection pressures of a lab-supply environment?

So why does your criticism #1 hold here? I'm no expert. I may be wrong.

It is easy to observe physical changes in selectively bred species. Those traits might survive for a very long time from a human observer's perspective - say, 100 years. The true test of evolution is much longer than that. Of course any cutoff point is arbitrary. If humans are wiped out tomorrow by an asteroid, we would still have had a two million year existence as homo sapiens. So you are correct to observe change/mutation immediately, but the jury is still out on whether it is "survivable" in the gene pool.

But let's say that the propensity of golden retrievers to get cancer is disadvantageous. It could take a thousand years before that trait dies out or is bred out. Here I'm not making a value judgment that cancer is bad, but merely recognizing the positive aspect that cancer leads to death and early deaths reduce the likelihood of reproduction. Benign traits can last indefinitely if they neither help nor hinder reproduction or survival. In geology they talk of geological time which does not consider things like a river changing its course. Geologists look at how and why the Grand Canyon was carved from a particular river. Widespread large changes in a species is similarly small potatoes in evolutionary time. To put it in a mathematical sense, evolutionary time is sufficient for the law of large numbers to hold with mutations that marginally affect survival and reproduction.

So with rats and pigeons, I'm quite sure that the availability of rich food sources and lack of predation are the chief causes of obesity. We will never live long enough to know what mutations aided their survival.

Asians are typically thin. I cannot tell you whether they have a genetic disposition toward leanness or whether economic and social factors lead to this. But in America, Asians are becoming more fat. This tells me that environmental factors are contributing to fatness in America not necessarily leanness in Asia.

Incidentally, this is also the confusion between weather and climate. People are making inferences from short run changes to long run phenomena.


It's natural selection through mutations that takes a very long time. This is because mutations are random and beneficial ones very rare.

But in a polymorphic population, i.e. a population whose certain members already possess a certain trait, that trait can propagate in a few generations thanks to natural or sexual selection. (Examples include the already mentioned Manchester moths, the recent Russian foxes, etc., or any experiments with bred animals.)

Survival of the Fattest isn't just a punk album anymore.

After reading Gary Taubes' Why We Get Fat I see most of these issues through a low carb perspective. By and large, it is only domesticated animals that get fat. A lion in the wild eating only meat will stay lean, but a dog or cat eating foods with rice, corn or grains as the base of their diet can trigger their bodies into a fat storage mode. Their insulin response is overwhelmed by starchy foods that they never truly adapted to. My 2 cents.

My additional 2 cents (see the comment below) is that there are some other factors involved; first, lions in the wild are eating herbivores which don't have access to manufactured feed in general - it would be interesting to see if their BMI changes when they eat domestic animals; and how to avoid changing that without altering the need for the chase, frequency of feeding, etc. Second, Ruth Ley have more to say about this, but I think there are some very different intestinal metabolisms in pure carnivores vs omnivores and herbivores. Domestic cats have been eating more like omnivores for a long time now; their weight gain appears recent. Research rats have long eaten basically the same alfalfa lab chow, the changes can't be explained by a recent increase in carbs.

My two cents from my personal n=1 experience. We have a female Maltese-Poodle mix which we feed dry, moist and canned commercial dog food. All contained grains and fillers of some sort. She developed sever allergies, became over weight, always had runny poop and at times refused to eat.

We finally figured out she was sensitive to grains, all grains. We switched her diet to a raw meat (low heat pasteurized and ground chicken that contains organ meat and bone), no grain, no fruit and vegetable one. She lost weight and is now at optimal weight for her size, her fur grew back completely, her poop is normal and most of her allergies have disappeared.

The only non-meat she eats now is grass when she finds some real fresh young blades.


It is funny that we think we can feed grain to dogs (or cows).

Why is it funny? Also, why say "we think we can" when you could just say "we do"?

Good point, I was going to add in something like "and expect no consequences" but that sounded a lot graver than I meant it to be.
Seems obvious that if you have to fool an animal into considering something food, it's got potential to turn out a little weird, that's all. Mad cow and all that being the obvious. I'll grant sometimes it can work out just fine.

"They" say that an all meat diet is not healthy for dogs -- but it is fine for cats. Dogs need some carbs in their diet.

My dog had a grain allergy. We put her on a food that used sweet potato for its carb source. There are a variety of mixes of protein and starch that are available.

I was curious about this point, so I tried to track down the details of the lab mice/rats growing fatter.
The only relevant article i could find from the references discussed that these animals had, for years (22+), been fed the same commercial product, Purina Certified Rodent Chow 5002. So what's in that?
Here's where it gets interesting. That has a well-defined fat, fiber, and protein content along with some trace elements and suchlike. But I cannot find a statement about its carb content. The best I can find is that its "carbohydrate can be derived from sugar or starch".

If one buys into the Gary Taubes thesis (and various slight variants of it) there remains a big issue here. Has the composition of the feed changed in a way which appears non-material if you are measuring the wrong things, but which has material impact on the extent to which the animals want to eat more of it during ad libidum feeding?
The could include:
- Has the precise carb mixture changed? (Fructose vs sucrose, sugars vs non-sugars, sweet vs non-sweet carbs)
- (Robert Lustig's issue): the extent to which the sugars/carbs are intrinsically bound to fiber, thus slowing their absorption and the size of the insulin spike
- (Mary Enig's issue): use of vegetable fats vs animal fats

This I think is the crucial case which needs to be examined to distinguish between carb diet issues and other possibilities (eg endocrine disruptors or virus).
All the other examples strike me as much messier and could very likely be the result of a trend of feeding ever more grain to animals that aren't built for grain, especially grain that has been bred to have so much starch bound to so little fiber. (My assumption is something like an ever increasing amount of grain in horse/chimp/cat/dog food as every year the providers see "well, the animals seem to live on x% grain, and it's cheaper than meat, so let's see how they do on x+1% grain).

Have there been changes in the feedstock grains from which the Lab Chow is composed over the years? Changes which, while not affecting gross analysis, alter the levels of bioagents like aminos or introduce new compounds ('Roundup Ready' comes to mind)? It might be worthwhile to look around for a stash of that chow from a decade or so ago and see what, if anything, has changed in the crops upstream from Purina which feed into that lab chow, as shown by differences in the two batches now.

“Obesity is a disease of the environment.” — Richard Jackson

There is an interesting book — Zoobiquity: What Animals Can Teach Us About Health and the Science of Healing — that includes significant parts on fat.

Barbara Natterson-Horowitz, a cardiologist at the University of California Los Angeles, writes:

Fattening in the animal world has enormous potential lessons for humans—including dieters looking to shed a few pounds and doctors grappling with obesity, one of the most serious and devastating health challenges of our time. ... They are mostly or completely dependent on humans for every meal, and we regulate both the quality and the quantity of everything that passes their lips and beaks. Consequently, we can’t really blame them for their weight problems. … And so we’re left with one conclusion: we, the species that both manipulates food to make it more unhealthful and has the intelligence to understand that we shouldn’t eat so much of it, are to blame. We’re responsible not only for our own expanding waistlines but for those of our animal charges as well.

I also covered a review of this book here:

There are two additional factors beyond the idea that diet and exercise are impacting each of these populations.

1. Antibiotics for growth promotion: Antibiotics have long been used for growth promotion in livestock (pigs, cattle); they also work in mice, for example. Low doses of antibiotics over time or a few spikes of antibiotics during juvenile years both lead to increased adiposity (Blaser et al, several publications). In the 50's, the world produced ~50-100 kg of antibiotics per year, but now, it is millions of tons (~30 or so). Antibiotics generally do not stay in the patient or animal, but flow through them bioactive. In fact, in the first major use of penicillin, the drug was recrystallized from urine for administration to the same patient (due to insufficient supply). As a result, there are large volumes of antibiotics in sewage, and perhaps elsewhere in the environment. There are a number of possible consequences of this; one that has not been fully explored is 'growth promotion' - increased adiposity - in humans and, incidentally, other animals.
Tying this to the next topic, the way the antibiotics serve in growth promotion appears to be through modulating the intestinal microflora to allow for a more rapid flow of nutrients into the animal. Why do the bacteria not adjust to this (they appear to have the capability to simply become resistant)? Why does the effect last over the lifetime of the animal? Nobody knows.

2. Obesity associated infectious agents: It has been demonstrated that, by taking the intestinal bacteria from a high-BMI mouse or a low-BMI mouse, one can impact the BMI of a mouse recieving those bacteria as its own microflora (Gordon et al publications). Similar studies have taken bacteria from humans and also shown cross species effects. If there were a large population of high-BMI humans, it might be that their bacteria infect the animals all around them, also raising their own adiposity. There may also be 'selfish genes' involved, crossing species and adjusting the metabolism of multiple bacteria in a convergent sense. This is a bit of the flip side of the first idea; it isn't the shared drug exposure, it is a selected infectious agent crossing populations as a zoonosis. It isn't impossible that both factors are working together.

I find these arguments much more compelling than the idea of diet and exercise, particularly in research settings and in wild animal populations.

1. I can guarantee you that incidental antibiotic exposure in laboratory mice is tightly controlled.

There are many transgenic mouse lines which use the presence or absence of an antibiotic (usually tetracyclines, one of the most common antibiotic types in use) to turn off/on genes. Experiments involving these animals would go to hell if there were trace amounts of antibiotics in feed or water.

2. Microflora have an obvious first-order effect on metabolism, but they are not easily transmissible. There is little chance of someone's gut flora "infecting" your intestines.

Furthermore, there is an incredible variation of intestinal flora within populations of humans.

Naive question: But is micro-flora not receptive to the typical fecal-oral route of e.g. pathogens? Too fragile?

I just sent my rats a memo to the effect of:

"If you rats don't have the willpower to lay off the carbs, you certainly aren't going to have the intestinal fortitude to finish the Skinner box."


You are in trouble with the tenure committee now.

Can we at least give it a name like the "Flynn effect," even though Jim Flynn is as thin as a rod. It will be tough as long as obese people keep being barred from academia. Yet I have a hope that a proper short-hand will be developed. The arc of history is long but it bends towards corpulence.

One other possible explanation (hinted at but not drawn out in the Aeon piece) is the increase in environmental noise and light, which disrupt sleep. And sleeplessness has been linked to obesity fairly conclusively.

"Lights Out" is kind of a fringe book and not very rigid in its methods, but it is very persuasive in some of its arguments. Anyone who has ever worked in horticulture can tell you how important light cycles can be.

I've always said, never count on a Tabby for their willpower.

So...more Fat Cats than ever?

We ARE the 1%

People are also getting taller. Tour an 18th century house or boat and you feel like a giant. Maybe what is happening is what happened with reptiles in the Triassic period. The planet gets hotter, the food supply for the dominant species becomes more plentiful and before long, geologically, they are giants. perhaps in 100,000 years, huamns will the size of building and house cats the size of school buses.

I was going to blame it on global warming, but you beat me to it.

my suggestion *is* the increase in avg temperature. It means less cold and therefore metabolic stress from burning calories keep warm is nit experienced. see

I heard that people are taller compared to the 1700s, but the same size as ancient humans.

Without doing any research (yet), we'll offer one prediction: all the listed species have also experienced an increase in longevity, which we'll base on this relationship.

Picking up on BenK's thoughts, the second is unlikely, but the first is promising. Antibiotics introduced into feedstock started to be introduced in the very late 1970s and became widespread in U.S. food production in the early 1980s. If one were looking for a correlation with weight increase across species, that would be the time frame in which the increases not associated with natural variation would be observed to begin.

There's another factor to consider as well. That was also the period in which high fructose corn syrup began to replace sugar in a lot of food production. That's significant because the high fructose corn syrup was a lot less costly than sugar, which resulted in lowering the cost of both food production and food for the consumer. And we all know what happens with quantity demanded in the situation where a supply curve shifts downward....

One consequence of that is that food producers would likely have increased the unit volumes of their products (let's call this "supersizing"). This is something that would primarily affect the human population, but not the animal populations, whose food wouldn't necessarily be produced with high fructose corn syrup. We would then predict that the weight of humans have increased proportionately more than those of the animal species as a result of this factor. If the combination of both antibiotics and cheaper food is responsible for weight gain in the human population, while only antibiotics are responsible for the weight gain in the animal species, it could be possible to isolate the effect of cheaper food upon the human population.

So, any master degree or doctoral students looking for an interesting thesis to investigate?...

Bad idea, and easily falsified. In the Netherlands hardly any HFCS is used but obesity is rampant - though with a time lag compared to the US.

The communicable disease idea is a better hypothesis.

Isn't the argument that the abundance of HFCS lowered the price (and thus increased the consumption) of sugars generally? So the US'ers switching to HFCS means that more cane sugar from antigua is available in Holland. it's not that HFCS is somehow worse for you than cane sugar.

Or perhaps more likely that US protectionism against foreign sugar keeps prices lower on the global market. But it still doesn't seem to hold up if we talk about a country like Brazil, where obesity is said to be increasing at an alarming rate (a minister recently said the country was in danger of becoming like the United States). The effects of global trade would seem more attenuated there. They eat sugar because they have good terrain and climate for producing it, and it tastes yummy. Maybe its simply food is cheaper.

HFCS is only cheaper in the U.S. because of price supports on sugar. In the U.S., we pay about 4X the world price for sugar, but HFCS is exempt from the price supports, so it is much cheaper than sugar. This carve-out was created for the soft drink industry, so they wouldn't be crippled by the high price of sugar. You can't use HFCS to make most types of candy (it doesn't set up into a solid like sugar does because HFCS is an invert sugar), so we've lost much of our candy industry to Canada and Mexico. I guess the candy industry didn't have enough political clout to avoid being gored by the sugar industry.

If I didn't have other things to do, I'd seriously consider becoming a sugar smuggler. I wouldn't have any ethical qualms about what I see as correcting an injustice.

I think that it was true at one time that HFCS was cheaper in the U.S. because of price supports for sugar, but corn producers used the sugar protectionism in the 80s to perfect their technology and no longer lobby for sugar supports. In the U.S. HFCS is cheaper than the global market rate for sugar. I think this genie is out of the bottle. The best HFCS opponents can hope for is ever-increasing mandates that gasoline be blended with more ethanol -- more food for fuel, less food for food.

(There is also the issue that HFCS are imperfect substitutes. HFCS is easier to use with some processed foods and my wife still refuses to squeeze a dollop of corn sugar into her morning tea)

HFCS is cheap because of crop insurance subsidies for corn, not technology. If the government money went away, there would be no HFCS.

"Control mice are typically allowed to feed at will from a controlled diet that has not varied much over the decades."

While that may be true, I am willing to bet that the food is sourced and manufactured differently now, probably by a subsidiary of one of the major food companies.

Another likely cause based on emerging research is the microbiome. There is the genome (raw code), the epigenome (external factors that determine how the code is executed), and what I would call the exo-genome: all of the genomes and epigenomes of the micro-organisms with which we are symbiotic. THEY digest most of our food. THEY determine how much nutrition and how many calories we absorb out of a given intake of food matter.

The soil has also become mineral depleted, so food today doesn't contain the same amount of minerals as it did in the past. This can possibly lead to overeating.

I used to find this implausible since a crop will not grow in ground without proper nutrition. It's a staple of horticulture and agriculture that even missing micronutrients create unhealthy and unproductive, or dead, plants. However, with the advances in hybridization and GMO, I'm not sure that's true anymore.

Jesus, it's not "implausible," it's fact! There are research studies. It's simple enough to measure the nutritional content of crops. As yields have gone up, nutritional value has gone down. It's indisputable.

Usually my comments are too long and boring to read to the end, but I thought this one was short enough to get there -- I was agreeing with Jonas, not disagreeing.

To be clear, my point was that once-upon-a-time if your soil was poor you didn't get poor crops, you got no crops. The whole fallow field, bury fish in with the crops, crop rotation thing? All those textbook pictures of the same kind of plant grown with and without micronutrients, etc.? But agriculture and green revolution advances (hybrids, new fertilizers) have changed the game. Here's a SA article about that, although I'm not seeing anything but assertion in it for the points about organic. Thanks for prompting me to look that up.

While true that nutrient density is decreasing, it is a bit misleading too. Breeding has increased the grain production per plant basically by increasing starch and increasing seeds per plant produced. The absolute volume of minerals put into seed per plant hasn't changed much. But when the number of seeds increases and the seeds increase in size (mostly starch), the mineral content is diluted by the starch bulk.

The same applies to less sweet fruits or tomatoes. Go buy a commercial variety of tomato plant and plant it beside the heirloom variety. Only allow the commercial variety to product as many tomatoes as the heirloom (probably 3-5 at a time). The commercial variety will not differ as greatly in flavor vs the heirloom. Allow another commercial variety to ripen 20-30 tomatoes simultaneously for easy harvesting and you get watery, flavorless fruit.

Surprised no one's mentioned the other chemical that has grown rapidly in the environment over the last several decades with known links to fat storage: estrogen.

Soy, growth hormones in beef, and water supply from BCPs, right? All things we really like, though.

Is estrogen readily absorbed through the gut?

Good question that someone will be able to answer well, but I'd guess there's at least a partial "yes" there since that's what oral contraception is based on.
But they might formulate it to facilitate absorption, if those are the right terms.

I haven't heard of any good gov't estrogen in the environment study -- has the EPA really studied it and found estrogen to not be a pollutant?

I understood it stays a long time in the environment.

It also affects sperm counts, like in fish, which are decreasing.
Probably a significant contributing factor, among others. But the most politically incorrect to discuss -- so one of the most likely, since the possible more PC causes seem not to be such big causes.

Space aliens bombarding the Earth with fat rays. For the obvious reasons ("To Serve Man").

If weight is increasing so uniformly, then gravity is increasing.

Took me about seven beats to get that one. . . . !

The lab mouse diet is controlled only for calories and nutrient content, not for all components of its composition. It's kibble made by agribusiness, not a controlled formula.

I would imagine at one time, lab mice/rats were fed butter, lard and/or tallow. Now it's canola, corn or soy oil. Their grains were fairly organic and most likely corn and long stalk wheat. Now it's GMO corn, soy and/or dwarf wheat. The sugar was cane or beet. Now it's high fructose corn syrup.

So yes, the calorie and nutrient content of their chow is the same, and the ingredients may sound the same, but they are vastly different.


The fact that you mention "GMO" as if it meant something as a category means you are clueless and should be ignored

Your certainty suggests you should be ignored.


Radio waves, cell phone towers, get out your tin foil hats!

Who knows, but I'll go with epigenetics. Human generations get progressively taller over periods of plenty. Like the humans, the control mouse population is now that many generations further separated from the Malthusian state of nature. Maybe the rats too. More food should mean more rats, but perhaps the rat population is not in equilibrium with the food source, but rather in equilibrium with the rat poison. Living the easy life until you eat something nasty.

The universe is expanding.

Is confirmation forthcoming from autopsies of rat fleas? Are rat fleas commensurately rotund? How about the plague in THEIR guts? Is plague bacteria so swollen it can't navigate into a human bloodstream?

Too much artificial light.

I read the comments to a previous citation of this study. The commenters were quite intelligent and a few of them had information about the laboratory animal situation. Two main points.

1. The feed formulations are changing constantly, despite claims that they are kept the same. Maybe researchers will try to keep the formulation the same over the span of an individual experiment, but the manufacturers are frequently changing the formulations for changing economic reasons.
2. The laboratory animals undergo a process -- over generations -- of winnowing out the obstreperously active animals. In other words, the ideal lab animals are docile, ergo somewhat less active in cages, and the problematic animals cause problems that lead to their being taken out of the lab animal gene pool. Consequently, there is a sustained increase in lab animal docility associated with gaining weight.

This is second-hand information, but seems quite plausible. Moreover, the lab animal aspect of the obesity trend is the key element -- the trends in other types of animals have various causes that aren't so hard to figure out.
If the lab animal obesity trend is explained by the above factors, the impact of the article is considerably reduced, but most people (who don't have direct experience with lab animals) will tend to mistakenly accept the proposition that the scientists are capable of the difficult feat of keeping the feed steady and gene lines immutable.

I always knew Baltimore was The Fire Swamp.

I recognize that mouse. It's from a study where scientists did gene alterations to one mouse to make it either much heavier or much lighter than the control.

As any true science acolyte on the web can tell you, everything is determined by calories in vs calories out. Therefore the only explanation is that rodents and domesticated animals are worried by overhearing us humans talk about the heat death of the universe, and so have decided to store as much energy as possible to forestall that eventuality. You can try explaining things like closed systems and description vs prescription to them, but understanding what thermodynamics actually is saying is probably reserved for higher order beings like ourselves.

That's a little implausible. I think border collies can get it.

Usually I start babbling about insulin response and their eyes glaze over.

Yeah, but so do mine. . . oh.

I wonder if air-conditioning could play a role. When I was a kid (around 1982) many places blasted air conditioning because it was ridiculously cheap. As we've become more energy conscious most businesses and residences have ticked the thermostat up a degree or two. The increase in heat could cause the animals to move around slightly less burning slightly fewer calories.

It seems like an environmental factor that could affect both mice on a steady diet and domestic animals.

I agree air-conditioning is the environmental factor driving the change.

Food got cheaper. Don't think it's any more complicated than that.

BTW if you don't want your cats to get fat/diabetic, don't give them a diet of primarily carbs. Get the Blue Buffalo wet or Halo dry foods.

What about cheap tuna and mice?

Mice are too fat.

Mice have diseases, tuna doesn't have the right mix of aminos and EFAs.

My parents fed the cat chicken for the last 10 - 12 years of its life. They'd buy a whole chicken, cook the best parts for themselves, boil the rest and feed it to the cat. She supplemented that diet with mice, and lived to be about 21 years old, as an indoor-outdoor cat.

She didn't get fat from it, either, but that's partly portion control and lots of outdoor exercise.

I wonder if control mice also exhibit sperm count decrease, as we humans do (well, we male humans that is). Maybe there's a lot of proto-oestrogens in the water, which would encourage an increase in body fat?

Clearly the answer is chemtrails. Maybe the control group of rats need tiny tin foil hats?

This explains why so few rats have PhDs.

I'm think there are different reasons for the different increases. Regarding the lab mice, a decade is ~33 generations, and that's more than enough time for selection to increase body size. It would be relatively trivial to increase the average weight of a population of dogs from 60 lbs to 68 lbs in a few generations, never mind 33. So then the issue is what would select for larger mice? Several possibilities come to mind (#3 seems to be the most straightforward):

1) Mice in captivity (especially males) can be incredibly aggressive towards each other. That's before you get to the infanticide. Being bigger certainly would help.

2) Larger body size often is correlated with higher fecundity. Depending on how one propagates the colony, this could be an issue.

3) Researchers probably won't pick the 'runty' ones, which skews the distribution. For propagation, 'stud' mice (males) are typically chosen. If there is a researcher bias towards picking the big ones....

Epigenetics or the microbiome could be involved (hard to rule out and not mutually exclusive), but, despite what some commenters are claiming, we have many examples across a wide range of animals that moderate phenotypic change can occur in 'observable' time, when there's strong selection. Animal breeders have breed significant change; the lab setting might be doing it accidentally.

Not sure how this could apply to people though, so I'm inclined to think that lab animal and human increases are merely coincidental.

I've heard that medicine is killing off some gut bacteria which contributes to obesity. Our sewage is getting into drinking water and causing weird things with fish. So a crazy theory (that I'll give a p<.05 of being true): our medicine that kills gut bacteria is feeding into the water source and getting into animals, messing with their bacteria and making them fatter.

On urine pollution:

A couple years ago I read (via Megan McArdle) that zoo animals were also getting fatter.

Maybe at this point we can stop treating the obesity epidemic as a morality play starring dem old debils Sloth and Gluttony, and instead start looking for hidden medical factors that could be causing this.

The truth is that animals go obese first. Human beings got obese second, after eating the fat animals that had been "bulked up" with chemicals prior to slaughter. Ingest the beef and ingest the chemicals.

Warren may be on to something. There is some evidence that the gut bacteria is different in obese people compared to those who have not been obese.

But we should examine the possibility that the Roswell aliens were part of a ranching project by a fat-consuming alien race to inoculate our environment to fatten up the feedstock on Earth in preparation for harvest at some point when we achieve an economically profitable level of ripening.

The herbicide glyphosate affects gut bacteria. Its increasing use could account for this finding.

Animals Fat? People Fat?

What has changed drastically since 1965?

The amount of corn in the diet, as an additive, as a sweetener and as a staple in the diet.

Look at any population that has used corn as a staple, over the last 1000 years, and you will find obesity. And the corn of today, starting in the 1900's is not the corn that was found in the America's when the first Europeans arrived. It has been bred to be stronger, sweeter and far more potent than the corn the natives planted. And they too, even then had problems with Diabetes, and when forced to rely on a diet of mainly corn, obesity.

Now its found in every food, even fast foods, Pet foods, and livestock foods.

The bacteria in the human gut has one type that, when antibiotics are administered, survive, and multiply- it craves the corn diet, and is easily spread, infecting animals as easily as humans. It is found on your teeth, found in your gut, found in your bloodstream and is the main suspect in hardening of the arteries, most gum diseases, and diabetes,

Take the corn out of the diet, and this bacteria is starved. Take out the upper section of the intestine, where the bacteria influences the gut to produce an abundance of two hormones linked to obesity, and type II diabetes, and you get rapid weight loss, and a 98 percent cure of type II diabetes.

Hey dummies, if people are getting fatter and animals are eating the scraps of food left over by those fat people - it's the same shitty food that's making the animals fat.

They get the same low quality food I am if I cant walk in my neighborhood neither can the dog.

Did you do tests for rats in a rural environment? there is more food waste in cities.

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