Radiation and Chemotherapy: Treatment or Cause?

The article, “How Cancer Shapes Evolution and How Evolution Shapes Cancer” explains cancer and cancer treatment from an evolutionary perspective. One topic of the article states that receiving cancer treatment through radiation or chemotherapy can actually worsen the cancer or allow a second cancer to develop. This is because “Although cytotoxic treatment can initially cause a major reduction of the tumor size, this also creates powerful pressure that will frequently select for clones that have intrinsic resistance to the regimen. This evolutionary ability of the tumor cells
thus results in regimen failure and regrowth of the cancer, populated by resistant cells” (Casás-Selves et al p. 6). As this quote explains, cancer treatment often only kills the least dangerous cancerous cells (the ones with the least resistance) and allows the better adapted clones to remain and grow more resistant.

Scientists are the University of California, San Diego, discovered an explanation for how this resistance occurs. Journalist Jamie Reno explains their findings saying, “Researchers found that two of the drugs — Erlotinib for lung cancer and Lapatinib for breast cancer — are effective for a while, but eventually stop killing cancer cells and begin prompting them to resist the drug and become more aggressive” (p.1). At this stage of resistance, treatment actually contributes to tumor growth due to a molecule called CD61. Researchers found that cancer treatment can cause this molecule to rise to the surface of the tumor and “spur tumor cells to acquire more stubborn, stem-cell-like properties, including an ability to survive almost anywhere in the body” (Reno p.1). 

Because treatment can increase the ability of cancer cells to survive throughout the body, secondary cancers can occur. These are cancer growths that can appear anywhere in the body and have three characteristics: “1) histologic features of first cancer and secondary cancer are different, 2) secondary cancer is within the area previously treated with radiation, and 3) the secondary cancer has a latency period of 5 years – that is, the secondary cancer develops five years or later after the first” (Loiselle p. 1). 

The idea that the means of treatment for cancer can either worsen the current cancer or cause a second type to develop is incredibly frightening. Fortunately, there is a potential solution on the horizon: a drug called Bortezomib. This drug “is introduced to the drug-resistant tumors treated by an RTK [chemotherapy] drug, it reverses stem-cell-like properties of the tumors and re-sensitizes the tumors to drugs that the cancer cells had developed resistance to” (Reno p. 1). These drugs are still going through clinical trials, but are appearing to be a promising addition to the current therapies that are used for cancer treatment. One of the researchers performing these clinical trials reports that in mice, “he has seen no recurrence of lung, breast or pancreatic cancer activity once the second drug is added” (Reno p. 1). In order to maximize the effectiveness of this process, oncologists plan to monitor patients drug resistance early in the treatment process and administer Bortezomib as early as resistance is detected (Reno p. 1).

Cancer treatment is still a new and highly imperfect process. Not only are current methods unreliable, but they can also make the cancer worse or cause it to reoccur. Fortunately, new drugs are being developed that can potentially help counteract the dangers of current treatments. If these new drugs are approved, there may be greater hope for cancer remission.

1. Casás-Selves, M., & DeGregori, J. (2011, December 2). How Cancer Shapes Evolution and How Evolution Shapes Cancer. . Retrieved April 23, 2014, from https://ctools.umich.edu/access/content/group/dd756836-7171-480e-b38d-66e2fc80511c/Readings/CasasSelves_DeGregori2011EvoEduOutreach.pdf

2. Reno, J. (2014, April 20). New Cancer Drugs Make Tumors Drug Resistant, More Aggressive. International Business Times. Retrieved April 22, 2013, from http://www.ibtimes.com/disturbing-discovery-new-generation-targeted-cancer-drugs-cause-tumors-become-drug-1573800

3. Loiselle, D. (2011, May 9). Secondary Malignancies After Radiation Therapy. Global Resource for Advancing Cancer Education. Retrieved April 22, 2014, from http://cancergrace.org/radiation/2011/05/09/secondary-malignancies/




The Lobbying Debate over the Agricultural Use of Antibiotics

Antibiotic resistance is becoming a major issue throughout the world. Many people consider overuse of antibiotics by humans the main cause of this growing resistance. Unfortunately, it is not this simple. Even people who avoid taking antibiotics for their own treatment are at risk of developing an antibiotic resistant infection. How could this be? The answer is found in our food: our meat and even our produce.

When animals are being raised on farms for food production, they are fed high doses of antibiotics, which promotes growth and prevents epidemics among them. By regularly giving food-producing animals these antibiotics, we are at risk of ingesting antibiotic resistant bacteria. Even eating fruits and vegetables is dangerous, because typically these foods are grown in manure that comes from animals who were fed antibiotics.

Obviously, this problem needs to be addressed, particularly by the Food and Drug Administration (FDA); However, little action has been taken thus far. A recent report done by the John Hopkins Center for Livable Future found that the main reason for this lack of progress is due to opposition from the farming industry. The report explained that, “The Center for Responsive Politics data, combined with the most recent lobbying filings, show that The American Farm Bureau, the large nonprofit representing the interests of the farm industry, has spent more than $3.3 million on lobbying in the first three quarters of 2013, partly to advocate for the use of antibiotics” (Conradis 2013). Lobbies such as The American Farm Bureau are pouring mass amounts of funding into lobbying against restraints on antibiotic use on animals. Because the government depends on support from these large, moneymaking interest groups, they are reluctant to pass legislation against antibiotic use. In an interview with Yale Environment 360, Robert Martin explained that the Obama administration began taking strides to combat the problem but “because of pressure from the industry, they [the Obama administration] abandoned that effort late last year before the election. Every [presidential candidate] gets so focused on winning Iowa and Ohio and Minnesota — states that are heavy CAFO states — that they abandoned that effort to inventory operations” (Yale Environment 360 2013).

Although the lack of progress is discouraging, there is a potential for change. As Martin stated, “In the last five years, Rep. Louise Slaughter of New York has sponsored the Preservation of Antibiotics for Medical Treatment Act (PAMTA), which would ban for use in animal agriculture the top seven antibiotics important in human medicine” (Yale Environment 360 2013). In addition, this bill would require that medicines be used for therapeutic [not growth] purposes only and be approved by the Secretary of Health and Human Services before use on animals. In general, the PAMTA would place restrictions on antibiotic use for food producing animals by regulating them with specific guidelines. (Library of Congress Summary 2013). These restrictions would decrease the likelihood of humans obtaining antibiotic resistant bacteria from food.

Unfortunately, the bill proposed by Slaughter has very little support thus far, yet antibiotic resistance continues to be a growing problem throughout the world. One of the steps to combatting this issue, is if Congress enacts restrictions on antibiotic use in agriculture. There is potential that as public concern heightens and puts more pressure on politicians, legislation could be passed. Until then, we wait and eat carefully.

(1) Conradis, B. (2013, October 25). News & Analysis. Farm and Pharmaceutical Lobbies Push Back Against Antibiotics Legislation. Retrieved April 16, 2014, from http://www.opensecrets.org/news/2013/10/farm-and-pharmaceutical-lobbies-pus.html

(2) Henneberger, M. (2013, October 22). Report: Feeding antibiotics to livestock is bad for humans, but Congress won’t stop it. Washington Post. Retrieved April 16, 2014, from http://www.washingtonpost.com/politics/feeding-antibiotics-to-cows-is-bad-for-humans-but-congress-wont-stop-it-new-report-says/2013/10/22/ecd2de08-3afd-11e3-a94f-b58017bfee6c_story_1.html

(3) Russo, C. (2013, November 19). How Industrial Agriculture Has Thwarted Factory Farm Reforms. Yale Environment 360. Retrieved April 16, 2014, from http://e360.yale.edu/feature/interview_robert_martin_how_big_agriculture_has_thwarted_factory_farm_reforms/2712/

(4) Library of Congress. (2013, March 13). GovTrack. Retrieved April 16, 2014, from https://www.govtrack.us/congress/bills/113/hr1150#summary/libraryofcongress


Could Using Your Water Bottle Be Making Your Children Fat?

Epigenetics seems to be a rising field of interest in the ecological and evolutionary biology world. I found this topic to be very interesting and as I looked more into it I found an article titled Obesity, Epigenetics, and Gene Regulation. This article focuses on epigenetic changes in the environment that affect the gene expression of obesity in agouti mice as well as its implications for humans. It is outlandish to think that it is possible that one of two genetically identical mice is small while the other is large and fat. However, through the complexities of epigenetics this is too possible.

In 2002 a scientist by the name of Randy Jirtle along with his postdoctoral student, Robert Waterland, conducted an experiment with agouti mice that clearly displayed the work of epigenetics right before their eyes. They began with several pairs of mice. These mice are named after a gene they carry, the agouti gene which makes them large and yellow as well as prone to cancer and diabetes [2]. When agouti mice breed they typically produce offspring that are identical to the parents (fat and yellow), however in this experiment a large number of the offspring turned out to be small and brown in color. Furthermore, the slender brown mice did not seem to have the same susceptibility to cancer and diabetes and lived through old age [2].

The researchers affected this gene without altering their DNA at all, they simply changed the diet of the mother. Before conception, Jirtle and Waterland fed the mother a diet rich in methyl donors, small chemicals that attach to genes and turn them off. These molecules are found in foods such as onions, beets, garlic, and food supplements given to pregnant women. The methyl donors then made their way to the chromosome of the embryo and then to the agouti gene. The mother passed the gene onto the offspring intact but because of her diet that was rich in methyl donors it was enough to turn off the gene.

There is evidence that environmental triggers can affect the behavior of an organism’s epigenome, turning a gene off or on. One suspected trigger is a chemical called bisphenol A found in water bottles and other plastic products. In this study, Jirtle and Waterland exposed the pregnant mice to this chemical and found that more offspring than expected turned out to be fat and yellow. This is due to to the fact that the bisphenol A caused DNA methylation at the agouti gene site to decrease by 31%. This supported the hypothesis that bisphenol A alters the genome by removing methyl groups from DNA.

This discovery is perplexing considering the fact that more and more Americans are becoming obese and this coincides with the widespread use of bisphenol A in everything from water bottles to dental sealants. A connection between the two has been observed and noted, however it cannot be determined for sure at this time [1]. Jirtle was one of the first to state that there is no definite relationship. Hopefully as we make more medical advances in the future this relationship can be determined definitely. Until then, make sure you consume foods rich in methyl donors and beware of plastic water bottles, they may make your future children obese!

Works Cited

1. Adams, J. (2008) Obesity, epigenetics, and gene regulation. Nature Education 1(1):128

2. Watters, Ethan. “May 2014.” Discover Magazine. Discover Magazine, 22 Nov. 2006.      Web. 17 Apr. 2014. <http://discovermagazine.com/2006/nov/cover&gt;.

Is cancer in our genes?

Many people have heard of the test for the breast cancer “gene,” but what does the test actually mean? Does it truly mean that you are at a higher risk to get breast cancer? Could it mean something else? Should people rely on more than that single test to judge their probability of getting breast cancer? All of these questions were addressed by Dr. Couch in the article “Breast Cancer: Predicting Individual Risk” published through the Mayo Clinic’s website. Being a woman combined with the amount of breast cancer awareness information released, this article peaked my interest. I am curious if and how genetics play a role in a person’s likelihood to get cancer later in life.

When doctors test for the breast cancer gene, they are looking for the genetic mutations BRCA1 and BRCA2. According to the article however, because these genes only account for a small portion of the total cases of breast cancer, the test results do not give a guarantee. A person who tests positive isn’t guaranteed to get breast cancer and on the other hand, a person who tests negative could still get breast cancer; genetics are more than meets the eye. Dr. Couch’s approach is to give his patients more than a general probability of getting breast cancer; he wants to personalize care to take each individual’s environment and genetic makeup into account. The proof behind Dr. Couch’s words stem from a study done on BRCA1 and BRCA2 mutation carriers. This study showed that the presence of DNA modifiers can take the 65% risk, the average risk of a patient with the BRCA1 or BRCA2 mutation, down as low as 30% or as high as 90%. This gives patients a better understanding of their personal risks of getting breast cancer. A woman with a risk around 90% may choose to undergo a radical mastectomy whereas a woman with a risk of 30% may chose to opt out of this procedure and keep a closer watch on the potential signs of breast cancer. Without this additional genetic information, patients are taking a larger risk in their decision to forego prophylactic surgery. This is because of the large uncertainty that lies in the basic 65% risk, as found by the BRCA1 and BRCA2 mutations alone, compared to a more specific 30% or 90% which stems from better genetic testing.

On a similar note, there is a way to genetically decide whether or not specific breast cancer prevention treatments are right for a patient, as stated in the article “Gene Variants Predict Response to Breast Cancer Drugs” on the National Institutes of Health, NIH, website. There are drug options for the preventative treatment of breast cancer, one of which is tamoxifen and another is raloxifene. These are drugs that are designed to block the effects of estrogen which, in turn, slows the growth of breast cancer tumors because estrogen promotes the growth of those tumors. However, these drugs also have very dangerous potential side effects which include blood clots, strokes, and endometrial cancer. Dr. James N. Ingle led a study based on the genetic markings of women who were considered at high-risk for getting breast cancer. They compared the genetics of women who remained cancer-free and those who eventually got breast cancer. The study revealed a difference in 2 SNPs (Single-nucleotide polymorphism) in women who got breast cancer while on the treatment compared to women who did not get cancer while also on the treatment. The two genes were called ZNF423 and CTSO. Those two genes in specific have a beneficial version and detrimental version. It turned out that women who had the beneficial version of both of the genes were approximately six times less likely to get breast cancer than women with both detrimental versions of the genes.

These discoveries are new to the study of breast cancer and can innovate the way that preventative breast cancer treatments are handled. It was actually proven that these genes, previously unrelated to breast cancer, are in fact related to the BRCA1 mutation. This information allows doctors to make the educated decision on whether or not to give women considered to have a high risk of getting breast cancer the preventative treatment. They are now able to do more genetic testing in order to know whether the treatment is worth the risk on a patient-by-patient basis.

All in all, it can be seen that a lot can be determined by our genes, especially pertaining to future diseases, namely cancer. Yes the breast cancer gene test, the test for the BRCA1 and BRCA2 mutations can help understand a person’s odds of getting breast cancer, but studying the DNA modifiers of each individual can help get more specific odds on the patient’s likelihood of getting breast cancer. On a similar note, patients can be tested for the beneficial or detrimental version of the ZNF423 and CTSO genes. This can also help doctors decide whether or not to give patients preventative treatments which have the potential for very negative side effects. The mere analysis of the BRCA1 and BRCA2 mutations, which used to be proper protocol for the screening of breast cancer, is no longer the best way to understand a patient’s likelihood of getting breast cancer. It is also not the best way to determine the best course of preventative treatment for patients. There are now more precise genetic tests that allow doctors to give the best possible prognosis. We have come a very long way in the study of genetics, but we still have so much more to learn.

Breast Cancer: Predicting Individual Risk:

Gene Variants Predict Response to Breast Cancer Drugs: http://www.nih.gov/researchmatters/july2013/07012013cancer.htm

Genetic Imprinting: Pregnancy and Beyond

The topic of genetic imprinting has been capturing the attention of evolutionary biologists in recent years. It was first introduced to the class by Stephen Stearns in his article “Evolutionary medicine: its scope, interest and potential.” Stearns describes the parent-of-origin imprinting effect as “the silencing in the parental germ line of genes expressed in the foetus and offspring; different genes are imprinted in mother and father. The father silences genes that would express the mother’s interests; the mother silences genes that would express the father’s interests; the normal result is an equilibrium at which both foetus and mother are healthy (3).” The rest of the article explores this genetic tug of war between maternal and paternal genes, but also introduces the third player in the game: the fetus. The fetus often sides with the father’s genetic interests; the father wants the best and strongest offspring possible, and the fetus also wants all of the mother’s attention and resources for itself. This can take a heavily biological and medical toll on the mother. Many say that pregnancy is one of the simplest and most natural things in the world- but just because it has been taking place since the dawn of humanity does not mean it is easy, safe, or sustaining for the mother. Instead of looking at pregnancy as a cornucopia, should we be viewing it as a risky tug of war- or even a host-parasite relationship?

Harvard University’s Dr. Haig has extensively researched this delicate resource balance between mother and child in relation to genetics. In his paper “Genetic Conflicts in Human Pregnancy,” Haig explores this genetic connection to pregnancy health risks and conditions, specifically regarding preeclampsia. Preeclampsia “occurs near the end of the second trimester and is characterized by a sharp rise in maternal blood pressure, heightened protein levels in the urine, swelling of the feet (edema), and, in advanced cases, obstruction of the blood supply to the mother’s vital organs” (2); this condition is extremely risky, and often involves premature delivery for the protection of the fetus. Haig theorizes that preeclampsia results from a fetal attempt to collect more and more resources in conditions of nutritional stress- which can arise when problems occur in the placenta, or if the mother is expecting twins or multiples. The placenta- which is controlled by paternal genes- then makes excess amounts of sFlt1, a protein that damages the mother’s endothelium, which causes the blood vessels to constrict Due to ease, more blood begins to flow to the placenta and away from the maternal tissues. In these cases, the mother’s tissues are drained, which can lead to kidney and liver failure, hemorrhaging, cardiac arrest and other damaging ailments (1). The paternal gene controlling the nutritional stress response causes the fetus to feed off of the mother, sucking the life and sustenance out of her-literally.

Gene imprinting can have impacts outside pregnancy. Dr. Lawrence Wilkinson of Cambridge University has done research on mice to connect Haig’s theories on gene imprinting to social behaviors. One behavior gene, Nesp55, is active in its maternal copy- the paternal copy is silent. Dr. Wilkinson and his colleagues found that “disabling the mother’s Nesp55 gene makes mice less likely to explore a new environment. Normally, the mother’s copy of Nesp55 may encourage the mice to take more risks on behalf of the group, whether that risk involves looking for food or defending the group (4). Wilkinson says that the gene imprinting effect on social behavior “Is a possibility, but it needs to be proved” (4).

Wilkinson and Haig’s research has only produced logical hypotheses. Further research is necessary to fine-tune and navigate the true connections and effects. But if scientists could identify the genes responsible for various pregnancy risks and psychological disorders, and control them as Dr. Wilkinson did, then solutions and treatment for patients could be attainable.


Works Cited
“Genetic Conflicts in Human Pregnancy.” The Quarterly Review of Biology 68.4 (1993): 495-532. Harvard Magazine. Harvard University. Web. 18 Apr. 2014.
Pettus, Ashley. “Prenatal Competition?” Harvard Magazine. Harvard University, Sept.-Oct. 2006. Web. 18 Apr. 2014.
Stearns, S. C. “Evolutionary Medicine: Its Scope, Interest and Potential.” Proceedings of the Royal Society B: Biological Sciences 279.1746 (2012): 4305-321. 7 Oct. 2012. Web. 18 Apr. 2014.
Zimmer, Carl. “Silent Struggle: A New Theory of Pregnancy.” The New York Times. The New York Times Company, 14 Mar. 2006. Web. 18 Apr. 2014.

Can We Get Rid Of Obesity?

Obesity has recently become an increasing issue around the world, becoming one of the leading preventable causes of death. Not only can it hinder and/or limit everyday activities, but it also increases the chances of developing various diseases such as diabetes, heart disease, and osteoarthritis. With so many sugary and fatty foods ready for consumption whenever we feel like it, it’s no wonder that obesity has become this big of an issue. The question is, can we ever stop it?

Perhaps learning more about why the human body grows fat after eating such foods can help to answer this question. Our bodies respond the way they do after we consume sugar because of the way the human body has evolved, or actually hasn’t evolved. Sugar has always been a part of the human diet since we were hunter-gatherers. Except back then humans got all of their sugar from fruits; the sweetest thing they had was honey, which by modern standards may not even be very sweet for many. Only recently have we been introduced to processed sugars and simple carbohydrates. Because sugar is so high in energy, we have evolved to crave it but our bodies did not evolve to digest large amounts of it quickly. And the result is mismatched diseases, or diseases that occur due to us not living the way in which our bodies are adapted (1). Obesity is one of these. Our bodies grow fat because foods that we eat everyday are filled with substances that our bodies cannot yet accommodate.

We can look at this issue through another point of interest: the gut microbiome. The gut microbiota, if in high diversity, are known to provide various benefits to our bodies such as protection against inflammation, boosting our immune system, and regulating digestion. Recently, a study seemed to find a correlation between gut microbiome diversity and metabolic health (and therefore body weight as well). The study put 49 overweight and obese participants on a low-calorie diet, and it was found that those who had low microbiota diversity at the start had significantly increased diversity as well as better metabolism by the end of the study (2). This shows a positive correlation between gut microbiota diversity and metabolic health, meaning that as diversity increases, metabolism improves, and this leads to better weight management. Low microbiota diversity can impact obesity in another way. There is a bacterium called Helicobacter pylori that is responsible for regulating gastric ghrelin, which controls hunger by increasing when you need to eat and decreasing when you are full. Essentially, if your gut contains low levels, or no levels, of H. pylori, your body’s ghrelin will not be regulated properly, therefore making you constantly hungry (3).

It might seem kind of weird that obesity is such a big problem; it’s common knowledge that excess body fat is bad for the health, plus the cure is so simple and right in front of us: just stop eating so many fatty and sugary foods and maybe even add in a little exercise to speed up the process. However, people already know this yet they still voluntarily make unhealthy choices. Waiting for the human body to evolve to the point where it can digest such foods without creating excess fat isn’t an option, as this will likely never happen. Consuming too much sugar not only causes fat but also causes high blood sugar, which can lead to diseases such as diabetes and heart disease. But these generally don’t occur until later in life, meaning it will not impact natural selection. Therefore, it seems that the only solution to obesity is in the people themselves, they themselves have to choose to stop eating so many sugary foods.

If you’re thinking that you can’t do it or if you don’t believe any of this, just look at Eve Schaub and her family (4). They went without sugar for a whole year, and although she admitted at first it was tough, her family eventually got used to the no-sugar life and ultimately even came to enjoy it (their overall health also greatly improved). Another example can be seen in the video below, where the mayor of one of America’s once most obese cities talks about how he made his town healthier.

In this video, Mayor Mick Cornett of Oklahoma City explains how he was able to help the people of the town drop a total of over 1 million pounds. Video from YouTube: http:// http://www.youtube.com/watch?v=raCIUeGUr3s

I believe that if more people became aware of the topics discussed in this post, then perhaps we can eventually see a change. If anything, do it for your gut microbiota. Why wouldn’t you want all of the health benefits they can give you (not to mention clear skin as well). Ultimately, the cure to obesity lies in the people’s hands; we are the only ones that can fix this problem. If the day ever comes that enough people realize this, that will be the day that the prevalence of obesity begins to decline.


Footnotes (Works Cited)

1. “How Our Stone Age Bodies Struggle To Stay Healthy In Modern Times.” NPR. NPR, 30 Sept. 2013. Web. 16 Apr. 2014. <http://www.npr.org/templates/transcript/transcript.php?storyId=227777434 >.

2. Greenwood, Veronique. “You Are Your Bacteria: How the Gut Microbiome Influences Health .” TIME. N.p., 29 Aug. 2013. Web. 17 Apr. 2014. <http://science.time.com/2013/08/29/you-are-your-bacteria-how-the-gut-microbiome-influences-health/ >.

3. Melanie. “Is Your Gut Making You Fat? How Gut Health Can Affect Weight.” Pickle Me Too. N.p., 21 May 2012. Web. 16 Apr. 2014. <http://www.picklemetoo.com/2012/05/21/is-your-gut-making-you-fat/ >.

4. Barclay, Eliza. “The Latest Wacky Food Adventure: A Year Without Sugar.” NPR. NPR, 11 Apr. 2014. Web. 16 Apr. 2014. <http://www.npr.org/blogs/thesalt/2014/04/11/300994012/the-latest-wacky-food-misadventure-a-year-without-sugar >.

Spillover and the Environment

Imagine for a second that you are a virus. You have food (your host), an ecosystem to live in, and are quite content. However, something happens and in one moment, you move. You enter someone, something new. That one moment that changed everything, is the spillover. A spillover is the moment when a virus is transferred from one species to another.

Infectious diseases are all around human beings. Infectious diseases are able to be transferred from one being to another, and in this way they are able to live within their own ecosystem of organisms. In the book, Spillover by David Quammen, infectious diseases, pathogens, are compared to predators. A predator is a beast that is able to eat its prey from the outside, whereas a pathogen is able to eat their prey from within.

Infectious diseases do not only transfer within one species; they can jump from species to species. The process is called zoonosis. Zoonosis and spillover are not the same thing. Zoonosis is a pathogen that is already known as being able to cross between different species, such as birds and humans; spillover is the moment of contact, the moment that a disease is first transferred. Zoonotic pathogens are able to exist in different species (Quammen, 2012).

Zoonotic diseases represent the unintentional things that human beings are doing to the planet. They represent the ecological and medical forces that humans are unleashing upon the world. Human caused ecological pressure and disruption are bringing wild animal pathogens closer into contact with human populations. Human technology and behavior are also spreading these pathogens widely and quickly, an example of this is an airplane. People can now travel all over the world on an airplane in a short amount of time and interact with other people and with natural and wild ecosystems, possibly spreading the disease while they do so (Quammen, 2012).

Human activity on the planet is causing harm to ecosystems, we are ripping different ecosystems apart with our actions. With modern technology this action of destroying ecosystems is even easier, and we are having an impact on the loss of diversity, a very important part in zoonosis. The more diversity that an ecosystem has and the more of a species that there is, the more un-likely it is for a pathogen to not come in contact and survive within a human. From all of the ecosystems that are being destroyed there are millions of unknown creatures that are being displaced, including viruses. Viruses can only duplicate themselves inside the living cells of another organism. So if the organism that they are adapted to is wiped out because of the destruction of a habitat then that viruses is going to do its best to survive, and that might mean adaptation to a new host. This might mean adaptation into a zoonotic disease and spilling over into another species. The disruption of natural ecosystems is unleashing pathogens into a wider and broader world. The pathogen much find a new host or go extinct. They need something to survive, and in some cases that something can be the human race, or a species closely linked with the human race, such as domesticated animals. This can yield to a pandemic (Quammen, 2012).

Spillovers and zoonotic diseases harm all species of the world. Spillovers do not only jump from a wild habitat into humans and the species that are linked with humans, but also from domesticated animals into the wild. Domestic animals and crops can serve as a reservoir of a pathogen, and that pathogen can then infect wild animals and plants. Pathogens from domestic organisms can have a significant impact on wild hosts, including wild hosts that are endangered or facing the threat of endangerment. For example domestic dogs have “spilt” a type of rabies into the endangered African wild dog and an endangered Ethiopian wolf and thus decimated their populations. A pathogen found in domestic dogs also lead to an epidemic of canine distemper in 1994 that devastated lion populations in the Serengeti. Human activity again plays a role in this, human activity dramatically modifies the environment, genetics, population and community structure of domestic organisms. Domesticated plants and animals are sometimes used by humans for agricultural purposes and are often kept in high density locations, which makes it easier to spread disease, and that can in turn be spread to undomesticated species (Power and Mitchell, 2004).

There was a study done by comparing the amounts of Avena fatua (wild oats) within a community. This study compared A. fauta with three other non-reservoir domesticated species. From this study it was discovered that through spillover that a particular pathogen found in A. fauta was five time more likely to be prominent within a community that had A. fatua, then in a community without. In addition when A. fauta was planted along with three other species the presence of A. fauta doubled the virus prevalence in the three other species, thus showing spillover. The presence of A. fauta dramatically altered disease dynamics in the other species and thus altered their communities (Power and Mitchell, 2004).

Contact between natural habitats and humans is happening at a fast pace. Technology is making this contact happen even faster. Forests are being taken down to make way for homes, developments and much more. Human beings are changing the face of the planet and thus bringing pathogens from wild animals and pathogens from domesticated animals closer together. This can change the structure of a community, not only physically but also what lives unseen within that community, such as diseases. Spillover happens, and with human intervention it is happening at more rapid pace then what it once did. Human beings, and domesticated animals are having more contact with wild habitats and thus exchanging zoonotic diseases.

Works Cited:
Power, Alison G., and Charles E. Mitchell. “Pathogen Spillover in Disease Epidemics.” The American Naturalist 164 (2004). Web. .
Quammen, David. Spillover. New York: W. W. Norton & Company, 2012. 20-42. Print.