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Edit to Anxiety Article (DELETED BY WIKI MODERATORS)
https://en.wikipedia.org/wiki/Anxiety

Evolutionary biology[edit] An evolutionary biology explanation for perpetuation of anxiety over time incorporates natural selection and suggests that organisms that are better equipped to deal with potential threats will have an increased likelihood for survival and inherit a fitness advantage. An evolutionary negative feedback loop displayed by trade-offs effectively placed constraints on expression of anxiety genes, preventing runaway selection for heightened anxiety. The line drawn between function and dysfunction for an anxious response to stimuli establishes a certain threshold for effectiveness, creating intermediary traits that have persisted throughout the course of evolution. Ancestral anxiety presents itself in modern day the same as it did thousands of years ago, differentiating between background noise and legitimate threat. The aforementioned threshold delineates an individuals' perception of stimuli and establishes the effective response. An individual can respond to the stimuli by either missing it, or initiating an alarm response. The evolutionary design for heightened anxiety response has, over time, up-regulated the gene responsible for initiating an alarm response to background noise. This is a result of humans effectively removing themselves from the food chain and eliminating predatory threats. The ancestral levels of anxiety have ultimately remained throughout evolution, indicating a transition of threat perception from life threatening to benign occurrences.

Individuals may be predisposed to certain anxiety disorders based on the evolutionary theory of antagonistic pleitropy. Genes that may have fitness advantages in relation to maintenance of anxiety may, in fact, have maladaptive fitness disadvantages in another scope of anxiety maintenance. In a study conducted by researchers Belsky & Pluess, it was noted that the presence of a shorter allele in the serotonin transporter-coding gene indicated both an increased predisposition for anxiety disorders in early childhood while also reducing the risk for anxiety disorders as the individual aged. The same serotonin transporter-coding gene is conveniently present in some primates and elicits similar function, suggesting evolutionary linkage.

FINAL DRAFT STARTS HERE: Evolutionary Aspects of Anxiety Disorders
Evolutionary Aspects of Anxiety Disorders

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Evolutionary Aspects of Anxiety Disorders:

For members of the millennial generation, conditions listed under the umbrella of anxiety disorders are not necessarily viewed as uncommon. Over the last century or two, increasing evidence has come to convince subsequent generations more and more of the existence of anxiety disorders. These disorders can range anywhere from common stage fright to the most extreme cases of obsessive-compulsive disorder. But where from and why exactly do these conditions arise? The answer, as this paper will describe, is actually rooted deep in the evolutionary history of mankind and gives natural explanations for things that are today considered problems. Coalescing theories of psychology and those of evolutionary biology have analyzed reasonable explanations for anxiety disorders in the context of natural selection, sexual selection, and evolutionary genetics.

Anxiety disorders are currently the leading form of mental illness worldwide, and for good reason. When analyzed in the scope of natural selection, the frequency of these disorders is certainly not unreasonable. As humans living in the present day, we are increasingly distancing ourselves from the natural chain of order. Particularly in what is considered to be the 1st world, humans do not have to deal with threats of predation or starvation. But think back to a time when the world was ruled by massive predators, when there was no infrastructure, and concepts of science and arithmetic did not exist. Early humans where fighting for survival. To say that stress and worry were quite literally the basis of our development would be an understatement. At its core, the function of anxiety in humans and others species is to “prepare the individual to detect and deal with threats” (Bateson, 2011). As such, it should come as no surprise that individuals equipped with copious mechanisms to deal with threats were not only more anxious as a result, but also better equipped for survival. In terms of natural selection, those that were more prepared for threats had a better chance of survival and therefore more opportunity to pass on those same genes, adding more anxiety to the gene pool.

The increase of anxiety in the gene pool however was not a never-ending process. The negative feedback loop displayed by trade-offs not only effectively placed physical constraints on early humans but also mental ones. The line drawn between function and dysfunction for a particular trait establishes a certain threshold for effectiveness, and an anxious response to stimuli is no exception (Bateson, 2011). While this ultimately limits the numbers those individuals that have an overzealous anxiety response and those with lack there of, it still leaves the large majority with intermediary anxiety traits. As humans evolved the necessity for this intermediate level of anxiety began to dissipate, however the traits remained in the gene pool and perpetuated throughout human development. This in-turn leaves the present human population with the ancestral traits that equates being preyed upon by a saber-tooth tiger to performing in front of a large audience. While comparing certain death to speaking in front of people may seem extreme, its biological link is quite prevalent. This ancestral anxiety presents itself in modern day the same as it did thousands of years ago, differentiating between background noise and legitimate threat. The overlap in the graphs above between the two distributions represents the amount of times the brain will miss the stimuli or simulate a false alarm. In those suffering from anxiety disorders, the right graph becomes the more recurrent reaction as the brain signals false alarms more frequently due to a low threshold for threat, resulting in a heightened level of anxiety. It is hypothesized that these lower threshold levels are becoming increasingly more prevalent in human populations due to the fact that they are not ever ousted from the gene pool as a result of natural selection like they may had been thousands of years ago.

Early humans did not only have to worry about surviving predation however, they also had to worry about surviving each other. In Scott Sherrington’s Rede Lecture 1993 the concept of the environment of evolutionary adaptation or EEA, refers to the habitat of our immediate ancestors (Price, 2003). During the human EEA, groups of approximately 50 hunter-gatherers would often travel and remain together as nomadic tribes. As in most social groups of any species, a hierarchy of power eventually evolves and so to do varying levels of reproductive success. The psychology of anxiety created by group living ultimately boils down to an individual’s response to a negative stimulus within the group that is viewed by the individual as worse than that of predation. The reasoning behind this heightened anxious response stems from the idea that one does not submit to a predator but can to a peer (Price, 2003). While this phenomenon inhabits the world of psychology, it can have real implications on the history of human evolution through sexual selection. Though an array of factors comes into play in regards to sexual selection, the primary contributors in early human populations place direct benefits and good genes at the forefront of selecting a mate (Nesse, 1999). In such small populations, the odds are not particularly in a given individual’s favor to begin with, especially when faced with competition within the group. For example, dominant individuals in the group would likely maintain higher reproductive success based on expressed characteristics that placed them atop the social hierarchy. These characteristics usually correlate to good genes and can provide the aforementioned direct benefits, leading to greater success. Conflicts for dominance in these groups would create compounding stressors and lead to an occurrence called prestige competition in which an individual would arise as dominant based on being more attractive to the rest of the group due to possession of certain beneficial traits. Unlike territorial species, humans that were not deemed attractive could not leave the social group and would have to remain with the pack for survival. These individuals would consequently become inherently submissive and have to play a subordinate social role (Price, 2003). The fear of the dominant individual(s) would ultimately give rise to same anxiety instigated by predation, however it would be prolonged for extended periods of time as a result of group living. When analyzed in the scope of competing between 50 people, stressors and anxiety do pose a very strong and direct affect on the constituents of the group (Nesse, 1999). Imagine however, the weaker, but still prevalent competition between the 6 billion people currently living on earth. With such vast networks of transportation and the advent of the Internet, the populous of the world has never been more interconnected. For those individuals possessing lower thresholds of threat, the monstrous anxieties of competition and reproductive success have never been higher in the course of human history. This often times leads to anxiety disorders in which individuals are overwhelmed with the same anxieties that affected early humans, but are now immeasurably amplified.

To gain a proper understanding of how these environmental factors affect the brain, one must observe the resulting reaction in the genotype space that can be observed in present day. In a large sample Virginia twin study performed by Kendler and his contemporaries, it was found that individuals may be predisposed to certain anxiety disorders based on the evolutionary theory of antagonistic pleitropy (Duncan & Kendler, 2010). Genes that may have fitness advantages in relation to maintenance of anxiety may in fact have maladaptive fitness disadvantages in another field of anxiety maintenance. In a study conducted by researchers Belsky & Pluess, it was noted that the presence of a shorter allele in the serotonin transporter-coding gene indicated both an increased predisposition for anxiety disorders in early childhood while also reducing the risk for anxiety disorders as the individual aged (Price, 2013). Interestingly enough, these findings actually diminish the possibility that natural selection was the sole proprietor of compounding anxiety throughout time. It does however support that general idea that genes that code for an increase or decrease in response to a threat have remained present throughout history and can still affect individuals in the present.

Among primates, the serotonin gene that is primarily linked to anxiety and depression disorders is only present in humans and macaques. For this reason, the macaques are a focal point of study for understanding the genetics of these heightened conditions of anxiety. Between both primates, those possessing the short allele for serotonin transcription are notably more anxious than those that posses the long (Watson et. al., 2009). Further, when studying only the monkeys, it was noted that individuals with the short allele would need to be bribed to observe pictures of dominant individuals while those with the longer allele would decline the bribery and view the image voluntarily (Price, 2013). This really puts ancestral factors into perspective especially when a trans-species study supports previous theories of dominance as well as natural selection in regards to evolutionary genetics.

The effects that various biological dynamics have on the evolution of anxiety in humans and other species proves that individuals suffering from anxiety disorders, for the most part, can blame a lot of their suffering on evolution. While the psychological aspect of anxiety plays an integral role in the presence of some of these disorders, it really all comes down to a deeper understanding of evolutionary biology to determine some of the ways we inherently think and act. In the case of anxiety, natural selection, sexual selection, and evolutionary genetics provide humans living in the present with important details about our past that can explain one of the major problems haunting our populations today.

REFERENCES Bateson, M. (2011). Anxiety: An Evolutionary Approach. The Canadian Journal of Psychiatry, 56(12), 707-715. Retrieved October 8, 2014.

J. Belsky, C. Jonassaint, M. Pluess, et al.2009 Vulnerability genes or plasticity genes? Molecular Psychiatry 14746754

K. K. Watson, J. H. Ghodasra, M. L. Platt, 2009 Serotonin transporter genotype modulates social reward and punishment in rhesus macaques PLoS ONE 4(1): e4156. doi:10.1371/journal.pone.0004156 L. E. Duncan, M. C. Keller, 2011 A Critical Review of the First 10 Years of Candidate Gene-by- Environment Interaction. Research in PsychiatryAmerican Journal of Psychiatry16810411049doi:10.1176/appi.ajp.2011.11020191.PMC 3222234. PMID 21890791.

M. A. Hofer, 2002Evolutionary concepts of anxiety, In: Textbook of Anxiety Disorders, D.J.Stein & E.Hollander, (Eds.), 5769American Psychiatric Publishing Inc., Washington, DC.

Nesse, R. (1999). Proximate and evolutionary studies of anxiety, stress and depression: Synergy at the interface. Neuroscience and Behavioral Reviews, 23(12), 895-903. Retrieved October 1, 2014.

Price, J. (2003). Evolutionary aspects of anxiety disorders. Dialogues in Clinical Neuroscience, 5(3), 223-236.

Price, J. (2013). New Insight Into Anxiety Disorders. In An Evolutionary Perspective on Anxiety and Anxiety Disorders (1st ed., Vol. 1 Ch. 1).

Changed Topic to Evolutionary Aspects of Anxiety Disorders
REFERENCES

Bateson, M. (2011). Anxiety: An Evolutionary Approach. The Canadian Journal of Psychiatry, 56(12), 707-715. Retrieved October 8, 2014.

J. Belsky, C. Jonassaint, M. Pluess, et al.2009 Vulnerability genes or plasticity genes? Molecular Psychiatry 14746754

K. K. Watson, J. H. Ghodasra, M. L. Platt, 2009 Serotonin transporter genotype modulates social reward and punishment in rhesus macaques PLoS ONE 4(1): e4156. doi:10.1371/journal.pone.0004156 L. E. Duncan, M. C. Keller, 2011 A Critical Review of the First 10 Years of Candidate Gene-by- Environment Interaction. Research in PsychiatryAmerican Journal of Psychiatry16810411049doi:10.1176/appi.ajp.2011.11020191.PMC 3222234. PMID 21890791.

M. A. Hofer, 2002Evolutionary concepts of anxiety, In: Textbook of Anxiety Disorders, D.J.Stein & E.Hollander, (Eds.), 5769American Psychiatric Publishing Inc., Washington, DC.

Nesse, R. (1999). Proximate and evolutionary studies of anxiety, stress and depression: Synergy at the interface. Neuroscience and Behavioral Reviews, 23(12), 895-903. Retrieved October 1, 2014.

Price, J. (2003). Evolutionary aspects of anxiety disorders. Dialogues in Clinical Neuroscience, 5(3), 223-236.

Price, J. (2013). New Insight Into Anxiety Disorders. In An Evolutionary Perspective on Anxiety and Anxiety Disorders (1st ed., Vol. 1 Ch. 1).

Request for Edit to Article AD Wiki
https://en.wikipedia.org/wiki/Alzheimer%27s_disease

The Alzheimer's article is semi protected against edits. I had to submit a request to edit the article, however I copied the edit below.

Insert: "As it stands, Alzheimer's is the only leading cause of death in America among the top ten that is neither curable or preventable."

Citation:

Tejada-Vera B. Mortality from Alzheimer’s disease in the United States: data for 2000 and 2010. NCHS data brief, no 116. Hyattsville, MD: National Center for Health Statistics. 2013

Improvements to Article AD Wiki
1) I believe the article could elaborate on recent research indicating grey matter atrophy in the brain correlating with cognitive levels in mild-cognitive impairment patients and AD patients.

2) The article lacks information regarding sever lack of research funding in comparison to other fatal illnesses.

3) The article fails to mention Alzheimer's being the only cause of death among the top 10 in America without a known way to prevent progression. — Preceding unsigned comment added by Fixler.3 (talk • contribs) 11:07, 1 October 2014 (UTC)

Annotated Bibliography
What is the evolutionary basis for the neurodegenerative condition Alzheimer’s Disease (AD) and its relation to human brain evolution?

Ashford, W. (2004). APOE genotype effects on alzheimer’s disease onset and epidemiology. Journal of Molecular Neuroscience, 23(3), 157-165. (2004, July 1).

This paper deals specifically with the genetics of infected individuals and their possession of the APOEe4 allele, an allele that frequents populations specifically with low genetic diversity. This allele tends to arise more frequently in low diversity populations as the gene pool has shrunk.

Braak, H. and Braak, E. (1996), Evolution of the neuropathology of Alzheimer's disease. Acta Neurologica Scandinavica, 94: 3–12. doi: 10.1111/j.1600-0404.1996.tb05866.x

This article hones in on the direct protein involvement in the brain that may become vulnerable to degeneration with age. Specifically, the A4 amyloid protein found in the cerebral cortex of healthy individuals is lacking in those suffering from Alzheimer’s. and could be correlated to clinical symptoms.

Finch, C. (1999). The evolution of Alzheimer disease, the reproductive schedule, and apoE isoforms. Neurobiology of Aging, 20(4), 407-428. (1999, August 1).

This paper analyzes the hypothesis that human hormone evolution could have severely impacted our susceptibility to Alzheimer’s. Unlike other primates, humans have developed an APOE isophorm associated with rapid brain development that and also Alzheimer’s progression.

Gili, T. et all. (2010). Regional brain atrophy and functional disconnection across Alzheimer's disease evolution. J Neurol Neurosurg Psychiatry, 82(58), 66-66. (2010, July 6).

This article summarizes the results of a study performed that analyzed healthy patients brains and compared them to those afflicted with Alzheimer’s. Results showed a similar regional pattern of brain disconnection between the posterior cingulate cortex and the medial prefrontal cortex and the rest of the brain. This indicates that the disconnection occurs before grey matter atrophy indicating a different kind of virulence.

Triskoff, S., & Verelli, B. (2003). PATTERNS OF HUMAN GENETIC DIVERSITY: Implications for Human Evolutionary History and Disease. Annual Review of Genomics and Human Genetics, 4, 293-340. (2003, June 4).

This article discusses the genetic basis of Alzheimers and discusses the potential genetic mutations that could result in Alzheimers susceptibility. Specifically the APOEe4 allele is associated with the disease and is more common in populations with lower genetic diversity such as those in developed countries where diversity is in decline.