brock health issue 6

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Dear Reader,

It is my pleasure to pres-ent to you the sixth issue of Brock Health! Brock Health is a student run academic magazine that was started in 2009 with the purpose of presenting scholarly and personal interest articles on issues related to health, biomedical applications, public health issues and opportuni-ties within Brock University. Brock Health emphasizes peer-to-peer ed-ucation and presents students with articles that highlight the most cur-rent and pressing research within Brock University and society as a whole.

Health is a term often mis-understood as something that re-fers purely to physical wellness. However, health is very broad and multi-dimensional. From a holistic perspective, the term health also includes areas that identify mental, occupational, environmental and social categories. Each of these di-mensions works in synchronous to produce a balanced and self-aware individual. In this issue, Brock Health hopes to share with you a balanced representation of health as major issues in every facet of the term is highlighted by our writers.

Our featured article for this semester sees Breanne Kramer tackle the popular topic of aging as she explores the possible use of telomerase in order to preserve cell life. Articles communicating the ENCODE project, three parent em-bryos and fetal programming will address the effect of interventions

before birth as it relates to the im-pact of disease development later in life. Global and environmental health is also a topic of interest as Puneet Nayyar explores emerging viruses while Ryder Damen pro-vides a sobering piece refl ecting on Canadian health. Among other top-ics, mental and physical health as it relates to preventative care is all explored in this issue. Finally, I am very excited to present to you our faculty spotlight and master’s high-light this issue as both Dr. Tsiani and Hisham Sharif’s research and stories are explored respectively.

This publication could not have been created without the sup-port of the wonderful people in-volved. I would like to thank Brock Health’s managing editors, Saumik Biswas, Amen Idahosa and Yas-meen Mann for all their hard work! Further, I would also like to thank Brock Health’s layout and graphic guru Scott Alguire for his expert advice and quality job on the lay-out and cover page. Thank you to Dr. Neil McCartney, The Faculty of Applied Health Sciences, BUSU and BUSAC for funding our maga-zine! A special thank you goes out to all our graduate editors who were not only fl exible but also incredibly punctual. Also, I would like to thank Dr. Kelli-an Lawrance and Joanne Boucher for their continued support towards this publication! This is my fi rst issue as the Editor in Chief and I appreciate all those who have made this transition smooth and success-ful! A fi nal biggest thank you goes out to Yumna Ahmed, last year’s Editor in Chief who continues to be a valuable and powerful support to the Brock Health team!

Live long and prosper and I hope you all have a wonderful time reading this issue!

Editor-in-ChiefGaibrie Stephen

Managing EditorsSaumik BiswasAmen IdahosaYasmeen Mann

Layout DesignScott Alguire Gaibrie Stephen

Editorial BoardSharmeel BhattiSaumik BiswasFranco CardoneJoyce ChongRyder DamenAmen IdahosaBreanne KramerYasmeen MannNathaniel MannellaColin MaslinkAmanda MilburnPuneet NayyarNiya Patel

Graduate EditorsPhuc DangDavid DodingtonKaitlyn LaForgeJenna LorussoRebecca MacPhersonYasmeen Mezil Amber MuirBecky Roberts

Graphic DesignScott Alguire

Faculty ConsultantKelli-an Lawrance (PhD)

Editor’s NoteGaibrie Stephen

Brock Health Team

Disclaimer: Brock Health is a neutral magazine. It is not strictly hardcore sciences nor public health issues; it is a platform for students to present scholarly, peer reviewed research in any topic related to health.

2November 2012 - Issue 6

• Running the Risks

• The ENCODE Project: Giving A New Meaning to “Junk DNA”.

• Two Moms and One Dad: A Potential Cure to Mitochondrial Disease

• Memory Consolidation and Stress: Therapeutic Advancements for PTSD Victims?

• Faculty Spotlight- Dr Evangelia Litsa Tsiani

• Fetal Programming

• Featured Article: Want to Live for 1,000 Years?: The Long and Short on

Telomeres

• TheCrossfitSystem

• Oversleep: Too much of a good thing?

• Master’s Highlight: Hisham Sharif

• Out With the Old, In With the New – New & Emerging Viruses

• If Brock was the World

• Hot Headlines

• Brock Health Team

• References

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Contents

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To what extent is exercise bad for your health? It is not uncommon to hear about traumatic team sport in-juries such as broken bones, sprains, or concussions, which damage play-ers’ careers, but what about solitary exercise? The less informed are led to believe that running is dangerous to your health instead of benefi cial. It is true that while running, your limbs are impacting the ground at anywhere from one and a half to fi ve times your body weight1. This stress has been suggested to be detrimental to joints and limbs due to the repetitive nature of the exercise1.

Articular cartilage, located at joints such as the knee, provide a smooth layer between interacting bones, but is avascular, meaning it receives no blood fl ow and heals at a rate much slower than other connec-tive tissues2. A study published by the American Journal of Sports Medicine tested the relationship between mara-thon running and articular cartilage damage, and found evidence suggest-ing that articular cartilage is capable of recovering and retaining its functional traits after a marathon3. The results suggested that running instigates bio-

chemical changes, such as fl uid shifts within the cartilage matrix, though no signifi cant morphological changes or structural defects were found in the cartilage after running3. Long term ef-fects of marathon running may prove to be damaging to your health, but as with all behaviour, moderation is a key factor and anything can become unhealthy if pursued in excess.

There is a general misconcep-tion that running is an activity that wears down joints and puts a damag-ing amount of stress on bones. In fact, running and physical activity in gen-eral has been known to improve bone density by stimulating osteoblasts and promoting bone growth, which is a key factor in preventing brittle bones and osteoporosis2. A study revealed a correlation between early physi-cal activity and bone mineral content later in life, suggesting that practising a physical lifestyle from a young age can benefi t bone density in individu-als later in life4. The implications of such a study are important in the pre-vention of degenerative bone disease, or osteoporosis.

Finally, what does running do for you, as a student? The Journal of Adolescent Health published a study that found when students ran a mini-mum of thirty minutes every morning for three weeks, there was a signifi -cant improvement in both objective and subjective sleep patterns and psy-chological functioning5. This study was conducted on a group of fi fty-one students with a mean age of eighteen. Participants showed a reduction in daytime sleepiness as well as a reduc-tion in sleep loss, combined with a longer duration of sleep. An improved mood and even greater self-esteem were noted in comparison with the control group.

The role of physical activ-ity on stress management is already established, but the added benefi ts of a regulated sleep schedule and emo-tional well-being make running an ideal activity for stressed and sleep-less students. The ebenefi ts of running certainly outweigh the risks. Not only does it help increase bone density, but it will keep you fi t, feeling good, and help you out in stressful times. Can’t sleep? Too stressed? Why not go for a run?

Running the RisksJoyce Chong

Interested in joining the Brock Health team?

Contact us at: [email protected]


Almost a decade ago, the study of genetics saw a major break-through with the completion of the Human Genome Project, a lengthy study that determined the makeup of human DNA, in terms of nucleotide sequence, and identified and mapped all of the 20,000-25,0000 genes with-in it1. Now, nine years later, a new ma-jor study has delved even further into what makes us who we are.

The ENCODE Project, or En-cyclopedia of DNA Elements Project, is a decade-long endeavor that aimed to outline all functional elements within the human genome, not just genes. A functional element refers to

a segment of DNA that encodes a cer-tain product (such as a protein or non-coding RNA) or has some biochemi-cal function2. By identifying these elements, a much broader understand-ing of the human genome would exist, which could lead to advances in our understanding of human disease from a genetic standpoint.

What the ENCODE Project found was revolutionizing. One major initial conclusion was that 80.4% of the human genome is involved in at least one biochemical event in at least one cell type2. This refutes the com-monly held belief that the vast major-ity of human DNA is “junk DNA”, or evolutionary relics that are of no use to us anymore3.

From a human disease per-spective, the results of the ENCODE project are indispensable. It was found that single nucleotide polymorphisms (single nucleotides on the genome that vary between individual humans) that have been previously associated with diseases are mostly located with-in the non-coding functional elements described in the ENCODE project, outside of protein-coding genes2.

When ENCODE data is compared to GWAS analyses, the potential for significant advance-ments can be seen. GWAS analyses, or genome-wide association studies, examine the DNA of people with and without a specific disease in an at-tempt to find regions on the genome that influence the risk of acquiring the disease4. It has been found that 76% of variable non-coding DNA that are linked to diseases are located close to

a transcription start site, which may suggest that it is alterations to how protein-coding genes are switched on and off, rather than alterations to the genes themselves, that cause many diseases5.

In addition, it has been found that 88.1% of DNA regions with non-coding variations associated with diseases and traits are active in the early stages of fetal growth. Many of these variations are associated with diseases that occur later in life. As a result, ENCODE data suggests that what occurs within the genome before birth may have an impact on getting diseases later in life6. Further dis-coveries include the observation that mutations leading to certain diseases tend to occur in sections of DNA read by proteins that regulate processes of those diseases, and the finding that cell types playing a role in specific diseases can be identified without any prior knowledge of the disease6.

Overall, the ENCODE Proj-ect has allowed for a major advance-ment in knowledge and understanding of human disease from a genetic per-spective. Although there is still much work to be done, we are one step clos-er to being able to fully understand the structure, role, and function of the hu-man genome, and how genomic vari-ants can impact human disease.

The ENCODE Project: Giving a New Meaning to “Junk DNA”Colin Maslink

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3 Parent Embryos: A cure for Disease?Franco Cardone

Anyone who has taken high school biology within the past 10 years knows of mitochondria as the “power house” of a cell responsible for energy production1. Mitochondria were at one point believed to be a type of bacteria that formed a symbiotic relationship with other organisms. For this reason, mitochondria have their own DNA, known as mtDNA, separate from the nucleus, and only the mother of a child passes on this mtDNA2. Mutations can occur in the mtDNA and while a single mutation in mtDNA may cause no harmful ef-fects, the accumulation of mutations can be the difference between a nor-mal life, and possibly an early death. A Stanford University publication cited over 191 different diseases that researchers believe to be a direct ef-fect of a mutation in mtDNA3. Mi-tochondria are found in nearly every cell type in the body, therefore these diseases can affect almost every sys-tem of the body from the cardiovas-cular system to the central nervous

system causing psychiatric issues. A specifi c example of a mitochondrial disease is Kearns-Sayre disease. This is a neuromuscular disease that para-lyzes eye muscles, causes chronic in-fl ammation in the retina and can lead to cardiac electrical defects. Mothers who are affl icted by mitochondrial disease have to live with the fear that they may be sentencing their child to a lifelong disease or early death by giv-ing birth to them. A solution to pre-venting these diseases has been within the grasp of science for many years. There are a few suggested treatments for mitochondrial disease such as ger-minal vesicle transport, metaphase chromosome transfer or even exer-cise4. However, the one most talked about in the media, especially in the United Kingdom, is that of Pronuclear Transfer4.

Pronuclear transfer involves transferring the nucleus of a zygote into another healthy zygote, from which the nucleus has been removed.

The embryo contains the nuclear DNA from two parents, the intended mother and father, and the cytoplasm, containing the mitochondria and the mtDNA of the donor female. This makes a three-parent embryo that will develop healthy mitochondria5. Two scientists by the name of McGrath and Solter were the fi rst to perform Pronuclear Transfer on mice, back in 19835. This concept has been proven to work in human embryos in recent work by the Mitochondrial Research Group at Newcastle University’s In-stitute for Ageing and Health6. How-ever, this research has yet to show the long-term developmental effects of Pro Nuclear transfer, but the answers are only years away.

Some people are uncomfort-able with Pronuclear Transfer ac-cording to an article published by the BBC; many are worried that such modifi cation would open the door for the dreaded “designer baby”7. Others believe that migrating around what nature has planned, is out of the scope of our intervention as a scientifi cally conscious society. With alternative options for starting a family such as adoption or surrogacy, there is specu-lation as to whether debating Pronu-clear Transfer is even worth the time and money8. Mitochondrial disease will continue to be one of the rarely talked about issues affecting a wom-en’s ability to give birth to a healthy child. We have the scientifi c capabili-ties to put an end to this issue within the near future. Now that there is con-fi rmation of the easy scientifi c pro-cesses involved, the diffi cult task of convincing politicians, ethical groups, and the public must commence for this solution to end mitochondrial dis-ease.


Memory Consolidation and Stress: Therapeutic Advances for PTSD Victims?Niya Patel One of the most intriguing processes in neuroscience is the mys-tery behind the making of memory. A key pathway involved in memory consolidation is emotional arousal. An individual is likely to recall emo-tionally arousing episodes in their life compared to recalling informa-tion that has no personal relevance1. People suffering from Post-Traumatic Stress Disorder (PTSD) generally have difficulty forgetting painful ex-periences in their life due to an emo-tional association with the traumatic memory. It is important to note that PTSD patients form strong memories in times of increased stress levels2. So the main idea trickles down to the as-sociation between stress and memory consolidation.

In order to understand memo-ry consolidation, it is important to first understand how the brain functions under stressful conditions. It has been proposed that the interaction between the amygdala and stress hormones stimulate memory formation. More-over, during a stress response the sympathetic nervous system (SNS) is activated, which in turn activates the hypothalamic-pituitary-adrenal (HPA) axis where hormones are re-leased from the pituitary gland in the brain3. The emotional experience during a stressful response heightens the release of stress hormones, spe-cifically glucocorticoids, known as cortisol in humans from the adrenal gland. The activation of the amygdala plays a crucial role in increasing at-tention, perception, learning, as well as memory1. During a stress response, the sympathetic nervous system is

activated to increase epinephrine lev-els, which binds to adrenoreceptors, activating cAMP production. Gluco-corticoids are able to enter the brain and bind to its receptors facilitating further release of norepinephrine. The activation of the noradrenergic path-way is thought to result in memory consolidation in other brain regions, where information during the stress response can be stored as long-term memory 4.

Kuhlmann and Wolf con-ducted a study where memory con-solidation was measured in relation to elevated cortisol levels5. Twenty-nine male university students were tested over two consecutive days in a dou-ble-blind placebo design test. The ex-perimental group was given three cor-tisol pills, while the control group was given 3 three placebo pills. Partici-pants were shown 30 photographs, 10 of which were categorized as positive, 10 negative, and 10 netural. Immedi-ate recall was tested and participants were instructed to return in 24 hours, where a second set of pictures were shown. Saliva samples were collected to measure cortisol levels at different time points of memory consolidation. Results showed that both groups had better recall of emotionally stimulat-ing pictures (negative and positive pictures) in comparison to the neutral stimuli over delayed recall. An in-teraction between emotional stimuli, cortisol treatment, and consolidation was observed. This study was able to manipulate cortisol levels in order to demonstrate memory enhancement to emotionally arousing stimuli under elevated cortisol levels, concurrently

impairing delayed-recall of neutral stimuli5. The positive correlation and outcome of this study being reviewed can be attributed to the cortisol pills given to the participants, inducing a stress response.

It is clear that there is an underlying process present that con-solidates emotionally arousing infor-mation into long-term storage, which is further enhanced during a stress response. The increase in cortisol in-teracts with adrenergic pathways, es-sentially strengthening memory con-solidation. The interaction between stress, glucocorticoids, hormones, and emotional stimuli holds great promise for further developing therapeutic ad-vancements in treating PTSD patients as researchers attempt to unravel the underlying cause of this disorder1. It provides insight on how memories are physiologically consolidated, ul-timately furthering our knowledge in neuropsychology and human behav-iour.

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Dr Evangelia Litsa Tsiani is an associate professor in the Depart-ment of Community Health Sciences at Brock University. Dr. Tsiani has been a professor at Brock University for 12 years, and her current under-graduate courses include “Principles of Human Physiology” and “Human Endocrinology”. In the past she has also taught a graduate course on “Cell Signaling Pathways in Health and Disease”.

Dr. Tsiani was born and raised in a small town in Greece near Mount Olympus (the home of ancient Greek Gods). She completed her Bachelor of Science in Physical Education and Sport Sciences from Aristotle Univer-sity of Thessaloniki, Greece. During this time, she worked in an exercise physiology lab for an undergraduate thesis, which solidifi ed her desire to pursue knowledge through research. Upon graduation, she worked for one year as a physical education teacher in a secondary school in Thessaloniki, Greece while studying and prepar-ing for a National Scholarship Exam. Her hard work paid off and she was awarded a prestigious, national three-year scholarship to study abroad. She completed her Master’s of Science degree in the Department of Physiol-ogy, at University College in London, England. Dr. Tsiani then moved to Canada to pursue her doctoral studies in the Department of Physiology, at the University of Toronto. Her main research interest was to examine skel-etal muscle insulin resistance and she was very excited to study at the same institution where insulin was discovered. She also chose to study in Canada because of the pictures she had seen of snow and she imagined many skiing opportunities around the

University of Toronto!

After moving to the Brock community and experiencing wine country fi rst hand, Dr. Tsiani became infl uenced by wine and the polyphenol compound found in red wine, resvera-trol. Her current research is focused on understanding the health effects of polyphenols such as resveratrol as well as other compounds found in food, wine, and herbs. Using cells grown in culture dishes in the lab, she exam-ines the effects of these compounds at the cellular and molecular levels.

One line of her current re-search is focused on the understand-ing of muscle insulin resistance, which is the main characteristic of Type II Diabetes. Specifi cally, she is investigating how we can prevent and inhibit muscle insulin resistance by using natural food components. Her other area of research interest includes the understanding the mo-lecular signaling pathways that lead to cancer cell growth and survival, as well as fi nding strategies to stop the growth of cancer cells. Dr. Tsiani is currently collaborating with other sci-entists from the University of Toronto and McMaster University in terms of both of these projects.

Dr.Tsiani loves academia and enjoys the everyday challenge of gaining new knowledge. She believes in the ancient Greek «Γηράσκω αεί διδασκόμενος», translated as “I Al-ways Learn as I Age”.

When not working in her lab or her offi ce, Dr. Tsiani is busy tak-ing care of her three children and driving them to their many extracur-ricular activities. She is married to an

accomplished clinician/scientist who works at the Juravinski Cancer Centre and shares the same interest in under-standing molecular mechanisms and cell functions! She also loves cook-ing, skiing, playing tennis, and read-ing for pleasure by the fi replace with a good glass of (yes, you guessed it) red wine!

Her advice for students is to aim high and to not be intimidated to set ambitious goals in life. With hard work, dedication, and persistence, students can achieve their dreams. She tells her students that they may be surprised at their own strength and potential: “you are smarter and stron-ger than you think”!

Written by: Amen Idahosa

Dr. Evangelia Litsa Tsiani BSc, MSc, PhD

FACULTY SPOTLIGHT


Fetal Programming Amanda Milburn

One out of every two adults in the United States is overweight and on top of that, one in every five is obese9. In addition, over the last 20 years the obesity epidemic in children has become an even greater problem with a 40% increase in childhood obe-sity worldwide 5. That accounts for an estimated 42 million preschool chil-dren in developed and developing na-tions that are overweight or obese and 92 million at risk to be2. With obesity rates in children continuing to climb, experts have started looking at the impact of the health of the parents on the children. Fetal programming is a theory defined as the influence of ma-ternal nutrition during critical early life periods of the offspring on later life wellbeing and metabolism7. It has been found that being overweight in the infancy to childhood stages sig-nificantly increases the risk for being obese in adulthood which we all know is linked to numerous metabolic risks and diseases such as type II diabetes 5;9.

Adverse effects have been found in offspring of mothers on a high fat (HF) diet or who have been defined as obese. Most studies discovered that offspring from a HF fed mother, in animal and human models, did not have a higher birth weight3;6;8;11. How-ever, that did not necessarily remain to be the case as they grew older. Rat offspring from obese mothers fed a HF diet had a higher percent body fat as well as a higher initial body weight at weaning (when they come off of their mother’s milk) compared to the control group on a standard diet9;;11. Offspring from HF-fed rat mothers that were fed a HF diet post-weaning showed an even higher percentage of fat body composition than those on a standard diet9;11. The offspring of obese mothers who were maintained on a standard diet still had a greater percentage of adipose tissue at 130 days old than the offspring from lean mothers on the standard diet9. Eating a HF diet throughout life, during preg-nancy and lactation has similar effects on offspring to simply eating a HF

diet during pregnancy and lactation5. In both cases, the offspring show an increase in body fat and body weight although when fed a regular or HF diet themselves but the results are highest for the offspring from mothers fed a HF diet throughout their life, preg-nancy and lactation5. It is evident that eating healthy is essential not only for ourselves but also for the health of our future generations.

One explanation may be epigenetic modification in which the DNA sequence of the offspring stays the same but phenotypes are differentially expressed due to DNA methylation which changes gene ex-pression10;1. Epigenetic modification ideally makes upcoming generations more fit in their surroundings so they can evolve to live a long and healthy life12;4. However, epigenetics can also act in a harmful manner by passing on negative traits, therefore making the offspring less fit and more suscepti-bility to disease12;4. Susceptibility to obesity can be passed on not only by the mother but also through second generation fathers coming from obese mothers.



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As a child, one of the most thrilling things to talk about is what your going to do when you grow up. You make plans about all of the im-portant things your going to do, and everything you will achieve. Your perception is as though you will live forever. Unfortunately, there comes a time in your life when your body becomes weak and frail, your mind becomes lost, and illness may strike in shorter intervals than it used to. Aging is an ample issue in our so-ciety; in which many people are becoming obsessed with looking and feeling younger, even in their elderly years. Cosmetic surgery and weight loss programs are on the rise, however these techniques are only temporary fi xes to the unsolv-able problem that is age. However, modern science tells us that there is something more to aging, some-thing very small called a Telomere.

Telomeres can be compared

to the plastic tip on your shoelace 1. Our genes are located in the nucleus of the cell, on small double twisted strands called chromosomes.The function of the telomeres, which sit on the the end of every single chromosome are to protect our data, make cell division possible, and hold mysteries as to how we age and develop cancer. A telomere is just a simple sequence of DNA made up of the same bases used for classic DNA strands; the exact sequence is TTAGGG1. The connection be-tween aging and telomeres lies in this: every time a cell divides, the telomere becomes shorter. When a telomere becomes extremely short, the chromosome ends will fuse to-gether and degrade the cell’s genet-ic map causing the cell to become either cancerous or die2. In DNA replication, after the strand has been unwound and separated, a molecule called DNA polymerase begins to make new strands with the help of small RNA pieces1. The prolem is,

these pieces of RNA take up a tiny space on the end of each new chro-mosome, making it shorter than the previous one1. In human blood cells, the length of telomeres range from 8,000 base pairs at birth to 3,000 base pairs as people age and as low as 1,500 in elderly people1. Each time a cell divides, an aver-age person loses 30 to 200 base pairs from the ends of that cell’s telomeres 1. The only thing produced in the body that can lengthen telo-meres is the enzyme telomerase 1. This enzyme is prevalent in young people to ensure that telomeres are not wearing down too fast1. Unfor-tunately, as we age, telomerase is not produced any longer, therefore the telomeres become shorter and the cells age1. A geneticist by the name of Richard Cawthon discov-ered that people who live shorter lives are associated with having shorter telomeres1. Among people over the age of 60, those who were plagued by heart disease and infec-tious disease were coincidentally those with shorter telomeres. The big question of this decades science is can telomerase prevent cells from aging? Can we inject telomerase into normal cells to induce immor-tality? Scientists have been very successful in making human cells divide much past their lifespan in laboratory experiments 1.

Cawthon concluded that those who had the longer telomeres in his study were living approxi-mately fi ve years longer than those who had the shorter telomeres1. This could mean that if scientists were able to stop telomere shortening completely, it would add between 10-30 years to the human lifespan 1.

Want to Live for 1,000 Years?: The Long and Short on Telomeres Breanne Kramer


This improvement would raise men’s life expectancy to about 86-106 years, and women’s 92-112 years based the current life expec-tancies at this time. Looking at other factors besides telomere shortening, oxidative stress and disease also contribute to human aging. Looking retrospectively at this century, the lifespan of both males and females has continued to increase dramati-cally over the years, and this would suggest that it will continue to move in an upward fashion. If the lifespan can be extended due to telomerase activity, as well as the absence of other factors it is hypothesized by Cawthon that the human lifespan could eventually reach 1,000 years1.

It is interesting to study the factors affecting telomere length, particularly because some of them can be controlled by lifestyle choic-es. Dietary factors have been stud-ied and it has been concluded that fiber intake is positively associated with telomere length, specifically in women2. This would imply that if one wants to extend their lifespan by extending their telomere length, they should eat foods high in fiber

such as whole grain cereal, celery, nuts, and beans. Another nutrient that can be taken in is an anti ag-ing peptide called Carnosine3 . Car-nosine has antioxidant properties, along with properties that suppos-edly prevent telomere shortening3. This protein can be found in various meats, or can be taken as a pill sup-plement. These dietary options are a great chance to extend your lifes-pan in young adulthood. It has also been found that paternal age can af-fect an offsprings telomere length Although this is not something we can control, it is another way to de-termine lifespan. Children who are born from older fathers have lon-ger telomeres than those born from younger fathers The reason for this phenomenon is telomeres in sperm lengthen with age, therefore older sperm produce offspring with lon-ger telomeres4. In today’s society where everyone wants to remain young, having an older father is a great advantage.

Finally, telomeres play a major role in the development of cancer. As telomeres become very short, the cell approaches death,

however it has the option of escap-ing this fate by converting itself into a cancer cell4 . The enzyme telomer-ase will then be activated, and the cancer cell will live on. Research-ers have recognized the presence of shortened telomeres in pancreatic, bone, lung, prostate, bladder, and kidney cancers1. The measurement of telomerase may be a new way to detect cancer1. If scientists could figure out how to stop telomerase, it may be possible to fight cancer by making cancer cells age and die1 . It is clear that this field of research is a emerging and promising.

Our knowledge of telomeres is limited, and we have a long way to go before humans could live for 1,000 years. However, current re-search has opened up a new branch of thinking, and new possibilities for extending and improving human life. It seems as though one day we will achieve our dream of extended youth, and will live to see much more than we do today.

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TheCrossfitSystemSharmeel Bhatti

A new revolutionary ex-ercise regime is gathering attention from coast-to-coast; from world star athletes to your average out of shape neighbours and more—it’s the Cross-Fit system. Have you heard about it?

The success of the CrossFit system largely stems from the fact that it can be modifi ed to fuel the needs of any user-regardless of their sex, lifestyle and age1. Due to this in-herent malleability, it’s believed to be the most effi cient method of getting fi t1.

The CrossFit system uses a wide variety of exercises-that can be mixed and matched to provide an endless number of workouts. The sys-tem caters to both broad and targeted fi tness goals2. Key exercises like the overhead squats and the butterfl y pull-ups focus on maximizing the repeti-tion count while engaging your hips, legs, core, back, and shoulders-which provides a challenge to even the fi ttest individuals. It combines weight train-ing, endurance training and gymnas-tics to provide effi ciency in reaching any fi tness goals2.

According to CrossFit re-searcher, the 10 main fi tness domains in the body are targeted by promoting neurological and hormonal response 4. These domains include respira-tory and cardio endurance, Stamina, Strength, Coordination, Flexibility, Power, Speed, Agility, Balance, and Accuracy3. By constantly varying, high-intensity, multi-joint functional movements the neurons are forced to constantly be fi ring and releasing high levels of hormones to support the physical workload being placed on the body3.

In the CrossFit system, the speed and the amount of weight be-

ing moved in each exercise is empha-sized rather than the proper form of the exercise4. This allows equal parts of tension of the exercise to be placed on the entire body, thus resulting in a balanced physique 2. As a result of these unique workout movements the user is prone to increased injury haz-ards. This is especially the case with inexperienced individuals as they are highly susceptible to injury4. Con-versely, learn the fundamentals of the CrossFit exercises from the profes-sionals drastically reduce injuries6. Ultimately, the risk of injury with this type of workout is the same as any other workout where the participant chooses to disregard the instructions. However, the CrossFit concept has gathered a fair amount of critique due to injury rates5.

CrossFit training is avail-able in a variety of ways, including affi liated gyms and free online con-tent3. There are currently over 2000 CrossFit gyms located around the world and The CrossFit Inc company, is verifying new affi liated gyms ev-eryday6. The CrossFit system is also

utilized in various professional fi elds. Police offi cers, professional athletes, and martial artists-readily employ the CrossFit system within their regular training 6. These gruelling workouts train the human body to respond with the most effi ciency1.

The long term presence of the CrossFit movement was made prevalent in 2007 with the launch of the fi rst annual CrossFit Games1. This competition challenges CrossFit elites to determine the fi ttest individual each year. The winner is awarded a mon-etary reward for their achievements1. This competition is sponsored by Reebok, who have also begun to pro-duce CrossFit gear3.

The intensity, the atmosphere and the challenge that CrossFit of-fers has gathered its loyal users. The rush obtained from the workouts has become an addiction for many, and for others-a reason to get up and take action towards a better and active life-style.


Oversleep: Too much of a good thing?Nathaniel Mannella

Sacrificing sleep for school-work is something University and College students know all too well. Staying up until the wee hours of the morning, and, on occasion, missing an entire night’s sleep to study is a common occurrence around campus-es across the country1. Most people are familiar with the effects of lack of sleep: a change in mood, loss of concentration and a decreased ability to retain or learn new information2. Studies have shown that it is more beneficial to sleep the night before a big exam, than to stay up late study-ing3. Post-secondary education is more demanding than ever before, and the effects can physically be felt by the body. As a university student, a good night’s sleep is absolutely es-sential now more than previous points in our lives, to cope with the demands

of daily life. But is there such thing as too much sleep? Will your health and well being be negatively effected by oversleeping?

It is recommended that healthy adults get an average of 8 hours of sleep per night, with young adults needing slightly more, at 9 hours per night4. A good night’s sleep is essential to revitalize the mind, and allow the body to recover from daily stressors. It’s easy to think that increasing one’s hours of sleep per night would allow for more focus, and feeling better throughout the day. However, almost the exact opposite has been proven to be true. The more sleep you get the night before, the sleepier you feel throughout the day. Excess sleep has also been shown to produce headaches and back pain

and it can also throw off one’s dietary schedule. Sleeping in too long could cause you to miss breakfast, decreas-ing cognitive function, something that is extremely important in school5. These complications are far from the worst of it though; oversleeping has been found to increase risk of obesity by 21%, cardiac disease by 38%, and diabetes by a whopping 50%6. Scien-tists have not fully made connections between the increased risks of these diseases and sleeping excessively, though a correlation has been shown relating increased morbidity to prob-lem sleeping. Researchers do caution, however, that there is no concrete evi-dence in these conclusions, and more laboratory results are needed before full acceptance of the problems asso-ciated with oversleeping7.

Oversleeping can be caused by multiple different diseases, such as hypersomnia, depression, or sleep apnea8. Occasionally, and more com-monly among young adults, sleeping for extended hours can be caused by poor sleep habits, excessive alcohol and drug use, laziness, stress, and the misconception that the more sleep you get, the better you will feel in the morning. Here is a simple recom-mendation for students: set the alarm. Keep a regular sleeping pattern, do not take naps throughout the day, and have the motivation to get up and start your day; it will make you feel a lot better. Remember, sleeping in is doing almost as much harm as only sleeping a few hours each night. So wake up!

13

Hisham Sharif, a highly determined and opportunistic cur-rent PhD student here at Brock Uni-versity, has gone above and beyond in developing his own pathway for success. As an undergraduate stu-dent of McMaster University in the Kinesiology Department, Hisham turned his focus to spinal cord in-jury research. He also completed his Masters Degree in Health Sci-ence Kinesiology for two years. Hisham has brilliantly managed to create a pathway that involves the application of his research and the ability to help individuals ev-ery day through rehabilitation.

Prior to his undergraduate studies, Hisham held a strong inter-est in biological sciences and was an active member in sports. He then di-rected himself towards kinesiology where he was introduced to the idea of combining rehabilitation with sci-entifi c research. Currently, Hisham works in the Spinal Cord Injury Lab here at Brock University. He is also a PhD candidate under the supervision of David Ditor, who runs the Spinal Cord Injury Lab. Upon completion of his PhD, Hisham’s goal is to work in an area that involves neuropro-tection and regeneration, aiming to repair damaged neuro cells. When asked for advice to give others enter-ing the study of rehabilitation, Hish-am suggested that when individuals enter this fi eld their main goal is to help others. However, along the way their path may become disor-ganized and diffi cult at times, which is why it is easy to begin focusing on methods rather than tasks. This implies that you do not forget the reason why you have entered this fi eld of rehabilitation, despite the workload that it may bring along.

“Focus more on research rather than purpose” Hisham cleverly stated. By this Hisham further explains that, when in this fi eld, allow yourself to continue to fi nd new discoveries that may benefi t mankind rather than fulfi lling a certain purpose. Hish-am concludes, “This is what will keep you motivated through it all”.

Still managing a healthy life-style, Hisham participates in boxing recreationally and beach volleyball throughout the summer. He enters his job everyday with a strong sense of motivation as he feels that he can have a positive impact on the lives of others daily. He describes a sense of incredible gratifi cation from helping people in the lab everyday. Hisham also mentioned that with his re-search, he is building more knowl-edge to help benefi t others in fu-ture years, forming a platform for long-term health benefi ts.

Written by: Yasmeen Mann



Master’s HighlightHisham Sharif

BA, MSc


Our world is dynamic and ever-changing, and we as humans are inclined to instinctively strive for perfection in everything that we do, and in doing so we become much more efficient at our tasks. Just like humans, viruses and diseases evolve over time to become more efficient, and ultimately much more difficult to detect1. The battle to permanently eradicate viruses is a long one, which ultimately may never see an end. Most people, at some point in their life, have experienced some kind of virus or disease, from some-thing as simple as the common cold to something more serious like ma-laria. These nuisances have been around since the dawn of civiliza-tion itself, and each time we try to destroy them, they return with a ven-geance, often having built immuni-ties to newly developed medicines2. Researches at Michigan State Uni-versity (MSU) conducted several experiments on different types of vi-ruses, and concluded they are always evolving: as the viruses encounter new medicines and challenges, they build immunities against previously

successful treatments3. It would fol-low that if viruses are constantly evolving, why are we working so hard to fight them? The reason for this is so we don’t become over-whelmed with a plethora of viruses and diseases. In fighting the viruses, we reduce the number of risk fac-tors we face, as opposed to fighting each and every one of them. As vi-ruses constantly adapt, we too must find new ways of combating them lest we are overtaken completely. A famous example of a new-ly emergent virus is the H1N1 Influ-enza Virus, better known as “swine flu”, which was responsible for in-ducing mass hysteria all around the world when news of a new, evolved strain broke in 2009. Although the influenza strain has been known for a long time (the influenza virus was responsible for the early 20th-century Spanish Flu pandemic), the H1N1strain is entirely different. As the colloquial name suggests, the typical influenza virus mutated into a composite strain of human, avian and swine genetic elements4, not only making it harder to detect, but

also tougher to treat for. One of the biggest challenges when faced with emerging viruses is finding the right cure swiftly. In the case of the 2009 H1N1 outbreak, the first vaccines were not distributed until October of that year; some eight months5 after the initial cases of the virus were re-ported. The challenge in synthesiz-ing an effective treatment against new viruses adds to the length of time before vaccines can be administered since the emergent virus is new, and new treatment must be discovered. Although viruses and diseases will continue to adapt to the changing world, there are measures for po-tentially limiting the risk factors. Studies suggest immuni-ties build naturally when a specific type of virus or disease is first en-countered. While it’s not usually recommended to go and contract as many viruses as you can for the best chance of immunizing yourself, there are many other ways to protect oneself against new and emerging viruses, the obvious example being to just stay hygienic! Poor hygiene is an invitation for diseases and virus-es to come and wreak havoc on our health. Using anti-bacterial soaps every time you use the bathroom is a sure way to eliminate bad pathogens. As the world changes, so too do the pathogens that litter it. While much great advancement in science and medicine are made daily, we are only human, and thus vulnerable still to a plethora of natural viruses and diseases. Will it ever be possible to eradicate the mean, ugly bad germs forever? Perhaps, but until that time we must try our best to stay clean, and most importantly, stay informed of emerging threats.

Out With the Old, In With the New - New & Emerging VirusesPuneet Nayyar

15

Living on campus in your fi rst year, it is easy to think that the world beyond the escarpment doesn’t exist – with the exception of the Pen Centre of course. In the spirit of that wonder-ful callowness, let us assume for 5 minutes that Brock University is the world and all its inhabitants, countries, and groups of people are equally rep-resented among our 18,000 students.

First off, Canadians in this world can be represented by the Neu-roscience students at Brock – there are about 90 of them1,2. Twenty-one of these Canadians are considered obese3. Nevertheless, these Canadians enjoy a long life expectancy of 80.8 years4, in comparison to the 61 fi rst-year nursing students from Mozam-bique who face a signifi cantly shorter life expectancy of 49.7 years4,5.

If you’re a student from the Faculty of Mathematics and Sci-ence, you live in Europe or Central Asia; we have 58 doctors to serve the approximate 1100 of you1,6. On the other hand, if you’re one of ap-

proximately 3000 students in the Faculty of Applied Health Sci-ences, you live in Sub-Saharan Af-rica; we have 3 doctors for you1,6.

The most common causes of death are heart disease (18 students per year), stroke (15 students per year), and lower respiratory tract infections (9 students per year)7. Twenty stu-dents are children under fi ve that have died this year, all of them being from low to middle income country. In a high-income country, one child of the same age group dies every fi ve years.

Infectious diseases run ram-pant in this student population. From a viral standpoint, 86 students are infected and living with HIV; four will die each year from it, seven more will become infected, one of those seven will be a child9. Looking at bacterial infections, an estimated 1,032 students are infected with Ma-laria, 825 of them are children from Africa – twice the population of fi rst year CHSC 1F90 students1,10. One of the most well known diseases will only affect 31 students; they will be

diagnosed with some form of can-cer11. In addition, 312 students will be diagnosed with depression12.

Perhaps the most shocking sta-tistics occur when you take a look at the basic health requirements. All 2,600 students with in the Faculty of Busi-ness have inadequate access to water1,

13. Add to them every single student in Applied Linguistics, Canadian Stud-ies, Classics, Dramatic Arts, English, History, Liberal Arts, French, Music, Philosophy, and Visual Arts, and you still have not reached the number of students that lack basic sanitation1,

13. Finally, the number of students in Kinesiology, Health Sciences, and Recreation and Leisure combined ap-proaches the number of people with-out access to health care systems1,8.

When applied to the Brock population, it is easy to see that there is a large population of people in the world who do not fi t the defi nition of health. When looking at groups of stu-dents in this article – large or small – it is important to remember that these diseases affect far more than a hand-ful of people; multiply each statistic in this article a little over 387,000 times, and you will begin to approach the real world prevalence rates.

Though we are not free and safe from disease, we have the oppor-tunity to study in a country free from water accessibility and sanitation is-sues, general poverty, and rampant, uncontrolled infectious diseases. As recipients of this luxury, it under-scores our responsibility to make a difference in world health care for those who do not have the opportunity to make a difference themselves.

If Brock was the WorldRyder Damen


HOT HEADLINES

Exercise may protect against brain shrinkage.

Article by: Anahad O’connor

Summarized by: Gaibrie Stephen

In a news report published in

the Journal of Neurology, a team at the University of Edinburgh followed a sample population of 600 individuals starting at

the age of 70. The participants provided information regard-

ing physical, mental and social activities that they engaged in throughout the day for a length

of 3 years. At the end of the period of time, using imaging

scans, scientists determined that the subjects who engaged in the most physical exercise had less

shrinkage and damage in the brain’s white matter. The white matter of the brain is associated with being the “wiring system” that coordinates communication between different regions of the

brain. This relationship was sustained even after scientists controlled for IQ, social class

and health status. The study only shows an association between

brain shrinkage and lack of physical activity so it is not pos-sible for researchers to rule out that people with less deteriora-tion in the brains were simply more likely to be physically

active.

Follow us on Twitter!

@BrockUHealth

Link Found Between Alzheim-er’s disease and Protein Regula-tion in the Brain- Hope for New

Treatments

Article by: Kobi Rosenblum,

Summarized by:Saumik Biswas

A new study was conducted to identify important factors that could be linked to Alzheimer’s

disease even before the irre-versible amyloid plaques are produced. The current study

compared mice that exhibited the human Apoe4 gene - a gene known as a main risk factor for Alzheimer’s- with a group of mice with the parallel Apoe3 gene, which does not form a

risk factor for the disease. Mice in the former group showed a

change in the regulating mecha-nism for protein generation

involving the eIF2alpha protein that damaged the cognitive abili-ties of those mice at a young age. This type of mechanism change is characteristic of aging, and so also hinted at the tendency

of these mice toward premature aging. This is the first time that a link has been found between the activity of eIF2alpha and the Apoe4 gene in relation to

Alzheimer’s disease. Modifica-tion treatments for the eIF2alpha

mechanism are being widely researched and are developing

quickly, and so the more we can understand about the connection

between this mechanism and Alzheimer’s, the more we can find ways to identify and slow

the progress of the disease.

Artery Damage, One Fatty Meal

At a Time

Article by: Avis Favaro

Summarized by: Yasmeen Mann

According to two Canadian

studies, a single junk meal has the potential to damage arter-

ies inside the human body. The participants of this upcoming research were required to eat

two meals. The first was salmon based, consisting mainly of

monounsaturated and polyun-saturated fats. A week later the second meal was given, com-posed of food similar to that

served in a fast-food breakfast, with mainly saturated fat and no Omega-3 fats. Research found that the arteries of participants dilated 24% less after the junk food meal and dilated normally after the healthy, salmon based meal. Another study found that the arteries’ ability to increase

blood flow under stress for students that ate a 900-calorie sandwich, was lowered by 15-

20%. This effect may be noticed after a sandwich from a fast food location as well.These findings advise that the food we eat at

home can significantly contrib-ute to our weight change and

cardiovascular health, meal by meal. Perhaps individuals can approach healthier substitutes.

Scott Alguire

THE TEAM

Puneet Nayyar

Sharmeel Bhatti Saumik Biswas

References

Nathaniel Mannella

Breanne KramerYasmeen Mann

Ryder Damen

Amen Idahosa

Niya Patel Colin Maslink Franco Cardone

Amanda Milburn Joyce Chong

Running the Risks

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Podiatric Medical Association, 98(1), 36-47.

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ENCONE Project: Giving a New Meaning to “Junk DNA”

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3 Parent Embryos: Potential Cure for Disease?

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Memory Consolidation and Stress: Therapeutic Advancements for PTSD Victims?

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Fetal Programming

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postnatal diet. J Physiol, 905-915.

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maternal obesity on insulin sensitivity and secretion in offspring. Diabetes Care, 15 (9), 1872-1876.

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Physiol Regul Integr Comp Physiol, 294, 528-538.

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11. White, C., Purpera, M., & Morrison C. (2009). Maternal obesity is necessary for programming effect of high-fat diet on offspring. Am J

Physiol Regul Integr Comp Physiol, 296, 1464-1472.

12. Wu, Q., & Suzuki, M. (2006). Parental obesity and overweight affect the body-fat accumulation in the offspring: the possible effects of a

high-fat diet through epigenetic inheritance. Obesity reviews, 7, 201-208.

Want to Live for a 1000 Years?: The Long and Short on Telomeres

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telomeres

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Nutrition (1273-1280)

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sciencedirect.com/science/article

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doi/10.111

The CrossFit System

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CrossFit-Think-Inside-The-Box

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Understanding_CF.pdf

3.Mitchell, B. (2008, August 16). Lawsit alleges crossfit workout damaging. Retrieved from www.marinecorpstimes.com/news/2008/08/

marine_crossfit_081608w/

3. Stewart, A. (2012, August 31). Is crossfit friend or fad?. Retrieved from http://www.bodybuilding.com/fun/crossfit-friend-or-fad.htm

4. Stoddard, G. (2011, October 11). Inside the cult of crossfit. Retrieved from http://www.menshealth.com/fitness/cult-crossfit

5. The editors of PureHealthMD (June 2010).CrossFit. Discovery Health Channel. Retrieved from http://health.howstuffworks.com/wellness/

diet-fitness/information/crossfit.htm

Oversleeping: Too much of a good thing?

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Health, 50(3),131-135.

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consequences

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Child Development. doi: 10.111/j.1467-8624.2012.01834.x

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magazine/article/0,9171,1147196,00.html

5. Simeon, J. T., & Grantham-McGregor, S. (1989). Effects of missing breakfast on the cognitive functions of school children of differing

nutritional status. The American Journal for Clinical Nutrition, 49, 646-653.

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com/2100-500368_162-4521622.html

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how-sleep-works/how-much-sleep-do-we-really-need

8. Ireland, J. T. (2011, March 28). Causes of oversleeping. Livestrong Foundation, Retrieved from http://www.livestrong.com/

article/127972-causes-oversleeping/

Out With the Old, In With The New

1. Burke DS. Recombination in HIV: An Important Viral Evolutionary Strategy. Emerg Infect Dis [http://wwwnc.cdc.gov/eid/

article/3/3/97-0301_article.htm]. 1997, Sep [2012].

2. Gary, J. (2007, December). Understanding evolution. Retrieved from http://evolution.berkeley.edu/evolibrary/news/071201_adenovirus

Meyer,J. (2012, January). “How Viruses Evolve”. Retrieved from http://news.msu.edu/story/10262/#

3.World Health Organization. Retrieved from http://www.who.int/topics/emerging_diseases/en/ [Retrieved Oct. 2012]

4.BodyAndHealth Canada (2011). Retrieved from http://bodyandhealth.canada.com/channel_condition_info_details.asp?channel_

id=2098&relation_id=74074&disease_id=350&page_no=1

5. Jacobson, S. (2009, October) “First Round of Swine Flu Vaccine Shipped to Texas, Other States” Retrieved from http://www.webcitation.

org/5kGGfFAUR

If Brock Was the World

1.Brock University Office of Institutional Analysis, (2011). Head count enrolment report fall 2011. St. Catharines, ON: Brock University.

2.Statistics Canada. Table 051-0001 - Estimates of population, by age group and sex for July 1, Canada, provinces and territories, annual

(persons unless otherwise noted), CANSIM (database).

3. Shields, M., Carroll, M. D., & Ogden, C. L. U.S. Department of Health & Human Services, Centre for Disease Control. (2011). Adult

obesity prevalence in Canada and the United States. Hyattsville.

4. The World Bank Group, (2012). Life expectancy at birth, total (years).

5. The World Bank Group, (2012). Health, nutrition and population statistics.

6. World Health Organization, (2006). Global atlas of the health workforce. France: WHO Press.

7. World Health Organization, (2008). World health statistics. France: WHO Press.

8. Shah, A. Global Issues (2011) Health Issues. Updated: September 22, 2011

9. UNAIDS, (2009). Aids epidemic update. Geneva: United Nations & WHO Press.

10. 2007 Human Development Report (HDR), United Nations Development Program, November 27, 2007, p.25.

11. International Agency for Research on Cancer, (2008). GLOBOCAN Database. World Health Organization.

12. Glover H., (2011) Global depression statistics. BMC Medicine 2011, 9:90 doi:10.1186

13. 2006 United Nations Human Development Report, pp.6, 7, 35

Hot Headline!

Exercise may protect against brain shrinkage.

1. O’Connor, Anahad. “Exercise May Help Preserve Memory and Thinking Skills - NYTimes.com.” Health and Wellness - Well Blog

- NYTimes.com. N.p., 26 Oct. 2012. Web. 27 Oct. 2012. <http://well.blogs.nytimes.com/2012/10/26/exercise-may-protect-against-brain-

shrinkage/?ref=health>.

Artery Damage, One Fatty Meal at a Time

1. Favaro, Avis. “Just one fatty meal can restrict bloodflow to arteries: studies | CTV News .” CTV News | Top Stories - Breaking News - Top

News Headlines. N.p., 30 Oct. 2012. Web. 30 Oct. 2012. <http://www.ctvnews.ca/health/just-one-fatty-meal-can-restrict-bloodflow-to-

arteries-studies-1.1017405>.

Link Found Between Alzheimer’s disease and Protein Regulation in the Brain- Hope for New Treatments

1. University of Haifa (2012, October 22). Link found between Alzheimer’s disease and protein regulation in the brain -- hope for new treat-

ments. ScienceDaily. Retrieved October 29, 2012, from http://www.sciencedaily.com¬/releases/2012/10/121022092855.htm

References

For more info please contact:[email protected]

Copyright © 2010 Community Health Science Council. This work is licensedunder the Creative Commons Attribution - Noncommercial-Share Alike 2.5

Canada License

You are free to copy, distribute, transmit, and adapt this magazine and itscontents, provided you attribute the work in an appropriate manner and donot use it for commercial purposes. Any derivative works must be licensedsimilarly. These conditions may be waived with the permission of the copy-

right holder.

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brock health issue 6

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