World First:

“To combat swine flu, for instance, we could make a precise, gene-modified pig to improve the animal’s resistance to the disease. We would do this by first, finding a gene that has anti-swine flu activity, or inhibits the proliferation of the swine flu virus; second, we can introduce this gene to the pig via pluripotent stem cells – a process known as gene ‘knock-in’. Alternatively, because the swine flu virus needs to bind with a receptor on the cell membrane of the pig to enter the cells and proliferate, we could knock out this receptor in the pig via gene targeting in the pig induced pluripotent stem cell. If the receptor is missing, the virus will not infect the pig.”

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Oxford University Press (2009, June 3). World First: Chinese Scientists Create Pluripotent Stem Cells From Pigs. ScienceDaily  –  Scientists have managed to induce cells from pigs to transform into pluripotent stem cells – cells that, like embryonic stem cells, are capable of developing into any type of cell in the body. It is the first time in the world that this has been achieved using somatic cells (cells that are not sperm or egg cells) from any animal with hooves (known as ungulates).

The implications of this achievement are far-reaching; the research could open the way to creating models for human genetic diseases, genetically engineering animals for organ transplants for humans, and for developing pigs that are resistant to diseases such as swine flu. 

The work is the first research paper to be published online June 3 in the newly launched Journal of Molecular Cell Biology.

Dr Lei Xiao, who led the research, said: “To date, many efforts have been made to establish ungulate pluripotent embryonic stem cells from early embryos without success. This is the first report in the world of the creation of domesticated ungulate pluripotent stem cells. Therefore, it is entirely new, very important and has a number of applications for both human and animal health.” 

Dr Xiao, who heads the stem cell lab at the Shanghai Institute of Biochemistry and Cell Biology (Shanghai, China), and colleagues succeeded in generating induced pluripotent stem cells by using transcription factors to reprogramme cells taken from a pig’s ear and bone marrow. After the cocktail of reprogramming factors had been introduced into the cells via a virus, the cells changed and developed in the laboratory into colonies of embryonic-like stem cells. Further tests confirmed that they were, in fact, stem cells capable of differentiating into the cell types that make up the three layers in an embryo – endoderm, mesoderm and ectoderm – a quality that all embryonic stem cells have. The information gained from successfully inducing pluripotent stem cells (iPS cells) means that it will be much easier for researchers to go on to develop embryonic stem cells (ES cells) that originate from pig or other ungulate embryos. 

Dr Xiao said: “Pig pluripotent stem cells would be useful in a number of ways, such as precisely engineering transgenic animals for organ transplantation therapies. The pig species is significantly similar to humans in its form and function, and the organ dimensions are largely similar to human organs. We could use embryonic stem cells or induced stem cells to modify the immune-related genes in the pig to make the pig organ compatible to the human immune system. Then we could use these pigs as organ donors to provide organs for patients that won’t trigger an adverse reaction from the patient’s own immune system.

“Pig pluripotent stem cell lines could also be used to create models for human genetic diseases. Many human diseases, such as diabetes, are caused by a disorder of gene expression. We could modify the pig gene in the stem cells and generate pigs carrying the same gene disorder so that they would have a similar syndrome to that seen in human patients. Then it would be possible to use the pig model to develop therapies to treat the disease. 

“To combat swine flu, for instance, we could make a precise, gene-modified pig to improve the animal’s resistance to the disease. We would do this by first, finding a gene that has anti-swine flu activity, or inhibits the proliferation of the swine flu virus; second, we can introduce this gene to the pig via pluripotent stem cells – a process known as gene ‘knock-in’. Alternatively, because the swine flu virus needs to bind with a receptor on the cell membrane of the pig to enter the cells and proliferate, we could knock out this receptor in the pig via gene targeting in the pig induced pluripotent stem cell. If the receptor is missing, the virus will not infect the pig.” 

In addition to medical applications for pigs and humans, Dr Xiao said his discovery could be used to improve animal farming, not only by making the pigs healthier, but also by modifying the growth-related genes to change and improve the way the pigs grow.

However, Dr Xiao warned that it could take several years before some of the potential medical applications of his research could be used in the clinic. 

The next stage of his research is to use the pig iPS cells to generate gene-modified pigs that could provide organs for patients, improve the pig species or be used for disease resistance. The modified animals would be either “knock in” pigs where the iPS or ES cells have been used to transfer an additional bit of genetic material (such as a piece of human DNA) into the pig’s genome, or “knock out” pigs where the technology is used to prevent a particular gene functioning. 

Commenting on the study, the journal’s editor-in-chief, Professor Dangsheng Li, said: “This research is very exciting because it represents the first rigorous demonstration of the establishment of pluripotent stem cell in ungulate species, which will open up interesting opportunities for creating precise, gene-modified animals for research, therapeutic and agricultural purposes.”


Journal reference:

Wu et al. Generation of pig induced pluripotent stem cells with a drug-inducible system. Journal of Molecular Cell Biology, DOI: 10.1093/jmcb/jmp003

GenengNews.com, New Rochelle, NY, June 2, 2009-Scientists around the world are accelerating their efforts to develop a vaccine against the H1N1 influenza virus (Swine flu) as rapidly as possible, reports Genetic Engineering & Biotechnology News (GEN). The need for such a vaccine received a strong impetus from the World Health Organization, which has issued a Phase 5 pandemic alert, a strong signal that the WHO believes a pandemic is imminent, according to the June 1 issue of GEN.

“It can take five or six months to come up with an entirely novel influenza vaccine,” says John Sterling, Editor in Chief of GEN. “There is a great deal of hope that biotech and pharma companies might be able to have something ready sooner.”

One company, Replikins, actually predicted over a year ago that significant outbreaks of the H1N1 flu virus would occur within 6-12 months. The predictions were based on correlations of flu virus specimens and PubMed documentation of major outbreaks during the past 90 years, focusing on concentrations of, and spacings between, replikins-the lysine and histidine residues in the hemagglutinin (HA) unit genetic sequences of the eight major genes in the influenza virus.  Replikins’ officials say the company’s PanFLuTM vaccine is ready for clinical trials.

Novavax plans to create a virus-like particle-based (VLP) vaccine against the H1N1 strain, which obviates the need for a live virus seed for manufacturing. The VLPs contain the proteins that make the virus’ outer shell and the surface proteins, without the RNA required for replication.

Other H1N1 vaccine programs covered in the GEN article include those at Medicago, VaxInnate, NanoBio, Vaxart, Pulmatrix, and Purdue University.

Following in the footsteps of tech, biotech and the Internet, genomics is shaping up to be the next investing boom.

GoogleNews.com, Forbes.com, June 3, 2009, by Jim Oberweis  —  The argument can be made that the surge of biotech development in the 1980s and 1990s was a result of increased government funding for programs like the National Institutes of Health, which bridged the gap between the academically possible and the commercially profitable.

From 1983 to 1993, the budget of the NIH increased 158%, rising from $4 billion to $10 billion. From 1993 to 2003, that budget increased another 163% to $27 billion. In addition to opening its purse strings, Congress also passed a series of laws that fostered the ability to profit from biotech discoveries.

In particular, the Bayh-Dole Act of 1980 permitted universities and small businesses to patent discoveries that evolved from NIH-funded research. Indeed, I think the biotech boom was a direct consequence of rising National Health Institute funding, cheap equity capital, and the ability to patent NIH-funded discoveries.

Under the Obama administration, NIH funding will explode once again, and there is a possibility that a similar wave of innovation will follow. In the last five years, under President Bush, NIH funding remained flat at $27 billion to $29 billion annually. The recently passed U.S. stimulus plan allocates $10.4 billion in additional NIH funding to be spent before September 2010, a windfall equaling roughly 30% of the annual budget. In addition to the immediate flush of cash, the allocation demonstrates the new administration’s commitment to public science funding. Research and academic institutions will benefit, as will the companies that support them.

No area is better positioned to benefit than genomics and personalized medicine. With knowledge of an individual’s genetic makeup, doctors will prescribe drugs with far better understanding of their efficacy for that particular individual.

The cost of obtaining one’s genotype through entire genome sequencing is plummeting: Sequencing cost $300 million in 2003, $1 million in 2007, $60,000 in 2008, is currently under $10,000, and will likely fall below $1,000 by the end of this year. Once below $300, gene sequencing will be cheap enough to be part of routine medical care. With costs this low, personalized medicine is just around the corner.

Just as with biotechs, making money from genomics could well prove elusive. Undoubtedly, genomics will produce an explosion of innovation. But finding the winners in advance is tricky business. Just like makers of picks and axes during the 18th-century California gold rush, makers of the tools that facilitate fast, cheap gene sequencing may be the safest bet.

Today, the two leading producers of gene sequencers are Life Technologies ( LIFEnews people ) and Illumina ( ILMNnews people ). Life Technologies is the product of a merger of Invitrogen ( IVGNnews people ) and Applied Biosystems ( ABInews people ).

Illumina, which is my preferred pick and a holding of the Oberweis Report’s Model Portfolio, appears to be leading the market. Even in this tough economic climate, I expect Illumina’s sales to grow by 30% in 2009. Shares trade for 35 times our 2009 earnings estimate.

By the end of 2009, both companies will likely benefit from the new NIH funding, of which $1 billion is allocated toward equipment purchases. In the longer run, affordability of gene sequencing will take the technology out of academic labs and into mainstream commercial labs. Indeed, 10 years from now, gene sequencers may be as ubiquitous as X-Ray machines. The risk remains that a better sequencing technology will eclipse Illumina’s and Life Technologies’, though I believe that the opportunity justifies the risk.

Last week I was at a dinner that featured a number of geneticists from the University of Chicago and a few consistent themes seemed to emerge. First, whole gene sequencing is on the threshold of being cheap enough to dominate genotyping technology and commercial implementations are likely to increase.

Second, cheap sequencing will drive the need for a better understanding of what to do with the data (right now, even if researchers isolate the genetic disorder that causes an ailment, they don’t necessarily have a way to do anything about it).

Third, genotyping will create the need for tools to store and analyze huge amounts of data. Currently, there is no good solution or standard methodology for its organization. An opportunity for Mr. Ellison and the folks at Oracle ( ORCLnews people )?

Genomics may be the “next big thing” after the Internet and biotech. Finding those who can make money early on will likely pay dividends to investors.

GoogleNews.com, June 3, 2009, by Sacha Pfeiffer, BOSTON – Harvard Medical School researchers say they’ve come up with a way to calculate how much money the health care system saves for every dollar spent on preventative medicine.

You know the saying “an ounce of prevention is worth a pound of cure”? Harvard’s Nancy Oriol wanted to put a dollar figure on just how much “cure” is delivered by the Family Van, a local mobile health clinic for the poor.

So she helped develop an algorithm that crunches national cost-savings data. And it calculated that each dollar spent on the van last year returned $36 in savings.

“Most people look at what we’re doing and they say, ‘Oh, what a cute little program. Isn’t that nice?’ ” says Oriol, dean of students at Harvard Medical School. “But how much do you think you save if you prevent one teenager from smoking? We’re now putting a number to that in a way that’s user-friendly. And we’re actually saving money.”

Oriol now wants to develop a web-based version of this “return on investment calculator” to put a value on other types of preventative health services. Oriol’s findings appear online in the June 2 issue of the journal BMC Medicine.

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Trying to mimic randomly occurring mutations that cause glioblastoma, Inder Verma and his team successfully used modified viruses to shuttle cancer-causing oncogenes into a handful of cells in the brains of adult mice. Individual cell nuclei are shown in blue, infected cells are shown in green. (Credit: Courtesy of Dr. Tomotoshi Marumoto, Salk Institute for Biological Studies) 

2009 ScienceDaily.com – Researchers at the Salk Institute for Biological Studies have developed a versatile mouse model of glioblastoma-the most common and deadly brain cancer in humans-that closely resembles the development and progression of human brain tumors that arise naturally.

“Mouse models of human cancer have taught us a great deal about the basic principles of cancer biology,” says Inder Verma, Ph.D., a professor in the Laboratory of Genetics. “By definition, however, they are just that: approximations that simulate a disease but never fully capture the molecular complexity underlying disease in humans.”

Trying to mimic randomly occurring mutations that lie at the heart of all tumors, the Salk researchers used modified viruses to shuttle cancer-causing oncogenes into a handful of cells in adult mice. Their strategy, described in the Jan. 4, 2009 online issue of the journal Nature Medicine, could not only prove a very useful method to faithfully reproduce different types of tumors but also to elucidate the nature of elusive cancer stem cells. 

The most frequently used mouse cancer model relies on xenografts: Human tumor tissue or cancer cell lines are transplanted in immuno-compromised mice, which quickly develop tumors. “These tumors are very reproducible, but this approach ignores the fact that the immune system can make or break cancer,” says first author Tomotoshi Marumoto, Ph.D., a former postdoctoral researcher in the Verma lab and now an assistant professor at the Kobe Medical Center Hospital in Kobe, Japan. Other animal models either express oncogenes in a tissue-specific manner or shut down the expression of tumor suppressor genes in the whole tissue. “But we know that tumors generally develop from a single cell or a small number of cells of a specific cell type, which is one of the major determinants of the characteristics of tumor cells,” explains postdoctoral researcher and co-author Dinorah Friedmann-Morvinski.

To sidestep the shortcomings of currently used cancer models, the Salk team harnessed the power of lentiviral vectors to infect nondividing as well as dividing cells and ferry activated oncogenes into a small number of cells in adult, fully immunocompetent mice. After initial experiments confirmed that the approach was working, Marumoto injected lentiviruses carrying two well-known oncogenes, H-Ras and Akt, into three separate brain regions of mice lacking one copy of the gene encoding the tumor suppressor p53: the hippocampus, which is involved in learning and memory; the subventricular zone, which lines the brain’s fluid-filled cavity; and the cortex, which governs abstract reasoning and symbolic thought in humans. 

He specifically targeted astrocytes, star-shaped brain cells that are part of the brain’s support system. They hold neurons in place, nourish them, digest cellular debris, and are suspected to be the origin of glioblastoma. Within a few months, massive tumors that displayed all the histological characteristics of glioblastoma multiforme preferentially developed in the hippocampus and the subventricular zone.

The ability of adult stem cells to divide and generate both new stem cells (called self-renewal) as well as specialized cell types (called differentiation) is the key to maintaining healthy tissues. The cancer-stem-cell hypothesis posits that cancers grow from stem cells in the same way healthy tissues do. Known as tumor-initiating cells with stem like properties these cells have many characteristics in common with normal stem cells in that they are self-replicating and capable of giving rise to populations of differentiated cells.

To test whether the induced glioblastomas contained bona fide cancer stem cells, Marumoto isolated cultured individual tumor cells in the lab. These cells behaved and looked just like neural stem cells. They formed tiny spheres-often called tumor spheres-and expressed proteins typically found in immature neural progenitor cells. When given the right chemical cues, these brain cancer stem cells matured into neurons and astrocytes. 

“They displayed all the characteristics of cancer stem cells, and less than 100 and as few as 10 cells were enough to initiate a tumor when injected into immunodeficient mice,” says Friedmann-Morvinski. Most xenograft models for brain tumors using tumor cell lines require at least 10,000 cells. 

“These findings show that our cancer model will not only allow us to start understanding the biology of glioblastoma but will also allow us to answer many questions surrounding cancer stem cells,” says Verma. Although the work described to date pertains to glioblastoma, Verma and his team are currently using this methodology to investigate lung, pancreatic, and pituitary cancers. 

Authors who also contributed to the work include Ayumu Tashiro, Ph.D., at the Kavli Institute for Systems Neuroscience at the Medical Technical Research Center in Trondheim, Norway; Miriam Scadeng, Ph.D., at the UCSD Center for Functional MRI in La Jolla; Yasushi Soda, Ph.D.; and Fred H. Gage in the Laboratory of Genetics at the Salk Institute.

This work was supported by the National Institutes of Health and in part by the H. N. and Frances C. Berger Foundation.


Press Release

06/2009

Genetic Re-disposition: Combined stem cell-gene therapy approach cures human genetic disease in vitro

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Genetically-corrected fibroblasts from Fanconi anemia patients (shown in green at the top) are reprogrammed to generate induced pluripotent stem cells, which, in turn, can be differentiated into disease-free hematopoietic progenitors, capable of producing blood cells in vitro (bottom: Erythroid colonies.)

Image: Courtesy of Dr. Juan-Carlos Belmonte, Salk Institute for Biological Studies.  

June 2009

La Jolla, CA-A study led by researchers at the Salk Institute for Biological Studies, has catapulted the field of regenerative medicine significantly forward, proving in principle that a human genetic disease can be cured using a combination of gene therapy and induced pluripotent stem (iPS) cell technology. The study, published in the May 31, 2009 early online edition of Nature, is a major milestone on the path from the laboratory to the clinic.

“It’s been ten years since human stem cells were first cultured in a Petri dish,” says the study’s leader Juan-Carlos Izpisúa Belmonte, Ph.D., a professor in the Gene Expression Laboratory and director of the Center of Regenerative Medicine in Barcelona (CMRB), Spain. “The hope in the field has always been that we’ll be able to correct a disease genetically and then make iPS cells that differentiate into the type of tissue where the disease is manifested and bring it to clinic.”

Although several studies have demonstrated the efficacy of the approach in mice, its feasibility in humans had not been established. The Salk study offers the first proof that this technology can work in human cells.

Belmonte’s team, working with Salk colleague Inder Verma, Ph.D., a professor in the Laboratory of Genetics, and colleagues at the CMRB, and the CIEMAT in Madrid, Spain, decided to focus on Fanconi anemia (FA), a genetic disorder responsible for a series of hematological abnormalities that impair the body’s ability to fight infection, deliver oxygen, and clot blood. Caused by mutations in one of 13 Fanconi anemia (FA) genes, the disease often leads to bone marrow failure, leukemia, and other cancers. Even after receiving bone marrow transplants to correct the hematological problems, patients remain at high risk of developing cancer and other serious health conditions.

After taking hair or skin cells from patients with Fanconi anemia, the investigators corrected the defective gene in the patients’ cells using gene therapy techniques pioneered in Verma’s laboratory. They then successfully reprogrammed the repaired cells into induced pluripotent stem (iPS) cells using a combination of transcription factors, OCT4, SOX2, KLF4 and cMYC. The resulting FA-iPS cells were indistinguishable from human embryonic stem cells and iPS cells generated from healthy donors.

Since bone marrow failure as a result of the progressive decline in the numbers of functional hematopoietic stem cells is the most prominent feature of Fanconi anemia, the researchers then tested whether patient-specific iPS cells could be used as a source for transplantable hematopoietic stem cells. They found that FA-iPS cells readily differentiated into hematopoietic progenitor cells primed to differentiate into healthy blood cells.

“We haven’t cured a human being, but we have cured a cell,” Belmonte explains. “In theory we could transplant it into a human and cure the disease.”

Although hurdles still loom before that theory can become practice-in particular, preventing the reprogrammed cells from inducing tumors-in coming months Belmonte and Verma will be exploring ways to overcome that and other obstacles. In April 2009, they received a $6.6 million from the California Institute Regenerative Medicine (CIRM) to pursue research aimed at translating basic science into clinical cures.

“If we can demonstrate that a combined iPS-gene therapy approach works in humans, then there is no limit to what we can do,” says Verma.

For information on the commercialization of this technology, please contact Dave Odelson at 858.453.4100, x 1223 (dodelson@salk.edu) in the Salk Office of Technology Management and Development.

Researchers who also contributed to the work include first author Ángel Raya, as well as Ignasi Rodríguez-Pizà, Rita Vassena, María José Barrero, Antonella Consiglio, Eduard Sleep, Federico González, Gustavo Tiscornia, Elena Garreta, Trond Aasen, and Anna Veiga of the Center for Regenerative Medicine in Barcelona, Spain; Guillermo Guenechea, Susana Navarro, Paula Río, and Juan Bueren of the Hematopoiesis and Gene Therapy Division, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas in Madrid, Spain; and Maria Castellà and Jordi Surrallés of the Department of Genetics and Microbiology, Universitat Autonoma de Barcelona.

About the Salk Institute for Biological Studies:
The Salk Institute for Biological Studies is one of the world’s preeminent basic research institutions, where internationally renowned faculty probe fundamental life science questions in a unique, collaborative, and creative environment. Focused on both discovery and mentoring future generations of researchers, Salk scientists make groundbreaking contributions to our understanding of cancer, aging, Alzheimer’s, diabetes, and cardiovascular disorders by studying neuroscience, genetics, cell and plant biology, and related disciplines.

Faculty achievements have been recognized with numerous honors, including Nobel Prizes and memberships in the National Academy of Sciences. Founded in 1960 by polio vaccine pioneer Jonas Salk, M.D., the Institute is an independent nonprofit organization and architectural landmark.

Press Releases

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Each neuron in the retina views the worlds through a small, irregularly shaped window. These regions fit together like pieces of a puzzle, preventing “blind spot” and excessive overlap that could blur our perception of the world.

Image: Courtesy of Dr. Jeffrey Gauthier, Salk Institute for Biological Studies. 

How the retina works: Like a multi-layered jigsaw puzzle of receptive fields

La Jolla, CA-About 1.25 million neurons in the retina — each of which views the world only through a small jagged window called a receptive field — collectively form the seamless picture we rely on to navigate our environment. Receptive fields fit together like pieces of a puzzle, preventing “blind spots” and excessive overlap that could blur our perception of the world, according to researchers at the Salk Institute for Biological Studies.

In the April 7 issue of the journal Public Library of Science, Biology, the scientists say their findings suggest that the nervous system operates with higher precision than previously appreciated and that apparent irregularities in individual cells may actually be coordinated and finely tuned to make the most of the world around us.

Previously, the observed irregularities of individual receptive fields suggested that the collective visual coverage might be uneven and irregular, potentially posing a problem for high-resolution vision. “The striking coordination we found when we examined a whole population indicated that neuronal circuits in the retina may sample the visual scene with high precision, perhaps in a manner that approaches the optimum for high-resolution vision,” says senior author E.J. Chichilnisky, Ph.D., an associate professor in the Systems Neurobiology Laboratories.

All visual information reaching the brain is transmitted by retinal ganglion cells. Each of the 20 or so distinct ganglion cell types is thought to transmit a complete visual image to the brain, because the receptive fields of each type form a regular lattice covering visual space. However, within each regular lattice, the individual cells’ receptive fields have irregular and inconsistent shapes, which could potentially result in patchy coverage of the visual field.

To understand how the visual system overcomes this problem, postdoctoral researcher and first author Jeffrey L. Gauthier, Ph.D., used a microscopic electrode array to record the activity of ganglion cells in isolated patches of retina, the tissue lining the back of the eye.

After monitoring hundreds of ganglion cells over several hours, he distinguished between different cell types based on their light response properties. “Often people record from many cells simultaneously but they don’t know which cell belongs to which type,” says Gauthier. Without this information, he says, he wouldn’t have been able to observe that the receptive fields of neighboring cells of a specific type interlock, complementing each others’ irregular shapes.

“The receptive fields of all four cell types we examined were precisely coordinated,” he says, “but we saw no coordination between cells of different types, emphasizing the importance of clearly distinguishing one cell type from another when studying sensory encoding by a population of neurons.”

Researchers who also contributed to the work include postdoctoral fellows Greg D. Field, Ph.D., Martin Greschner, Ph.D., and Jonathon Shlens, Ph.D., all in the Chichilnisky Laboratory, as well as postdoctoral researcher Alexander Sher, Ph.D., and professor Alan M. Litke, Ph.D., both at the Santa Cruz Institute for Particle Physics, University of California, Santa Cruz.

This work was supported by the National Institutes of Health, the National Science Foundation, the Chapman Foundation, the Helen Hay Whitney Foundation, the Burroughs Wellcome Fund, the Deutscher Akademischer Austauschdienst and the McKnight Foundation.

Johns Hopkins University Bloomberg School of Public Health (2009, June 3). Vision Impairment Costs Billions Lost In Productivity. ScienceDaily. –  Corrected vision impairment could prevent billions of dollars in lost productivity annually, according to a study by researchers from the Johns Hopkins Bloomberg School of School of Public Health, the International Centre for Eyecare Education, the University of New South Wales and the African Vision Research Institute. 

Researchers estimate that nearly 158 million people globally suffer with vision impairment resulting from uncorrected refractive error, which can usually be eliminated with a pair of eyeglasses and an eye examination. This is the first study to estimate the productivity loss from uncorrected refractive error and is published in the June 2009 issue of the Bulletin of the World Health Organization.

“The economic gains that could be made if eyeglasses were provided to everyone in need are substantial,” said Kevin Frick, author of the study and an associate professor with the Bloomberg School’s Department of Health Policy and Management. “Our research estimates $269 billion in productivity lost and nearly 158 million people are vision-impaired because of uncorrected refractive error-which is correctable. The Western Pacific region, which includes China and Vietnam, has the highest estimated number of cases of uncorrected refractive error at 62 million and is responsible for almost half of the potential loss of productivity. The Southeast Asia region, encompassing Bangladesh, India and Nepal, has 48.7 million cases.”

Frick, along with colleagues, used conservative assumptions and national data to estimate the purchasing power, parity-adjusted gross domestic product loss for individuals with impaired vision and blindness, and for individuals with normal sight who provide them with informal care. Researchers found that uncorrected refractive error has a potentially greater impact on the global economy than all other preventable vision disorders despite low-cost interventions such as eyeglasses.

“Apart from the moral obligation, this research indicates that there is a tremendous loss of human potential and lost productivity associated with avoidable blindness and impaired vision due to uncorrected refractive error,” said Frick.

“Potential lost productivity resulting from the global burden of uncorrected refractive error” was written by TST Smith, KD Frick, BA Holden, TR Fricke and KS Naidoo.


Journal reference:

TST Smith, KD Frick, BA Holden, TR Fricke and KS Naidoo. Potential lost productivity resulting from the global burden of uncorrected refractive error. Bulletin of the World Health Organization, June 2009