Lance Armstrong: The Final Cheat?

Transcription

Lance Armstrong: The Final Cheat?
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Vol 19 | Easter 2013 | University of Cambridge
A Production of The Triple Helix
The Science in Society Review
The International Journal of Science, Society and Law
Lance Armstrong:
The Final Cheat?
Chimeras in Research:
How Far Should We Go?
Medically Supervised
Drug Injection Sites:
More Harm than Good?
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TABLE OF CONTENTS
What does
personalised
treatment bring?
Royalty-free image
16
MSDIS
22
Strategies to decreade
illegal drug use
Flickr: Dirty Bunny
CC-BY 2.0
Thomas J. Evans
Lance Armstrong: The Final Cheat?
Cambridge Articles
9
The Path Towards Personalised Treatment:
Multiple Sclerosis
Samantha Johnson
Grace Petkovic
12 Chimeras in Research: How Far Should We Go? International Features
16
20
22
Medically Supervised Drug Injection Sites:
More Harm than Good? Veggie Delight Black Athletic Superiority:
Fact or Fiction?
Does it really exist?
Wikicommons, PD.
Cover Article
4
Black Athletic
Superiority
CAMBRIDGE
9
Multiple
Scelrosis
Julia Romanski, Brown
Rashmi Jain, UC San Diego
Kaylin Keerd Muskat, UC San Diego
Front Cover photo taken by David Iliff. License: CC-BY-SA 3.0,
featuring the breakaway group of the 2012 London Olympic Road Race, 28 May 2012.
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Red: Overpopulation Event. ©The Triple Helix, Cambridge.
Green: Explanation by Harrison Keely, stock.xchng. ©sxc.hu.
Purple: Woman Using Computer by Ariel da Silva Parreira, stock.xchng. ©sxc.hu.
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2 THE TRIPLE HELIX Easter 2013
Science in Society Sixth Formers Conference
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THE TRIPLE HELIX Easter 2013 3
CAMBRIDGE
Lance Armstrong: The Final Cheat?
Thomas J. Evans
Reproduced from [22].
4 THE TRIPLE HELIX Easter 2013
© 2013, The Triple Helix, Inc. All rights reserved.
CAMBRIDGE
“Everybody wants to know what I’m on. What am I on? I’m on
my bike busting my ass six hours a day. What are you on?”
Lance Armstrong, 2001 Nike TV advert
H
is story was too good to be true. When Armstrong
won his second Tour de France title, having been
diagnosed with brain, lung, and testicular cancer
just four years earlier, the CEO of Nike joked that “If a
script writer had come up with a story resembling what
you have just achieved, even the Hollywood studios would
have refused” [1]. With good reason, too, for his success was
quite simply unprecedented. Rumours of doping abounded,
but after Armstrong’s seventh consecutive win in 2005, he
hit back at the cynics and skeptics. “I’m sorry for you”, he
said. “I’m sorry you don’t believe in miracles” [2].
But they were right to question this miracle. Last year
the United States Anti-Doping Agency (USADA) published
a report claiming there was “no doubt that Mr. Armstrong’s
career was fuelled from start to finish by doping” [3]. The
evidence, comprising first-hand eyewitness accounts of his
cheating, was compelling and overwhelming; it was “the
most sophisticated, professionalized, and successful doping
programme the sport has ever seen” [3]. The Union Cycliste
International (UCI) stripped Armstrong of his titles, declaring,
“Lance Armstrong has no place in cycling. He deserves to
be forgotten” [4]. This January, after months of denial and
silence, he turned himself in, announcing on public television
that he “viewed this situation as one big lie that I repeated
a lot of times” [5].
Armstrong’s preferred method of cheating was blood
doping. The World Anti-doping Agency (WADA) defines
this as “the misuse of certain techniques and/or substances
to increase one’s red blood cell mass, which allows the body
to transport more oxygen to muscles and therefore increase
stamina and performance” [6].
It was the most sophisticated,
professionalized, and
successful doping programme
the sport has ever seen.
In particular, Armstrong used human recombinant
erythropoietin, or EPO [3]. A naturally occurring hormone
secreted by the kidneys, EPO secretion is responsible for
erythropoiesis (red blood cell production). By injecting
synthetic EPO into his body, Armstrong was able to stimulate
endogenous erythropoiesis, boosting the amount of oxygen
delivered to his tissues, and providing him with a huge
competitive advantage in his brutal endurance races.
Thankfully, EPO doping is detectable. It can be discovered
by a simple and reliable urine test, which uses the separation
of endogenous and synthetic EPO by isoelectric focusing (a
method of protein analysis) to infer whether or not an athlete
Computer model of erythropoietin (EPO), a hormone that induces red blood cell production. Reproduced from [23].
© 2013, The Triple Helix, Inc. All rights reserved.
THE TRIPLE HELIX Easter 2013 5
CAMBRIDGE
has cheated [7]. However, poorly timed tests can miss cheats
[8]. More recently, WADA has developed technology to
overcome this inherent temporal error in urine samples by
using a “biological passport”, which enables longitudinal
monitoring of athletes [8]. EPO-doping results in elevated
haematocrit levels, the percentage of blood occupied by red
blood cells. This tends to reduce the level of reticulocytes
(immature red blood cells) in the blood. By tracking the
amount of haemoglobin and reticulocytes in the blood over
has contributed to the evolution of “an arms race between
regulators and the cheats” [9]. This increased detection pressure
on athletes drives them to hunt for new techniques that are
more likely to go unnoticed by the regulators.
Currently, the solution seems to be gene doping [10].
Former WADA president Dick Pound agrees, once saying:
“You would have to be blind not to see that the next generation
of doping will be genetic” [11].
Gene doping is the “non-therapeutic use of genes, genetic
elements and/or cells that have the capacity to enhance
athletic performance” [12]. It has its roots in gene therapy:
the introduction of a healthy, therapeutic gene (transgene)
that codes for a specific protein in order to replace a mutated,
non-functional gene. This sort of gene transfer has been a
promising angle as a means to cure diseases [10]. But now
that gene therapy is starting to become a clinical reality, it is
increasingly being viewed as open to abuse by athletes [10].
For example, in 1997 it was showed that EPO gene
“You would have to be
blind not to see that the next
generation of doping will be
genetic.”
Detection of EPO doping through urine testing involves the separation of
endogenous and synthetic EPO by isoelectric focusing, the principle of which is
described above. Reproduced from [24].
time and comparing it to the biological passport, WADA
can infer EPO-use by values that sit outside a given range
of natural variability specific to the athlete [8].
However, rigorous anti-doping strategies such as the
biological passport, which since its implementation by the
UCI in 2010 has already caught at least eight cyclists [8],
6 THE TRIPLE HELIX Easter 2013
transfer in non-human primates resulted in increased red
blood cell levels [13]. More recently, a clinical gene therapy
technique known as Repoxygen has been developed, that
uses EPO gene transfer to treat severe anemia associated
with renal failure [14].
But athletes could also exploit the same technology in
order to boost their haematocrit [10]. Since the protein is
not exogenous but is actually synthesized within the athlete
by the transgene, it would be very difficult to distinguish
between the naturally-occurring protein and the transgene’s
protein [10], which means that cheats could go ahead to
compete and win titles totally free from the fear of tests.
Gene doping has the capability to give athletes the upper
hand in the arms race.
However, the risks of gene doping are serious. In 2004,
a team from the University of Pennsylvania experimentally
introduced the EPO gene into macaque monkeys [15]. The
macaques developed polycythemia (thick, sluggish blood
due to too many red blood cells), but to make matters worse,
some then developed auto-immune anaemia: their immune
system had attacked both the EPO from the transgene and
the endogenous EPO, causing low hematocrits. In the end,
the anemia was so severe the animals were euthanized.
Nevertheless, if these risks can be overcome, the potential
of gene doping is alluring, and it extends to numerous other
genes. HGF, a gene implicated in angiogenesis (blood vessel
development) is a potential target [10]: increased angiogenesis
facilitates increased oxygen supply to muscles; as is IGF-1,
which can trigger muscle hypertrophy (tissue growth) [10],
enabling athletes to run faster, jump higher, and throw further.
In an approach that seems perhaps more akin to science fiction
than to reality, an exciting target are the pain relief genes
such as the one that encodes glutamic acid decarboxylase,
© 2013, The Triple Helix, Inc. All rights reserved.
CAMBRIDGE
which acts to block transmission of pain signals through
triggering the expression of the inhibitory neurotransmitter
GABA (gamma-Aminobutyric acid). [10]
Some view gene doping as no different to any other
form of cheating: it provides an unfair advantage, plain
and simple. Thomas Murray, chairman of WADA’s ethics
panel, agrees. He believes it fundamentally “violates our
understanding of what should make for success in sports”
[16]. However, some argue that sport itself is inherently
technological: from the training shoe to keyhole joint surgery,
athletes benefit from technology, so why not let athletes
use gene doping? [17] Armstrong didn’t believe that what
he did was cheating. “The definition of cheat is to gain an
advantage on a rival or foe that they don’t have. I didn’t
view it that way. I view it as a level playing field.” [5]
Gene doping in athletics
might be the tip of the iceberg
in terms of gene transfer
technology affecting society.
Furthermore, gene doping can be a means of
democratizing sport. It eliminates genetic predispositions
and allows those who work hard to win, which is surely fairer
than the somewhat genetically determined and elitist status
quo? The fundamental dilemma is whether doping itself is
wrong. Society is inconsistent with respect to its attitudes
towards drug use: millions drink caffeine everyday, but
until 2004 it was on the WADA Prohibited List. And how
about legal performance enhancers, such as creatine? Where
and how do we draw the line? Some believe that science
and technology has the ability to make sport more fun, so
the use of performance enhancers is “more an expression
of the spirit of sport” than an attempt to undermine the
integrity of it. [18]
Gene doping in athletics might be the tip of the iceberg
in terms of gene transfer technology affecting society. What
are the limits of gene doping? Whilst it currently remains in
the realm of athletic performance, it seems likely that people
might also wish to introduce genes for improved intellectual
performance, if such genes exist. This is not beyond reason:
the phenomenon of “intellectual doping” exists today. In a
situation analogous to gene doping, therapeutic drugs such
as modafinil, Ritalin, and Adderall, which are designed to
treat conditions like ADHD and insomnia, are being misused
by students in order to improve cognitive performance [19].
If left unregulated, the societal implications of these “smart
drugs” are profound. It could result in a two-tier education
system whereby those who can afford such drugs are at
a great advantage compared to those who cannot [19].
Economically, the use of such drugs by the ageing workforce
could enable many to postpone retirements, which whilst
beneficial to them, would have negative implications for
youth employment. [20]
The adverse reaction towards Lance Armstrong’s
wrongdoings is a reflection of society’s perception of doping.
In a situation analogous to gene doping, therapeutic drugs such as modafinil, Ritalin, and Adderall, which are designed to treat conditions like ADHD and
insomnia, are being misused by students in order to improve cognitive performance [19]. Reproduced from [25].
© 2013, The Triple Helix, Inc. All rights reserved.
THE TRIPLE HELIX Easter 2013 7
CAMBRIDGE
Doping is banned by the WADA; the punishment for
being caught, as seen in the case of Lance Armstrong, is
not just the loss of a lifetime’s work, but also a cold, harsh
rejection by society. However, as doping technologies become
more sophisticated, they begin to propose some fundamental
philosophical questions about the ethics of doping.
The power of gene doping is remarkable: it is an
opportunity for mankind to dispel the limits on human
potential. Lance Armstrong said that “one of the redeeming
things about being an athlete is redefining what is humanly
possible” [21]. Will our attitudes towards doping one day
shift in alignment with his? Gene doping seems like the
magic ingredient for sporting success, even if the risks are
high and the techniques frowned upon. For society, there
are some serious questions to answer. Ultimately, social
mores change over time, as exemplified just last year with
the legalization of marijuana in the US states of Washington
and Colorado. One wonders: in the future, will public opinion
on doping change too?
Thomas Evans is a first year student studying Natural Sciences
(Biological) at Fitzwilliam College.
Reproduced from [26].
References:
1. The Telegraph. “Pain is temporary … quitting lasts forever”. [Internet] 2004
July 25 [cited: 2013 January 23] Available from: http://www.telegraph.co.uk/
sport/2383525/Pain-is-temporary...-quitting-lasts-forever.html
2. BBC Sport. Lance Armstrong: fall of a sporting hero. [Internet] 2012 October
11 [cited: 2013 January 24] Available from: http://www.bbc.co.uk/sport/0/cycling/19907683
3. USADA. Reasoned Decision of the United States Anti-Doping Agency On
Disqualification and Ineligibility. [Internet] 2012 October 10 [cited: 2012 November
25] Available from: http://d3epuodzu3wuis.cloudfront.net/ReasonedDecision.pdf
4. BBC Sport. Lance Armstrong stripped of all seven Tour de France wins by UCI
[Internet] 2012 October 22 [cited: 2012 November 25] Available from: http://www.
bbc.co.uk/sport/0/cycling/20008520
5. BBC Sport. Lance Armstrong & Oprah Winfrey: interview transcript [Internet]
2013 January 18 [cited: 2013 January 24] Available from: http://www.bbc.co.uk/
sport/0/cycling/21065539
6. WADA. Questions and Answers on Blood Doping. [Internet] 2011 September [cited: 2012 December 5] Available from: http://www.wada-ama.org/en/
resources/q-and-a/blood-doping/
7. WADA. WADA Technical Document – TD2007EPO. [Internet] 2007 April 5
[cited: 2012 December 6] Available from: http://www.wada-ama.org/rtecontent/
document/td2007epo_en.pdf
8. Patrick, K. Passport to clean competition. BMJ 2012 May 22; 344:e2077
9. Nature Editorial. A Level Playing Field? [Internet] 2008 August 6 [cited: 2012
December 4] Available from: http://www.nature.com/nature/journal/v454/n7205/
full/454667a.html
10. Baoutina A, Alexander IE, Rasko JEJ, Emslie KR. Potential Use of Gene
Transfer in Athletic Performance Enhancement. Mol Ther 2007 October; 15 (10):
1751-1766
11. Reuters. New illegal drugs available in run-up to Games [Internet] 2012
April 20 [cited: 2012 November 27] Available from: http://www.reuters.com/
article/2012/04/20/us-olympics-london-doping-idUSBRE83J1A320120420
12. WADA. The 2008 Prohibited List. [Internet] 2007 September 22 [cited: 2012
December 2] Available from: http://www.wada-ama.org/rtecontent/document/2008_list_En.pdf
13. Svensson EC, Black HB, Dugger DL, Tripathy SK, Goldwasser E, Hao Z, Chu
L, Leiden JM. Long-term erythropoietin expression in rodents and non-human
8 THE TRIPLE HELIX Easter 2013
primates following intramuscular injection of a replication-defective adenoviral
vector. Hum Gene Ther 1997 Oct 10;8(15): 1797-806
14. Science News. Barry, P. Finding the Golden Genes. [Internet] 2008 August 13
[cited: 2012 December 6] Available from: http://www.sciencenews.org/view/generic/id/35185/title/Finding_the_golden_genes
15. Gao G, Lebherz C, Weiner DJ, Grant R, Calcedo R, McCullough B, Bagg A,
Zhang Y, Wilson JM. Erythropoietin gene therapy leads to autoimmune anemia in
macaques. Blood 2004 May 1; 103: 3300-3302
16. Brownlee, C. Gene Doping: Will athletes go for the ultimate high? Science
News 2004 October 30; 166 (18): 280-281
17. The Washington Post. Miah A. Enhanced Athletes? It’s Only Natural. [Internet]
2008 August 3 [cited: 2012 December 6] Available from: http://www.washingtonpost.com/wp-dyn/content/article/2008/08/01/AR2008080103060.html
18. The Boston Globe. Rothman J. Just what’s wrong with doping? [Internet]
2012 July 15 [cited: 2012 December 6] Available from: http://www.bostonglobe.
com/ideas/2012/07/14/what-really-wrong-with-sports-doping/qO1GZhk7ay36zoh8GMM18N/story.html
19. BBC. Do cognitive-enhancing drugs work? [Internet] 2011 November 9 [cited:
2012 December 6] Available from: http://www.bbc.co.uk/news/health-15600900
20. Academy of Medical Sciences, the British Academy, the Royal Academy
of Engineering and the Royal Society. Human Enhancement and the future of
work. [Internet] 2012 November [cited: 2012 December 6] Available from: http://
royalsociety.org/uploadedFiles/Royal_Society_Content/policy/projects/humanenhancement/2012-11-06-Human-enhancement.pdf
21. Fast Company. What’s possible? [Internet] 2001 March 31 [cited: 2013 January
24] Available from: http://www.fastcompany.com/64040/whats-possible
22. ~Xtinalicious. [image on the internet]. http://www.flickr.com/photos/xtinamilan/3282943169/ under CC-BY 2.0 license.
23. Image from Wikimedia. [image on the internet]. http://commons.wikimedia.
org/wiki/File:Erythropoietin.png under CC-BY 2.0 licence.
24. Mrbean427. [image on the Internet]. http://commons.wikimedia.org/wiki/
File:Isoelectric_focusing_contribute2.jpg under the CC-BY 2.0 licence
25. Wikimedia. [image from the internet]. http://commons.wikimedia.org/wiki/
File:Ritalin_Methylphenidat.jpg under the CC-BY 2.0 licence.
26. Wladyslaw. [image from the internet]. http://commons.wikimedia.org/wiki/
File:Tour_de_Doping.jpg under the CC-BY 2.0 licence
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CAMBRIDGE
The Path Towards Personalised Treatment:
Multiple Sclerosis
Samantha Johnson
M
ultiple Sclerosis (MS) is an autoimmune disease that
affects approximately 1.3 million people worldwide
and is renowned for its huge variation in disease
progression [1]. Whilst sufferers are diagnosed with one
of four broad types of the disease (Relapsing-Remitting,
Primary Progressive, Secondary Progressive or Benign),
individuals with the same type of MS won’t necessarily
experience the same symptoms in the same way. Significant
individual variation results in unpredictable responses to
disease-modifying drugs, and so developing drugs that are
widely effective, even within a particular type of MS, is
challenging [2].
Personalised medicine could be the answer to improve
patients’ prognosis through more effective treatment and
reduced clinical trial costs via earlier patient stratification.
However, other factors mean this could be a slow process and
the cost to the pharmaceutical and healthcare industry would
be high; therefore, one must ask how near to personalised
medicines are we and is this solution justified?
The cause of MS is uncertain but the mechanism involves
the migration of the body’s defensive lymphocytes (white
blood cells) across the blood-brain-barrier, despite the absence
of infection. These cells behave in an autoreactive manner.
The lack of the usual protective action of controlled cell death
allows inflammatory attacks, which result in patches, known
as plaques, of demyelination - the loss of the insulating layer
of myelin around nerve axons [3].
Plaques occur in many regions of the central nervous
system (CNS) and demyelination is believed to be due to the
activation of microglia in inflammation, which destroy the
Personalised medicine could
be the answer to improve
patients’ prognosis.
cells making the myelin through the cell-surface associated
tumour necrosis factor α (TNFα) [3,4]. Therefore, unlike many
neurodegenerative diseases where specific regions of the
Reproduced from [12].
© 2013, The Triple Helix, Inc. All rights reserved.
THE TRIPLE HELIX Easter 2013 9
CAMBRIDGE
Reproduced from [14].
brain are primarily affected, the pathophysiology of MS can
be widespread in the CNS and depends on an individual’s
immune system. This may explain the diversity of the disease
symptoms seen to affect many functions including the motor,
sensory, visual, and autonomic systems [3].
Ascertaining why the disease progression varies so
much is less understood. The classification of types of MS is
a clinical separation based on the frequency of and recovery
from attacks and its basis in disease mechanism is unclear
[5]. It has, however, been suggested that it depends on the
accumulation of axon degeneration and damage [3]. Some
data tentatively suggests that disease progression is largely
age-dependent as the initial type of MS diagnosed has no
significant influence on the age at which patients reached
particular disability landmarks; however, these findings do
not preclude the considerable individual variability in age
at disability milestones [6]. The genetic basis is also debated
as some data supports genetic heterogeneity, implying
the varied progression arises from separate mechanisms
in several genes, but most analysis concludes that MS is a
single disease and the T-cell mediated inflammation variation
is due to different immunological responses with varied
mechanisms [3].
Recently Ottoboni et al. used samples of white blood
cells and RNA probes to determine if the expression of
various genes is regulated differently in MS patients. This
could provide a new biomarker to determine the MS disease
course. Currently treatments are usually tested on highlyselected subject populations [2] which may not represent all
the patients in a particular type of MS who are consequently
prescribed the drug. Therefore, the drugs can seem effective
at slowing attacks in clinical trials and in some patients, but
in others the response may be poorer than expected, hence
the clear advantage for treatments that are more tailored
to the individual’s disease.
10 THE TRIPLE HELIX Easter 2013
After studying untreated MS patients, along with two
groups undertaking different treatments used to manage
MS (glatiramer acetate and interferon-beta), the experiments
uncovered two subsets of subjects (MSA and MSB) that
can be differentiated by a single transcriptional signature
in all the three subject groups (i.e. both treatments and the
untreated). MSA subjects overexpressed particular genes and
this overexpression was the same in all groups, suggesting that
the underlying nature of the disease may not be fundamentally
altered by either treatment. Moreover, the genes involved
were required in pathways that activated lymphocytes and
the MSA patients showed a more active disease course [2].
The paper addresses the research’s shortcomings, having not
done any longitudinal studies, meaning that an individual
may fluctuate between the two subsets over time, but clearly
states the discovery’s potential for personalising patient care
and enhancing our understanding of MS [2].
Doctors could argue that personalised medicine has
always been practised by considering age, sex and family
history in diagnosis, and adapting treatments correspondingly
to co-morbidities, the patient’s lifestyle and economic
circumstances [7]. However, the modern approach of
processing and analysing aggregated data can lead to the
generic treatments based on the ‘average patient’ which,
as previously mentioned, can lead to treatments being less
effective in individuals than patients are led to believe [7].
Pharmacogenomic experiments, such as those by Ottoboni
et al, can allow the stratification of a single disease into
redefined disease subsets or the disease can be approached
entirely at the individual level by assessing the patient’s
individual biological make-up and its interaction with the
environment. Personalised medicine promises more precise
treatments but at the cost of more precise information. Currently
many ‘omics’ (genomics, transcriptomics, proteomics) support
stratification approaches but individual assessment will require
more complex methods – for example, specific data for an
individual can be generated for a snapshot of time but not
necessarily how it interacts over time [7]. The 1000 Genomes
Project enables personalised medicine research and so far
has mapped 38 million single nucleotide polymorphisms
(SNPs) which are thought to be the cause of variation between
individuals of the same species [8].
Personalised medicine
promises more precise
treatments but at the cost of
more precise information.
Genetic sequencing may underpin personalised medicine
yet there is uncertainty about how effective the observation of
individuals’ expression levels will be in clinical medicine or
predicting therapy responses [9]. There are claims that gene
expression studies of therapy responses do not fully enable
the potential impact of global collaborations as pharmaceutical
companies do not share their data with each other to improve
their sample size and communication with basic bioscience
is not effective enough, hence it is unlikely to implement
the predicted effects of personalised medicine [9].
© 2013, The Triple Helix, Inc. All rights reserved.
CAMBRIDGE
Expansion of the diagnostics industry will help resolve the need for
fewer side effects and more productive screening. Image reproduced from [14].
Reiss, on the other hand, suggests that whilst
pharmaceutical companies may limit this advance in medicine
by currently using a ‘one-therapy-fits-all’ business model,
the increased demand for biomarkers would provide new
research and potential profit for companies to counter
their reluctance to adapt these models [10]. Furthermore,
stratification using biomarkers could enable clinical trials to
be conducted with more accurate patient populations, where
those with adverse reactions could be identified earlier, such
that the total number and duration of clinical trials could be
reduced [10]. This presents advantages for all the involved
parties: pharmaceutical companies may initially have to
adapt their business strategy but the potential new research
Personalized medicine
will inevitably become a
mainstream therapy of the
future.
fields and reduced costs in clinical trials could outweigh
these losses and patients will have more effective treatments
discovered at a faster rate.
Previously, personalised medicine fell short of its high
expectations due to asynchronous advances in the relevant
areas [11]. There are still companies providing generic
solutions, as these are the most cost effective solutions for
less specific conditions; however other companies have
References:
1. World Health Organisation, Multiple Sclerosis International Federation. Atlas
multiple sclerosis resources in the world 2008. Geneva Switzerland: WHO Press;
2008. 56 p.
2. Ottoboni L, Keenan BT, Tamayo P, Kuchroo M, Mesirov JP, Buckle GJ, Khoury
SJ, Hafler DA, Weiner HL, De Jager, PL. An RNA Profile Identifies Two Subsets
of Multiple Sclerosis Patients Differing in Disease Activity. Sci Transl Med. 2012
September 26; 4(153): 153ra131 doi: 10.1126/scitranslmed.3004186
3. Compston A, Coles A. Multiple sclerosis. Lancet. 2008 October 25;
372(9648):1502-17
4. Zajicek JP, Wing M, Scolding NJ, Compston DA. Interactions between oligodendrocytes and microglia. A major role for complement and tumour necrosis factor
in oligodendrocyte adherence and killing. Brain. 1992 Dec; 115(Pt 6):1611-31
5. Kremenchutzky M, Rice GP, Baskerville J, Wingerchuk DM, Ebers GC. The
natural history of multiple sclerosis: a geographically based study 9: observations
on the progressive phase of the disease. Brain. 2006; 129(3): 584–94.
6. Confavreux C, Vukusic S. Age at disability milestones in multiple sclerosis.
Brain. 2006 March; 129 (3), 595-605.
7. Harvey A, Brand A, Holgate ST, Kristiansen LV, Lehrach H, Palotie A, Prainsack
B. The future of technologies for personalised medicine. New Biotechnology. 2012
September; 29 (6): 625- 633.
© 2013, The Triple Helix, Inc. All rights reserved.
recognised the benefit of highly differentiated products
in personalised medicine despite the higher cost. DNA
sequencing is becoming more affordable and accurate and
so the technology required to develop these medicines
effectively is also available [11]. Therefore, pharmaceutical
companies now have the technology and drive to adapt to
producing personalised medicines and it will inevitably
become a mainstream therapy of the future [11].
Increased pressure from regulatory authorities and
patients, for fewer side effects and diagnostic tests to determine
who the drug will be most effective for, is also steering
healthcare towards personalised medicine [11]. This demand
has been known to slow down the approval of new therapies,
and the time it takes to reach patients, demonstrating an
opposite argument to that given by Reiss; however, increased
collaboration and expansion of the diagnostic market could
resolve this problem in the long term. It may also benefit
small and medium-sized enterprises, which typically develop
biomarkers or diagnostic tests to complement specific drugs
already in clinical use, perhaps developed by a larger partner
company [9], thus expanding the pharmaceutical industry
away from a few key players, which many believe would
create a fairer economical market.
It therefore seems that personalised medicine is the
inevitable next step to effectively treat major diseases
complicated by individual variation, such as MS. It will not
be a simple step, as it requires collaboration in the scientific
industry, between basic bioscience research, diagnostic
companies and ‘big pharma,’ but the financial and clinical
benefit that will ensue from this seems a justified incentive.
Whether or not one agrees with the increasing prevalence
of genetic screening, it is hard to doubt the positive outcome
it could have in these circumstances. The expansion of
pharmaceutical companies into supporting diagnostic
technologies could be an economical advance in the healthcare
industry, and, although treatments may initially be costly, as
the understanding of biomarkers advances the reduced cost
of trials should make personalised medicine an affordable
and desirable solution.
Samantha Johnson is a 3rd Year student studying Natural Sciences
at Trinity Hall.
8. 1000 Genomes Project Consortium, Abecasis GR, Auton A, Brooks LD, DePristo
MA, Durbin RM, Handsaker RE, Kang HM, Marth GT, McVean GA. An integrated
map of genetic variation from 1.092 human genomes. Nature. 2012 November 1;
491 (7422):56-65. doi: 10.1038/nature11632
9. Mesko B, Zahuczky G, Nagy L. The triad of success in personalised medicine:
pharmacogenomics, biotechnology and regulatory issues from a Central European
perspective. New Biotechnology. 2012 September; 29 (6):741-750. doi: 10.1016/j.
nbt.2012.02.004
10. Reiss T. Implications of personalised medicine for the health economy. Abstracts of the 14th European Congress on Biotechnology; 2009 September 13-16;
Barcelona, Spain. New Biotechnology. 2009 September; 25 (Supplement) S16-17.
doi: 10.1016/j.nbt.2009.06.042
11. Desiere F, Spica VR. Personalised Medicine in 2012: Editorial to the Special
Issue of New Biotechnology on ‘‘Molecular diagnostics & personalised medicine’’.
New Biotechnology. 2012 September; 29 (6) 611-612.
12. Sebastian Kaulitzki [image on the Internet]. http://office.microsoft.com/en-us/
images/results.aspx?qu=neuron&ex=2#ai:MC900438727| Royalty Free image.
13. David Hall [image on the Internet]. http://commons.wikimedia.org/wiki/
File:Dna-SNP.svg under CC-BY 2.0 license.
14. Gravitywave [image on the Internet]. http://www.flickr.com/photos/gravitywave/7715395/ under CC-BY 2.0 license.
THE TRIPLE HELIX Easter 2013 11
CAMBRIDGE
Chimeras in Research: How Far Should We Go?
Grace Petkovic
E
xperiments from Japan suggest that a new technique
could revolutionize organ transplantation donation.
However, it would also raise multiple scientific and
ethical concerns, as the organisms used would be humannonhuman chimeras. Chimeras are organisms made up of
cells or tissues derived from more than one fertilized egg.
In 2010, Professor Nakauchi, of the Center for Stem Cell
Biology and Regenerative Medicine, in Tokyo showed that
organs made up of the cells of one species can potentially
be grown in a different species [1]. These proof-of-principle
experiments (to show an idea is possibly workable) used
mice, which were genetically modified so that they could not
generate a sufficient pancreas. To try to generate a pancreas,
the team injected induced-pluripotent stem cells (iPSCs)
from rats (contra mice) into blastocysts (these contain cells
that go on to become the early embryos) of these mice. iPSCs
are formed by inducing differentiated cells into the stem
cell state [2]. The team found that these rat iPSCs seemed to
fill the “developmental niche” in the mice – making up the
majority of the pancreas. The resulting animals were rat-mice
chimeras. Unlike hybrids, in chimeras, the cells maintain
their distinct species identity. The team now hopes to use
this technique, which they term ‘blastocyst complementation’, to generate animals, which could act as human organ
donors. For example pigs could grow human pancreases.
Organs made up of the
cells of one species can
potentially be grown in a
different species .
Whilst chimeras have been used in research for decades
[3], this technique could effect their transition from laboratory to industry – one can envisage “organ-farms” growing
human-animal chimeras. This aim is still some way from
being achieved [4] – the greater size and developmental
differences between pigs and humans vs. rats and mice
could create experimental difficulties. Furthermore, immune
rejection could still be an issue as the supporting tissues (e.g.
Reproduced from [13].
12 THE TRIPLE HELIX Easter 2013
© 2013, The Triple Helix, Inc. All rights reserved.
CAMBRIDGE
blood vessels) would be pig, not human, in origin. Such a
move would also entail addressing the following questions:
1. Is the creation of humanoid chimeras ethically acceptable?
2. Should such chimeras be patentable?
3. Does the creation of humanoid chimeras raise any scientific concerns?
1. Is the creation of humanoid chimeras ethically acceptable?
There are two common ethical objections to the creation of humanoid chimeras, as discussed by Karpowicz,
Cohen and Van Der Kooy (Karpowicz and Van Der Kooy
are research biologists; Cohen is a bioethicist) in their article
on human-nonhuman chimeras [5]:
Moral taboos argument
This argument proposes that the repugnance felt by
some individuals to the idea of creating humanoid
chimeras is a justification that the very creation of
such organisms is morally wrong. However, many
would disagree that emotion can be regarded as
justification for ethical decisions; rather it is the
rationale behind the emotion that should be investigated. Furthermore, moral taboos are not always
universal (consider the example of polygamy[6]).
Thus, the fact that some view chimeras as a taboo
is not in itself reason to prevent their creation.
The moral taboo argument is often linked with
the “unnaturalness” argument. This is a way of
explaining the potential relevance of repugnance for
informing ethical decisions. The “unnaturalness”
argument essentially proposes that the natural state
of things is the “correct” state. Thus the creation
of humanoid chimeras, and the blurring of species
boundaries, would be viewed as an explanation of
why such chimeras should not be created. However,
the weakness of such an argument is evident when
one considers recent medical advances such as
xenotransplants and genetic engineering, which
are also “unnatural” (as is, arguably, most medical
intervention) but are not viewed, on the whole,
as morally questionable.
Human Dignity argument
The human dignity argument proposes that there
is something, needing protection, that differentiates humans from other species. It is often evoked
in debates about euthanasia and cloning but an
exact definition is missing. This lack of definition
is not in itself a refutation of the argument, but
does cause difficulties in interpretation. Human
dignity seems to be a combination of different factors including emotionally complex views of the
world, sophisticated language and more. Though
harder to define, the human dignity argument
appears more compelling than the moral taboo
argument so raises the question: does the creation
of humanoid chimeras denigrate human dignity?
To answer this, one must consider what human
© 2013, The Triple Helix, Inc. All rights reserved.
dignity should encompass. Those factors - language,
emotions, social structure - that contribute to human dignity seem to all involve the brain. Few
would argue that a human liver differentiates a
human being. Thus, perhaps humanoid chimeras
that do not involve the brain would not violate
this human dignity argument. However, neural
chimeras raise more interesting problems.
Would animals with human neurons have an
increased capacity for human thought or exhibit
more human-like qualities? One study on chicks
and quails showed that when regions of the quail
brain were excised and transplanted into chicks then
some of the chicks exhibited quail-like behavior
in their crowing vocalization [7]. However, this
experiment involved whole areas of the brain being
transplanted. This is very different from blastocyst complementation where the neurons would
instead develop fully in the host organism, not
the donor organism. The different developmental
environments in the two techniques are likely to
be significant, but more investigation is needed.
Reproduced from [14].
2. Should chimeras be patentable?
The development of such new technologies, and potentially of an industry, that could spring from the use of
humanoid chimeras poses the question of whether humanoid
chimeras could or should be patented [8]. In fact, the issue
has already begun to play out in the USA.
Humanoid chimeras may act
as a ground for trans-species
viral development.
In 1997, Stuart Newman and Jeremy Rifkin undertook to
file a patent application on embryos and full-term organisms
that were humanoid chimeras. Their aim was, surprisingly,
to prevent the creation of such organisms; either by enforcing a patent, were it issued, or by initiating a ban on patents
of human-nonhuman chimeras [9]. After various revisions,
the application was rejected in 2005.
Arguments against the patenting of humans in the USA
THE TRIPLE HELIX Easter 2013 13
CAMBRIDGE
are founded both on conflict with the 13th Amendment’s
prohibition of slavery and the constitutional right to privacy.
This right to privacy, in part, allows a person control over
when and where they procreate. A patent would allow the
holder to control the reproduction of their product; were
the product “human” then the “human product’s” right to
privacy and the right of a patent-holder to control product
reproduction would be at odds [10]. However, ultimately
these arguments only show why humans cannot be patented. They do not show where and whether a boundary
line between humans and other animals should be drawn.
Animals are frequently neutered or entered into breeding
programs, with little to no uproar that this is against their
rights. But when is an animal human enough to have these
rights? Almost nobody would argue that a man with a pig
heart transplant is no longer classified as human, and few
would argue that a pig with a human pancreas should be
classified as human – but what of the potentially murkier
scenarios e.g. a chimpanzee with human neurons?
At the moment, the U.S. patent office is having to decide
what it is to be human and the question has sizeable ramifications for the biotechnology industry. Without patents,
there is little incentive for biotech companies to develop
potentially life-saving technologies such as those proposed
by Prof. Nakauchi. However, as the old definitions of human
(a species with human cells/genes/46 chromosomes) become
outdated, science is waiting on society for a decision as to
how far it can go in pushing these barriers.
3. Scientific concerns?
The creation of such chimeras may also raise scientific concerns. This is suggested by studies on human-pig
chimeras generated by injecting fetal pigs with human T
cell-depleted bone marrow cells i.e. hematopoietic stem cells
[11]. These are multipotent cells that can differentiate into
different types of blood cell. The chimeric pigs were studied
6-12 months after birth. They were found to contain human
blood cells and pig blood cells, but also fused human-pig
cells i.e. hybrid cells. These hybrid cells made up 60% of
the non-porcine blood cells.
Possible scenarios such as chimpanzee with human neurons blur the increasingly murky definitions of being ‘human’. Images reproduced from [15] & [16].
14 THE TRIPLE HELIX Easter 2013
© 2013, The Triple Helix, Inc. All rights reserved.
CAMBRIDGE
Crucially, the hybrid cells contained Porcine Endogenous Retrovirus (PERV) DNA. In vitro studies showed
that these hybrid cells could infect human cells with the
virus. Whilst in vivo results may be different (PERV viruses
have previously been found to infect human cells in vitro
but then failed in vivo [12]) – it raises the possibility that
humanoid chimeras may act as a ground for trans-species
viral development. One might speculate that the risk of swine
flu etc. could increase. However, more work is needed on
this area to quantify such risks in vivo.
Thus, recent research on blastocyst complementation and
its potential applicability to humans highlights the need for
science and society to address the use of humanoid chimeras
in research. The biological definitions of humans and other
species are in flux and eventually these questions will need
to be answered in order to direct research.
Grace Petkovic is a third year student studying Natural
Sciences (Physiology, Development and Neuroscience) at St John’s
College.
Humanoid chimeras may act as a ground for trans-species viral development. One might speculate that the risk of swine flu (pictured above) etc. could increase.
Reproduced from [17].
References:
1. Koyayashi T, Yamaguchi T, Hamanaka S, Kato-Itoh M, Yamazaki Y, Ibata M,
et al. Generation of Rat Pancreas in Mouse by Interspecific Blastocyst Injection of
Pluripotent Stem Cells. Cell. 2010 Sep 3; 142 (5): 787-99
2. Takahashi K, Yamanaka S. Induction of Pluripotent Stem Cells from Mouse
Embryonic and Adult Fibroblast Cultures by Defined Factors. Cell. 2006 Aug 25;
126 (4): 663-76
3. Behringer RR. Human-Animal Chimeras in Biomedical Research. Cell Stem
Cell. 2007 Sep 13;1(3):259-62
4. Solter D. Viable Rat-Mouse Chimeras: Where Do We Go from Here? Cell. 2010
Sep 3; 142(5): 676-8.
5. Karpowicz P, Cohen CB, Van der Kooy D. Developing human-nonhuman
chimeras in human stem cell research: ethical issues and boundaries. Kennedy Inst
Ethics J. 2005 Jun;15(2):107-34
6. Barber N. Explaining Cross-National Differences in Polygyny Intensity
Resource-Defense, Sex Ratio, and Infectious Diseases. Cross-Cultural Research.
2008 May 1;42(2):103-17
7. Balaban E, Teillet M, Le Douarin N. Application of the quail-chick chimera
system to the study of brain development and behavior. Science. 1988 Sep
9;241(4871):1339-42.
8. Rabin S. The human use of humanoid beings: chimeras and patent law. Nature
Biotechnology. 2006;24(5):517-9.
© 2013, The Triple Helix, Inc. All rights reserved.
9. Newman, SA. My attempt to patent a human-animal chimera. L’Overvatoire de
la génétique/Centre de bioéthique, IRCM. 2002
10. Weiss, R. U.S. Denies patent for a too-human hybrid: Scientist sought legal
precedent to keep others from profiting from similar ‘inventions’. The Washington
Post 2005 Feb 13
11. Ogle BM, Butters KA, Plummer TB, Ring KR, Knudsen BE, Litzow MR, et al.
Spontaneous fusion of cells between species yields transdifferentiation and retroviral transfer in vivo. FASEB J [Internet]. 2004 Jan 8 [cited 2012 Dec 10]; Available
from: http://www.fasebj.org/content/early/2004/03/05/fj.03-0962fje
12. Denner J. Is Porcine Endogenous Retrovirus (PERV) Transmission Still Relevant? Transplantation Proceedings. 2008 Mar;40(2):587-9
13. Uwe Gille [image on the Internet]. http://commons.wikimedia.org/wiki/
File:Intracardial-injection-rat.JPG under CC-BY 2.0 license.
14. Ryan Somma [image on the Internet]. http://www.flickr.com/photos/ideonexus/2481197228/ under CC-BY 2.0 license.
15. Belgianchocolate [image on the Internet]. http://www.flickr.com/photos/frankwouters/50824323/ under CC-BY 2.0 licence.
16. Microsoft Office Clipart. [image on the internet]. http://office.microsoft.com/
en-us/images/results.aspx?qu=brain&ex=1#ai:MC900055181| Royalty Free Image
17. C. S. Goldsmith and A. Balish, CDC [image on the internet]. http://commons.
wikimedia.org/wiki/File:B00526-Swine-flu.png under CC-BY 2.0 licence.
THE TRIPLE HELIX Easter 2013 15
BROWN
Medically Supervised Drug Injection Sites:
More Harm than Good?
Julia Romanski
W
hile the harms of illegal injection drug use are
universally recognized, no single strategy exists to
reduce or prevent drug abuse. Relatively recently,
a new drug policy paradigm has surfaced: that of harm
reduction, which seeks to mitigate the consequences of illicit
drug use. One example of a harm reduction mechanism is
a medically supervised drug injection site (MSDIS). In an
MSDIS, people inject drugs under the supervision of medical
staff who intervene in the case of an overdose. The goals of
MSDIS’s are to reach the target population, encourage the
use of treatment services, improve health while reducing
risky behaviors, reduce the incidence of infectious disease
such as HIV, reduce overdoses and overdose deaths, reduce disorder, and avoid an increase in crime [2]. The most
comprehensive studies on MSDIS’s have been on the sites
in Sydney, Australia and Vancouver, Canada, which both
opened in the early 2000s. In order for these pilot sites to
retain their legal exemptions from drug laws, they must
show that they are achieving the objectives. However, there
is overwhelming evidence that many of these aims have not
conclusively been met. Moreover, evidence suggests that
MSIDS’s have a negative impact on public safety and the
health of drug users.
the heroin drought [3].
Furthermore, in Sydney, there were more police officers
deployed to the area around the MSDIS when it opened,
leading to a dispersion of drug users into neighboring areas
and therefore an artificial decrease in discarded needles [3].
Data for ambulance callouts clearly shows this displacement
effect. In the state of New South Wales, where the King’s Cross
MSDIS is located, there was a 61% reduction in ambulance
callouts for heroin overdoses from 2000 to 2007, with an 81%
reduction in the King’s Cross area [3]. However, only a 45%
reduction was seen in neighboring Darlington and Surrey
Hills, indicating possible displacement [3]. An evaluation
by the NSW Bureau of Crime Statistics and Research also
showed that percentage reductions in crime rates in King’s
Cross, where the injection center is located, were on par
with the rest of Sydney under heroin drought conditions
[3]. However, greater reductions would be expected if one
takes into account the increase in policing [3]. These medically supervised drug injection facilities may not be fulfilling
the goals of decreasing public drug use and its associated
crimes, and may actually be exacerbating these problems
since decreases in public drug use and crime were lower
than expected [3].
The data would have
had to show that drug
use rates fell below the
declining baseline in
order to conclude that the
MSDIS reduced public
drug use.
Impacts on Individual Drug Users
While supporters of medically supervised drug injection
sites believe that MSDIS’s provide a safe environment for
Impacts on Public Safety
Several evaluations of MSDIS’s after the year 2000 have
claimed that these sites contribute to decreases in public
drug use, public disorder, and crime, but they failed to mention two key confounding factors possibly responsible for
these decreases: the heroin drought that began in 2000 and
increased policing around drug injection facilities [3]. For
example, in Australia, the heroin drought reduced heroinrelated deaths by 60% to 70% from 2000 to 2010 due to a
significantly lower supply [3]. Therefore, the data would
have had to show that drug use rates fell below the declining baseline in order to conclude that the MSDIS reduced
public drug use [5]. In the 2007 evaluation of the King’s Cross
MSDIS in Sydney, KPMG, a consulting firm, claimed that
the drug injection site had contributed to the 48% reduction
in discarded needles (a measure of public drug use) from
2000 to 2007, a reduction that could also be attributed to
16 THE TRIPLE HELIX Easter 2013
Reproduced from [15].
© 2013, The Triple Helix, Inc. All rights reserved.
BROWN
drug users to inject, this is not being taken advantage of by
the vast majority of drug users [3]. At the Sydney facility
the 7% of clients who attended the facility most regularly
injected outside the MSDIS 80% of the time [3]. The next
26% of more frequent attendees injected outside the MSDIS
95% of the time [3]. Together, these groups were responsible
for 92% of injections in the center, leaving few injections for
the remaining 67% of the clientele [3]. This indicates that a
significant number of injections still happened outside the
MSDIS. While some policy makers and members of communities where drug use is high advocate opening more
injection sites, existing ones, such as the Sydney MSDIS, see
usage significantly below full capacity [3].
Based on the number of injections in the Sydney MSDIS,
the effective number of lives
saved by the facility would
amount to only four in nine
years of operation.
Although the purpose of MSDIS’s is to decrease the
problems associated with injection drug use, these sites may
be doing more harm than good. What is most troubling is
evidence that the proximity of medical staff may promote
risk-taking behavior among drug users. For example, the
Sydney MSDIS sees a 32-fold higher rate of drug overdose
inside the facility than outside [3, 4]. Although the KPMG
evaluation attributed the higher overdose rate to the clientele
being high-risk [6], Drug Free Australia’s analysis of the
Sydney MSDIS data controlled for this confounding factor
by comparing the clients’ overdose history with overdose
rates inside the facility. Further, an evaluation by SAHA,
an advisory firm, incorrectly used the non-fatal overdose
rates inside the facility to calculate the number of lives saved
without correcting for the fact that overdose rates were so
high inside the facility [3, 7]. Instead, it concluded the lives
saved by the Sydney MSDIS to be 25 per year [3, 7]. A more
accurate way of estimating the number of lives saved is by
using known facts about drug users: 100 heroin users inject
100,000 times per year on average and the mortality rate
for heroin users is 2% per year [3, 4]. Based on the number
of injections in the Sydney MSDIS, the effective number of
lives saved by the facility would amount to only four in nine
years of operation [3, 4]. Similar rates of lives saved were
calculated for Insite, the MSDIS in Vancouver, Canada [5].
This implies that MSDIS’s may not be saving as many lives
as some people believe they are.
Reproduced from [16].
© 2013, The Triple Helix, Inc. All rights reserved.
THE TRIPLE HELIX Easter 2013 17
BROWN
Reproduced from [17].
How Drug Policies Have Been Shaped by Possibly False
Assertions
The statements and findings in science and the media are
very influential in garnering public support for MSDIS’s as
well as shaping drug policies, despite the possibility that
MSIDS’s do more harm than good [1]. One year after the
Sydney MSDIS was opened, its medical director misinformed
the public by telling the media that the facility had saved
more than a hundred lives [6]. In a study from the major
scientific journal The Lancet, the researchers claimed that
Insite, which opened in 2003, was responsible for the decrease in overdose deaths [5, 8]. However, they included
2001, a peak year in drug overdose deaths, in the baseline [5,
8]. Between 2001 and 2002, drug overdose deaths dropped
precipitously and between 2002 and 2005 overdose deaths
actually increased in Vancouver [5]. By including 2001, a
peak year in drug overdose deaths, the cited decrease in
overdose deaths may not have been representative of the
upward trend that continued after the opening of the MSDIS
[5]. Another common claim regarding client health is that
MSDIS’s prevent HIV, but not all studies are in agreement.
Reliance on these possibly false assertions of lives saved,
either by averting fatal overdoses or reducing HIV prevalence,
can be seen in the reasons for judgment from the appeal to
the Supreme Court of Canada to keep Insite open following
the Minister of Health’s decision to close it:
“Insite saves lives. Its benefits have been proven.
There has been no discernable negative impact on
the public safety and health objectives of Canada
during its eight years of operation. The effect of
denying the services of Insite to the population it
serves is grossly disproportionate to any benefit that
18 THE TRIPLE HELIX Easter 2013
Canada might derive from presenting a uniform
stance on the possession of narcotics.” [9]
Perhaps harm reduction is not the best method for controlling the problem of injection drug use. In its 2001 report the
United Nations International Narcotic Control board stated:
“The operation of [supervised injection] facilities, where addicts inject themselves with illicit
substances, condones illicit drug use and drug
trafficking and runs counter to the provisions of
the international drug treaties” [4].
The effectiveness of harm reduction ought to be questioned.
Sweden used to have the highest level of drug use in Europe
but now it has the lowest level among OECD countries
thanks to a restrictive drug policy that focuses on prevention with a low emphasis on harm reduction [4]. In contrast,
Australia, which focuses on harm reduction, has the highest
rate of illicit drug use among OECD countries [4]. In 2000, a
three-year average of lifetime prevalence of drug use among
15-64 year olds in Sweden was found to be 12% while in
2004, the lifetime prevalence of cannabis alone was 33.6%
in Australia [11-12]. Why has harm reduction become the
dominant ideology in so many countries? Much of it has to
do with misinterpretation of data as discussed above. The
politicization of what ought to be a science-based issue has
caused individuals and policy-makers to overlook evidence
that medically supervised injection sites may not be the best
option for drug policy [1].
Some MSDIS supporters claim that MSDIS’s could be
restructured to fulfill their objectives. Arguably, more referrals
could be made, which would connect drug users to treatment. However, this is not a strong argument for opening
© 2013, The Triple Helix, Inc. All rights reserved.
BROWN
more MSIDS’s as there are many negative consequences,
such as the promotion of risk-taking behavior, associated
with these facilities. MSDIS’s by their very nature encourage,
condone and enable drug use [4, 6]. According to a former
Sydney MSDIS client:
Additionally, many drug users suffer from mental health
conditions that can be treated with medicine and behavioral
therapy. Treatment puts faith in the individual to stop using
drugs, rather than condoning and encouraging the use of
drugs like MSDIS’s do.
“[Drug users] feel a lot more safer (sic), definitely
because they know they can be brought back to
life straight away. […] So in a way they feel it is
a comfort zone, and no matter how much they
use, if they drop they will be brought back.” [6]
Treatment should also include
screening for diseases that
may be transmitted through
syringe sharing, such as HIV/
AIDS and hepatitis B and C,
which could provide a gateway to treatment and prevent
further transmission.
This risk-taking behavior consequently increases the profits
of local drug dealers [3, 4]. The whole idea of harm reduction is inherently wrong, because it is akin to placing an
invisible net under a bridge; such a net would save those
trying to commit suicide but it would not solve their underlying depression [13]. Similarly, MSDIS’s do not solve
the problem of drug injection, but rather promote drug use
as evidenced above.
Alternatives
The alternatives to harm reduction are prevention and treatment, in addition to tougher policing. One must consider
the idea of distributive justice: funds must be allocated in
a way to help the greatest number of people in the greatest
possible way. For example, the $2.5 million used each year
by the Sydney MSDIS could fund 109 drug rehabilitation
beds or 700 naltrexone implants for a year [4]. Naltrexone
blocks opioid receptors in the brain, leading to reduced
activation by opioids such as heroin [10]. It has been shown
to reduce the risk of relapse [10], and to boost the immune
system, which is weak in addicts with blood-borne illnesses
[3]. Treatment should also include screening for diseases
that may be transmitted through syringe sharing, such as
HIV/AIDS and hepatitis B and C, which could provide a
gateway to treatment and prevent further transmission [14].
References
1. Mangham C. A Critique of Canada’s INSITE Injection Site and its Parent
Philosophy: Implications and Recommendations for Policy Planning. The Journal
of Global Drug Policy and Practice [Internet]. 2010 [cited 2012 Oct 15]. Available
from: http://www.globaldrugpolicy.org/Issues/Vol%201%20Issue%202/A%20
critique%20of%20Canada’s%20INSITE.pdf
2. Davies G. A Critical Evaluation of the Effects of Safe Injection Facilities. The
Journal of Global Drug Policy and Practice [Internet]. 2007 [cited 2012 Oct 15].
Available from: http://www.globaldrugpolicy.org/Issues/Vol%201%20Issue%20
3/A%20Critical%20Evaluation.pdf
3. Drug Free Australia. Analysis of KPMG Evaluation of the Sydney Medically
Supervised Injection Centre [Internet]. 2010 Oct [cited 2012 Oct 15]. Available
from:
http://www.drugfree.org.au/fileadmin/library/Policies__Legislation_and_law/
DFA_Analysis_Injecting_Room_2010.pdf
4. Drug Free Australia. The Case for Closure [Internet]. 2003 [cited 2012 Oct
15]. Available from: http://www.drugfree.org.au/fileadmin/Media/Reference/
DFA_Injecting_Room_Booklet.pdf
5. Pike G, Santamaria J, Australia V, et al. Analysis of the 2011 Lancet study on
deaths from overdose in the vicinity of Vancouver’s Insite Supervised Injection
Facility. Drug Free Australia [Internet]. 2011 [cited 2012 Oct 15]. Available from:
http://www.drugfree.org.au/fileadmin/Media/Global/Lancet_2011_Insite_
Analysis.pdf
6. Christian G. Blinded by the Dominant Ideology. Quadrant Online [Internet].
2010 Nov [cited 2012 Oct 15]; 54 (11). Available from: http://www.quadrant.org.au/
magazine/issue/2010/11/blinded-by-the-dominant-ideology
7. KPMG. Further evaluation of the Medically Supervised Injecting Centre during
its extended Trial period (2007-2011) Final report [Internet]. 2010 Sep 14 [cited
2012 Oct 15]. Available from: http://www.health.nsw.gov.au/resources/mhdao/
pdf/msic_kpmg.pdf
8. Marshall B, Milloy M, Wood E, et al. Reduction in overdose mortality after
the opening of North America’s first medically supervised safer injecting
facility: a retrospective population-based study [Internet]. 2011 Apr [cited
2012 Oct 15]. Available from: http://www.sciencedirect.com/science/article/pii/
© 2013, The Triple Helix, Inc. All rights reserved.
Conclusion
The debate on MSDIS’s must be depoliticized to examine
the scientific evidence objectively. The merits of MSDIS’s
have been overstated and their flaws excluded in scientific
literature, the media, and political rationale, to the detriment
of injection drug users. The implementation of MSDIS’s is
not justified if one considers that they are not proven to
decrease crime, HIV rates, or overdose deaths, and may
actually exacerbate some of these outcomes. Administrators
and government officials should seriously consider the
termination of MSDIS’s and the reallocation of funds to
reliable prevention and treatment programs.
Julia Romanski is majoring in Biology at Brown University. She
first became interested in this topic when she participated in a
debate about whether or not large cities ought to have medically
supervised drug injection sites.
S0140673610623537
9. Canada (Attorney General) v. PHS Community Services Society. Supreme Court
of Canada [Internet]; 2011 Sept 30 [cited 2012 Oct 15]. [134] Available from: http://
scc.lexum.org/en/2011/2011scc44/2011scc44.html
10. SAMHSA. Division of Pharmacologic Therapies. Naltrexone [Internet]. 2012
[cited 2012 Oct 15] Available from: http://www.dpt.samhsa.gov/medications/
naltrexone.aspx
11. Lafrenière G. National Drug Policy: Sweden [Internet]. 2002 [cited 2012 Oct
15]. Parliament of Canada. Available from: http://www.parl.gc.ca/Content/SEN/
Committee/371/ille/library/gerald-e.htm
12. Ross J, editor. Illicit drug use in Australia: Epidemiology, use patterns and
associated harm. (2nd Edition). National Drug & Alcohol Research Centre
[Internet]. 2007 [cited 2012 Oct 15]. Available from:
http://www.nationaldrugstrategy.gov.au/internet/drugstrategy/publishing.nsf/Co
ntent/17B917608C1969ABCA257317001A72D4/$File/mono-63.pdf
13. Kay B. Insite clinic enables drug users and helps spread human misery.
National Post [Internet]. 2011 May 18 [cited 2012 Oct 15]. Available from: http://
fullcomment.nationalpost.com/2011/05/18/barbara-kay-insite-clinic-enables-drugusers-and-helps-spread-human-misery/
14. National Institute of Drug Abuse. DrugFacts: Treatment Approaches for
Drug Addiction. National Institutes of Health [Internet]. 2009 [cited 2012 Oct 15].
Available from: http://www.drugabuse.gov/publications/drugfacts/treatmentapproaches-drug-addiction
15. REPRODUCED WITH PERMISSION. Pike, G; Santamaria, J; Australia, V, et
al. Analysis of the 2011 Lancet study on deaths from overdose in the vicinity of
Vancouver’s Insite Supervised Injection Facility. Drug Free Australia. [Internet]
2011 [cited 2012 Oct 15]. Available from: http://www.drugfree.org.au/fileadmin/
Media/Global/Lancet_2011_Insite_Analysis.pdf
16. Dirty Bunny [image on the Internet]. http://www.flickr.com/photos/
angrybee/7380216/ under the CC-BY 2.0 license.
17. United States Drug Enforcement Administration. [Internet] [cited 2012 Dec 20].
Available from: http://www.justice.gov/dea/pr/multimedia-library/image-gallery/
heroin/heroin_powder.jpg
THE TRIPLE HELIX Easter 2013 19
UCSD
Veggie Delight
Rashmi Jain
A
bout 30 years ago, vegetarians in the U.S. were few
and far between, and the concept of vegetarianism
was widely seen as odd; many thought that a vegetarian diet was not really possible. Today, however, the
number of vegetarians is increasing rapidly. In 1994, the
percentage of the American population that was vegetarian was between 0.3 and 1%; in a 2012 poll, that number
has risen to 5% [6,9]. Although the number is still not a
staggeringly high proportion of the population, the fact is
that it is growing quickly. This is reflected in many facets
of modern society. For example, many fast food restaurants
now offer “veggie burgers” and different food companies
are creating new food products to cater specifically to the
vegetarian and vegan populations.
The annual health care costs
of meat consumption rival
the annual costs of treating
smoking-related illnesses.
Historically, vegetarianism began largely as a moral
aversion to the consumption of animals. Many have made
arguments for or against the consumption of meat with
justification from the Bible; people argued about God’s intent and whether or not He meant for man to eat meat. In
the 6th century B.C., Pythagoras (founder of the Pythagorean Theorem of mathematics), established a group that
refrained from eating meat for moral and spiritual reasons,
which related to the afterlife [8]. Many Eastern cultures
also embrace vegetarianism for religious reasons. Today,
people’s reasons for abstaining from meat vary greatly, from
religious to environmental, but there is also overwhelming
scientific evidence that giving up meat confers significant
health benefits.
It is true that a diet lacking in meat makes obtaining
certain necessary vitamins and minerals difficult. Vitamin
B12 and Vitamin D are two examples [11]. Vitamin D is
only naturally found in some foods, like fish, mushroom
and eggs. Thus, many vegetarians and vegans must rely on
fortified foods or vitamin supplements to get the Vitamin
D that they need [5].Vitamin B12, which is generally only
present in animal products, needs to be supplemented in the
diets of vegetarians and vegans as well [5]. People whose
diets do not include meat also sometimes lack adequate
zinc and iron because the zinc and iron in plant products
are more difficult for the body to absorb than those from
animal products. The iron found in animal products like
meat and fish is called heme iron, and that found in plant
foods like legumes, nuts and seeds is called nonheme iron.
The body does not absorb nonheme iron as well as it does
heme iron, but nutrients like Vitamin C help in absorption
of nonheme iron [5]. Finally, a vegetarian or vegan diet can
20 THE TRIPLE HELIX Easter 2013
make it difficult to obtain proteins, since animal and meat
products are rich in amino acids and proteins [11]. However,
despite these setbacks, when a vegetarian or vegan diet
is planned in a healthy and safe way, such that the body
receives sufficient amounts of all the nutrients and vitamins
that it needs, a meatless diet can actually have an extremely
positive and beneficial effect on the body.
Studies showed that glucose
sensitivity increases,
metabolism is improved,
and blood pressure is
lower in those that follow
meatless diets.
Additionally, numerous studies have linked meat consumption with adverse health effects. Societies that have high
meat consumption exhibit higher levels of cholesterol and
higher rates of heart disease than societies in which meat
consumption is lower. In one study published in the Journal
of American Medical Association, when meat was added
to the diet of vegetarians, their cholesterol levels increased
by 19% and their blood pressure increased by 3% [7]. High
cholesterol and blood pressure are associated with health
conditions like heart disease, diabetes, and obesity. One
report states that in the United States, the annual health care
costs of meat consumption rival the annual costs of treating
smoking-related illnesses [2]. All of these are relevant issues
in today’s society. High healthcare costs and the ubiquity
of illnesses like heart disease and diabetes are dominant
topics of concern in the developed world. It is possible that
reduced meat consumption may serve to alleviate, and at
least partially provide a solution to, these problems.
Doctors have been
promoting vegetarian diets
to their patients due to the
numerous benefits that
these diets have been shown
to confer.
Many studies show the positive effecvts of a diet vwithout meat. In one study, conducted on overweight women,
the results showed that those who followed a vegan diet
lost more weight than those who did not follow the diet.
Various parameters were tested, and in those who followed
the vegan diet, factors that contributed to the greater weight
loss included increased glucose tolerance, and increased
insulin sensitivity [1]. This means that glucose levels were
© 2013, The Triple Helix, Inc. All rights reserved.
UCSD
Reproduced from [12].
lower in those who followed the vegan diet; they responded
more to insulin, which basically lowers glucose levels by
causing cells to take up glucose from the blood. This suggests that physiologically, a vegan diet has an effect on
how the body responds to and deals with glucose; this has
significant implications for societies in which diabetes is a
major issue. Furthermore, the vegan diet may lead to more
weight loss because it has a higher thermic effect -this refers
to the amount of energy required to metabolize the food itself
[1]. In other words, a vegan or vegetarian diet may simply
keep the body healthier because metabolizing these foods
increases the body’s metabolic rate. Other studies showed
that people who follow vegetarian diets have lower blood
pressures, and that following a vegetarian diet can therefore
be beneficial for people with hypertension [4].
These types of studies have important implications.
They show how a diet without meat affects the physiology
of the body and how it changes the way the bodily processes
work. In this case, the studies showed that glucose sensitivity
increases, metabolism is improved, and blood pressure is
lower in those that follow meatless diets. Understanding
specifically how diets without meat affect body functions can
help to explain why these diets help alleviate the symptoms
of different kinds of diseases.
In a study conducted on people with rheumatoid arthritis,
one group was put on a vegan diet for the first few months,
and then was gradually converted to a lactovegetarian diet
(allowed to consume milk products). The other group ate an
ordinary diet (presumably with regular amounts of meat).
The group that was put on the diet in this study showed
significant improvements in the symptoms of rheumatoid
arthritis, and the improvements were present even after
one year. In the group with the regular diet, almost none
of the symptoms showed any significant improvement. A
possible explanation for these results is that in people who
switch to vegetarian diets, the composition of fatty acids in
the body changes. Fatty acids are involved in the formation
of molecules that facilitate the inflammatory response; in
people who switch to vegetarian diets, the changed fatty
acids may produce molecules with reduced inflammatory
activity, which results in less pain and arthritis symptoms
[3]. Many similar types of studies can attest to positive effects of a diet lacking in meat on diseases like diabetes,
heart disease, hypertension, obesity, and even cancer [10].
There is abundant literature that proves that a diet
without meat is significantly healthier than one that does
contain animal products, and this is a widely accepted fact in
the scientific community as well. Doctors have been promoting vegetarian diets to their patients due to the numerous
benefits that these diets have been shown to confer. Diets
without meat are beneficial in part because people who follow these types of diets have different physiologies in some
ways than those who do not. Various studies have shown
the effects of meatless diets on, among others, glucose levels,
blood pressure, and cholesterol levels. All of these are key
factors that are not in check in those who suffer from diabetes, heart disease, hypertension, etc. which are major health
problems in many countries in the world. Although it may
not be practical to suggest that everyone must completely
eradicate meat from their diet in order to remain healthy,
the benefits that meatless diets confer do seem to suggest
that it might be time to start at least limiting meat intake.
References
poll/156215/Consider-Themselves-Vegetarians.aspx
7. SCIENCE WATCH - Health Effects of Meat [Internet]. NYTimes.com; 1981
Aug 18 [cited 2012 Dec 23]. Available from: http://www.nytimes.com/1981/08/18/
science/science-watch-health-effects-of-meat.html
8. Shapin, S. Vegetable Love [Internet]. The New Yorker; 2007 Jan 27 [cited 2012
Dec 23]. Available from: http://www.fas.harvard.edu/~hsdept/bios/docs/shapin_
vegetable_love.pdf
9. Stahler, C. How Many Vegetarians Are There? [Internet]. The Vegetarian
Resource Group; 1994 [updated 2000 Aug 30; cited 2012 Dec 23]. Available from:
http://www.vrg.org/nutshell/poll.htm
10. Vegetarian Diets Can Help Prevent Chronic Diseases, American Dietetic
Association Says [Internet]. Science Daily; 2009 Jul 3 [cited 2012 Dec 23]. Available
from: http://www.sciencedaily.com/releases/2009/07/090701103002.htm
11. Vegetarianism Nutrition [Internet]. NYTimes.com; 2011 [cited 2012 Dec 23].
12. http://www.oregon.gov/DAS/PEBB/PublishingImages/newsletter/
wellnessarchive/fruit000004461830med30080320.jpg
1. Barnard ND, Scialli AR, Turner-McGrievy G, Lanou AJ, Glass J. The effects of a
low-fat, plant-based dietary intervention on body weight, metabolism, and insulin
sensitivity. Am J Med 2005 Sept; 118(9): 991-997.
2. Brody, J. Health Cost of Meat Diet is Billions, Study Says [Internet]. NYTimes.
com; 1995 Nov 21 [cited 2012 Dec 23]. Available from: http://www.nytimes.
com/1995/11/21/science/health-cost-of-meat-diet-is-billions-study-says.html
3. Kjeldsen-Kragh J, Haugen M, Borchgrevink CF, Laerum E, Eek M, Mowinkel
P, Hovi K, Forre, O. Controlled trial of fasting and one-year vegetarian diet in
rheumatoid arthritis. The Lancet 1991 Oct; 338(8772): 899-902.
4. Margetts BM, Beilin LJ, Armstrong BK, Vandongen R. Vegetarian diet in mild
hypertension: effects of fat and fiber. Am J Clin Nutr 1988 Sept 1; 48(3): 801-805.
5. Marsh K, Zeuschner C, Saunders A. Health Implications of a Vegetarian Diet: A
Review. American Journal of Lifestyle Medicine 2012 May/June; 6(3): 250-267.
6. Newport, F. In U.S., 5% Consider Themselves Vegetarians [Internet]. Gallup;
2012 Jul 26 [cited 2012 Dec 23]. Available from: http://www.gallup.com/
© 2013, The Triple Helix, Inc. All rights reserved.
Rashmi Jain is a 2nd-year student, majoring in Bioengineering, at
University of California, San Diego. She is interested in pursuing
a career in the health care field in the future.
THE TRIPLE HELIX Easter 2013 21
UCSD
Black Athletic Superiority:
Fact or Fiction?
Kaylin “Kai” Keerd Muskat
E
very Boston Marathon since 1990 has been won by a
Kenyan. Every man’s world record at every standard
track distance is held by an athlete of African descent
[1]. In the 2012 Racial and Gender Report Card, African
Americans made up 67% of players in the National Football
league and 78% of athletes in the National Basketball Association [2,3]. It seems logical, almost blatantly obvious,
to extrapolate that “black” athletes are genetically superior
to their “white” competitors. Not surprisingly, individuals
across the ethnic spectrum, including both African Americans and Caucasians, find it logical as well. Wasn’t genetic
evidence found confirming the legitimacy of the former
assertions? It seems so straightforward and natural, but
it’s simply wrong; a cultural invention.
African American dominance
in the athletic world is
not the result of inherent
“racial” superiority, but
the consequence of a more
complex commingling of
environmental, structural, and
ideological influences.
Ironically, the genetic superiority theory can be invalidated precisely because of its inherent illogicality due to its
reliance on the socially-constructed (not biological) notion
of race. The rationale behind the myth’s dissemination and
its verisimilitude is part of the pervasive re-circulation of
racial stereotypes throughout history. African American
dominance in specific sectors of the athletic world—track
and field, football, and basketball—is not the result of inherent “racial” superiority, but the cultural consequence of a
more complex commingling of environmental, structural,
and ideological influences [4]. Although many studies
attempting to corroborate the genetic superiority theory
claim to be socially objective and racially indifferent—even
asserting that proof of the genetic superiority theory is not
a stereotype of black hyperphysicality, but a celebration of
the strength and stalwartness of the black community—they
disavow how the maintenance of the racial myth systematically channels African American youth into athletics and
diverts their attention away from academic aspirations and
career-minded goals where they will statistically find more
success. In a society where images and representations
have real, material consequences, the genetic superiority theory assists in sustaining and perpetuating a covert
national structure based on racial segregation and somatic
exploitation.
22 THE TRIPLE HELIX Easter 2013
Biological Advantage, Not Racial Advantage
Race itself is not a biological, but a social construct and
therefore, attempts to assign genetic significance to murky,
arbitrarily defined racial categories is axiomatically incoherent. Some phenotypic characteristics, such as the flower
color of pea plants studied by famous geneticist Gregor
Mendel, are due to genes expressing themselves in an eitheror basis. In this type of inheritance pattern, the dominant
allele for purple flowers is singularly expressed regardless
of whether or not it is coupled with a recessive allele for
white flowers. Human skin color, however, cannot be used
to separate people into distinct biological categories. Skin
pigmentation is expressed in the human population across
a graded spectrum as a result of multiple alleles combining
to have a cumulative corollary on phenotype. Genetically,
traits determining skin color are indistinct so racial groups
themselves are a result of a dubious, indistinguishable
classification system [5]. As further proof of the biological
meaninglessness of the socially constructed notion of race,
the scientific community has overwhelmingly come to the
consensus that more genetic variation is present within the
so-called racial groups than across them [4]. Therefore,
right from the start, the genetic superiority theory is invalidated because it relies on an arbitrary, socially defined
system of racial categorization historically deployed by the
nation-state to perpetuate inequality based on the hierarchal
ranking of bodies [6].
Many contemporary studies upholding the genetic
superiority theory assert the existence of a genetic racial
predisposition to athletic greatness rather than a genetic
biological advantage entirely independent of race and contingent on environmental factors and the efficacy of training
regimes [4]. If one is endowed with a higher proportion of
oxidative muscle fibers—which use up oxygen slowly but
efficiently to generate energy in the form of ATP—their body
make-up is more conducive to endurance-based athletics
such as long-distance running or biking. In contrast, a
person with more glycolytic muscle fibers—which utilize
glycogen to generate ATP quickly, but rather inefficiently—
allow for fast, short bursts of contraction such as sprinting,
throwing, jumping, or punching [7]. Jon Entine’s “Taboo:
Why Black Athletes Dominate At Sports And Why We’re
Afraid To Talk About It” argues “functional differences”
in “physique, musculature, metabolic efficiency, hormone
levels and reaction time” differentiate between the so-called
racial groups. Entine is a senior research fellow at the Center
for Health and Risk Communication at George Mason University as well as founder and director of the university’s
Genetic Literacy Project. Entine’s research is typical of contemporary studies asserting the genetic superiority theory
in that purported anatomical, physiological, and statistical
idiosyncrasies are used to prove the existence of genetic
racial demarcations as opposed to simply confirming the
© 2013, The Triple Helix, Inc. All rights reserved.
UCSD
advantages of inheriting certain biological characters and
training in severe climates [1].
In addition, even if an individual possesses an opportune biological endowment, the efficacy of training regimes
and individual dedication are the ultimate determining
factors behind athletic success at the elite level. Entine
argues that while environment and training regimes play
an important role, an individual’s genetic endowment
supersedes the ability of climate and training in determining the competitive potential of division 1 and world-class
athletes. Entine refuses to ascribe the majority of the
Kenyans’ success in endurance running to the fact that
these athletes, the majority from the mountainous regions
of Eldoret, Kenya, are extremely dedicated and train vehemently at high-altitude. There seems to be an obsessive,
single-minded compulsion for Entine and proponents of
racial science in general to prove that “blacks” specifically
are genetically endowed with innate running, jumping, and
basketball-playing abilities. For instance, the Sherpas—an
ethnic group living at the base of the Himalayas in Nepal
with cultural and geographic ties to Indians, Mongolians,
and Pakistanis—often summit Everest multiple times per
year as guides and “pack” animals, a once-in-a-lifetime
accomplishment for the majority of hikers. In 2004, native
Pemba Dorjie scaled the 29,035 foot monolith in 12 hours
and 45 minutes, an incredible feat considering it takes the
average hiker months to ascend due to the need to acclimatize to changes in altitude at various base camps. Despite
having “amassed sports credentials at least as impressive as
the Kenyans,” no one ascribes the incredible athletic accomplishments of the Sherpas to their “Asian-ness” but rather
attributes their athletic propensity to living and training in
an extreme environment. As evidenced by the previous
example, if other racialized groups dominate in a particular
athletic sector, their success is immediately attributed to
climate, lifestyle, and work ethic without recourse to the
possibility of genetic racial affinity. Essentially, without
the context of slavery, Jim Crow segregation, and a system
relying on institutionalized racial hierarchy that still operates today, individuals categorized socially as “black”
would not be overwhelmingly targeted as possessing innate
racial abilities [4].
The Perniciousness of the Myth: Its Social Ramifications
for Black Student Athletes
The benevolent goal of sport as a team-building recreation
and promoter of active, healthy lifestyles becomes provisional when the misguided belief of genetic superiority
and idealistic, over-representations of money-laden African American superstar athletes in the media cause young
African Americans to disproportionately place intellectual
and cultural growth secondary to the pursuit of unlikely
aspirations of athletic fame, glory, and wealth. [8] In 2003,
a study by the Center of the Study for Athletics found that
44% of African American football players (in contrast to 20%
of non-African American football players) at 42 division
1 colleges expected to become professional athletes even
though the NFL recruits on average only 2.3% of collegiate
athletes. [4] Despite the improbability of being drafted by
professional leagues out of college, the genetic superiority
myth helps maintain the distorted perception specifically
© 2013, The Triple Helix, Inc. All rights reserved.
Reproduced from [12].
among African American youth that athletics has the highest
potentiality of prosperity and happiness.
Moreover, the university’s academic mission is often
supplanted by athletic commercialism. The legendary football coach from Alabama Paul “Bear” Bryant said publicly,
“I used to go along with the idea that (athletes) on scholarship were “student-athletes,” which is what the NCAA calls
them. Meaning a student first, an athlete second. We are
kidding ourselves, trying to make it more palatable to the
academicians. We don’t have to say that and we shouldn’t.
At the level we play, the boy is really an athlete first and a
student second.” [4] The Center for the Study of Race and
Equity in Education performed a four-year study of athletes
from schools that incorporate the ACC, Big East, Big 10, Big
12, Pac 12, and SEC. The results revealed that only 50.2%
of African-American athletes graduated in 6 years and
96.1% of schools graduated African-male student athletes
lower than the student-athlete population as a whole [9]. In
summation, many African Americans leave the university
without a degree and disenchanted; the only fruits of their
labor and reapings of their college experience are cynicism,
disappointment, and disillusionment.
Conclusion: Is Science Corrupt?
Throughout history, scientists asserting the existence of a
genetic athletic predisposition based on race were generally not incompetent racists with overtly discriminatory
agendas. Researchers who utilized comparative anatomy
in the 19th century weren’t unqualified bigots, but upstanding physicians, scientists, and sexologists of their time who
followed punctilious research methodologies to gather
and present their data. The problem was the studies were
invariably linked and dependent on dominant ideologies of
white supremacy and widely-accepted cultural stereotypes
of black mental inferiority and degeneracy. Eugenics appeared as a scientific discipline around the same time as
white social, political, and economic domination was being
challenged with the threat of miscegenation (interracial
marriage), immigration, and a black population seeking the
vote and political clout. Although the Civil War officially
ended slavery with the ratification of the 13th amendment
in 1865, the continued Jim Crow segregation and discrimination that characterized the lives of free African Americans
THE TRIPLE HELIX Easter 2013 23
UCSD
Reproduced from [13].
ated myths of the past stressing black hyperphysicality and
by association, black mental inferiority [4].
Science offered a natural,
genetically-based argument for
African American inferiority
that justified exploitation and
eased anxiety.
was a troublesome, socially precarious contradiction and
source of uneasiness for the privileged “white” elite who
assisted in their exploitation. Science offered a natural,
genetically-based argument for African American inferiority that justified exploitation and eased anxiety. Studies
resonated so well with dominant cultural presumptions and
productions about race that it was “virtually uncontested
from inside the mainstream of science.” [10]
Similarly, the recent increase in studies supporting
black athletic superiority is not an overtly racist assault
against the African American community, but rather is
suggestive of a more fundamental fear and subtle paranoia
about race still present in society. The recent economic
downturn combined with African American ascendancy in
the marketplace (as a result of affirmative action policies and
financial scholarships to universities) has increased racial
antagonisms across the U.S. and once again is causing the
country to target African Americans as scapegoats for its
economic woes. Not surprisingly, the sports world, one of
the few places African Americans have been able to find
success, has recently revived the same nervous, unsubstantiReferences
1. Holt J. Nobody Does It Better. The New York Times [Internet]. 2000 Apr 16:1
[cited 2012 Dec 26]; Available from: http://www.nytimes.com/books/00/04/16/
reviews/000416.16holtlt.html
2. Lapchick R. The 2012 Racial and Gender Report Card: National Football
League. Orlando (FL): Institute for Diversity and Ethics in Sport (University
of Central Florida); 2012 Sep 51p; Available from: http://dl.dropbox.
com/u/11322904/2012%20NFL%20RGRC.pdf
3. Lapchick R. The 2012 Racial and Gender Report Card: National Basketball
Association. Orlando (FL): Institute for Diversity and Ethics in Sport (University
of Central Florida); 2012 Jun 51p; Available from: http://web.bus.ucf.edu/
documents/sport/2012-NBA-RGRC.pdf
4. Earl S. Race, Sport, and the American Dream. Durham: Carolina Academic
Press; 2007.
5. Cain ML, Campbell NA, Jackson RB, Minorsky PV, Reece JB. Campbell
Biology. 9th Edition. San Francisco, CA: Pearson Benjamin-Cummings; 2010.
6. Murillo R. “Rethinking Race and Nation” in Black is a Country by Nikhil
Sing [unpublished lecture notes]. Ethnic Studies 1A: Intro Population Histories,
University of California San Diego. 2012 Nov 14.
7. Fortes G. Types of Skeletal Muscles: Fast and Slow, Glycolytic and Oxidative
24 THE TRIPLE HELIX Easter 2013
Using science as a means of confirming racial genetic
advantage is especially pernicious because of its ability to
naturalize structures of inequality. Racial genetic superiority becomes an indubitable, meticulously researched fact
and both whites and African Americans internalize this racism as truth and subsequently shape their self-perceptions,
decisions, and behaviors around it. In “Taboo,” Entine’s
concluding statement of the first chapter attempts to show
how black athletic superiority is a positive finding that
doesn’t seek to discriminate, but honor the small wonders
of diversity and unite humanity, “After all, in the end, for all
our differences, we are far, far more similar. That’s Taboo’s
only real message.” The claim is reflective of most modern
proponents’ views on the athletic superiority myth in its assertion of racial indifference and unintentional dependence
on subconscious racial bias that, as shown, can have deleterious effects. The statement has truth to it, but Entine’s logic
is inverted. Entine argues that although racial groups are
biologically distinct, we are socially on a level playing field.
However, the stark reality is that even though race doesn’t
exist biologically, race is a powerful social construction for
perpetuating inequality that continues, although subtly and
probably inadvertently, to discriminate and marginalize
people of color to the periphery [11].
Kai is a pre-medical student at UC San Diego considering a
major in Physiology and Neuroscience or ethnic studies. An
introductory Ethnic Studies class interested her in the function
of race in society and how the social construction continues to
structure and influence the nation. A desire to be informed and
be vocal of social and cultural injustice combined with an interest
in biology inspired her to dispel the mythology in athletics of black
athletic superiority.
[unpublished lecture notes]. Bild 2: Multicellular Life, University of California San
Diego. 2012 Nov 8.
8. Simiyu NW. Triple Tragedy of the Black Student Athlete. The Sport
Digest [Internet]. 2010 [cited 2012 Dec 20]; 17(3): 1-6. Available From: http://
thesportdigest.com/archive/article/triple-tragedy-black-student-athlete
9. Black Athletes’ Graduation Rates Weak, According to the University of
Pennsylvania Study. The Huffington Post [serial online]. 2012 Dec 3[cited 2012
Dec 20]. Available from: http://www.huffingtonpost.com/2012/12/04/penn-studiesafrican-american-graduation-rates_n_2236867.html
10. Somerville SB. Queering the Color Line: Race and the Invention of
Homosexuality in American Culture. Durham and London: Duke University
Press; 2000. P. 15-38.
11. Bogin B. Book Review: “Why Black Athletes Dominant at Sports and Why
We’re Afraid to Talk About It.” American Journal of Physical Anthropology
[Internet]. 2001 Feb [cited 2012 Dec 12]. Available From: http://www.jonentine.
com/reviews/American_Journal_Physical_Anthropology.htm
12. Bob Ramsak / piran café [image on the Internet]. http://www.flickr.com/
photos/brightblightcafe/2781335721/ under the CC-BY 2.0 license.
13. http://www.loc.gov/exhibits/odyssey/archive/08/0829001r.jpg
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