Shattering the Vegetarian Myth: Meat Consumption Was Intrinsic to Human Evolution

Apologies for the absence. It takes time to finish one life and start another.

At least this dragged me back into the scene: Kathy Freston's "Shattering the Meat Myth: Humans Are Natural Vegetarians." The piece is, and I hesitate to write this in an age where one's Google News feed bears a striking resemblance to The Onion, a breathtakingly poor scrap of doggerel. Even for ill-researched propaganda, this beast is remarkable in its reckless and wanton distortion of not only science, but of history as well.

This rebuttal in no way touches upon the relative morality or nutrition of diets that include or exclude animal products. In fact, the article came to my attention via Facebook by a respected friend and colleague who takes a valid moral stance against meat consumption. However, with 20,000 other Facebook Likes at the moment, I cannot let the grotesque inaccuracy of the arguments from biology stand. To crib from Samuel L. Jackson's character in Pulp Fiction, "Well, allow me to retort!"

Freston argues as follows (and by all means, read the original to evaluate my summary).
1. The inclusion of meat in the human diet is a product of agricultural civilization (circa 10,000 years ago) and is incompatible with a plant-based biochemistry that dates back "at least tens of millions of years." Prior to the rise of herding, "we may have needed a bit of meat… in times of scarcity."
2. "Humans are herbivores" because we lack physical adaptations that make it easy to tear flesh and hide, such as overdeveloped canine teeth and claws. We resemble the other great apes in that we process food with our hands and must have similarly had "a largely plant-based diet."
3. Humans have "never adapted" to a meat-inclusive diet because meat-eaters have a higher incidence of heart disease, cancer, and diabetes.

Freston's deeply flawed arguments can be attacked from historical, evolutionary, and logical angles. Let's get the observed history out of the way so we can get on to the evo.

A History of Meat Consumption
Let us assume, for the purposes of clarity (since Freston surely provided little), that the "natural" state of humanity refers to traits expressed prior to civilization and its concomitant horrors. Freston has asserted that, before the advent of agriculture-dependent herding 10,000 years ago, humans consumed only small quantities of meat in times of hardship.

Um. But.

This ignores the physical record of at least 70,000 years of hunting. Hunting big things. From some of the earliest human art on cave walls depicting the hunt, to no shortage of archaeological sites riddled with thousands of mammoth bones (one example), remains of other large and small mammals, deep middens of fish bones and mollusk shells, and so on. By about 10,000 years ago, we were in part responsible for the disappearance of nearly every large mammal in the Western Hemisphere by eating them toward extinction.

South African cave art. Photo Credit San Felszeichnung, from Wikimedia Commons.

Of course, then civilization struck and, well… a grand total of zero of the remotely successful cultures on the planet, now or in recorded history, have categorically excluded meat from their diet. Jared Diamond has a little more to say on the subject.

But let's throw Freston a bone (hah) and examine her argument in the time frame of millions of years. What does biology have to say?

Pretty Much The Same Thing
Freston views humanity through the lens of our closest living relatives, the other great apes, so let's follow. Our sister group, the two chimpanzee species, eat lots of lovely fruits and vegetable bits. Er, and also insects, birds, and mammals including other primates and small relatives of cows and pigs(!). Meat only comprises about 5% of their caloric intake, but for a species relying on its hands, primitive tools and wits, it's seriously impressive that they can muster as much.

Is Freston correct that the human gut tract is like the intestines "of other herbivores" in being very long? No, we're rather intermediate on the spectrum between hypercarnivores and herbivores. Incidentally, carnivore gut tracts are not particularly short "so they can quickly get rid of all that rotting flesh they eat" - another of the bountiful instances in which Freston's sensationalism throws science on the fire. Carnivores have a short and efficient intestinal tract in that they don't need to process large quantities of generally indigestible plant fibers. Our barrel-shaped rib cages, rather than the conical arrangement exhibited by primates that consume more plant matter, in part reflects this reduction in gut length.

Freston laments the absence of wicked claws and fangs (actually, in primates the size of the canine teeth is strongly correlated with social structure rather than with diet) and such. If only humans had a way of compensating for that!

Oh. Right. The whole running and tools thing.

A proper treatment is well beyond the scope of this post, but the evolution of the human body plan from that of a four-footed ancestor appears to have been driven in large part by selective pressure on the ability to run long distances efficiently - and later, while holding tools. Our legs and feet are superbly adapted to long distance running. The NYT has a decent, if brief summary of a few of these characters, and there's a skeletal outline of the endurance running hypothesis over at Wiki. This ability may be nearly 2 million years old, dating back to Homo erectus.

There are a couple reasons for us to run long distances: to poach kills (in fact, that's how we got tapeworms from large cats and hyenas), and to run prey into the ground. Turns out we're pretty good at that (awesome Attenborough video!). We run, we track, and unlike many of our large prey, we can sweat to cool off in the chase. Persistence pays off.

Might meat consumption have put evolutionary pressure on not only our body plans, but on our developmental timing as well? Humans wean their offspring at a very early age relative to other great apes (2 years and change in humans / 5 in chimps / 7 in orangutans, which consume very little animal protein). This is a pattern common to carnivorous mammals (PLoS ONE original). Carnivores wean their offspring faster than do herbivores due to improved milk quality and/or the ability of the offspring to eat high-energy meat. After weaning, females again become receptive to mates; the upshot is that a shorter weaning period increases reproductive capacity.

The preponderance of evidence suggests that Freston's thesis could not be more wrong. The increased means to acquire and utilize meat was likely one of the major driving forces behind the evolution of our bipedal body plan optimized for endurance running, our ability to make and manipulate tools, and our developmental timing. There are other human relatives that were more clearly geared toward eating tough plant matter. They didn't make it.

But It'll Still Kill You
Meat is an extremely efficient source of nutrients, including proteins, fats, vitamins, and minerals. When combined with leafy greens and other nutritious foods and an active life style, it helps build healthy bodies. In the short term. In the long term, the consumption of, in particular, red and processed meats is linked to increased risk of cardiovascular disease, certain cancers, and diabetes.

Apparently needing a screamingly ludicrous sound bite from an otherwise distinguished individual, Freston concludes her sad crusade with this gem from Dr. William Roberts, editor of the American Journal of Cardiology. In its entirety: "Although we think we are, and we act as if we are, human beings are not natural carnivores. When we kill animals to eat them, they end up killing us, because their flesh, which contains cholesterol and saturated fat, was never intended for human beings, who are natural herbivores." Coupled with another MD suggesting that "our bodies have never adapted to [eating meat]," it begs the obvious question: why did our ancestors eat meat - and as we have seen above, they certainly did - if it predisposed them to disease? The answer, again, rests in timing.

Except in cases of gross excess and sedentary life styles, these pathologies tend to strike late in life. Specifically, they largely affect post-reproductive (or nearly so) individuals. If you die at 55 from a heart attack but raise ten vigorous, meat-fed offspring, you still have dramatically higher fitness than a vegetarian who lives to 90 but raised five offspring before menopause. Additionally, during the course of human history, "post-reproductive" is a luxury that an incredibly small portion of the population would ever live to see; those disorders would be invisible to natural selection. The MDs' argument is completely vacuous. While they may mean well, I won't stand by to see them misinform the public in order to do so.

It's good to be back.

[Note: Desmond Morris tackled the evolution of humans as a balancing act between carni- and herbivory in his classic The Naked Ape.]

A Day Late and a Dollar Short

Please forgive the absence. June was spent running analyses and putting together my talk for the Joint Meeting of Ichthyologists and Herpetologists (nerds working on fishes and reptiles/amphibians, respectively) in Providence. Two glad tidings: I have returned to wax scientific on subjects, and I was honored to receive the ASIH Stoye award in General Ichthyology at the conference. Before the year is out, I will write an article here on the same: what the interrelationships of batoid fishes, my study group (skates, rays and allies), can tell us about widespread convergent evolution and the effects of the end-Cretaceous extinction event on their current patterns of diversification.

Speaking of mass extinction...

This one has been a while coming. Toward the end of last year, several science news outlets picked up a striking article in the journal Biological Conservation. In short, it suggested that current guidelines for setting minimum population sizes for protected species, like the black rhinoceros, are at least an order of magnitude (10x) too low to adequately protect them from extinction in this century. The current guidelines adhere to a "50/500" rule, in which a minimum of 50 adults are required to avoid the negative effects of inbreeding, and a minimum of 500 to be able to adapt to long-term environmental changes or rebound from a catastrophic event.

Ten times too low. Put a big, flashing exclamation point at the end of that one. Horrifying corollaries are immediately evident: many species are already too far gone to be preserved in the long term even if we dropped everything to triage them now, and species we think we've done a bang-up job of protecting to date may just need one calamity to drop them below that point of no return. In light of the political difficulties - an understatement by any measure - of maintaining even today's meager/modest conservation measures, a tenfold increase will never happen. These species, humble to majestic, mountain gorilla (~400) to desert pupfish (42!), are going away sooner than we'd like.

It is not an encouraging picture.


Black rhinoceros. Photo credit John and Karen Hollingsworth, USFWS, from Wikimedia Commons.

This is not a political blog, so we'll leave the issue behind and look at what these numbers mean. Why do we need X number of animals to avoid catastrophe? The first barrier, inbreeding, is intuitively obvious: offspring are produced by close genetic relatives. Put another way, the two copies that an individual carries of each her genes have a high probability of being identical by descent, or having come from the same ancestor (grandma) independently through each parent. Gross, yeah. But why is this necessarily a bad thing? Every human has two identical copies - alleles - of at least some genes, and we're not all running around with horrible genetic abnormalities. Things go south (no pun intended; I am from Texas after all) when you deal with genes that have a healthy version and a defective one.

At many gene locations in your DNA, you have one healthy allele and one defective one. In most cases, the normal copy steps up and does a stalwart job compensating for the freeloader. You'll never notice that one copy is bad, and so we call that copy a recessive, or hidden allele. That's the good news. The bad news is that they're ticking time bombs on a generational timescale. When you reproduce, one of those alleles is "drawn" at random to end up in your sperm or eggs. If you pass on the healthy version, great, your child will be A-OK for that gene. If not, you'd better hope that your mate contributes a healthy copy to pull the weight for your freeloader. If two recessive alleles end up in the offspring, she won't be able to make that gene's normal protein product. The effects may be mild, and even desirable to some: blond hair or blue eyes. Or instead, they may cause a serious genetic malady like cystic fibrosis or sickle cell anemia. If you have one healthy and one hidden, defective allele for a disease-associated gene, you are a carrier. Everyone on the planet is a carrier for an unknown, but probably not inconsiderable, number of genetic disorders. This is the basis behind genetic testing, which is becoming cheaper and more widely available every year.

The rest is easy to follow. If you're a cheetah and there are only a handful of your species left (the cheetah-reality is not that dire), the odds that you are closely related to any other cheetah you see are much higher than they are for a species with larger population sizes, like industrialized humans. If you mate with that cheetah, your odds of having the same set of alleles from a common ancestor are high, and an increasing proportion of offspring will either have two healthy or two defective copies of a gene - allele fixation. You can see how the situation degrades quickly once disease traits become universal in a population. Lost genetic diversity takes a long, long time to be recovered.

The second, higher requirement for a minimum viable population size (the 500 of the 50/500 rule) is trickier to understand. It builds on the concept of inbreeding, but the higher number of organisms keeps a larger gene pool - the total genetic variation in a population - available into the future. High genetic variation gives a population options, so to speak, in the face of environmental change. There may be warmer-adapted cheetah alleles that would do better under increased temperatures, or slightly faster cheetahs that can better keep up with Thomson's gazelles, which are under similar pressures. Perhaps most importantly, it provides options for [pathogenic] disease resistance.

Viruses, bacteria, and other parasites are engaged in a constant arms race with their hosts at a molecular level. Genetic variability goes a long way to ensure that at least some cheetahs will survive a potent disease, while if they are genetically homogeneous, a single bacterial strain that has "figured them out" can wipe out the whole population in one fell swoop. As a great recent example, humans of European descent have a much higher incidence of a genetic mutation called CCR5-delta32 that provides resistance to HIV. This mutation also appears to confer resistance to the great historical European plagues. That is, some Europeans had this mutant allele and became resistant to plague, while other didn't and were selected against. If Europe's population had been much smaller, this mutation may have never arisen and the entire continent could have been taken out in one of those dread epidemics.

A grim picture, to be sure. The next steps are political, but having been introduced to the science, hopefully you are in a better position to weigh the costs and benefits of conservation measures for yourself.

Here's to an educated democracy.

This reView of Life(?): Viruses, Part 2

The first decade of this brave new century was characterized by dramatic upheavals, often violent, in politics, business... and film. Perhaps through widespread disillusionment in the wake of crises in security and finance, perhaps merely the pendulum swinging back from the fantastic (read: "divorced from reality") flavors of storytelling in the 1980s - early 90s, the public has rushed to embrace the gritty and believable. Joel Schumacher's candy-colored Batman films were usurped by Christopher Nolan's dark masterpieces, achieving almost ridiculous commercial success. Peter Jackson breathed life into a vision of The Lord of the Rings that eschewed most of the magic and occasional levity of the book, and also featured a rather mundane, if attractive, aesthetic. Additional existing franchises and concepts from other media leapt to the big screen or were rebooted, and surprisingly often attempt to feature some "scientific" hook to enhance the believability of the tale. One of the rising stars of this movement is our enigmatic acquaintance, the virus.

Viruses are now almost universally implicated as the nefarious causal agent in modern zombie tales or close cousins, such as the animalistic, deranged "infected" in 28 Days Later. Alas, the point of this article is not to tackle the questionable physiology of a zombie (actually, that sounds like a good one for another day), but rather to touch on Hollywood's mixed success in portraying the pathology of viruses.


The virus in 28 Days Later is particularly terrifying in that, 30 seconds after exposure, a victim is reduced to a hemorrhaging, raging volcano of virus-laden fluids. One infected person in a crowd can effect some sick parody of The End Times in mere minutes. Viruses in many other films spread with similar urgency, in some cases reanimating a corpse within two minutes of exposure (Dawn of the Dead reboot). What does the real world have to say about this?
©2002, 20th Century Fox.

Viruses are constrained by the same physical laws that the rest of us are, regardless of your definition of "life." A generic viral life cycle, and there are all sorts of bizarre variants, goes something like this:
 1) find a host cell;
 2) enter the host cell, or inject genetic material;
 3) use own or hijacked machinery to replicate genes and coat proteins;
 4) stay forever, or have all your copies erupt out of the host cell;
 5) repeat.

Each of these steps requires time, particularly step (3). This is even more of a problem for related scifi concepts involving rapid gains of animal/plant/fungal tissue, or what I call "The Werewolf Problem." I'll leave that for another day.

The window of time between initial exposure and the point at which symptoms first emerge is called the incubation period. During incubation, viruses are reproducing and spreading through host cells but are at insufficient numbers to make much of an impact. Yet. So how long is this timetable? Clearly 30 seconds for complete system takeover is unrealistic.

The fastest acting human virus, as far as I have been able to discover, is the stringy little fiend below, ebola. The incubation period of ebola is 2 - 21 days, but usually 5 - 18 [source: Emerging infectious diseases 9(11):1430-7; via Wikipedia]. The fastest.


Ebola virus. Photo Credit Centers for Disease Control, from Wikimedia Commons.

A common pattern of viral strategies is a correlation between their agressiveness and their ability to be transmitted. Ebola and similar viruses have evolved a strategy that is very much living (yes, I said it) on the edge. They emerge, spread and kill so quickly that they run the risk of not being able to find a new host and suffering local extinction. Compare this to the less common strain of the virus that causes AIDS, HIV-2. HIV-2 often degrades the immune system more slowly than does HIV-1, leading to higher long-term survival rates. It also is less successful at being transmitted between people. For an analogy in honor of the ongoing NBA finals, it may only shoot 60% from the field compared to HIV-1's 80%, but gets an extra five minutes of playing time. The natural world is full of these trade-offs, in which organisms fine-tune their life strategies over time.

The ones that fail? Well. We don't see those guys anymore.

On that note, next time I will likely bring up some recent, distressing speculations about the fates of endangered species.

This reView of Life(?): Viruses, Part 1

There are no absolutes in science. The closest you'll get is in physics, but most of the so-called Laws remain either fundamentally unexplained and/or not quite what we thought they were. If asked to name one "obvious truth" about the natural world, I suspect most folks would immediately come up with something about gravity. "If I let go of this cute kitten, it will fall." But would you believe that we have almost no idea why this is so? We have nothing but competing theoretical frameworks for why things fall, and to get more technical, why gravity should exactly equal an object's inertia. No [prevailing] idea whatsoever. To make matters worse, gravity appears to "misbehave" at astronomical distances. The concepts of dark matter and dark energy are stabs at explaining why our observations of big objects' movement through the universe do not at all conform to expectations under gravitational theory, and our most distant manmade satellites are typically not where we expected them to be. The explanations could be mundane... or not.

Biology is far messier, if much better understood. In fact, as a biologist it is difficult to even define our field! Think on this for a moment: how would you define life? Which set of characteristics makes something living, from people to peas to protists? Let us consider two different candidates.

The first is from NASA, whose stalwart crew of scientists are engaged in the very business of finding weird, unexpected kinds of life out there in the big empty.

"Life is a self-sustained chemical system capable of undergoing Darwinian evolution."


For a different perspective, let's go to the textbook I'm using to teach non-majors intro bio this summer, Essential Biology by eds. Campbell, Reece & Simon.
"The set of common characteristics that distinguish living organisms, including such properties and processes as order, regulation, growth and development, metabolism, response to the environment, reproduction, and the capacity to evolve over time."

Clearly there's something going on behind the scenes to have two such dramatically different definitions. NASA's definition is more inclusive, which is to be expected when anticipating exotic forms of "life," but what exactly are the textbook makers ruling out?

Why, it is your friend and mine, the pesky little bugger that's had me coughing and cursing for the last week: the virus.

Viruses and bacteria are together responsible for most human infectious diseases, but are fundamentally very different things. A bacterium is an organism by any definition, composed of a single discrete unit called a cell. Its arrangement into wholly or semi-autonomous cells puts it in the same league as all other life (by the textbook definition) on Earth: it grows, it divides, it responds to stimuli, and as an imperfect reproducer its populations are capable of change over time.

The virus is not a cell. Writers for pop media often get this dead wrong. For example, consider an episode of the current Fox television series Fringe. The show features both surprisingly excellent characters and some of the mostly howlingly terrible "science" I've ever seen. A sluglike parasite used in assassinations was revealed to be a genetically engineered supersized cold virus "cell." Sigh.

Viruses are actually a diverse grab-bag of maybe-organisms consisting, at a minimum, of genetic information and a protective coat. The info can be stored either as DNA, as in all cellular life on Earth, or as its chemical cousin RNA. The coat is made of protein and sometimes fats. A virus is basically the nasty hacker of the biosphere: it comes into contact with some cellular organism, injects its genetic material, and hijacks that cell's machinery to make more copies of the virus. In some cases, the cell basically explodes in order to release a swarm of new viruses. Other, more sinister viruses actually incorporate themselves into the host's DNA and "hitch a ride." Potentially forever. A good deal of the so-called "junk DNA" in your genome is actually viral information: some dormant, some not so much!

How do you fight something like that? We have antibiotics against cellular organisms, like bacteria: chemical compounds that selectively interfere with the pest's way of life. Not so with viruses. Antibiotics have zero effect on them, and are actually counterproductive in that they give rise to resistant strains of bacteria that can then feel free to rise up and take on humanity. Vaccination is currently the best defense against viruses, since the limited supply of drugs that can actually hamper the viral life(?) cycle often do a good deal of damage to the patient's cells too.

So. What do viruses lack that makes some consider them non-living? Do they possess order/structure? Of course; take a look at this micrograph of swine flu. So does ice, great. Reproduction? Check, but so does fire. Evolution? Yes oh yes. Metabolism? That one's a maybe, since it hijacks a host cell's metabolic machinery. The "problem" lies in virus' inability to directly grow (although they self-assemble) and, more importantly, maintain an internal environment different from what's outside their coat.
Swine flu (H1N1). Photo Credit C. S. Goldsmith and A. Balish, CDC, from Wikimedia Commons.

Okay, I could buy that, except some bacteria run into the same problem when they face certain stresses. In these circumstances they form spores, which are dormant, hardcore, last-chance structures used to ride out what would otherwise be certain death. Some important causes of human disease form spores, like the agents behind anthrax and botulism. Spores do not have metabolism, do not reproduce, do not grow, do not maintain that internal environment... they are basically virus-like, waiting for favorable circumstances before developing back into bacteria. While a bacterium may form a spore while it waits for nutrients to come along, viruses wait for new host cells.

Personally, I side with NASA and find it hard to call spores and viruses nonliving. There is a tremendous gulf between viruses and uncontroversially nonliving particles, far greater than that between viruses and some bacterial stages. At worst, viruses are renegade bits of life. Hypotheses of the origins of viruses, events which have probably occurred innumerable times through the history of life on Earth, usually stipulate these bits of genetic information "going rogue" and escaping the cell with the bare minimum of machinery for propagating themselves. Once they're out in the biosphere, evolution takes over and all hell breaks loose.

And that's what life is all about.

Next time: touching again on the misrepresentation of viruses in pop culture, particularly movies.