Home » cooking

Category Archives: cooking

Earlier Evidence for Erectus’ Use of Fire

1600 words

I hold the position that the creation and management of man-made fire was a pivotal driver in our brain size increase over the past 2 my. However, evidence for fire use in early hominins is scant; a few promising locations have popped up over the year, the most promising being Wonderwerk Cave in South Africa (Berna et al, 2012). Much more recently, however, it was discovered in Koobi Fora, Kenya, that there was evidence of fire use by Erectus 1.5 mya (Hlublik et al, 2017).

Hlublik et al (2017) identified two sites at Koobi Fora, Kenya that have evidence of fire use 1.5 mya, and Erectus was the hominin in that area at that time. Hlublik et al (2017) conclude the following:

(1) Spatial analysis reveals statistically significant clusters of ecofacts and artifacts, indicating that the archaeological material is in situ and is probably the result of various hominin activities during one or a few occupation phases over a short period of time. (2) We have found evidence of fire associated with Early Stone Age archaeological material in the form of heated basalt (potlids flakes), heated chert, heated bone, and heated rubified sediment. To our knowledge this is, to date, the earliest securely documented evidence of fire in the archaeological context. (3) Spatial analysis shows the presence of two potential fire loci. Both loci contain a few heated items and are characterized by surrounding artifact distributions with strong similarities to the toss and drop zones and ring distribution patterns described for ethnographic and prehistoric hearths (Binford 1983; Henry 2012; Stappert 1998).

This is one of the best sites yet for early hominin fire control. This would also show how the biologic/physiologic/anatomic changes occurred in Erectus. Erectus could then afford a larger brain and could spend more time doing other activities since he wasn’t constrained to foraging and eating for 8+ hours per day. So, clearly, the advent of fire use in our lineage was one of the most important time frames in our evolutionary history since we could extract more energy from what we ate.

Carmody et al (2016) identified ‘cooking genes’ that were under selection between 275-765,000 ya. So we must have been cooking, in my opinion, before 765,000 ya, which would have then brought about the genetic changes due to a large shift in diet—which would have been cooked meat/tubers. Man’s adaptation to cooked food is one of the most important things to occur in our genus, because it allowed us to spend less time eating and more time doing. This change to a higher quality diet began in early Erectus (Aiello, 1997), which then shrank his teeth and gut. If Erectus did not control fire, the reduction in tooth size needs to be explained—but the only way it can be explained is through the use of cooked food.

Around 1.6 my there is evidence of the first human-like footprints/gait (Steudel-Numbers, 2006Bennett et al, 2009). This seems to be the advent of hunting parties and cooperation in hominins to chase prey. The two new identified sites at Koobi Fora lend further credence to the endurance running hypothesis (Carrier, 1984Bramble and Lieberman, 2004; Mattson, 2012), since without higher quality nutrition, Erectus would not have had the anatomic changes he did, nor would he have the ability to hunt due to being restricted to foraging, eating, and digesting. Only with higher quality energy could the human body have evolved. The further socialization from hunting and cooking/eating meat was also pivotal to our brain size and evolution. This allowed our brains to grow in size, since we could have high-quality energy to power our growing set of neurons.

The growth pattern of Nariokotome boy (formerly called Turkana boy) is within the range of modern humans and does not imply that he had a growth pattern different from that of modern humans (Clegg and Aiello, 1999). It’s interesting to note that Nariokotome boy, one of the best preserved Erectus fossils we have discovered to date, had a similar growth pattern to modern humans. Nariokotome boy is estimated to be about 1.6 million years old, so this implies that we had similar high-quality diets in order to have similar morphology. It is also interesting to note that Lake Turkana is near Koobi Fora in Kenya. So it seems that basic human morphology emerged around 1.5-1.6 mya and was driven, in part, by the use and acquisition of fire to cook food.

This is in line with the brain size increase that Fonseca-Azevedo and Herculano-Houzel (2012) observed in their study. Metabolic limitations of herbivorous diets impose constraints on how big a brain can get. Herculano-Houzel and Kaas (2011) state that Erectus had about 62 billion neurons, so given the number of neurons he had to power, he’d have had to eat a raw, herbivorous diet for over 8 hours a day. Modern humans, with our 86 billion neurons (Herculano-Houzel, 2009; 2012), would need to feed for over 9 hours on a raw diet to power our neurons. But, obviously, that’s not practical. So Erectus must have had another way to extract more and higher-quality energy out of his food.

Think about this for a minute. If we ate a raw, plant-based diet, then we would have to feed for most of our waking hours. Can you imagine spending what amounts to more than one work day just foraging and eating? The rest of the time awake would be mostly spent digesting the food you’ve eaten. This is why cooking was pivotal to our evolution and why Erectus must have had the ability to cook—his estimated neuron count based on his cranial capacity shows that he would not have been able to subsist on a raw, plant-based diet and so the only explanation is that Erectus had the ability to cook and afford his larger brain.

Wrangham (2017) goes through the pros and cons of the cooking hypothesis, which hinges on Erectus’ control of fire. Dates for Neanderthal hearths have been appearing later, however nowhere near close enough to when Erectus was proposed to have used and controlled fire. As noted above, 1.6 mya is when the human body plan began to emerge (Gowlett, 2016) which can be seen by looking at Nariokotome boy. So if Nariokotome boy had a growth pattern similar to that of modern humans, then he must have been eating a high-quality diet of cooked food.

Wrangham (2017) poses two questions if Erectus did not control fire:

First, how could H. erectus use increased energy, reduce its chewing efficiency, and sleep safely on the ground without fire? Second, how could a cooked diet have been introduced to a raw-foodist, mid-Pleistocene Homo without having major effects on its evolutionary biology? Satisfactory answers to these questions will do much to resolve the tension between archaeological and biological evidence.

I don’t see how these things can be explained without entertaining the fact that Erectus did control fire. And now, Hlublick et al (2017) lends more credence to the cooking hypothesis. The biological and anatomical evidence is there, and now the archaeological evidence is beginning to line up with what we know about the evolution of our genus—most importantly our brain size, pelvic size, and modern-day gait.

Think about what I said above about time spent foraging and eating. Looking at gorillas, for instance, they have large bodies partly due to sexual selection and the large amounts of kcal they consume. Some gorillas have been observed to have consumed food for upwards of 10 hours per day. So, pretty much, you can have brains or you can have brawn, you can’t have both. Cooking allowed for our brains as we could extract higher quality nutrients out of our food. Cooking allowed for the release of a metabolic constraint—as seen with gorillas. It wouldn’t be possible to power such large brains without the addition of higher quality nutrition.

One of the most important things to note is that Erectus had smaller teeth. That could only occur due to a shift in diet—masticating softer foods leads to a subsequent decrease in tooth and jaw size. Zink and Lieberman (2016) show that although fire-use/cooking was important for mastication. Slicing meat and pounding tubers improved the ability to breakdown food by 5 percent and decreased masticatory force requirements by 41 percent. This, too, led to the decrease in jaw/tooth size in Erectus, and the advent of cooking with softer/higher-quality food led to a further decrease ontop of what Zink and Lieberman (2016) state, although Zink and Lieberman (2016: 3) state that “the reductions in jaw muscle and dental size that evolved by H. erectus did not require cooking and would have been made possible by the combined effects of eating meat and mechanically processing both meat and USOs.” I disagree and believe that the two hypotheses are complimentary. A reduction would have occurred with the introduction of mashed food and then again when Erectus controlled fire and began cooking meat and tubers.

In conclusion, the brain size increases that are noted in Erectus’ evolutionary history need to be explained and one of the best is that he controlled fire and cooked his food. There are numerous lines of evidence that he did, mostly biological in nature, but now archaeological sites are beginning to show just how long ago erectus began using fire (Berna et al, 2012; Hlublick et al, 2017). Many pivotal events in our history can be explained by our shift in diet to softer foods due to the advent of cooking, like smaller teeth and jaws to the biologic and physiologic adaptations that occurred after the shift to a new diet. Erectus is a very important hominin to study, because many of our modern-day behaviors began with him and by better understanding what he did and created and how he lived, we can better understand ourselves.


The Evolutionary Puzzle of Floresiensis

1600 words

Back in October, I wrote that floresiensis is either descended from Erectus or habilis, since those were the only two hominins in the region. Yesterday a study was published titled The affinities of Homo floresiensis based on phylogenetic analyses of cranial, dental, and postcranial characters (Argue et al, 2017), in which Argue et al argue that floresiensis was not descended from a shipwrecked Erectus, as is a popular view. Another theory is that floresiensis is descended from habilis. The third theory is that floresiensis is Homo sapiens with a pathology, but that has been disproven (Falk et al, 2009). It was commonly thought that the LB1 floresiensis specimen was a pathological human inflicted with Laron syndrome which is a type of growth hormone deficiency (Laron and Klinger, 1994).

Argue et al found that floresiensis and erectus had completely different bone structures, particularly in the pelvis and jaw. They now believe that the theory that floresiensis is a derived form of an erectus that swam or rafted to Flores has been defintively refuted. They found that floresiensis was a sister species to habilis. So either a common ancestor of floresiensis or habilis swam to Flores from Africa, or floresiensis evolved in Africa and swam to Flores. They used new phylogenetic techniques to ascertain that floresiensis is stil a part of our lineage, but shows no phylogenetic relationship to erectus on the tree.

According to Baab (2016), biogeography shows that Indonesian erectus is the best fit with what is currently known. She says if floresiensis was derived from erectus that it “implies some degree of body size reduction and more marked brain size reduction.”

Kubo, Kono, and Kaifu (2013) conclude that the evolution of floresiensis from early Javanese erectus is possible when comparing the brain cases of both specimens. However, if floresiensis descended from habilis, then the brain size reduction wouldn’t be as marked (and is still due to island dwarfism, just not on as large of a scale as it would be if floresiensis were descended from erectus). The LB1 specimen also shows the closest neural affinities to early Asian erectus (Baab, Mcnulty, and Harvati, 2013; but see Vannuci, Barron, and Holloway, 2013 for the microcephalic view). Weston and Lister, (2009) showed that there was a 30 percent reduction in brain size in Magalasy hippos, which lends credence to the insular dwarfism hypothesis for floresiensis. Craniofacial morphology also shows that floresiensis evolved from Asian erectus (Kaifu et al, 2011).

The teeth of unknown hominin found at Mata Menge are intermediate between floresiensis and erectus, being 600,000 years older than where floresiensis was found (van den Bergh et al, 2016). This lends credence to the hypothesis that floresiensis is derived from erectus. Furthermore, insular dwarfism is seen in primate species isolated on islands, with changes in body size seen in child populations even on large islands not far from the mainland (Bromham and Cardillo, 2007, Welch, 2009). Genetically isolated on islands, primates can become bigger if the parent population was smaller, or smaller if the parent population was bigger. This is due to differing energy demands relative to the parent population, along with differing predators/prey.

The island rule even holds in the deep sea. As is the case with islands, the deep sea is also associated with decreased food availability. Looking at several species of gastropods, McClain, Boyer, and Rosenberg (2006) found that the island rule held in small-bodied shallow species. They were found to have larger bodied deep-sea representatives, with the same being true for large bodied deep-sea gastropods. Further, island dwarfism in elephants on the islands Sicily, Malta, Cyprus; mammoths on the California channel islands; and red deer on the island Jersey involved body mass changes of 5- to 100-fold over 2,300 to 120,000 generations (Evans et al, 2012).

So the overall hypothesis that island dwarfism is still intact, albeit if floresiensis is derived from habilis, the reduction in brain/body size would be smaller than if floresiensis evolved from early Asian erectus.

Further evidence for brain/body size reduction due to less food availability is noted by Daniel Lieberman in his book The Story of the Human Body: Evolution, Health, and Disease (Lieberman, 2013). While talking about the evolution of floresiensis on page 123 he writes:

The same energetic constraints and processes also affect hunter-gatherers . 62

And in the 62nd footnote on page 391 he writes:

Several human “pygmy” populations (people whose height does not exceed 150 centimeters, or 4.9 feet) have evolved in energy limited places like rain forests or islands. Perhaps the small size of the Dmansi hominins from Georgia also reflected selection to save energy among the first colonists of Eurasia.

Either way, if floresiensis evolved from erectus or habilis, considerable reductions in brain size have to be explained, since the smallest erectus brain ever found is 600 cubic centimeters while the smallest habilis brain ever found is 510 cubic centimeters (Lieberman, 2013: 124), with floresiensis having a brain 417 cubic centimeters (Falk et al, 2007).

What is most important about the insular dwarfism hypothesis in regards to the evolution of floresiensis is the effect of energy reduction/food availability and quality in regards to populations isolated on islands from parent populations. Floresiensis was able to survive on about 1200 kcal by shrinking, needing to consume about 1400 kcal during lactation compared to 1800 kcal for an erectus female who needed about 2500 kcal during lactation (Lieberman, 2013: 125). The cognitive price for the reduction in the brain size of floresiensis is not known, but since brains are so energy expensive (Aiello and Wheeler, 1995; Herculano-Houzel and Kaas, 2011; Fonseca-Azevedo and Herculano-Houzel, 2012), the reduction seen in floresiensis is no surprise.

Energy is one of the most important drivers for the evolution of a species, the evolution of floresiensis is one major example of this. Whether floresiensis evolved from habilis or erectus, reduced energy on the island caused the brain and body size of floresiensis to get smaller to cope with fewer things to eat. Keep in mind that habilis was a meat-eater as well, and with lower-quality energy on the island, the brain would have to reduce in size as it’s one of the most expensive organs in the body. As I’ve been saying for a long time now, the quality of energy is most important to the evolution of a species—especially Man. Cooking was imperative to our evolution, and with a lower-quality diet, we, too, would evolve smaller brains and bodies to compensate for reduced energy consumption since our brains take 25 percent of our daily energy requirements to power despite being 2 percent of our overall body weight.

The evolution of floresiensis shows how important energy is in the evolution of species. Its biggest implication—no matter if floresiensis evolved from habilis or erectus—is how important diet quality is to evolution, as I’ve noted here, here, here, here, here, and here. Without our high-quality diet, we, too, would suffer the same body/brain size reductions that floresiensis did.


Aiello, L. C., & Wheeler, P. (1995). The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Current Anthropology,36(2), 199-221. doi:10.1086/204350

Argue, D., Groves, C. P., Lee, M. S., & Jungers, W. L. (2017). The affinities of Homo floresiensis based on phylogenetic analyses of cranial, dental, and postcranial characters. Journal of Human Evolution. doi:10.1016/j.jhevol.2017.02.006

Baab, K. L., Mcnulty, K. P., & Harvati, K. (2013). Homo floresiensis Contextualized: A Geometric Morphometric Comparative Analysis of Fossil and Pathological Human Samples. PLoS ONE,8(7). doi:10.1371/journal.pone.0069119

Baab, K.L. (2016). The place of Homo floresiensis in human evolutionJournal of Anthropological Sciences, 94, 5-18.

Bergh, G. D., Kaifu, Y., Kurniawan, I., Kono, R. T., Brumm, A., Setiyabudi, E., . . . Morwood, M. J. (2016). Homo floresiensis-like fossils from the early Middle Pleistocene of Flores. Nature,534(7606), 245-248. doi:10.1038/nature17999

Bromham, L., & Cardillo, M. (2007). Primates follow the ‘island rule’: implications for interpreting Homo floresiensis. Biology Letters,3(4), 398-400. doi:10.1098/rsbl.2007.0113

Evans AR, Jones D, Boyer AG, Brown JH, Costa DP, et al. (2012) The maximum rate of mammal evolution. Proc Natl Acad Sci USA 109: 4187–4190.

Falk, D., Hildebolt, C., Smith, K., Morwood, M. J., Sutikna, T., Jatmiko, … Prior, F. (2007). Brain shape in human microcephalics and Homo floresiensis. Proceedings of the National Academy of Sciences of the United States of America, 104(7), 2513–2518.

Falk, D., Hildebolt, C., Smith, K., Jungers, W., Larson, S., Morwood, M., . . . Prior, F. (2009). The type specimen (LB1) of Homo floresiensis did not have Laron Syndrome. American Journal of Physical Anthropology,140(1), 52-63. doi:10.1002/ajpa.21035

Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109

Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution. Brain, Behavior and Evolution, 77(1), 33–44.

Kaifu, Y., Baba, H., Sutikna, T., Morwood, M. J., Kubo, D., Saptomo, E. W., . . . Djubiantono, T. (2011). Craniofacial morphology of Homo floresiensis: Description, taxonomic affinities, and evolutionary implication. Journal of Human Evolution,61(6), 644-682. doi:10.1016/j.jhevol.2011.08.008

Kubo, D., Kono, R. T., & Kaifu, Y. (2013). Brain size of Homo floresiensis and its evolutionary implications. Proceedings of the Royal Society B: Biological Sciences,280(1760), 20130338-20130338. doi:10.1098/rspb.2013.0338

Laron, Z., & Klinger, B. (1994). Laron Syndrome: Clinical Features, Molecular Pathology and Treatment. Hormone Research,42(4-5), 198-202. doi:10.1159/00018419

Lieberman, D. (2013). The Story of the human body – evolution, health and disease. Penguin.

Mcclain, C. R., Boyer, A. G., & Rosenberg, G. (2006). The island rule and the evolution of body size in the deep sea. Journal of Biogeography,33(9), 1578-1584. doi:10.1111/j.1365-2699.2006.01545.x

Vannucci, R. C., Barron, T. F., & Holloway, R. L. (2011). Craniometric ratios of microcephaly and LB1, Homo floresiensis, using MRI and endocasts. Proceedings of the National Academy of Sciences of the United States of America, 108(34), 14043–14048.

Welch, J. J. (2009). Testing the island rule: primates as a case study. Proceedings of the Royal Society B: Biological Sciences,276(1657), 675-682. doi:10.1098/rspb.2008.1180

Weston, E. M., & Lister, A. M. (2009). Insular dwarfism in hippos and a model for brain size reduction in Homo floresiensis. Nature, 459(7243), 85–88.

Diet Or Socializing—What Caused Primate Brain Size To Increase?

1100 words

The social brain hypothesis argues that the human brain did not increase in size to solve increasingly complex problems, but as a means of surviving and reproducing in complex social groups (Dunbar, 2009). The social brain hypothesis is one of the most largely held views when it comes to explaining primate encephalization. However, an analysis of new phylogeny and more primate samples shows that differences in human and non-human primate brain evolution come down to diet, not sociality.

Diet is one of the most important factors in regards to brain and body size. The more high-quality food an animal has, the bigger its brain and body will be. Using a larger sample (3 times as large, 140 primates), more recent phylogenies (which show inferred evolutionary relationships amongst species, not which species is ‘more evolved’ than another), and updated statistical techniques, Decasien, Williams, and Higham (2017) show that diet best predicts brain size in primates, not social factors after controlling for body size and phylogeny (humans were not used because we are an outlier).

The social scheme they used consisted of solitary, pair-living, harem polygyny (one or two males, “a number of females” and offspring), and polygynandry (males and females have multiple breeding partners during the mating season). The diet scheme they used consisted of folivore (leaf-eater), frugivore-folivore (fruit and leaf eater), frugivore (fruit-eater) and omnivore (meat- and plant-eaters).

None of the sociality measures used in the study showed a relative increase in primate brain size variation, whereas diet did. Omnivores have bigger brains than frugivores. Frugivores had bigger brains than folivores. This is because animal protein/fruit contains higher quality energy when compared to leaves. Bigger brains can only evolve if there is sufficient and high-quality energy being consumed. The predicted difference in neurons between frugivores and folivores as predicted by Herculano-Houzel’s neuronal scaling rules was 1.08 billion.

The authors conclude that frugivorous primates have larger brains due to the cognitive demands of “(1) necessity of spatial information storage and retrieval; (2) cognitive demands of ‘extractive foraging’ of fruits and seeds; and (3) higher energy turnover and enhanced diet quality for energy needed during fetal brain growth.” (Decasien, Williams, and Higham, 2017). Clearly, frugivory provided some selection pressures, and, of course, the energy needed to power a larger brain.

The key here is the ability to overcome metabolic constraints. Without that, as seen with the primates that consumed a lower-quality diet, brain size—and therefore neuronal count—was relatively smaller/lower in those primates. Overall brain size best predicts cognitive ability across non-human primates—not encephalization quotient (Deaner et al, 2007). Primate brains increase approximately isometrically as a function of neuron number and its overall size with no change in neuronal density or neuronal/glial cell ratio with increasing brain size (in contrast to rodent brains) (Herculano-Houzel, 2007). If brain size best predicts cognitive ability across human primates and primate brain size increases isometrically as a function of neuron number with no change in neuronal density with increasing brain size, then primates with larger brains would need to have a higher quality diet to afford more neurons.

The results from DeCasien, Williams, and Higham (2017) call into question the social brain hypothesis. The recent expansion of the cerebellum co-evolved with tool-use (Vandervert, 2016), suggesting that our ability to use technology (to crush and mash foods, for instance) was at least as important as sociality throughout our evolution.

The authors conclude that both human and non-human primate brain evolution was driven by increased foraging capability which then may have provided the “scaffolding” for the development of social skills. Increased caloric consumption can afford larger brains with more neurons and more efficient metabolisms. It’s no surprise that frugivorous primates had larger brains than folivorous primates. Just as Fonseca-Azevedo and Herculano-Houzel (2012) observed, primates that consumed a higher quality diet had larger brains.

In sum, this points in the opposite direction of the social brain hypothesis. This is evidence for differing cognitive demands placed on getting foods. Those who could easily get food (folivores) had smaller brains than those who had to work for it (frugivores, omnivores). However, to power a bigger brain the primate needs the energy from the food that takes the complex behavior—and thus larger brain—to obtain. This lends credence to Lieberman’s (2013) hypothesis that bipedalism arose after we came out of the trees and needed to forage for fruit to survive.

Brain size in non-human primates is predicted by diet, not social factors, after controlling for body size and phylogeny. Diet is the most important factor in the evolution of species. With a lower quality diet, larger brains with more neurons (in primates, 1 billion neurons takes 6 kcal per day to power) would not evolve. Brain size is predicated on a high-quality diet, and without it, primates—including us—would not be here today. Diet needs to be talked about a lot more when it comes to primate evolution. If we would have continued to eat leaves and not adopt cooking, we would still have smaller brains and many of the things that immediately came after cooking would not have occurred.

Since we are primates we have the right morphology to manipulate our environment and forage for higher quality foods. But those primates with access to foods with higher quality have larger brains and are thus more intelligent (however, there are instances where primate brain size increases and decreases and it comes back to, of course, diet). Sociality comes AFTER having larger brains driven by nutritional factors—and would not be possible without that. Social factors drove our evolution—no doubt about it. But the importance of diet throughout hominin evolution cannot be understated. Without our high-quality diet, we’d still be like our hominin ancestors such as Lucy and her predecessors. Higher quality diet—not sociality, drives primate brain size.


DeCasien, A. R., Williams, S. A. & Higham, J. P. Primate brain size is predicted by diet but not sociality. Nat. Ecol. Evol. 1, 0112 (2017).

Deaner, R. O., Isler, K., Burkart, J., & Schaik, C. V. (2007). Overall Brain Size, and Not Encephalization Quotient, Best Predicts Cognitive Ability across Non-Human Primates. Brain, Behavior and Evolution,70(2), 115-124. doi:10.1159/000102973

Dunbar, R. (2009). The social brain hypothesis and its implications for social evolution. Annals of Human Biology,36(5), 562-572.

Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109

Herculano-Houzel, S. (2007). Encephalization, neuronal excess, and neuronal index in rodents. Anat. Rec. 290, 1280–1287.

Lieberman, D. (2013). The story of the human body: evolution, health and disease. London: Penguin Books.

Vandervert, L. (2016). The prominent role of the cerebellum in the learning, origin and advancement of culture. Cerebellum & Ataxias,3(1). doi:10.1186/s40673-016-0049-z

Genetic Changes from Cooking

2600 words

The debate about cooking’s role in human evolution is ongoing. Some people may rightly say “Cooking it not a selection pressure.” This is true. However, it doesn’t say much. The advent of cooking was one of the most important events in human history as it released the constraint on brain size due to predigesting our food outside the body. This seminal event in our history here on earth is one of the main reasons we are here today. In the articles I wrote two months ago on how and why we are so intelligent, I forgot to bring up two important things—the thermic effect of food (TEF) and our gut microbiota and its relationship with our brain. The importance of these variables in regards to cooking cannot be overstated. The subject tonight is cooking and how it benefitted us metabolically and our gut microbiota that partly drive our brain and behavior.

Cooking was beneficial to us not only because it released constraints on brain size due to how nutrient-rich meat was as well as other foodstuffs that were then cooked, but because it’s possible to extract more energy out of cooked food compared to non-cooked food. When erectus began controlling fire around 1-1.5 mya (Herculano-Houzel, 2016: 192) this allowed for the digestion of higher-quality foods (meat, tubers, etc) and this is the so-called ‘prime mover’ for the brain size increase in hominids over the past 3my.

The introduction of cooked/mashed foods changed the shape of the ridges on our skull which serve as attachments for the facial muscles responsible for chewing. The saggital crest on the cranium and zygomatic eminences in the cheeks exist in great apes but not us. Further, molars and canine teeth reduced in size while brain size double in erectus. Our jaw bones decreasing in size shows that we didn’t need to have as forceful of a bit due to the introduction of cooked foods 1-1.5 mya (Herculano-Houzel,2016: 193).

Along with the introduction to a diet with softer foods, smaller teeth and intestines then followed. So brain size and teeth size are not correlated per se, neither are brain size and gut size. However, the relationship between all three is cooking: cooking denatures the protein contained in the food and breaks down cell walls, gelatinizing the collagen in the meat allowing for easier chewing and digestion. So the fact that tooth size and brain size do not have a relationship throughout our evolution is not a blow to the cooking hypothesis. The introduction of softer foods is the cause for both the decrease in tooth size and gut size. Cooking is a driver of all three.

Fonseca-Azevedo and Herculano-Houzel (2012) showed that the availability of kcal from a raw diet is so limiting that without a way to overcome this limitation, modern Man would not have been able to evolve. Our brains would not have emerged if not for the advent of cooking. Indeed, Herculano-Houzel and Kaas (2011) showed that the outler is not our brains being bigger than our bodies, great apes have bodies too big for their brains, reversing a long-held belief on our brain-body relationship. Cellular scaling rules apply for all primates, so knowing this, the Colobinae (old-world monkeys) and the Pongidae (gorillas, chimpanzees, and orangutans) favored increases in body size, in line with the ancestor that we share with great apes, while our lineages showed gains in brain size and not body size, possibl due to a metabolic limitation of having both a big brain and body. Indeed, the amount of neurons a brain can hold along with how big a body can realistically get impedes the relationship between the brain and body. You can have either brains or brawns, you can’t have both.

We should then look for when genetic changes in our genome occurred from cooking. Carmody et al (2016) show that these genetic changes occured around 275-765kya. We know that differing nutrients change gene expression, so, over time, if these changes in gene expression were beneficial to the hominin lineage, there would be positive selection for the gene expression. Carmody et al (2016) took 24 mice and fed them either cooked or raw foods for 5 days. Two hours into the 5th day, mice were ‘sacrificed’ (killed) and their liver tissue was harvested and immediately (within 60 seconds of death) were flash frozen for later analysis. They evaluated differential gene expression for cooked/raw food, calorie intake (raw/fed), energy balance of the consusmer (weight gain/loss over 5 days of feeding), and food type (meat/tuber). The diet consisted of either organic lean beaf round eye toast or sweet potato tubers cooked or raw. They gave restricted rations to evaluate the effect of a cooked diet with negative energy status (this is important).

They cooked the meat until it gelatinized (around 70 degress celsius), which is equivalent to medium well-done. They were then given the same diets, cooked/raw, free-fed or restricted sweet potato tubers or meat. The mice were weighed during periods of inactivity and the food they refused to eat was weighed to monitor fresh weight than freeze-fried to monitor dry weight.

The most interesting part of this experiment, in my opinion, was that the mice that were free-fed with cooked diets consumed less kcal than the mice that were free-fed raw diets. They discovered that free-fed cooked diets led to the maintenance of body weight, whereas the free-fed raw diet led to weight loss. This confirms that cooked food gives more energy than raw food, which was itelf a critical driver in our evolution as humans.

When they looked at the livers of the sacrificed mice, they found that the mice that were fed meat showed liver gene expression patterns that were more similar to mice fed a human diet than mice that were fed tuber. The mice that were fed cooked food showed similar gene expression to mice fed a human diet and more similar to the human liver than in the mice fed the raw food. Even more interestingly, the mice fed tuber or raw foods exhibited liver expression patterns more similar to mice fed a chimpanzee diet and gene expression patterns noticed in non-human primates. Their analysis on the gene expression from cooked/raw diets compared to another data set showed that these genes that were expressed went under selection between 275-765kya.

Food type and preparation were associated with significant changes in gene expression, but those related to cooking were shown to have evidence of possible selection in the timeframe state by Carmody et al. These results also show that along with cooking increasing the bioavailability of foods, habitual cooking would have led to less energy spent on immune upregulation. This energy could then be used for other bodily processes—like our increasing brain size/neuronal count.

Carmody et al show that the biological evidence for cooking is 2mya, archaeological evidence 1mya, hearths 300kya, not too many Neanderthals controlled fire until 40 kya, and the earliest direct evidence we have of cooking appears around 50kya. We can obviously look at physiological, metabolic and diet differences between hominins and infer what was eaten. Now with looking at changes in gene expression, we can pinpoint when the positive selection began to occur. The biological evidence, in my opinion, is the best evidence. We don’t need direct physical evidence of cooking, we can make inferences based on certain pieces of knowledge we have. All in all, this new study by Carmody et al show that 1) cooking definitely predated modern humans and 2) many different hominins practiced cooking. This evidence shows that cooking for ancient hominins occurred way earlier than the archaeological record suggest.

Now, remember how the mice free-fed on a cooked meat diet ate less yet maintained their weight? There is a reason for this. Protein is the most filling macro (followed by fat, fiber then CHO). So it’s no surprise that the mice at less of the cooked meat. What was a surprise was that the mice maintained their weight eating less kcal then the mice that ate a raw foods diet. This is yet more evidence that cooking released us from the metabolic constraints of a raw, plant-based diet.

For those who have some knowledge of human metabolism, you may have heard of the thermic effect of food. The thermic effect of food is the amount of energy expenditure above the basal metabolic rate due to the cost of processing food and its storage. So if you’re cooking food before you ingest it, you bypass a lot of the processing that happens internally after digestion, allowing you to extract close to 100 percent of the kcal contained in the food. Due to cooking’s effects on foods, since we our bodies have to use some of the energy we consume to function and process the kcal, getting higher quality food was beneficial to us since we could have more for our bodily functions and to power our growing brains. Since we were able to get higher quality calories from cooked food, the effects of TEF weren’t as large, which was yet another constraint that we bypassed with a cooked diet. A cooked diet is more efficient than a raw one in more ways than one.

One more thing I forgot to mention in my series of articles on the benefits of cooking and human evolution is the effect it had on our microbiome. The completion of the Human Microbome Project (HMP) was imperative to our understanding of the trillions of bacteria that live in our guts. It was commonly stated that the bacteria in our guts outnumbered regular bacteria with a 10:1 ratio. However, Sender, Fuchs, and Milo (2016) showed that on average, there is about a 1:1 ratio with about 30 trillion normal bacteria and 39 trillion gut bacteria, some people possibly having double the amount of gut bacteria in comparison to regular bacteria, but nowhere on the level of 10:1 that has been stated for the past 40 years.

The human microbiome has undergone a substantial change since the divergance of humans and chimpanzees (Moeller et al, 2014). Over the course of our evolutionary history, our microbiome has become specialized to animal-based diets. Wild apes have way more diversity in their gut microbiota than humans do, indicating that we have experienced a depletion in our microbiota since our divergence with chimpanzees. This comes as no surprise. With the introduction to cooked foods, our microbiota became adapted to a new selective pressure. Over time, our gut microbiota became less diverse but more and more specialized to consume the food we were eating. So the introduction to a cooked diet both changed our gut microbiota as well as giving our bodies enough energy to power itself and its processes, the brain and our gut microbiota that are imperative for our development.

All that being said, some people may say “Cooking isn’t a selective pressure; neither is bipedalism nor tool-making”, and they would be correct. However, human tool-making capacities reflect increased information-processing capabilities (Gibson, 2012). So, clearly, there were some changes in our brains before the use of tools. This change was the advent of bipedalism which allowed our bodies to conserve 75 percent more energy in comparison to knuckle-walking (Sockol, Racihlen, and Pontzer, 2007). This was yet another constraint that we bypassed and allowed our brains to grow bigger. When we left the trees, we then became bipedal and that therefore increased the availability of edible foodstuffs for us. This increased our brain size, and as we learned to make tools, that increased our information-processing capabilities.

Cooking, of course, is not a selective pressure. What cooking did, however, was release the use from the metabolic constraints of a raw, plant-based diet and allowed us to extract all of the nutrients from whatever cooked food we ate. This event—one of the most important in human history—would only have been possible with the advent of bipedalism. After we became bipedal we could then manipulate our environement and make tools.

I figure I may as well touch on the Expensive Tissue Hypothesis (ETH; Aiello and Wheeler, 1995) while I’m at it. The ETH states that since our guts are metabolically expensive tissue—as well as our brains—that there was a trade off in our evolutionary history between our brains and guts. However, Navarette, Schaik and Isler (2011) showed that the negative correlation was with fat-free mass and brain size—not with the gut and brain size. However, as I noted earlier in this article, our guts reduced in size due to diet quality, e.g., softer foods. So while the correlation is there for the brain size increase/gut reduction, it is not causal. Diet explains the gut reduction and brain size increase, but the brain size increase did not cause the gut reduction.

In sum, genetic changes from cooking occured between 275-765kya. But we controlled fire and began to cook between 1-2mya (archaeological evidence says 1-1.5 mya while biological evidence says 2 mya). Cooking led to differences in gene expression and then positive selection in the hominin lineage. Mice that were fed a raw diet showed gene expression similar to a chimpanzee fed a raw diet while mice fed a cooked diet showed gene expression like that of a human. This is huge for the cooking hypothesis. What this shows is that while the gene expression occurred while we started cooking, the actual positive selection didn’t occur in our genomes for about 1my after we began cooking. This is more evidence that cooking released us from metabolic constraints, as mice that were fed a cooked diet maintained their weight even when eating less kcal than mice fed raw foods.

When thinking about the evolution of Man and our relationship with fire, we should not forget about how the body uses some of the kcal is ingests for bodily processes. Furthermore, we cannot forget about our microbiome which evolved for an animal-based diet. Those two things both cost caloric energy. The advent of cooking released us from the energetic constraints of a raw, plant-based diet as well as gave our microbiome higher quality energy. When we take both the TEF and our microbiome into account, we can then begin to put 2 and 2 together and state that along with cooking freeing us from the metabolic constraints that apes have to go through due to their diet, it also benefitted our microbiome and gave our bodies higher quality energy to power it.

We would not be here without cooking. Thank cooking for our dominance on this planet.


Aiello, L. C., & Wheeler, P. (1995). The Expensive-Tissue Hypothesis: The Brain and the Digestive System in Human and Primate Evolution. Current Anthropology,36(2), 199-221. doi:10.1086/204350

Carmody, R. N., Dannemann, M., Briggs, A. W., Nickel, B., Groopman, E. E., Wrangham, R. W., & Kelso, J. (2016). Genetic Evidence of Human Adaptation to a Cooked Diet. Genome Biology and Evolution,8(4), 1091-1103. doi:10.1093/gbe/evw059

Fonseca-Azevedo, K., & Herculano-Houzel, S. (2012). Metabolic constraint imposes tradeoff between body size and number of brain neurons in human evolution. Proceedings of the National Academy of Sciences,109(45), 18571-18576. doi:10.1073/pnas.1206390109

Gibson, K. R. (2012). Human tool-making capacities reflect increased information-processing capacities: Continuity resides in the eyes of the beholder. Behavioral and Brain Sciences,35(04), 225-226. doi:10.1017/s0140525x11002007

Herculano-Houzel, S. (2016). The Human Advantage: A New Understanding of How Our Brains Became Remarkable. doi:10.7551/mitpress/9780262034258.001.0001

Herculano-Houzel, S., & Kaas, J. H. (2011). Gorilla and Orangutan Brains Conform to the Primate Cellular Scaling Rules: Implications for Human Evolution.

Moeller AH, Li Y, Mpoudi Ngole E, Ahuka-Mundeke S, Lonsdorf EV, Pusey AE, et al. Rapid changes in the gut microbiome during human evolution. Proceedings of the National Academy of Sciences. 2014;111(46):16431–35.

Navarrete, A., Schaik, C. P., & Isler, K. (2011). Energetics and the evolution of human brain size. Nature,480(7375), 91-93. doi:10.1038/nature10629

Sender, R., Fuchs, S., & Milo, R. (2016). Revised estimates for the number of human and bacteria cells in the body. doi:10.1101/036103

Sockol, M. D., Raichlen, D. A., & Pontzer, H. (2007). Chimpanzee locomotor energetics and the origin of human bipedalismProceedings of the National Academy of Sciences,104(30), 12265-12269. doi:10.1073/pnas.0703267104