How Our Brains Got So Big

Contributed by Robert Havranek

Humans have a considerably larger brain size than would be predicted for an animal our size, and this considerable brain size has helped shape the evolution of humanity. But how did this increase occur?

One idea about how our brains increased in size is the expensive tissue hypothesis. Our brain consumes 20% of our energy demands at rest, so it’s a very energetically expensive organ. In order to increase the size of the brain, the expensive tissue hypothesis suggests that our bodies had to divert energy from other systems—like the muscles or gut—to our brains. Our brains exclusively use glucose as its form of energy, and recent research from anthropologists at Duke University has found evidence in our genes for the expensive tissue hypothesis. They compared the amount of proteins that bring glucose into brain and muscle cells and found that humans demonstrated significantly more mutations for genes that increased the expression of glucose transporter proteins in the brain and had fewer mutations that increased the expression of the glucose transporters in the muscles. In contrast, chimpanzees had greater glucose transporter expression mutations in muscles but not in the brain when compared to humans. The differential expression of glucose transporters in humans and chimps means that chimps are much stronger than humans because more energy is going to their muscles than their brains. A recent study comparing the strength of chimps and macaques to the strength of university basketball players found that the apes could pull much more weight than humans. We (modern humans) last shared a common ancestor with chimps more than 7 million years ago, when the evolutionary line between modern chimps and modern humans split. After that, selection must have acted to shape the use of glucose, and thus muscular strength, differently in these two evolving lineages. Together, these two studies support the expensive tissue hypothesis, where humans directed more energy to their brain for enhanced cognitive abilities.

Diverting energy away from the muscles to the brain may be a method that allowed our ancestors’ brains to expand, but how exactly did evolution select for a big brain in the first place?

One major hypothesis is called the cultural intelligence hypothesis. This emphasizes the importance of sociality, communication and social learning in selecting for a larger brain. Social communication and learning may have been selected for because they allow for cooperative food gathering strategies such as group hunting and foraging. Communication also would have facilitated the development of tools. If you can learn to make an effective spear, which allows you to hunt larger prey and feed more people, then your offspring and kin would benefit, in terms of increased survival and reproduction. Your offspring would only have a higher fitness, however, if you can teach them how to make the spear and they can pass on that information to other generations. This passing on of information across generations is called culture and is similar to the transmittance of heritable alleles, thus we can talk about culture and biology as simultaneously shaping our evolution.

Our ability to run long distances coupled with our ability to make tools and pass on the information of how to make tools both increased our behavioral ability to hunt, giving us a fitness advantage. Our behaviors can then increase or decrease fitness, which would shape a population’s expressed phenotypes (both biological and cultural phenotypes) resulting in evolutionary changes. Those evolutionary changes influence our biology, which interacts with our culture to further shape behavior. Of course, all of this is going on in the context of the environment, which determines if a particular trait is going to increase you and your offspring’s chances of survival and reproduction.

Thus culture can augment the heritable transformation of alleles that increase the fitness of organisms. The development of culture and transmission of knowledge increasingly shaped our fitness and evolution. The simultaneous effect of biological and cultural selection forces shaped our evolution and lead to an increase in brain size in our ancestors and allowed the genus Homo to arise.

Click the following link to visualize how biocultural evolution occurs: Biocultural Co-evolution

The interaction of culture (which facilitated learning and effective hunting) and biological changes (which diverted more energy to the brain) with behavior may have allowed for the size of our ancestors’ brains to increase, resulting in the nearly three pound organ that we see today. These are only a few hypotheses on how the brain expanded, and they are not mutually exclusive. They all may have played some aspect in the evolution of our present-day brains. However, the main point is that no one specific factor played a role in our brain expansion. Instead, a confluence of factors has shaped who we are today.


For more information, check out these sites!

“Bigger Brains: Complex Brains for a Complex World.” Smithsonian Institute 11/28/2015. Web.

Babbitt, Courtney C., et al. “Genomic Signatures of Diet-Related Shifts During Human Origins.” Proceedings of the Royal Society of London B: Biological Sciences (2010). Print.

Bozek, Katarzyna, et al. “Exceptional Evolutionary Divergence of Human Muscle and Brain Metabolomes Parallels Human Cognitive and Physical Uniqueness.” PLoS Biol 12.5 (2014): e1001871. Print.

Fedrigo, O., et al. “A Potential Role for Glucose Transporters in the Evolution of Human Brain Size.” Brain, Behavior and Evolution 78.4 (2011): 315-26. Print.

Jabr, Ferris. “How Humans Evolved Supersize Brains.” Quanta Magazine 2015. Web.

Reader, Simon M., Yfke Hager, and Kevin N. Laland. “The Evolution of Primate General and Cultural Intelligence.” Philosophical Transactions of the Royal Society of London B: Biological Sciences 366.1567 (2011): 1017-27. Print.

Roberts, Roland G. “Jocks Versus Geeks—the Downside of Genius?” PLoS Biol 12.5 (2014): e1001872. Print.

Somel, Mehmet, Xiling Liu, and Philipp Khaitovich. “Human Brain Evolution: Transcripts, Metabolites and Their Regulators.” Nat Rev Neurosci 14.2 (2013): 112-27. Print.

Evolution and Autism

Contributed by Suranjana Dey, Tiffany Ding, Jane Chang, Paul Nguyen

Evolution by natural selection requires the heritability of different characteristics that let some individuals produce more children, possibly because they survive longer. This might make you think that natural selection is “selecting” for traits that make individuals stronger and “better”. This isn’t necessarily true. Consider individuals suffering from autism. Individuals suffering from autism spectrum disorders (ASD) exhibit impaired social behavior, difficulty with communication, and a tendency to engage in repetitive behaviors. Evolutionary biologists are interested in how autism, which is a disorder that makes it difficult to find a mate and start a family, originated in humans. From an evolutionary perspective, a condition that decreases fertility is not expected to persist for long. However, autism continues to persist and, arguably, is arising at a faster rate.

Evolutionary biologists have honed in on one observation in particular. Autistic individuals are more likely to be males and have an interest in repetitive behaviors and mechanical actions. Men were usually the hunters in ancient hunter-gatherer societies. Hunters had to be able to predict the patterns of game movement through the seasons (a repetitive behavior), endure solitude while hunting (an antisocial state), and make and invent tools (a mechanical action). Thus, it has been hypothesized that the autistic brain is an example of an extreme male brain that initially evolved to cope with the demands of hunting. In hunter-gatherer societies, these traits allowed males to survive and provide for their families (Crespi 2013). However, these traits no longer provide the same benefits in the context of our modern world.

Evo-Bio Graphic

Another evolutionary explanation focuses on the rapid evolution of human cognition. Humans’ life histories consist of the longest period of neurodevelopment (about 25 years). Evolutionary biologists posit that autism is simply the stagnation of neurodevelopment and the persistence of a “child-like” state:

Heterochronic model for autism in regards to its restricted interests and repetitive behavior.


Developmental heterochronic model with respect to local vs. global processing in autistic individuals

This hypothesis focuses on the observation that autistic traits, such as being self-centered (averse to social interaction) and enjoying repetitive behaviors, are similar to the characteristics of a 3-year-old child. According to this hypothesis, as the genes that control life history have evolved to give humans an extended childhood, they have also become more susceptible to deleterious mutations that result in the exaggerated child-like state seen in autism (Ploeger et al., 2011). Furthermore, the AUTS2 gene has recently been implicated in the origins of ASD. In general, the AUTS2 gene appears to play a role in the rapid evolution of human cognition, which suggests the same genes that may be favorable in terms of cognition can also impact non beneficial traits (Oksenberg et al, 2013): These observations suggest that ASD could be an evolutionary by product of the rapid evolution of human cognition.

Figure 4: What happens when AUTS2 is knocked down?

For more information see:

  1. Crespi, B. 2013. Developmental heterochrony and the evolution of autistic perception, cognition and behavior. BMC Medicine 11 (119): 1-11.
  2. Ploeger, A., and Galis, F. 2011. Evolutionary approaches to autism-an overview and integration. Mcgill J Med 13 (2): 38-43.
  3. Oksenberg, N., Stevison, L., Wall, J.D., Ahituv, N. 2013. Function and Regulation of AUTS2, a Gene Implicated in Autism and Human Evolution. PLOS Genet 9 (1): 1-9.


  1. Gallup, G.G., Jr., and Hobbs, D.R.. 2011. Evolutionary medicine: Bottle feeding, birth spacing, and autism. Medical Hypothesis 77 (3): 345-46.
  2. Tordjman, S., Somogyi, E., Nathalie, C., Kermarrec, S., Cohen, D., Bronsard, G., Bonnot, O., Weismann-Arcache, C. Botbol, M., Lauth, B. 2014. Gene x Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms. Front Psychiatry 2014 (5): 1-17.
  3. Lomelin, D.E. 2010. An Examination of Autism Spectrum Disorders in Relation to Human Evolution and Life History Theory. Nebraska Anthropologist. Paper 57: 73-81.
  4. Oksenberg, N., and Ahituv, N. 2013. The role of AUTS2 in neurodevelopment and human evolution. Trends in Genetics 29 (10): 600-608.




Helicobacter pylori and you.

Contributed by Thomas Partin and Austin Piccolo

Species do not live in a world separate from each other. Organisms interact with other organisms everyday, and over time adapt to each other accordingly. Often, the evolution of two species can become strongly linked to each other, for better or worse. Heliobacter pylori is a bacteria that thrives in the acidic conditions of the human stomach. It causes stomach ulcers and is strongly correlated with gastric cancer. As recently as the 1980’s, the idea of a bacteria being able to survive in the stomach’s harsh conditions and being responsible for this disease was so controversial that it took one doctor intentionally infecting himself to prove its role in stomach ulcers. That doctor later won the Nobel prize in medicine for his work.

H. pylori did not first start infecting humans in the 80’s though. H. pylori and humans have been living (and battling) together for millennia. The earliest humans also played host to H. pylori. One way this can be shown is a creative use of a phylogenetic tree. Scientists sampled many different strains of H. pylori, and used them to create an ancestral tree of the different strains. They then compared the tree they made to geographic locations of their samples. What they found was that lineages of H. pylori matched perfectly with the migration patterns of ancient humans as they moved out of Africa. Newer strains of H. pylori are found where humans migrated to most recently. The strains were carried and dispersed based on how early humans moved around the globe.

This intimate relation between H. pylori and humans provides a great opportunity to explore coevolution. Humans and H. pylori have been locked in an arms race for thousands of years. H. pylori colonization poses serious health consequences to the host, which creates a selective pressure for humans that can prevent H. pylori infection. Likewise, the human body is an incredibly hostile environment towards foreign invaders like H. pylori, which creates a strong selective environment for H. pylori cells that can overcome human defenses. There is evidence this selective pressure is so strong that H. pylori begins adapting specifically to the host after initial colonization. Although not an innate aspect of human biology, antibiotics are another human defense against H. pylori. Antibiotic use creates a selective pressure for H. pylori that is so strong that resistant strains can develop remarkably quickly after attempted treatment.

Please watch the below video to learn more!

For further information see:

Linz, B., Ballouxm, F., Moodley, Y., Manica, A., Liu, H., Roumagnac, P., Falush, D., Stamer, C., Prugnolle, F., van der Mer, S.W., Yamaoka, Y., Graham, D.Y., Perez-Trallero, E., Wadstrom, T., Suerbaum, S., Achtman, M. 2007. An African origin for the intimate association between humans and Helicobacter pylori. Nature 445: 915-918

Gao, W., Cheng, H., Hu, F., Li, J., Wang, L., Yang, G., Xu, L., Zheng, X. 2010. The Evolution of Helicobacter pylori Antibiotics Resistance Over 10 Years in Beijing, China. Helicobacter. 15: 460-466.

Oh, J.D., Kling-Bäckhed, H., Giannakis, M., Xu, J., Fulton, R.S., Fulton, L.A., Cordum, H.S., Wang, C., Elliott, Glendoria., Edwards, J., Mardis, E.R., Engstrand, L.G., Gordon, J.I. 2006. The complete genome sequence of a chronic atrophic gastritis Helicobacter pylori strain: Evolution during disease progression. PNAS. 103: 9999-10004.

Blecker, U., Landers, S., Keppens, E., Vandenplas, Y. 1994. Evolution of Helicobacter pylori Positivity in Infants Born From Positive Mothers. Journal of Pediatric Gastroenterology and Nutrition. 19: 87-90

Kennemann, L., Didelot, X., Aebischer, T., Khun, S., Drescher, B., Droge, M., Reinhardt, R., Correa, P., Meyer, T.F., Josenhan, C., Falush, D., Suerbaum S. 2011. Helicobacter pylori genome evolution during human infection. PNAS. 108: 5033-5038.

Marshall, B.J., Warren, J.R. 1984. Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulcers. The Lancet. 323: 1311-131.

Avasthi, T.S., Devi, S.H., Taylor, T.D., Kumar, N., Baddam, R., Kondo, S., Suzuki, Y., Lamouliatte, H., Mégraud, F., Ahmed, N. 2011. Genomes of Two Chronological Isolates (Helicobacter pylori 2017 and 2018) of the West African Helicobacter pylori Strain 908 Obtained from a Single Patient. Journal of Bacteriology. 193: 3385-3386.

Why You Should Thank Your Food Allergies

Contributed by Jimmy Shah, Sanjana Rao, and Laura Galarza


Did you know that over 15 million Americans suffer from food allergies today? Consider this. Every 3 minutes, a food allergy reaction sends someone to the ER. Given these severe, potentially life-threatening medical conditions that have no known cure, we think studying the origins of food allergies can have significant clinical implications. So what exactly is a food allergy?

Food allergies manifest as adverse immune system reactions to harmless food substances. Once the allergen enters the body, it will be recognized by and bind to serum immunoglobulin E (IgE) – antibodies found in the lungs, skin, and mucosal membranes. IgE is attached by FcɛRI surface receptors on mast cells, an immune cell that helps the body create inflammatory responses. Interestingly, studies have shown that the high-affinity IgE-FcɛRI receptor binding is involved in responding to not only allergen exposure, but also parasite invasion.

Symptom severity is correlated with IgE antibody concentration

Symptom severity is correlated with IgE antibody concentration

After the binding occurs, the allergen will cause antibody cross-linking on the mast cell surface and lead to something called mast cell degranulation, which means the mast cell will release its internal pro-inflammatory molecules, like histamines, leukotrienes, and prostaglandins, into the bloodstream. This will cause the onset of the allergy symptoms many of us may know well (especially in the pollen-rich spring) – sneezing, itching, coughing, hives, GI discomfort, etc. The most severe of these is anaphylaxis, a rapid and potentially life-threatening body state where blood pressure is lowered and emergency symptoms arise as a result. This brings us to our central question: why would evolution naturally select for us to be allergic to food that sustains us? The anomaly of food allergies and their past, present, and future benefits remain largely poorly-defined. However, research shows us that IgE antibody recognition of the allergen and shared defense mechanisms play a significant role in evolving allergic responses over time.


Although not fully understood, allergic responses are thought to have evolved from an immune defense mechanism against parasite invasion and other harmful toxin colonization. For years, scientists saw allergies as genetic accidents where aberrant IgE antibody production was just a mishap. But given the conservative nature of evolution, the IgE antibody class couldn’t have just arisen to be destructive only in the case of genetic disorders. Even if they did, evolution wouldn’t keep them around if they were solely harmful. In 1991, Margie Profet created the toxin hypothesis – the idea that responding to toxins and allergic reactions occur in very similar ways, that allergies are inherently toxic or affiliated with toxic substances, and that allergic responses mostly involve symptoms by which toxins are expelled (sneezing, vomiting, coughing, etc.) Last month, scientists at Stanford published evidence supporting the sustained positive evolutionary pressure to keep these IgE antibodies around. First, they found that in normal mice, previous exposure to venom allowed for greater survivability following a lethal venom injection, as compared to mice who were only treated with control solution. Then, they tested the role of the allergic pathway. Specifically, they studied three different types of mice responding to bee venom injections – mice without IgE, mice without IgE receptors on mast cells, and mice without mast cells at all. Unlike the normal mice, the three mutants did not benefit from previous venom exposure, since they did not have the key immunological players coordinating allergic response (Tsai, 2015). Although allergies have become less threatening in our daily lives, this allergic-type, IgE-associated immune response provides support for the idea that allergic responses are closely linked to the ways in which our bodies fight off toxins, long ago and today.

In another study published in October 2015, researchers at the London School of Hygiene & Tropical Medicine hypothesized that there must be some molecular similarity between parasites and allergen proteins, as the same branch of the immune system is found to kick in in both circumstances. After extensive data analysis, the team found that 2,445 known parasite proteins were structurally and sequentially (think base pairs A, C, T, G) similar to those found in the portion of the allergen that is prone to immune system attack. Further, measuring human cell immune response to a protein from a parasitic worm that was similar to a protein from a prevalent pollen allergen family revealed that blood serum reacted against both worm infection and the allergen via the same antibody mechanism (Tyagi, 2015).


Overall, the precise origin of food allergies has yet to be defined. However, we can infer that thousands of years ago, our ancestors may have consumed foods that contained harmful proteins or mimicked harmful substances, so allergies may have very well evolved to protect us. For example, someone could have ingested a raw plant that looked like a poisonous plant in the same family, so his body was on high alert. The IgE response naturally kicked in and perhaps was sustained throughout several generations as a heritable characteristic because it gave certain individuals an advantage over others in surviving and reproducing. As a result, those advantaged individuals likely passed on these beneficial traits, so eventually the proportion of individuals with these advantageous characteristics increased because those who didn’t, would lesser survivability.

This beneficial defense mechanism is not a novel idea – if unwanted substances enter the body, whether it just appears to be harmful or actually is, the organism’s ability to survive is potentially at stake. Thus, evolution would select for mechanisms by which these substances can be fought internally and expelled from the body. It therefore makes perfect sense that evolution would select for allergic responses as a means to protect one against destructive parasites and toxins.

Ultimately, food allergies account for $25 billion dollars in health costs each year, and cause 30,000 cases of anaphylaxis, 2,000 hospitalizations, and approximately 150 deaths annually. This significant burden on our population’s health warrants study of how allergic responses occur and the reasoning behind why they do. In doing so, perhaps we can find a cure! But for now, keep in mind that food allergies aren’t necessarily all bad and that they might actually be shielding you from something far worse.


Brandtzaeg, Per. 2010. Food Allergy: Separating the Science from the Mythology. Nature Reviews Gastroenterology & Hepatology 7, no. 7: 380–400.

Fitzsimmons, Colin Matthew, Franco Harald Fakone, and David William Dunne. 2014. Helminth Allergens, Parasite-Specific IgE, and Its Protective Role in Human Immunity. Frontiers in Immunology 5: 61.

Gross, Michael. 2015. Why did evolution give us allergies? Current Biology, no. 2: 53-55.

Liu, Andrew H. 2015. Revisiting the Hygiene Hypothesis for Allergy and Asthma. Journal of Allergy and Clinical ImmMatricardi, P. M. 2014. Molecular Evolution of the Allergy. Allergologie 37, no. 10: 423–24.

Machado, D. C., Horton, D., Harrop, R., Peachell, P. T. and Helm, B. A. (1996), Potential allergens stimulate the release of mediators of the allergic response from cells of mast cell lineage in the absence of sensitization with antigen-specific IgE. Eur. J. Immunol., 26: 2972–2980. doi: 10.1002/eji.1830261224

Platts-Mills, Thomas A. E. 2012. Allergy in Evolution. New Trends in Allergy and Atopic Eczema, edited by J. Ring, U. Darsow, and H. Behrendt, 96:1–6.

Ratnaparkhe, Milind B., Tae-Ho Lee, Xu Tan, Xiyin Wang, Jingping Li, Changsoo Kim, Lisa K. Rainville, et al. 2014. Comparative and Evolutionary Analysis of Major Peanut Allergen Gene Families. Genome Biology and Evolution 6, no. 9: 2468–88.

Sicherer, Scott H., and Hugh A. Sampson. 2009. Food Allergy: Recent Advances in Pathophysiology and Treatment. Annual Review of Medicine 60, no. 1 (2009): 261–77.

Tsai, Mindy, Phillip Starkl, Thomas Marichal. 2015. Testing the “toxin hypothesis of allergy: mast cells, IgE, and innate and acquired immune responses to venoms. Elsevier. Vol. 36: 80-87.

Tyagi, Nidhi, Edward Franell, Colin Fitzsimmons, Stephanie Ryan. Comparisons of Allergic and Metazoan Parasite Proteins: Allergy of the Price of Immunity. PLOS Computational Biology.

Wang, Jing, Litao Yang, Xiaoxiang Zhao, Jing Li, and Dabing Zhang. 2014. Characterization and Phylogenetic Analysis of Allergenic Tryp_alpha_amyl Protein Family in Plants Journal of Agricultural and Food Chemistry 62, no. 1: 270–78.

Zusi, Karen. 2015. An Evolutionary Basis for Allergies. The Scientist.

Human Mate Choice: How We Choose Our Mates

Contributed by So Heui Kim

image This black and white photo was created by using the sandwich technique. I randomly chose the faces from a magazine. The third negative is a photo of human cells. My intention was to create a photo that illustrates how our cells and the genes within them are involved in our mate choice.

Despite a lot of interest, it is not clear what traits determine what mates humans choose. It sometimes seems that each individual has different preferences. Humans can be influenced by many factors, including parental guidance, the environment, education, attractiveness, and the media. Some research suggests that despite these influences, human mate choice is based on genetic similarity.

The major histocompatibility complex is believed to take a huge role in human immune system. The MHC molecules bind pathogen-derived peptide fragments and display them on the cell surface to be recognized by the T cells (Janeway, Travers, Walport et al, 2001). These MHC molecules help our body to recognize and eliminate the harmful pathogens. Therefore, maintaining MHC diversity is a key to human survival. The more diversity there are in MHC molecules, the more pathogens will be killed.
In “Major histocompatibility complex peptide ligands as olfactory cues in human body odor assessment”, researchers found out that humans have the ability to detect and evaluate body odor by MHC peptides. In the experiment, human volunteers were asked to apply two different solutions of MHC peptide ligands under their armpits. Then, the participants had to decide which armpit smell they preferred. Participants preferred their body odor more typical of individuals with an MHC profile like their own. This result strongly supports the findings that humans with similar MHC alleles also have similar perfume preference. Unlike when smelling armpits, women prefer the odor of shirts worn by men with different MHC alleles. By mating with a person who has dissimilar MHC genotype, they will maintain their offspring’s MHC diversity.

Wearing perfume is considered one way to attract a mate. Based on the results from the experiments above, we can consider how MHC should impact perfume selection. From the armpit experiment, we can predict that people will prefer to wear perfumes that are similar to their MHC peptides. In “Evidence for MHC-correlated perfume preferences in humans”, researchers found that there is a strong correlation between one’s MHC and their perfume choice. In the first experiment, participants were asked if they liked the smell or not. In a second experiment, participants were asked if they liked the smell, and if they wanted their mates to smell like that. From these experiments, they found out that people sharing specific MHC alleles also share preference for specific perfume odor. In other words, there was a strong correlation between MHC type and one’s preference for the perfume ingredients such as musk, rose, or cardamone. Although this research could not assess which odors were related to MHC, it provides the basis for studies that can test the relationship between the MHC and perfume in more detail. If we can find which odors are related to MHC, we can analyze what perfumes can attract potential mates. If so, we can wear perfumes to not only enhance our body odors, but also to attract our mates.

For more information, please see:

Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001. The major histocompatibility complex and its functions.

Milinski M, Cory I, Hummel T, Boehm T. 2013 Major histocompatibility complex peptide ligands as olfactory cues in human body odour assessment. Proc R Soc B 280: 20122889.

Milinski M, Wedekind C. 2001 Evidence for MHC-correlated perfume preferences in humans. Behav. Ecol. 12, 140–149.

The Evolution of Bitter Taste

Contributed by Jonathan Adcock, Hana Ahmed, Robert Bruner, Farhan Momin, Andrew Shibata

How Bitter Taste Works

Specialized bitter taste receptors are concentrated at the back of the tongue. Upon eating a bitter food, these receptors are activated, and and a signal is sent to to the brain that leads to the perception of a bitter taste. Bitter taste receptors are encoded by the TAS2R gene family. This family includes nearly 25 genes and psuedogenes (genes that are no longer functioning) that are concentrated in bundles on chromosomes 3, 5, and 7. Extensive studies have been performed in order to determine which molecules in bitter foods can activate these receptors. Scientists have found that many of the compounds that activate the bitter taste receptors are chemicals produced by plants. Many of these compounds were also found to be toxic and if consumed could lead to illness or death.

How Bitter Taste Evolved

Our ancestors and other animals have not always been able to taste bitter foods. The bitterness sensation is thought to have evolved 200 million years ago. The prevalent hypothesis is that bitter taste evolved by random gene mutation events which caused the formation of the TAS2R gene family and the bitter taste receptors on the tongue that could bind to toxic chemicals. Animals possessing these mutations were able to  taste toxins in their food. These toxins would have tasted bad to the animal, and thus, the animal would learn to avoid the toxic food in the future. Animals with the mutations that produce the TAS2R gene family would be be better adapted to their environment because they can avoid toxic and poisonous foods that could cause sickness or death in the animal. Animals not possessing these mutations would still be susceptible to ingesting naturally occurring poisonous chemicals. Because these animals have improved survivability in comparison to other animals without the TAS2R genes, animals that could taste bitter foods would be better able to reproduce and pass the functional TAS2R genes to their offspring, who in turn would have increased survivability, be better able to reproduce and pas the TAS2R genes to their offspring. Organisms possessing the TAS2R genes have a higher fitness than organisms that do not posses this gene family. Thus, the TAS2R gene family would have been selected for via natural selection and became the ability to taste bitter foods would have become dominant in the population.

This is especially true in the case of the thyroid-inhibiting toxin, PTC. PTC is known to decrease thyroid hormone, which regulates metabolic function. PTC can also lead to liver damage and a host of other medical problems that would eventually lead to death. Being able to taste the PTC toxin would have allowed our ancestors to to avoid toxic foods that if ingested would ultimately lead to their death. Because of this, the ability to taste the PTC toxin would be passed on to the next generation and contribute to the increased fitness of the following generation. In this way, the bitter taste genes would become selected for and would become prevalent in the population.

How the Evolution of Bitter Taste Affects Me Today

Although variation in taste facilitated the evolution of primates and other animals, in modern human society it can be detrimental. With the advent of agriculture, there is less need for tasting of bitter food. Highly nutritious vegetables are known to activate the bitter taste receptors. Instead of doing their intended evolutionary job of protecting from toxic materials, the bitter taste receptors are preventing some people from getting an adequate daily amount of nutritious vegetables due to their aversive taste.

Additionally, some individuals have extremely high sensitivity to bitter tastes resulting from higher rates of expression of the TAS2R gene. These individuals are known as “supertasters”.  Supertasters can be found in the highest frequency in parts of Asia, Africa, and South America. This may be because these areas originally possessed a higher concentration of toxic plants and animals in comparison to other areas. In order to compensate for the increase in potential toxins, the individuals living in this area might have benefited more from bitter taste receptors. Today, many supertasters dislike a wide variety of vegetables such as cabbage and soy, and favor sweet items over bitter vegetables. This not only leads to increased chance of obesity and diabetes, but because of the avoidance of vegetables there is increased risk for GI diseases such as colon cancer. Not all side effects are bad though. Supertasters have a higher dislike for alcohol, carbonated beverages, and smoking. Avoidance of these items is actually quite beneficial in boosting heath.

Next time you don’t feel like eating your vegetables, you can blame it on evolution!

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More Reading…

Campbell, M. C., P. A. S. Breslin, A. Ranciaro, S. A. Tishkoff, D. Drayna, D. Zinshteyn, G. Lema, T. Nyambo, J.-M. Bodo, S. Omar, J. Hirbo, and A. Froment. “Evolution of Functionally Diverse Alleles Associated with PTC Bitter Taste Sensitivity in Africa.” Molecular Biology and Evolution 29.4 (2012): 1141-1153.

Wooding, Stephen. “Evolution: A Study in Bad Taste?.” Current Biology 15.19 (2005): R805-R807.

Are Humans Still Evolving?

Contributed By Kevin Childress, Ricardo Acevedo, and Crystal Seales

Can we be at the mercy of evolution?

A common misconception about evolution is that humans are no longer evolving. It’s very easy to think that because we seem to be the masters of the world around us, there is no need for the human species to be changing anymore. However, if we just look at some examples, we can see that humans are indeed not immune to the power of natural selection. For example, only certain human populations, mainly from pastoral/cow farming heritage, have the ability to digest milk at older ages. If you contrast those humans with humans from East Asia, you see that a large majority from East Asia cannot digest milk due to the lack of dairy in their ancestor’s diets. (For more information, see a recent post on lactase).

But let’s take a look at a more “drastic” example, the pygmy humans. They represent a population of humans around the world that have an unusually small body size that is well proportioned. They are found in certain African, Southeast Asian and South American populations, so they aren’t just an isolated group of people. The groups found in Central Africa are known to be the shortest humans on Earth! These pygmy populations tend to grow at a slower rate than other humans, and they normally stop growing at just 13 years old!

So why are they short? Well, genetic testing has shown that these groups evolved separately from one another. Currently, many hypotheses are being investigated. The most recent one is that this is an adaptation that allows the pygmies to stop growing at an earlier age, and thus reproduce at a younger age. This is plausible because less resources are put into their growth, allowing for more energy to be available to reproduce at an earlier age.  Understandably, however, the hypothesis is highly debated. Others believe that earlier reproduction times and a smaller body size evolved to compensate for a lack of  food and resources in their environment. A shorter stature could also help the pygmies navigate their surroundings and regulate their body temperatures more efficiently.

These hypotheses are an attempt by researchers to explain why the pygmy populations differ physically from the rest of the human species. Even though evidence doesn’t support a specific hypothesis at this time, the current data illustrates that evolution is a force that will continue to influence our species.

Check out our video on the topic!

For more info, see :

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