Globalization has eradicated great power war, dedev reverses

Other Impacts

Jan C., Senior Expert working in the Unit of Scientific Advice of the European Centre for Disease Prevention and Control, European Journal of Public Health, Vol. 22, Issue 1, pp. 5-6, “Economic crisis and infectious disease control: a public health predicament”, http://eurpub.oxfordjournals.org/content/22/1/5.full

Great Recession proves

Meredith, Reporter, Nature.com, December, “Financial crisis hits developing world disease research”, http://www.nature.com/news/financial-crisis-hits-developing-world-disease-research-1.9550

Venetia, Lecturer @ the Faculty of Health and Caring Professionals @ the Technical Education Institute in Athens, Greece, Health Science Journal, Vol. 7, Issue 2, “Economic crisis and health. The role of health care Professionals”, http://www.hsj.gr/volume7/issue2/722.pdf

Economic crisis and vulnerable groups ¶ Poor social groups are those who are mainly ¶ affected by the repercussions of the crisis, since ¶ socioeconomic factors play a major role in the ¶ psychological health level of the population. ¶ Income inequalities, occupational status and ¶ productivity capacity are important indicators for ¶ the sense of well‐being and the overall health of ¶ the individuals.26,27 It is worth mentioning that ¶ high‐income countries, compared to those with ¶ low‐income, have low fertility and mortality rates ¶ and increased life expectancies while the disease ¶ map to some extent is totally different from the ¶ low‐income countries which are faced with high ¶ mortality rates from infectious diseases and ¶ maternal and childhood mal‐conditions.28 ¶ The major cause of inequality and relative ¶ poverty is unemployment. Income equality seems ¶ to improve social cohesion and reduce the social ¶ divisions. A rise in unemployment which leads to ¶ lower income can harm nutritional intake and ¶ quality of life.29 ¶ Social and public health policies that can cover ¶ the most important health determinants by reducing unemployment, minimizing income and¶ wealth inequality, showed evidence of improved ¶ population health as presented in comparative ¶ studies of policies on health inequalities form 8 ¶ different European countries.30

International cooperation is key to contain disease

Board on Global Health 2004. P208 http://www.nap.edu/catalog.php?record_id=10915

As the world becomes more conscious of microbial threats to health, countries are increasingly recognizing the necessity of reporting outbreaks promptly and cooperating fully in international efforts to contain them. Indeed, if there is one piece of good news to be noted from last year’s epidemic, it is the fact that—as David Heymann and Guenael Rodier observe in this chapter—an array of diagnostic and surveillance tools, coordinated strategies of containment, and international collaboration among scientists and public health authorities were in this case able to control the outbreak of SARS, even in the absence of curative drugs or vaccines. Nevertheless, last year’s experiences further reinforce the lessons that HIV/AIDS, influenza, Ebola, malaria, and a host of other persistent and emerging infectious diseases have already made clear—that the health of any one nation cannot be isolated from the health of its neighbors, and that public health challenges in any locality have the potential to reverberate swiftly around the globe. Karen Monaghan’s paper for the National Intelligence Council, which concludes this chapter, summarizes the continuing threat that SARS may still pose, as well as the challenges that lie ahead for attempting to contain any further deadly outbreaks of SARS or other infectious diseases in the future.

Norberg 3

[Johan Norberg, Fellow at Timbro (Swedish think tank), 2003, In Defense of Global Capitalism, p. 189 ]

Personally, I believe we have more to expect from philanthropic capitalists than from politics. Capitalism does not force people to maximize their profit at every turn; it enables them to use their property as they see fit, free of political considerations. Microsoft’s Bill Gates, the very personification of modern capitalism, himself devotes more to the campaign against disease in the developing countries than the American government does. Between November 1999 and 2000, through the $23 billion Bill and Melinda Gates Health Fund, $1.4 billion went to vaccinate children in developing countries for common diseases and to fund research into HIV/AIDS, malaria, and TB, for example, in developing countries. That is a quarter of what all industrialized nations combined devoted to combating disease in the developing countries. So the fact that Bill Gates is worth more than $50 billion should give the poor and the sick of the world reason to rejoice. Clearly they would stand to gain more from a handful of Gateses than from the whole of Europe and another couple of WHO.

No Impact

Bad methodology is the cause of fears that viruses are getting more severe

Garske ‘9 (Garske T, Legrand J, Donnelly CA, et al. Assessing the severity of the novel influenza A/H1N1 pandemic. BMJ. 2009; 339: b2840. Friday 17 July 2009 00.00 BST
Another issue is the time delay between becoming ill and dying. Early in an epidemic, people may have caught the virus, but their illness won't have had time to run its course. Put bluntly, at a particular point in time there will be people who are going to die, but who are still alive at the time statistics are calculated. Mathematically, this type of bias is called censoring. Censoring tends to have its strongest effect early in a pandemic when a disease is spreading faster and faster. It has the effect of making the illness look milder at first, then more serious later as the first wave of patients either die or recover. This happened in the SARS epidemic, and caused unwarranted fears that the virus was becoming more severe.

Influenza won’t cause mass death- basic countermeasures solve

- Collignon ‘9 (Monday, 25 May 2009 Take a deep breath, Swine Flu’s not that bad by Peter Collignon Peter Collignon is an Infectious Diseases Physician and Microbiologist and Professor, School of Clinical Medicine, Australian National University.
We need to also consider what killed most people when new and virulent Flu pandemics spread across the world previously. It is not the Flu virus itself. Most deaths were likely the result of secondary bacterial infections especially Staphylococcus aureus and pneumococcus. The high death rate in 1919 was because there were no antibiotics developed yet. In the late 1950’s (Asian Flu), it was because there was a lack of available and active antibiotics — penicillin resistance had developed and spread rapidly in Staphylococcus aureus by then. Antibiotic resistance is a major and rapidly growing international problem, especially in developing countries. However in Australia we are fortunate because we still have a variety of antibiotics (especially injectables) that will work against nearly all strains of bacteria that might complicate Flu and cause pneumonia. We also know we can slow or stop the spread of Flu virus, even in households with close personal contact by good hygiene, hand care (alcohol hand rub and soap and water), masks and other general infection control measures.

Humans will adapt

Gladwell 95 (Malcolm, The New Republic, July 17, Excerpted in Epidemics: Opposing Viewpoints, p. 29)

In Plagues and Peoples, which appeared in 1977. William MeNeill pointed out that…while man’s efforts to “remodel” his environment are sometimes a source of new disease. They are seldom a source of serious epidemic disease. Quite the opposite. As humans and new microorganisms interact, they begin to accommodate each other. Human populations slowly build up resistance to circulating infections. What were once virulent infections, such as syphilis become attenuated. Over time, diseases of adults, such as measles and chicken pox, become limited to children, whose immune systems are still naïve.

Diseases are short term – They evolve to be benign and don't cause extinction

AMNH 98 – (The American Museum of Natural History “How did Hyperdisease cause extinctions?” http://www.amnh.org/science/biodiversity/extinction/Day1/disease/Bit2.html)
It is well known that lethal diseases can have a profound effect on species' population size and structure. However, it is generally accepted that the principal populational effects of disease are acute--that is, short-term. In other words, although a species many suffer substantial loss from the effects of a given highly infectious disease at a given time, the facts indicate that natural populations tend to bounce back after the period of high losses. Thus, disease as a primary cause of extinction seems implausible. However, this is the normal case, where the disease-provoking pathogen and its host have had a long relationship. Ordinarily, it is not in the pathogens interest to rapidly kill off large numbers of individuals in its host species, because that might imperil its own survival. Disease theorists long ago expressed the idea that pathogens tend to evolve toward a "benign" state of affairs with their hosts, which means in practice that they continue to infect, but tend not to kill (or at least not rapidly). A very good reason for suspecting this to be an accurate view of pathogen-host relationships is that individuals with few or no genetic defenses against a particular pathogen will be maintained within the host population, thus ensuring the pathogen's ultimate survival.

No disease is powerful enough or could mutate to cause extinction

Gladwell 99 (Malcolm, The New Republic, July 17 and 24, 1995, excerpted in Epidemics: Opposing Viewpoints, p. 31-32)
Every infectious agent that has ever plagued humanity has had to adapt a specific strategy but every strategy carries a corresponding cost and this makes human counterattack possible. Malaria is vicious and deadly but it relies on mosquitoes to spread from one human to the next, which means that draining swamps and putting up mosquito netting can all hut halt endemic malaria. Smallpox is extraordinarily durable remaining infectious in the environment for years, but its very durability its essential rigidity is what makes it one of the easiest microbes to create a vaccine against. AIDS is almost invariably lethal because it attacks the body at its point of great vulnerability, that is, the immune system, but the fact that it targets blood cells is what makes it so relatively uninfectious. Viruses are not superhuman. I could go on, but the point is obvious. Any microbe capable of wiping us all out would have to be everything at once: as contagious as flue, as durable as the cold, as lethal as Ebola, as stealthy as HIV and so doggedly resistant to mutation that it would stay deadly over the course of a long epidemic. But viruses are not, well, superhuman. They cannot do everything at once. It is one of the ironies of the analysis of alarmists such as Preston that they are all too willing to point out the limitations of human beings, but they neglect to point out the limitations of microscopic life forms.

Any mutation will lower the risk

MacPhee and Marx 98 (Ross, American Museum of Natural History and Aaron Diamond, AIDS Research Facility and Tulane University, “How Did Hyperdisease Cause Extinctions?”, http://www.amnh.org/science/biodiversity/extinction/Day1/disease/Bit2.html)
It is well known that lethal diseases can have a profound effect on species' population size and structure. However, it is generally accepted that the principal populational effects of disease are acute--that is, short-term. In other words, although a species many suffer substantial loss from the effects of a given highly infectious disease at a given time, the facts indicate that natural populations tend to bounce back after the period of high losses. Thus, disease as a primary cause of extinction seems implausible. However, this is the normal case, where the disease-provoking pathogen and its host have had a long relationship. Ordinarily, it is not in the pathogens interest to rapidly kill off large numbers of individuals in its host species, because that might imperil its own survival. Disease theorists long ago expressed the idea that pathogens tend to evolve toward a "benign" state of affairs with their hosts, which means in practice that they continue to infect, but tend not to kill (or at least not rapidly). A very good reason for suspecting this to be an accurate view of pathogen-host relationships is that individuals with few or no genetic defenses against a particular pathogen will be maintained within the host population, thus ensuring the pathogen's ultimate survival.

Responses solve

Ensom 3 (Jim, Crisis Management Trainer at Business Continuity Consultants, Former Editor of Survive Magazine, Former Journalist for the BBC, June 20, http://www.globalcontinuity.com/article/articleview/94/1/30/)
In reaching these landmarks in the containment of SARS, the most severely affected countries and areas have identified and rapidly corrected long-standing weaknesses in their health systems in ways that will mean permanent improvements for the management of all diseases. In addition, systems of data collection and reporting, and new patterns of openly and frankly communicating information to the public will hold the world in good stead when the next new disease emerges and the next influenza pandemic breaks out.

Your evidence is media hype

Rooks 06 – (Kyle, thesis paper, School of Journalism, Media and Cultural Studies Cardiff University, “An Epidemic of Epidemics: A Case for Public Relations Role in Mitigating Health Scares,” http://slb.cf.ac.uk/jomec/resources/KyleRooks_MAIPR2005_2006.pdf)
Health scares are rife in today’s society, ironically persisting during a time of unparalleled health. Capturing the headlines and the public’s imagination, these scares have a detrimental impact on public health as the ensuing panic invokes stress – which does a number of harmful things to our health – and influences public health policy through the misappropriation of government resources. The ongoing panic in the UK surrounding the measles, mumps and rubella (MMR) vaccine, one of the safest and most effective preventative health measures, highlights both the importance of being able to effectively frame and communicate risk and the glaring inability of health authorities to maintain trust in the vaccine. With the media and pressure groups perpetuating health scares to satisfy their agendas, and the scientific community poorly positioned from a traditional standpoint to rebut scaremongering tactics, this study endeavours to determine how a public relations (PR) strategy can cut through misperceptions in order to foster a reasoned dialogue and appropriate public action to health risks.

Technological advances mean diseases aren’t existential threats anymore

Jeffrey Taubenberger, M.D. PhD medical college of Virginia and virologist at the Department of Molecular Pathology at the Armed Forces Institute of Pathology, 12/11/2005, “Can We Stop the Next Killer Flu?” Washington Post, Lexis

And then the tide turned back. Drug-resistant bacteria began flourishing. HIV became pandemic. Scientists began talking of "emerging" diseases. They come from the rain forest, from the dark recesses of tropical caves, from foul duck ponds and fetid chicken coops. They take advantage of a world of abundant human and animal meat. It would appear from the unfolding concern over avian flu, and from recent outbreaks of panic over other pathogens -- SARS, for example -- that civilization is increasingly vulnerable to pandemics, and that the human face of the future will be covered with a mask. By overcrowding the planet, by ravaging our environment, by jetting promiscuously around the world with all manner of microbes in tow, by overprescribing antibiotics and helping breed superbugs, we've set ourselves up for a plague. That's the basic argument. But here's another possibility: That we're at a turning point in the war between people and germs. That we've learned, just in the past half-century or so, how to read the code of life. That we've developed techniques, just in the past two decades, to discern the complete genetic code of an organism. That, just in the last few years, we've started to figure out the innermost secrets of microbes and what turns some of them into pathogens. Jeffrey Gordon, who studies intestinal bacteria at Washington University in St. Louis, says: "We have the tools in the year 2005 to define the genetic evolution of a lot of these pathogens, particularly in the case of viruses like flu. It's a race between our society, our politics, our societal will and the viruses." No one knows how the race will turn out, but the advantage at the moment is not necessarily on the side of the microbes. We're on to their game. Or, to use a more appropriate metaphor, we're not a bunch of sitting ducks.

Epidemics don’t cause extinction they eventually evolve into milder strains so they don’t kill their hosts

Jeffrey Taubenberger, M.D. PhD medical college of Virginia and virologist at the Department of Molecular Pathology at the Armed Forces Institute of Pathology, 12/11/2005, “Can We Stop the Next Killer Flu?” Washington Post, Lexis

We also don't know what would happen to the virulence -- the deadliness -- of the avian flu if it did become a human contagion. Contagiousness and virulence are often at cross-purposes. Ebola, a frightening filament-like virus that causes uncontrolled bleeding throughout the victim's body, burns so hot as a disease that it usually kills people before they have much of a chance to spread it. Emerging viruses that are initially highly lethal, such as avian flu in the human cases seen so far, often evolve toward lower virulence for their own survival. Even the merciless 1918 virus evolved into a milder strain. Jahrling, the virologist, says: "The equilibrium seems to be toward lower virulence, toward an accommodation with the host. It's not smart to kill your host."

What does Jahrling think will happen in the case of avian flu? "We can't prognosticate evolution," he says.

We can keep our eyes open. If, based on genetic flu research like Taubenberger's, scientists knew exactly which mutations were critical to the emergence of a pandemic strain of flu, and if health officials carefully monitored the strains evolving in the influenza hot spots of Southeast Asia, China and Indonesia, it might be possible to snuff out a dangerous strain before it could spread.

No impact – anything virulent enough to be a threat would destroy its host too quickly

Joshua Lederberg, professor of genetics at Stanford University School of Medicine, 1999, Epidemic The World of Infectious Disease, p. 13

The toll of the fourteenth-century plague, the "Black Death," was closer to one third. If the bugs' potential to develop adaptations that could kill us off were the whole story, we would not be here. However, with very rare exceptions, our microbial adversaries have a shared interest in our survival. Almost any pathogen comes to a dead end when we die; it first has to communicate itself to another host in order to survive. So historically, the really severe host- pathogen interactions have resulted in a wipeout of both host and pathogen. We humans are still here because, so far, the pathogens that have attacked us have willy-nilly had an interest in our survival. This is a very delicate balance, and it is easily disturbed, often in the wake of large-scale ecological upsets.

Viruses will never cause extinction

Don Brownlee, Department of Astronomy, UW, Seattle, Nature, International Weekly Journal of Science, 423, June 19, 2003, A walk to the gallows, http://www.nature.com/nature/journal/v423/n6942/full/423803a.html

The threat of specifically designed killer viruses or diseases seems more credible, and new biological threats are sure to cause havoc in the future. But can even the most deadly designer bugs cause total human extinction? The nastiest viruses are usually not very successful because they kill their host before they can be transmitted. Life is actually pretty robust, the product of the tough taskmaster of evolution. Viruses have been attacking bacteria in the oceans for billions of years and, even though they outnumber their hosts by orders of magnitude, the viral attackers can never completely win.

A2: Pandemic

Flu outbreaks are down now and vaccines are already being prepared for the next flu.

Blumenthal, 3/19/11 (Susan, former US surgeon general, “Flu in the 21st Century,” http://www.huffingtonpost.com/susan-blumenthal/fighting-the-flu-in-the-2_b_837526.html)
This is why the recent news from Hong Kong is so worrisome. Fortunately, as of yet, sustained human-to-human transmission has not occurred with this avian flu strain. Scientists monitor circulating flu strains to determine which are the most prevalent in preparation for formulating the next year's mix for the flu vaccine. According to a recent article in Nature (24), work is now underway to prepare for a possible future resurgence in the H2N2 strain, which circulated widely in the 1950s and 60s. This year, the primary form of flu in circulation worldwide is the "garden variety" seasonal flu, which in actuality is numerous different strains that change every year. Today, international influenza occurrence is generally low but increasing in Canada and Europe with a recent marked rise in rates in Mongolia, the Republic of Korea, Sri Lanka, Madagascar and Cameroon. In the U.S., flu activity, which typically peaks in late January to February, has risen since the early fall, but there is a lower incidence of the flu this year (particularly the H1N1 strain) than there was last year (25). However, despite the disease's severe consequences in some people, the flu is still viewed by many as a fairly mild illness.

Research is already producing vaccine breakthroughs.

Blumenthal, 3/19/11 (Susan, former US surgeon general, “Flu in the 21st Century,” http://www.huffingtonpost.com/susan-blumenthal/fighting-the-flu-in-the-2_b_837526.html)
Researchers at Oxford have recently found a promising candidate to provide universal protection against the flu (42). The vaccinate targets T-cell production in the body, elicited by a protein less susceptible to mutation that sits on the inside of the flu virus, rather than the external proteins that current flu vaccines use. Preliminary results also show that the vaccine is more effective in older people than the traditional vaccine, a great breakthrough that would help the segment of the population that has the highest mortality rate from influenza (43). The good news is that research is currently underway to revolutionize flu vaccine technology in the 21st century. Given the impact of the seasonal flu every year and the potential health and economic threat posed by a pandemic, this must be a public health priority. However, the long term safety and effectiveness of new approaches must be determined before these techniques can be mainstreamed. While scientists pursue these new advances, currently available flu vaccines and healthy habits will continue to be the best defense against influenza. Everyone over the age of 6 months (there are some exceptions) should get vaccinated for the seasonal flu annually (protection against H1N1 is included in this year's vaccine) and practice good hygiene such as washing your hands, sneezing/coughing into the crook of your arm, and staying away from others if you are sick. Hopefully, with more public awareness and investments in scientific research and innovation, the nightmare scenario of a global flu pandemic will be found only in the history books.

Research is already underway to develop better, faster immunization techniques.

Blumenthal, 3/19/11 (Susan, former US surgeon general, “Flu in the 21st Century,” http://www.huffingtonpost.com/susan-blumenthal/fighting-the-flu-in-the-2_b_837526.html)
Thankfully, research is now underway to develop faster, better ways of producing flu immunizations as well as to design delivery mechanisms that can be used across age groups (e.g., nose drops, preservative free multi-dose vials) to further promote their use and availability. To be licensed, a new flu immunization must be shown to be safe and effective, to elicit antibodies, and to prevent influenza. In a recent paper published in the New England Journal of Medicine (34), researchers from the National Institutes of Health (NIH) described eight different strategies that scientists are exploring to improve flu vaccines in the 21st century: 1. Growing inactivated influenza vaccines in mammalian cell cultures rather than chicken eggs. Mammalian cell-culture has several advantages to the current method of vaccine production that uses chicken eggs. In the event of an avian influenza outbreak among chicken flocks, there may be insufficient egg supply to produce large quantities of vaccine; the cell culture method overcomes this limitation, giving manufacturers greater control over the production process and allowing them to increase surge capacity for vaccine production in the event of a pandemic (35,36). However, this technique may not significantly reduce the amount of time it takes to produce vaccines. A cell cultured live attenuated vaccine is currently in late-stage pre-clinical development but more work must be done before it can advance to clinical testing. 2. Enhancing the effectiveness and reach of existing vaccines with adjuvants. Adjuvants are substances (e.g. oils or aluminum salts) (37,38) that are added to vaccines to amplify the body's immune response to an antigen (e.g. a foreign particle such as a flu virus). The body's immune response to certain influenza strains may not be robust enough to protect it from the health damaging effects of the flu virus; adjuvants help to overcome this by stimulating the production of high levels of antibodies that can defend the body against the virus's infection. Additionally, adjuvants may act to expand the amount of vaccine available, since less of the active ingredient is needed per dose of vaccine, allowing limited supplies of active ingredient (e.g. purified virus protein) to be stretched over a greater volume of doses (39). While adjuvant based vaccines have been approved for use in Europe, they have not been approved by the FDA for administration in the United States. Currently, next generation adjuvants using purified bacterial outer membrane proteins and toll-like receptors are in the early stages of clinical testing in America.

3. Developing new live attenuated vaccines. In contrast to vaccines that contain the inactivated (killed) influenza virus, live attenuated vaccines contain a live virus that scientists have altered so that it stimulates the immune response without doing harm to the body. A promising candidate for this type of vaccine is based on altering or deleting the influenza NS1 protein, which works to prevent the virus from replicating while it enhances the body's immune system defenses. 4. Creating next generation vaccines with DNA recombinant techniques. Producing vaccines with DNA recombinant technology eliminates the need for chicken eggs or mammalian cell cultures, thereby significantly speeding up production time (40). When the genetic sequence of a particular influenza virus's HA (its distinctive outer marker) is identified, scientists can use this information to more rapidly produce a vaccine without having to adapt viruses to grow in eggs. They can use the DNA to create HA proteins in the lab for use in vaccines. A clinical trial of such a DNA recombinant vaccine for seasonal flu has recently been completed for use in people over the age of 18 and is currently under review by the FDA. 5. Utilizing non-infectious virus-like particles for vaccine production. This technique uses recombinant viral vectors to produce proteins found in the influenza virus, which then self-assemble to form particles that resemble wild-type viruses themselves but are non-infectious. The method is still under development but has reached testing in phase-2 clinical trials. 6. Using other harmless "carrier" viruses as vectors to deliver influenza proteins to the immune system. Not every virus causes disease in humans. This novel vaccination method uses harmless viruses that are still capable of entering human cells, piggybacking them with influenza proteins so that they will help the body develop immunity to the wild influenza virus. Early trials of nasal spray and pill versions of this type of vaccine are showing promise. 7. Creating DNA-based vaccines. Injecting DNA directly into the muscles of animals, where it subsequently encodes the critical HA or NA influenza proteins, has resulted in positive immune responses. So far, this technique has not worked as well in humans. Further research must prove the efficacy of DNA based vaccines in human studies before researchers proceed to scale up this prevention method. 8. Developing a "universal" vaccine. This approach, the "Holy Grail" of vaccine development, involves the creation of a "universal vaccine" capable of conferring long lasting immunity across multiple strains of the influenza virus. The flu virus is a wily adversary that mutates often. It is this frequent genetic misspelling of the influenza virus that makes it so hard to conquer; because the virus changes so often, a new vaccine must be developed every year to prevent its widespread transmission. But certain highly conserved virus proteins (those that tend to survive most mutations and are present across strains) could be the targets for a universal vaccine, and these are now the subject of several clinical trials (41). The question of whether lifelong protection against all strains of flu could be achieved with a universal vaccine remains unanswered. That is why research should also pursue a vaccine strategy that would confer full or partial protection with periodic immunizations against seasonal strains as well as emerging pandemic ones.

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