Evolution

Arman Saeedi

The theory of evolution explains the origins of all life on earth. Evolution itself is the change in inherited characteristics of organisms over several generations. The mechanism that controls the evolutionary process is known as natural selection . Coined by Charles Darwin, natural selection states that organisms of a certain species that have favorable characteristics will thrive and reproduce, passing their genetic information down to their offspring; meanwhile, those with unfavorable characteristics will die out due to their inability to live long enough to reproduce. This process is driven and shaped by the organisms environment. Evolution does not conflict with my spiritual beliefs. Humans cannot prove or disprove the existence of a higher power; agnosticism is the belief system that states that humans cannot know with certainty if there is or is not such a higher power, so it does not even attempt to answer that question. Science aligns itself with my beliefs in that I consider evolution as a process that perhaps occurred alongside the coming of Adam and Eve. Maybe Adam and Eve were sent to Earth around the same time human evolution was catching up. Evolution is certainly an observable science. There is bountiful of data backing the theory of evolution, and it is something that has led to various advancements in our knowledge as humans , particularly in areas such as medicine. For this reason, it is a more valuable outlet for intellectual curiosity than religion as it provides room for growth as a species that yearns to learn more about the universe and yields more palpable findings. Dr. Moalem introduces the book by stating his four tenants. The first diminishes any thinking that we may be alone at any given time. No matter the location or the time, we are surrounded by thousands of living organisms; our digestive systems are filled with millions of bacteria that assist in the absorption of food. As there are organisms that are helpful, there are also many that can cause harm. Nature does not favor one or the other because both are simply trying to survive and reproduce. This sets up Dr. Moalems second point. Evolution is not an independent process. Earth

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contains millions of life forms, ranging in complexity, all driving towards the same two basic goals: survival and reproduction. The survival of an organism may mean the death of another or many others, and this is what ultimately drives evolution. Dr. Moalem writes evolution in any one species can create pressure for evolution in hundreds or thousands of other species. And that, when it happens, will create evolutionary pressure in hundreds or thousands of other species (xiv). The third misconception that Moalem dismisses is the idea that mutation is an innately bad thing. Mutation is change. Mutations that harm an organisms chance of survival are quickly removed from the gene pool. Those that help an organism survive lead to the evolution of a new trait (Moalem XV). Natural selection is the underlying process that filters out the bad from the good. The final point Dr. Moalem makes is that DNA isnt a path set in stone. Its more like the type of the stone one is given to make ones own path . It certainly influences ones life drastically, but the way in which it does is wholly dependent on ones environment, choices, and parents. DNA is simply the recorded history of every organism that preceded a current organism. Evolution is the printing press that writes that history. There is one underlying theme that needs to be understood: Survive. Reproduce. Hemochromatosis is a hereditary disease introduced to the genome somewhere along the long line of human evolution. Dr. Moalem introduces the disease in first chapter of his book, Ironing it Out. In laymans terms, the disease prevents the body from feeling full from the metabolism of iron. The condition is sometimes referred to as iron overload. When left untreated, hemochromatosis can lead to a serious of health complications such as liver failure, heart failure, diabetes, arthritis, infertility, psychiatric disorders, and possibly even cancer. Armand Trousseau first described it in 1865; over a century later, a strong correlation was found between the gene for hemochromatosis and those of Western European descent. If your ancestors are

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Western European, the odds are about one in three, or one in four, that you carry at least one copy of the hemochromatosis gene (Moalem 3). This discovery opened doors for epidemiologists to look into for any hints of why a disease so deadly would be naturally selected. Iron is a driving force in the metabolism of almost all life. Its an essential mineral for many of the processes that are carried out in the complex systems within life; however, too much can spell trouble. It just so happens that parasites, cancer cells, and bacteria also thrive on our iron. This explains why there are innate processes that also control the level of iron absorbed in the digestion of food . In fact many of the openings vulnerable to infection are flagged iron no -fly zones by the body (Moalem 7). For even added protection in these areas, proteins known as chelators lock up iron molecules and prevent their use. Saliva and mucus are two examples of fluids rich with chelators. The immune system is even smart enough to make sure to lock away iron that could be used against someone during periods of illness and to pump the body full of illness-fighting proteins in whats called the acute phase response. There are some interesting trends found in history. Vikings are said to have spread the disease through Northern Europe. It may have evolved as a mechanism to minimize iron deficiencies in poorly nourished populations (Moalem 14). Its further thought to have been spread through the founder effect or inbreeding. The bubonic plague leaves trails to understanding hemochromatosis. Stephen Ell, a professor at the University of Iowa, wrote, Iron status mirror*ed+ mortality (11). Women who lost iron through menstruation, children, and the elderly who lacked iron were spared in greater numbers when compared to healthy adult males. A more recent outbreak in 1625 indicated a ratio of up to 2:1 deaths between males and females aged 14-44, respectively. One nuance between those with hemochromatosis and those without is at a cellular level: macrophages, cells designed to find and eliminate invaders, have much less iron in a person who has hemochromatosis. When the plague hit in the fourteenth,

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Arman Saeedi

those afflicted with hemochromatosis were suddenly more favored by evolution. Natural selection can be a very short-term process. In this instance, the gene that guaranteed surviving the plague was selected for even if it was a death sentence in forty years. There were recurring outbreaks up until the nineteenth century that embedded this gene even further into Northern and Western European populations. Something that I found very interesting was the fact that the understanding of the hemochromatosis virus led to the revival of long dismissed medical practice known as bloodletting. In modern medicine, the practice of bloodletting is called therapeutic phlebotomy. It was shunned as a savage and barbaric treatment, but is now realized as one of the effective treatments for hemochromatosis and several other diseases. This leads to me to inquire: how many other outdated/ridiculed medical practices have been reintroduced as effective treatments? Dr. Moalem begins his second chapter, A Spoonful of Sugar Helps the Temperature Go Down with, The *WHO+ estimates that 171 million people have diabetes and that number is expected to double by 2030 (23). As shown in the previous chapter, for a disease to continue existing, it must have or it had an evolutionary benefit for the species. Diabetes, or diabetes mellitus, focuses on one substance and how the body manages it. Sugar is the culprit, but more specifically blood sugar known as glucose. Insulin and glucose go hand-in-hand. Using insulin, a hormone produced by the pancreas, glucose is stored in the liver, muscles, and fat cells to be used as energy at a later time. Diabetes breaks this process. One of the first noticeable symptoms of the disease tends to be the pungently sweet smell of the urine of someone that has it. Moalem writes, In the past Chinese physicians actually diagnosed and monitored diabetes by looking to see whether ants were attracted to someones urine (24). The sugary urine of those with diabetes attracted more ants. Left unmanaged, diabetes can lead to rapid dehydration, coma, and death. The problems dont stop

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there. Even with careful management, long-term complications of diabetes include blindness, heart disease, stroke, and vascular disease eventually leading to gangrene and amputation. Diabetes has two main types. Type 1 diabetes, commonly called juvenile diabetes, is thought by some researchers to be an autoimmune disease in which the body attacks its very own cells responsible for the production of insulin. No insulin means no glucose can be stored. Currently type 1 diabetes requires external insulin through either daily injections or insulin pumps. The second type of diabetes, sometimes referred to as adult-onset diabetes, behaves a little differently. The pancreas is still able to produce insulin, but it is often not enough or the bodys tissues become resistant to it, ultimately interrupting the absorption of glucose. Like hemochromatosis, diabetes has links to certain populations. The Pima Indians of the southwestern United States, for example, have a staggering rate of diabetes --- nearly half of the adults (Moalem 26). One theory is that the sugar and carbohydrate heavy diet of the Western world is too much for their historic metabolisms that relied on heavily on hunted meats. The correlation of type 1 diabetes is vastly different. It presents itself very commonly in people of Northern European descent with Finland having the highest rate of the disease and reducing as one goes south. And like hemochromatosis, when theres correlation between a genetic disease and specific populations, a look at evolutionary history may provide insight on why or how nature selected for said disease. The answer lies in the Younger Dryas, a rapid transition in the earths climate into an ice age. In this chapter Dr. Moalem pointed out two methods that have been observed as ways to survive the cold; he wrote, eliminating water and driving up sugar levels to deal with the cold: Grapes do it. Now we know frogs do it (44). This quote refers to the osmotic change in grapes and frogs as

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they attempt to survive freezing conditions. The elimination of water is an instinctual response. Water expands when it freezes. Eliminating water makes sense when an organism attempts to survive freezing conditions, which is why humans tend to get an urge to urinate when cold. It is also a complementary way to drive up sugar concentration without adding sugar. As blood sugar goes up the freezing point of blood decreases allowing an organism to withstand much colder temperatures. Frequent urination, another symptom of diabetes, results in low internal water levels. Together, they are a recipe for cold-resistance. Another interesting connection has been found in areas of different weathers. During colder months, especially in cold countries, diabetes diagnoses are significantly higher than during warmer months in warmer countries. When all the pieces are put together, its easy to see natural selection favoring diabetesafflicted humans during the short and violent ice age called the Younger Dryas. Those who had it also had the advantage of being able to survive and reproduce . Another interesting finding was the connection of cold weather as a risk factor for a stroke. Correlations such as this one can help preventative measures. This chapter made me wonder: Will natural selection slowly work its way into removing previously useful diseases that have since lost their evolutionary advantage? The Cholesterol Also Rises, Moalems third chapter, addresses the evolutionary need for, well, high cholesterol, and it all ties into vitamin D. Vitamin D is a vital component of the body that assists with bone growth and maintenance . It is also used to manage sufficient levels of calcium and phosphorus in our blood, and it has recently been found to be crucial in the proper *functioning+ of the heart , the nervous system, the clotting process, and the immune system (Moalem 50). Deficiency of the vitamin can lead to osteoporosis in adults and a disease called rickets in children that harms bone growth and causes deformity. Not only that, someone who is vitamin D

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deficient may contract diseases such as different cancers, diabetes, heart disease, arthritis, psoriasis, and mental illness to name a few. American milk started to be fortified with vitamin D once the deficiency and rickets were found to be related; theres also a much more natural source in the body: cholesterol. The word cholesterol often has a negative connotation , but it is a substance required by the body for a variety of processes. For example, cholesterol is required to make and maintain cell membranes. As Dr. Moalem writes, It helps the brain send messages and the immune system to protect us against cancer and other diseases (51). In addition to this, cholesterol is the precursor of many hormones such as estrogen and testosterone. The body also uses cholesterol to manufacture vitamin D through a process very similar to photosynthesis in its dependence on the sun. Ultraviolet B is the type of sunlight necessary for the body to convert cholesterol to vitamin D . It is interesting to note that the body is so efficient at making the vitamin that it is able to store enough, when it does get sufficient sun exposure, to get by in the darker months. As UVB rays are able to convert cholesterol into vitamin D, they are also ruthless destroyers of another important substance by the name of folic acid or folate , depending on its form. Folic acid helps in replicating DNA in cell division, which is especially important during pregnancy. This link was first proposed in the mid-1990s when an Argentinian pediatrician reported that three healthy women all gave birth to children who had neural tube defects after using indoor tanning beds during their pregnancies (Moalem 52). Historically, the evolution of humanity brought along with it changes in skin color. The skin is the largest organ of the human body. It is involved in the functioning of the immune, nervous, and circulatory systems as well as metabolism. The skin is important in protecting the bodys folate as well as hosting a step in the manufacturing of vitamin D. The human species is believed to have originated in Africa and expanded

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Arman Saeedi

outwards. Skin color, being dependent on a populations sun exposure, is darker in environments where more protection against the suns rays was needed . To prevent folic acid deficiency, an evolutionary preference in Africa arose towards darker skin, but as some population groups moved northward, where sunlight was less frequent and less strong, having dark skin started to get in the way of vitamin D production (55). Simply put, skin color is a tipping scale under the wrong conditions. Darker skin doesnt have any additional benefit in mild to moderate sun exposure and it even hinders vitamin D production, whereas lighter skin quickly burns or in some cases contracts melanoma, a deadly skin cancer, in moderate to severe exposure. So dark skin did provide some added protection for those living in the appropriate place, but how did those populations possibly produce enough vitamin D? When theres a will, theres a way. Or so the saying goes. These populations of dark skinned had yet another evolutionary stress, and in response apolipoprotein E, ApoE4, introduced itself to the human species. ApoE4 works by increasing the available amount of cholesterol to be converted to vitamin D , effectively countering the deficiency caused by reduced sun exposure. Interestingly enough, the same evolutionary pressure introduced the adaptation to the light-skinned people of Europe who were not blocking out UVB rays because of their skin; rather , they werent getting any of the essential sunlight to begin with. In the same way as in Africa, the ApoE4 gene keeps cholesterol levels high in northern Europeans to ensure sufficient production of vitamin D. As with the previously discussed diseases, it comes with its disadvantages. ApoE4 may be necessary for survival in Africa near the equator where sun exposure is plenty, but as Moalem points out, what happens when those with the adaptation move to New England or similar places where the sunlight is scarcer and less intense? (66) Now, this population is hurt by not having enough vitamin D and having excess cholesterol that isnt being converted due to the lack of sunlight . The high cholesterol

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caused by the adaptation may be necessary in some environments where it is actively converted to maintain vitamin D levels, but when it builds up, it can result in higher risks of heart disease, stroke, and in Caucasians, even Alzheimers disease. In fact until vitamin D fortified milk, there was a substantially higher incidence rate of rickets in African Americans. This chapter also touched on two very interesting ideas: the explanation of the high rate of high blood pressure among African Americans and a gene that expressed rapid metabolism. When looking at African Americans, doctors immediately assumed that elevated incidence of high blood pressure was a common trait between all blacks . They were wrong. Blacks living in Africa do not have the same rate of hypertension as people of African descent in America (Moalem 65). Why is that? History holds the answer once again; it seems that a very unnatural selection took place during the period of time slave traders imported Africans through what is known as the middle passage. These horrible conditions often didnt provide enough water for the slaves and resulted in many deaths, and again natural selection favored those that could survive . The Africans that retained high levels of salt were able to withstand harsher levels of dehydration and reproduce, spreading the trait down to the next generation. In another case, a patient became ill when she took her prescription cough syrup . After a closer look, she was found to carry many copies of the CYP2D6 gene causing her to metabolize the drug much more rapidly. Of course doctors consider racial backgrounds in their diagnosis of certain conditions, but how often is a doctor able to account for genetic differences such as the CYP2D6 gene? It would be very interesting if in the future, technology allowed complete and relatively fast access to a persons genetic information. It would certainly allow for much more effective approaches at attacking disease and infections.

Evolution

Arman Saeedi

Chapter IV, titled Hey, Bud, Can You Do Me a Fava? focuses on an enzyme deficiency known as Favism. Greek philosophers often warned against the consumption of fava beans and superstitions against eating *them+ were common throughout the Middle East (Moalem 73). Favism is an inherited enzyme deficiency carried by upwards of 400 million people making it the most common enzyme deficiency in the world. Severe reactions to the deficiency combined with the consumption of fava beans or certain drugs that contain similar compounds can result in rapid anemia . Modern scientists supposedly first noticed the connection during the Korean War. Antimalarial drugs, specifically primaquine, were observed to cause the development of anemia in soldiers that were prescribed to it. Ten percent of African American soldiers developed anemia, and those of Mediterranean descent tended to develop a more severe version of the disease, hemolytic anemia. Moalem describes the disease, their red blood cells were literally bursting (74). Anemia, when left untreated, can cause several problems. It can lead to kidney failure, heart failure, and in some instances even death. The mechanism behind mechanism behind favism is a little complex. Fava beans contain compounds: vicine and convicine. Together, these compounds produce free radicals in the body, especially hydrogen peroxide. Dr. Moalem explains how if the hydrogen peroxide isnt cleared out with the help of G6PD , it starts to attack your red blood cells, ultimately breaking them down which sounds a lot like hemolytic anemia. The gene that expresses the G6PD protein production and indicates whether or not someone has the deficiency goes by the same name. It is carried on the X chromosome and therefore tends to be more common in men. The first fava beans date back around 8,500 years in Nazareth. It is believed that cultivation of fava beans continued to spread first to the Middle East and then even farther to places like the eastern Mediterranean, Turkey, and Italy. Even more interesting is that if you marked up a map to show where favism is most common and

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Arman Saeedi

then overlaid that with the areas where the fava bean cultivation is most common there lies an astounding similarity. Favism is most common in North Africa and Southern Europe; the two places happen to be the locations most of the cultivation occurred . Which begs the question: why does a population that has the largest fava bean consumption also have a genetic mutation that causes it tons of problems? One mustnt look too far in order to understand the evolutionary benefit of this deficiency, but several things need to be understood. Various organisms have differing ways by which they ensure the continuance of their species. Some plants, for example, have evolved to grow edible fruits, and it was no mistake. The fruits contain seeds. Animals that eat the fruits spread the seeds, and the cycle starts all over again. Other organisms such as infectious agents like malaria have evolved towards other transmission methods. In ancient times, doctors thought, many diseases were caused by unhealthy vapors emanating from still water (Moalem 88). Hippocrates coined the term miasma for this perceived phenomenon. The doctors were right in finding a correlation between higher rates of infections and the vapors, but for the wrong reasons. Mosquitos, being the efficient disease transport systems they are, thrived in those environments; as a result, the disease rates were significantly higher near such areas. J.B.S. Haldane first suggested the idea that people with sickle-cell anemia had better natural resistance to malaria. Researchers today seem to agree that *G6PD deficiency+ may also provide protection against malaria (Moalem 90). Lab studies showed that malaria preferred healthy blood cells to those that were G6PD deficient, which explains why certain populations would select for this mutation; however, it leaves the questions as to why those populations would also cultivate fava beans . Even when a non-deficient person eats the beans, they experience added protection, and when a deficient person eats fava beans, the parasite is done for. Another very cool aspect about the gene is that one may be partially deficient . In areas where the

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Arman Saeedi

mutation is common, a large number of women are at least partially deficient, because the gene is only passed on the X chromosome of which women have two. Partialdeficiency provides malarial protects without causing extreme reactions to the consumption of fava beans. More surviving pregnant women equals natural selection at work. It is truly interesting the way fava beans exploit a genetic mutation to provide medicinal value. Fava beans are one example of herbal remedies; however, humans have been relying on herbal remedies since, well, probably before there were humans (Moalem 91). Findings show that Neanderthals may have used plants for healing as far back as 60,000 years ago. Morphine, one of the most powerful modern painkillers, is derived from the same source that Ancient Greeks got opium milk from. Countless other medicines have been derived from natural plant toxins. All of this raises some questions as well: are all medicines derived from plants and more importantly, are unknown genetic factors possibly the reason so many of them have side effects that affect only a small number of people? It must be a very long and arduous process when determining the safety of a newly proposed drug. It might just so happen to be fatal to some unknown population. Dr. Moalems next chapter Of Microbes and Men strays somewhat from human evolution towards the discussion of microbial evolution. The recurring theme, survive and reproduce, is ever most emphasized when Moalem writes about multiple parasites and infectious diseases in this chapter. The Guinea worm, or Dracunculus medinensis, is the first parasite that introduces the readers to the chapter. When water fleas ingest the larvae of the worm, they effectively contaminate that water supply with the disease. Humans, unaware of the infected fleas, drink the water; the parasite is able to travel from the small intestine into the body. The larvae then grow and mate. Moalem describes the process writing, About a year after infection, adult females ---

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now two to three feet long, about the diameter of a piece of spaghetti and full of new larvae themselves --- make their way to the skin of the person carrying them (95). Here is where it gets interesting. The first visible sign of infection is the appearance of a blister on the skin. As the worm makes its way out of the skin, it ruptures the blister causing great pain. Instinctually, the host responds by applying cool water to the area, which actually triggers the worm to emit thousands of larvae, starting the process anew. There are different kinds of relationships that our body shares with the organisms that inhabit it. When both an organism and the host it inhabits are benefitted, it is a symbiotic relationship. For example, colonies of gut flora dominate the resources in someones intestines keeping more dangerous and harmful agents such as Neisseria meningitides, Staphylococcus aureus, and Streptococcus pneumoniae at bay. They may inhabit someone at any given time, but the symbiotic relationship with gut flora provides some level of protection. Another example is a species of bacteria that assist in the digestion of ice cream and other dairy products. Guinea worm has been discovered in Egyptian mummies. Some researchers even believe the possibility of a link to the fiery serpent that struck the Israelites during their forty-year desert adventure. One thing is for sure: infection rates have gone down tremendously as time passed. Former president Jimmy Carter has led a two-decade effort to spread understanding about the parasites method of reproduction to every corner of the world, ensuring that its victims avoid water when looking for relief and that its potential victims avoid water that could be infected (Moalem 96). Through education, infection rates dropped from 3.5 million in 1986 to a mere 10,674 in 2005. Understanding a diseases relationship to humans opens up new paths of prevention and defense. The evolutionary mechanism at play is host manipulation. What seems to be dragged straight out of a science fiction movie happens everyday at the microbial level .

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In one case, a parasitic worm used host manipulation to control the behavior of the spider it had infected. Through the release of certain chemicals, it modified the spiders web building patterns and essentially looped one portion. This resulted in a sturdy environment in which the parasite leeched the remaining energy from the spider, killing it, and began its cocoon. Another organism that this mechanism can be observed in is Toxoplasma gondii. This specific parasite has a limitation, however, it can only reproduce inside of cats. T. gondii is still very capable of infecting almost every warmblooded animal, but it is only able to undergo sexual reproduction and produce new oocysts, or spore cells, within cats. Infected cats are not only home to the new parasites, but they are also partially responsible in their distribution. Oocysts get transferred through droppings. For an organism so small, oocysts are pretty durable and able to survive for up to a year in droppings. The cycle continues when rodents, birds, or other animals ingest the oocysts (Moalem 106). The infection can also spread through the ingestion of an infected animal, and humans are at risk when eating undercooked meat or poorly washed vegetables. The T. gondii distributes itself making its home in muscle and brain cells; however, in order to reproduce, it must make its way back into a cat. This is where host manipulation comes into play once again . Scientists have observed when a mouse eats infected cat droppings, the parasite behaves in the usual manner, moving into the mouses muscle and brain cells, but theres more. The mouse becomes fat and lethargic. Then it loses its natural fear of predators --- of cats (Moalem 106). Certain studies have actually shown infected mice being drawn to the scent of cat urine. The cat gets a free meal, and the parasite hitches a ride, ready to reproduce again. Moalem cites other research showing the possibility of a connection between *OCD+ disorders and streptococcal infections in children (112) and correlations between STD infection and increased sexual promiscuity in hosts (113).

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Arman Saeedi

Inhibition of Staphylococcus aureus, or staph for short, resulted in the accidental discovery of penicillin by Alexander Fleming in 1928. Within eight years, forty percent of all staph strains had developed resistance to penicillin. Ten years later, resistance grew to a whopping 80% of all staph. Scientists developed methicillin to counter this resistance in 1959. A similar trend followed. Just two years after the introduction of the specialized antibiotic, the first incident of methicillin-resistant staph, known as MRSA, was reported (Moalem 117). Currently, MRSA afflicts many patients in hospitals around the world and treatment has switched to yet another class of antibiotics containing vancomycin, and as expected resistant strains of the disease popped up once more. The first case of VRSA was reported in 1996 in Japan. Evolutionary stress pressures bacteria to select for resistances against our countermeasures . Something to note about infectious diseases is the degree to which they destroy their host, also known as virulence. Virulence ranges widely from hardly dangerous (common cold) to rapidly, horribly fatal (Ebola) (Moalem 118). Paul Ewald believes that the mode of transmission plays an important role in the influencing the virulence of a given parasite. Microbes can spread in three basic ways: close proximity like through the air or physical contact, using an intermediate organism, usually a mosquito, fly, or flea, or traveling through contaminated food or water (Moalem 118). According to Ewald, diseases that spread through close proximity face evolutionary pressure to reduce virulence. They depend on their hosts ability to spread them around through physical contact or close proximity. This explains why the common cold is unlikely to ever evolve to kill humans. It attains its basic goals of survival and reproduction fairly easily while allowing the host to function to a great extent. The flip side, when an infectious agent isnt dependent on the hosts mobility for transmission virulence tends to be favored by evolution. In the case of malaria, the chance of being bitten by a mosquito rises when the host is heavily incapacitated, and each bite ingests more

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parasites. Mosquitos are able to feed on the immobile host, and the pathogen spreads successfully. Cholera, another disease independent from mobility, spreads easily through unprotected water supplies when soiled clothes or bed linens are washed in rivers, ponds, and lakes, or through sewage runoff (Moalem 119). Following the trend, cholera has a high virulence. The possibilities that this understanding of microbial evolution brings with it are fascinating. Humans may some day be able to steer evolution in their favor by reducing the virulence of pathogens. Ewalds theory is that by removing the modes of transmission that dont require human participation , evolutionary pressure will allow for reduced virulence. A series of cholera outbreaks in 1991 hold promising evidence. Ewald spoke of the possibility of essentially domesticating those disease organisms , making them into mild versions of what was there before (121). This would mean using our knowledge of evolution to steer all disease towards a state of low virulence, akin to strains contained in vaccinations. Can we potentially come to an evolutionary singularity with harmful organisms using our knowledge of evolution? Dr. Moalems next several chapters did not involve particular diseases; rather they discussed various scientific discoveries that changed human understanding of evolution significantly. In Jump Into the Gene Pool Dr. Moalem explains the concepts of mutations and jumping genes, a completely novel idea proposed and later discovered by Barbara McClintock. The gene pool contains many mysteries of life. What is interesting is how less than 3 percent of your DNA contains instructions for building cells (Moalem 128). Scientists coined the term junk DNA for the other 97% that isnt actively used in protein production. New research is proving them wrong. A new look at human cells, specifically the mitochondria within them, has scientists believing that mitochondria independent, parasitic bacteria that evolved a mutually beneficial relationship with some of our pre-mammal evolutionary predecessors (Moalem 129).

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Mitochondria have their very own inheritable DNA, or mtDNA. Researchers currently think up to a third of human DNA is from viruses. The possibility that human evolution not only adapted to viruses and bacteria, but also has integrated them into the genome is mind-blowing. Barbara McClintock decided to stir up some controversy of her own. For the longest time, previous consensus between researchers was that DNA was a set-in-stone blueprint for the production of the proteins that would continue for the course of an organisms life and that mutations, or changes in DNA, were both rare and random. In the 1950s, McClintock managed to produce evidence that under the right conditions , parts of the genome mutated. She discovered significant changes like whole sequences of DNA moving from one place to another. She noticed several trends. Dr. Moalem writes, First of all, they relocated to certain parts of the genome more often than to other parts. Second, these active mutations appeared to be triggered by outside influences, by changes in the environment that threatened the survival of the corn , like extreme heat or drought (137). This would mean that these mutations are neither rare nor random. When she presented her discovery, the scientific community responded with skepticism and scorn. Over thirty years later, after her discovery had changed human understanding of mutations, McClintock was awarded a Nobel Prize. Her discovery of jumping genes opened even more doors. In one experiment milk-shunning E. coli was deprived of all food excluding lactose. Much more rapidly than previously thought possible, the strain developed mutations that allowed *it+ to lose *its+ lactose intolerance (Moalem 141). The scientist behind the experiment wrote that E. coli may have a mechanism for the inheritance of acquired characteristics, a phrase incorrectly belonging to disdained Lamarckian ideology. Another blow to the disbelievers is the possibility of retroviruses or viruses and their capability to carry DNA

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from somatic cells to germ cells, something previously thought impossible according to the Weismann barrier. Moalem points out, If so, that would theoretically open the door to the idea that acquired adaptations could be passed on to future generations (143); Lamarckian ideology is making a comeback. Scientists have also linked the brain and immune systems to jumping genes. The individuality of jumping genes brings great possibilities for different combinations. For example in the immune system, B-cells seek out the instruction for a specific antibody in their DNA and mix-and-match through what is called V(D)J recombination, essentially rewriting their own genetic code in a very specialized manner. V(D)J recombination leaves a unique little loop when it reconnects the remaining strands of DNA. Until recently, scientists thought genetic information flowed in only that one direction, DNA to RNA to protein (Moalem 149). Retroviruses, like HIV, have proven otherwise. Made up of RNA, retroviruses utilize an enzyme called reverse transcriptase to reverse the information flow and literally change DNA. Logically speaking, if a retrovirus was able to break through the Weismann barrier and encode itself into the DNA of germ cells, that organisms offspring is born with the virus permanently encoded in its DNA (Moalem 149). Speaking of which, it was previously mentioned that up to one third of human DNA came from viruses so it makes sense to assume some retroviruses have succeeded in breaking that barrier. Another incredible similarity was noticed, this time between a type of jumping gene and retroviruses. Retrotransposons are copy-and-paste genes and the mechanism they use to insert themselves in mirrors the one retroviruses use. Reverse transcriptase is used in both processes to paste the genes into the DNA. Jumping genes may very well be descendants of viruses. The idea that humans are made from DNA that contains viruses and bacteria that have evolved to integrate themselves into us is absolutely out of this world . Persisting viruses is what Luis Vilarreal calls viruses that have migrated into our

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genome over millions of years and may have become our partners in evolution (Moalem 151). Persisting viruses have invested in us and share a stake in our survival. For this reason, they come to the rescue and allow for fast-forward evolutionary adaptations when it is needed for survival. The study of jumping genes has completely revolutionized researchers view on junk DNA to accept the possibility and probability that it is the key to a library of genetic information for jumping genes to choose from. Where does this research lead now and is it possible that evolution is speeding up exponentially? Could humans perhaps use their knowledge to steer evolution in certain direction that would be beneficial such as immunity to more diseases? The next chapter of Dr. Moalems book Methyl Madness: Road to the Final Phenotype introduces the study of epigenetics and methyl markers . New research is paving way for a completely new dimension in genetics. Connections have been found between obese children and their pregnant mothers eating habits. This isnt to say the expecting mothers eating habits produced some kind of genetic change that was passed on to the offspring, rather certain compounds have been discovered to to attach themselves to specific genes and suppress their expression (Moalem 156). The DNA does not change, but its expression certainly does. This groundbreaking research, called epigenetics, is focused on how children can inherit and express traits from their parents without a change in their DNA. Sensory information received by an expectant mother influences the expression of certain genes in a child. Not only is methylation present during pregnancy, but methylation has also been observed in maternal interactions after birth. An experiment on showed the suppression of a gene, agouti, during prenatal care was expressed in the phenotype of the offspring. This process, methylation, is when a methyl group binds to a gene and changes the way that the gene expresses itself without actually changing the DNA (Moalem 158). This isnt completely new

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Arman Saeedi

thinking either. Researchers have long noticed the ability of some organisms to produce offspring customized to the mothers prenatal experiences. Theyve always known it, but they were unable find an explanation. Epigenetics was the answer. In one observed example, environmental factors affected the desert locusts tendency to be a loner or group with others. Other experiments show evidence of methylation post-birth. In an experiment with rats, nurtured pup lost the methyl markers that would have blocked the development of a part of their brain (169) which led to more confident pups. In contrast, pups with harsher mothers often experienced lower self-esteem and confidence. As an evolutionary advantage, epigenetics is akin to a weather forecast. It hints to the possible hardships that an offspring may face and responds by triggering the methylation of certain genes. This certainly may at least partially explain the epidemic of childhood obesity. Western diets are high in calories and fats while simultaneously lacking important nutrients. Pregnant mothers who do not have good nutritional habits during the first two weeks of their pregnancy are signaling their embryos that there will be scarce nutrients. This can lead to a smaller baby at birth, and trigger a thrifty metabolism designed to conserve any calories it gets. In ancient times when food was sometimes hard to come by, these epigenetic markers would certainly have provided benefit to newborns, but in most developed countries they are superfluous and result in harmful effects. Its funny that Lamarck was ridiculed for a theory that was wrongly credited to him, and now modern research may be providing evidence that supports that very same theory due to methylation. There is also so little that we know as of yet about the science of epigenetics. The fact that methylation can occur near transposons and even be carried to where it jumps, muting a genes expression, is a slightly worrying concept. Needless to say, the study of epigenetics has great potential, which leads me

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Arman Saeedi

to ask: is it possible for epigenetic science to advance far enough to allow for live genetic modification? If researches can find what stresses trigger which methyl markers , then who knows what the possibilities are? The last chapter of Dr. Moalems eye-opening book discusses a question almost everyone has: why do we age? Thats Life: Why You and Your iPod Must Die attempts to tackle this hard question. Aging has been speculated to simply be a product of wear and tear through the years, but with recent research isolating genetic factors responsible in the aging related disease, progeria, researchers began to wonder if there was a genetic variable that causes humans to age. Progeria is a disease that accelerates aging substantially. Those afflicted with it tend to die in t heir early 30s. To answer that, the Hayflick limit was discovered. The limit says that, cells only divide a fixed number of times before they up and quit . . . in humans the limit is around fifty-two to sixty (Moalem 185). Telomeres are behind the Hayflick limit. With every cell division, a tiny bit of DNA is lost. To protect the truly important information, chromosomes have what are called telomeres at the end of each strand. Different species have different life expectancies and for good reason. Short life expectancies have a lack of evolutionary pressure to develop DNA repairing mechanisms whereas long life expectancies have the opposite. So why would any species evolve to have a limit on cell division? The answer is cancer. The Hayflick limit is essentially a defense mechanism in place that is meant to stop unchecked cancer growth before it gets too out of hand. Once a cancer cell divides 52-60 times, its stopped dead in its tracks, but it doesnt always work that way. Successful tumors manage to circumvent this natural mechanism by activating an enzyme called telomerase, which prevents the shortening of telomeres, effectively rendering the Hayflick limit null. So the evolutionary advantage of the Hayflick limit that is added protection against cancers comes with the trade-off of aging. Aging also

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Arman Saeedi

provides other benefits, although to the species as a whole rather than the individual. For one, it allows room for evolution, and secondly, it eliminates individuals that have become laden with parasites preventing them from infecting the next generation (Moalem 191). Scientists have been working on a method to detect telomerase activity in order to more effectively locate tumor growth. Telomerase is not exclusive to cancer cells. In fact, stem cells, cells that can turn into any other kind of cell, also utilize telomerase to fix their telomeres. Stem cells have great potential to cure disease, and have so much room for research. I hope to witness the benefits that stem cell research brings to the species during my life. With our ever-growing knowledge of biology, is aging anything we could alter or slow down within our lifetimes? Is there a possibility of reversing aging, and would those in power even allow such discoveries to be released to the public? Dr. Moalem explained various aspects of biology and how history can leave hints and clues to discovering connections between almost everything. I believed in evolution prior to reading this book; however, t his book certainly taught me things I have

not heard of before, and I believe some of the discoveries mentioned in the book will lead to medical advances that will take our species very far. At the same time, each discovery raises ten more questions and so on. I mean, the Human Genome Project had just been completed, when suddenly epigenetics blew up. Out of nowhere, there was this whole another mechanism by which genes expressed themselves, which sparked the start of the Epigenetic Human Genome Project . The other thing that fascinated me was the idea of viral and bacterial integration in our DNA. I cant help but think life itself is more of a living, breathing organism than every species spanning across the three domains. It is mind boggling the once independent organisms work in every single one of our cells now, or that viruses have embedded their genetic information into our DNA

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Arman Saeedi

so that maybe a helpful sequence can be selected for in a time of dire need . Science is an incredible thing, and its good that humans have such a thirst for knowledge, because if we dont discover the mysteries of the universe, then who will? Its depressing to think so much could be left unknown, and as a species I feel that we will never stop at least not willingly in our efforts to conquer knowledge.