Spring Newsletter
November 2004 No. 23
1 From
the Editor
2 From the President's Desk
3 Research
- Retina Internnational Conference
4
Two Otago
Medical Students carry out Retinal Research
5 Treatments - Macugen on track for FDA approval
6 Address by Dr Marion Maw, Chair of
the Retina NZ Scientific & Medical Advisory Board
7 Coping - Ready Anything Easily Just
Point
8 People
- Tim Prendergast - A Golden Paralympic
9 Profile of Mary Dobbie
10
Branch News, Letter, Notice
1 From the Editor
This will be the last time I edit the Retina newsletter. A few months ago
I indicated my intention to retire from this most interesting and enjoyable
job and a new Editor has now been found. She is Susan Mellsopp
of
Hamilton, also a Retina member. Resigning as Editor also means that I am
no longer a part of Retina's Executive committee.
I have now been editing quarterly newsletters for the blind for the past 15
years, so it will seem strange for a while but old habits and interests die
hard. I will still be reading scientific papers and articles about low
vision and blindness due to retinal disorders and occasionally write about
things that interest me.
I leave in place a most talented and younger committee, all of whom are
committed to Retina's mission, so I will enjoy hearing about what's
happening through this newsletter. It has always been my intention to
bring you the latest published scientific research about the retina,
information about how to cope, news from the Executive and branches, and
letters from and articles about our members. As you will realise
by now,
we have a lot of wonderful members, both young and old, many of whom have
successfully re trained for different careers once their retinal disorder
has been diagnosed. This issue features two of them Tim Prendergast, a
young sportsman in his twenties and Mary Dobbie,
still going strong at the
age of ninety one.
For the first time I have been able to introduce a 'Treatments' section,
both articles being about Macular degeneration. But sadly, so far there is
virtually no treatment available for people with any type of RP. However,
a publication caught my eye in the Journal of Biological Chemistry that
something as simple as a zinc imbalance in the body may be the cause of RP.
If this is proved to be so, then perhaps RP's can retain their sight by
simply taking a zinc supplement! But every different type of RP
inheritance will require a different type of treatment and each one has to
be proved by years of animal and human trials before it can be released for
general use.
I will still be one of the Retina peer supporters and would love to hear
from any of you if you want to chat or write or email me about your vision
problems. In this way I have got to know so many of you over the years
since Retina started in 1988. So I'll sign off now by wishing you all the
very best in life and hoping that you all have a wonderful Christmas holiday.
June Ombler
Apt. C16,
Rita Angus
Village, 66 Coutts Street, Kilbirnie,
Wellington.
Phone: 04 387 4553; Email: < jombler@xtra.co.nz >
2 From the President's Desk
Actually, my new computer has taken over my dining table until I get the old
one off my desk. The old computer decided it was full and was finding
ordinary tasks too onerous.
It has been a busy time for Retina NZ since the last newsletter. Now the days
are longer and brighter, I hope you have your sunglasses on whenever you
venture outdoors. One of the lectures I attended at the Retina International
conference was about how people with retinal disorders are more susceptible
to damage from sunlight. So we need to protect our eyes to preserve whatever
sight we have.
We had a very successful AGM and conference in Christchurch in September. Some visitors
came for just part of the day, but more than 50 people were there at any
time. My thanks go to Peter, Petronella and Pip of
Christchurch who helped to organise the event.
Peter had just arrived back from an overseas trip and wasn't due back at work
until the Monday, but he came in on the Friday to set up. Some of the day is
covered elsewhere in this newsletter, but we do have tapes available if
anyone particularly wants to hear what was said.
The Executive met again early on Sunday for a meeting. One task we had to complete
was to appoint a new editor. Sue Mellsopp of Hamilton will be taking
over that function later this month and I am sure she will introduce herself
in the next issue. We managed to give June Ombler a
flower spray and a book for her many years of hard work, but she did not want
a fuss made. Watch out next year for an article about June and her many
experiences. She was a founding member of NZ Retinitis Pigmentosa
Society in 1988, and it is her energy and driving force which has made Retina
NZ the organisation it is today. She has served as
Vice President, President, Secretary, International
Delegate and latterly as Editor. She leaves a legacy to be proud of.
Although there has been little change in the membership of the Executive,
many of you are new, so I asked the Executive to send me a couple of lines
about themselves.
Janet Palmer who is our National Secretary, lives in
Wellington,
with her husband, Keith, and has 2 adult children. She manages a secretarial
service, and her interest is music. Janet enjoys singing and belongs to two
choirs.
Camille Guy is our Vice President. A freelance journalist and oral historian,
writing regularly for the NZ Listener and University of Auckland's
Ingenio magazine. Lost central vision due to myopic
retinopathy about four years ago. Uses JAWS screen reader on computer.
Fraser Alexander from Auckland As a member of the Retina New Zealand
Executive since 1998 "I have been privileged to be involved at a time
when our organisation's membership has grown
massively, our peer support programme has been
implemented successfully and we have built significant relationships with
allied agencies and decisionmakers of significance
with
respect to our goals and missions. I have Choroideremia
and work full time in fundraising and study part time towards a Master of
Business degree".
Elizabeth East from the Kapiti Coast
myopic macular degeneration. Enjoys using her well developed communication,
networking and administration skills gained in previous employment in the HR
field to run the telephone based peer support scheme.
Denise Keay from Wellington has worked in a wide range of
policy or human resource management positions, primarily in the public
sector. With a history of retinal detachments and other visual problems
associated with high myopia, Denise has a particular interest in the welfare
of those whose levels of visual impairment have a major impact on their
everyday lives (employment, housing, transport, friendships, leisure, health,
and well being) but who are not eligible for any form of assistance from
established agencies like the RNZFB and whose attempts to help themselves are
all too often met with rebuffs or derision.
Kaye Clark from Wellington Kaye is the only fully sighted member of the
Executive and brings her research and policy analyst background skills to
Retina NZ. She is representing us on the recently formed Vision NZ group, a
collaboration of organizations working together to reduce vision loss.
Lynn Keogh from Dunedin
is Chairperson/Secretary of Otago/Southland Branch.
"I am also a member of the Retina Peer Support team. At present I am
trying to upgrade the website with the help of Robert Strong".
I work as an accountant in Christchurch.
When I have any spare time left from Retina stuff, I love to get outside in
the garden as well as walking and exercise. I am active in Toastmasters, and
would like some time over to play my piano and flute. Roll on Christmas
break!
Kaye Newton
Phone: 03 3795 807
Email: president@retina.org.nz
3
Research
Retina Internnational
Conference
"Focus on Seeing 2004" - The 13th Bi-Annual World Congress of
Retina International (RI) in conjunction with the RI Continuing Education Programme and General Assembly,
June 30/July 3
Reported by Fraser Alexander, Retina NZ International Delegate
The NZ delegation of Kaye Newton, Fraser Alexander and Christina van der Wal represented Retina New
Zealand at each of the forums above held in Noordwijk,
The Netherlands in early July this year. The event was attended by about 550
people from all over the world. Many of the world's leading scientists from a
large range of disciplines from molecular biology to electrophysiology, from
genetics to prosthetics and from optobionics to optometrics presented their findings in the search for
treatments and cures for retinal degenerative and other ophthalmic conditions .
The conference kicked off with the continuing education day which proved to
be an excellent chance to learn from fellow Retina International delegates on
topics ranging from fundraising to forming a SMAB. Electronic copies of
presentations are available from me on request. The Continuing Education day
is an excellent forum for sharing ideas on how to achieve the key objectives
of Retina International at a national level. As Kaye and I agreed, New Zealand
performs above the odds in peer support and public education, given the scale
of our resources but we need to improve our game in areas such as patient
database management and research collaboration.
RETINA INTERNATIONAL GENERAL ASSEMBLY
Kaye Newton and I represented Retina New Zealand
at the Retina International (RI) General Assembly. There are now 21 countries
that are full members of RI, all of which attended the event, and another 20
countries are at various stages of preparing for full membership. As more
patient groups develop around the world, not only are more RP sufferers
supplied with information and support but also, in time, some of these
countries may be able to develop their own research programmes
and contribute to the worldwide goal of finding cures and treatments.
Due to the quantity of business to be covered, the RI General Assembly was a
long day, beginning at 8.30 am and concluding not long before 7.00 pm. The
minutes of the meeting can be found by going to www.retina
international.org and following the links to conferences. I will now summarise some of the key decisions made.
* Regarding having more than one organisation from
a country: More than one from a country may be accepted as full members, as
long as the aims and objectives substantially differ from those of the
existing member.
* The officers of the management committee were appointed. The size of the
management committee was increased and all candidates appointed.
* Presentations were made by the hosting and bidding countries for the 2006
and 2008 World Congress. I remain totally confident New Zealand can undertake the hosting of the
2010 Congress and look forward to Retina New Zealand making a bid at the 2006
Congress in Brazil.
* If you go to the Website you will note that Retina International has
adopted a new logo, quite different from the old one as it is thought to be
outdated. While member countries are expected to use the new logo, it can be
used alongside, rather than in replacement of, our Retina NZ logo.
RETINA INTERNATIONAL WORLD CONGRESS
After a night discovering the flavours of Amsterdam, the next day
dawned as day one of the World Congress. A Retina International World
conference is about the latest advances in scientific and medical research,
low vision aids and issues related to vision loss caused by retinal
degenerative diseases. Essentially, it is for people with retinal dystrophies
and their families along with vision care professionals and others interested
in learning about retinal degenerative conditions and other related diseases
of the retina.
The Retina International environment offers a unique opportunity to:
* learn from leading scientists, ophthalmologists, and ophthalmology
researchers about treatment initiatives and how patients and their families
can practically assist the development of treatments and cures.
* participate in coping seminars that enlighten and encourage and
enthusiastically promote the ideologies of lateral thinking and embracing
technology.
* visit informative exhibits of equipment, research programmes
and rehabilitation techniques.
* participate pro actively in international networking opportunities that
result in mutual benefits involved with advocacy, knowledge sharing, peer
support and collaborative programmes.
As usual, the tone of the scientific presentations was very upbeat about
progress in the laboratory and now, for the first time, we received news that
a number of clinical trials have started or are planned. We also received
"hot off the press" good news that the EU (European Union) has
approved (subject to contract negotiations) providing Euro 10 million to fund
retinal research in several European countries.
Apart from the good research news, there is also the growing realisation that finding cures and treatments for RP in
the laboratory is only the start of a long process that continues through
enormously expensive clinical trials, to various stages of government
approval and the need to get pharmaceutical companies involved in the process
of making treatments available to patients. Over the coming years we will
hear much more on these subjects.
RESEARCH FINDINGS SUMMARISED
Saving central vision
The breaking news released at the congress was the identification and
characterization of a rod derived cone protection factor by Dr Thierry Leveillard and colleagues of the Pierre
and Marie Curie
University in Paris. Researchers have long suspected that
the death of cone cells in Retinitis Pigmentosa is
a secondary process. RP is primarily a disease of the rod photoreceptors,
causing night blindness and loss of peripheral (side) vision. The central
vision loss only occurs later in the disease process when difficulties with
reading and other fine focus visual tasks begin. They suspected that the
death of the rod photoreceptors somehow causes the death of the cones and Dr Leveillard 's
findings now confirm this theory. His team discovered a cone viability
factor, (RdCVF) that is expressed by the rods and
as the rods die and stop producing this trophic
factor, the cones start to die as well. His team have
identified the gene that codes for RdCVF and they
have successfully manipulated the gene expression in a mouse model of RP.
This exciting discovery offers new treatment possibilities for Retinitis Pigmentosa.
Carriers of genes for retinal degeneration
Professor Ed Stone of the University
of Iowa was one of the
keynote speakers. He is a leading researcher in the field of Ophthalmogenetics and his new theory on the rate of
carriers for RD should be a wake up call to all health officials and
planners. Dr Stone estimates that one in five people in the general
population are carriers of a genetic mutation for retinal degeneration. This
is more than a tenfold increase in the previous estimation of one in eighty
in the population.
Age related Macular Degeneration
Dr Stone's group at Iowa
are also responsible for the exciting new discovery of a gene linked
to Age related Macular degeneration (AMD). The gene Fibulin
5 is normally involved in the production of a protein called elastin. This type of protein helps to produce elastic fibres that maintain the integrity of tissues like skin
and blood vessels. These are also found in Bruch's
membrane which underlies the RPE layer in the retina. Although only 2% of the
402 patients screened had the gene mutation, the findings were
"scientifically significant". Researchers are now generally in
agreement about the genetic predisposition in AMD, which probably then
becomes manifest in the presence of appropriate environmental factors.
Excellent papers on genetic, environmental and other aspects of AMD were
given by Professors Alan Bird, Joe Hollyfield, Paulus De Jong and various
other speakers.
Micro arrays
The buzz word at the congress was definitely the "chip". These
micro arrays can be used to screen for gene mutations in a few hours.
Although they will only identify known gene mutations they will certainly
assist in rapid linkage for isolated RP cases that may not be amenable to
traditional linkage studies. A call was made to RI delegates to join an international
consortium to fund the RP chip.
Vitamins, carotenoids and other supplements
There is still no final word on the effect of Lutein
on rate of visual loss. The results of the 5 year trial may shed some light
on this. The fact that Lutein supplementation does
increase the density of the macular pigment is undisputed. Patients taking
extra Lutein state that the addition of Lutein decreases sensitivity to sunlight. Consult your
eye specialist before embarking on any supplementation. Remember that high doses
of Vitamin A should never be taken by pregnant women or smokers.
Retinal and cortical implants
There has been definite progress in both the artificial retina and the
cortical chip implanted into the visual cortex of the brain. While neither of
these will be commercially available in the next 3 years, the results
presented at the congress were truly encouraging.
Hope for the future
Dr Gerald Chader, Chief Scientific Officer of the
American Foundation Fighting Blindness gave an elegant paper to the plenary
session titled Retinal Degeneration: Progress in Basic Science and Movement
to Clinical trials. Dr Chader again inspired the
gathering with appropriate expressions of optimism and challenging calls for
collaboration with scientists and ophthalmologists. Clinical trials are in
progress RIGHT NOW! Proof of principle for several types of therapies has
been established. Other basic work in the field of gene therapy,
transplantation, stem cell research, pharmaceutical research, nutrition and
electronic implants, show varying degrees of promise. We can treat a few
human RD conditions and in many cases we can cure RD in animal models.
What do we need to do to meet the challenge?
Retina New Zealand,
in conjunction with its Scientific and Medical Advisory Board is developing a
patient database which will increase the likelihood of a New Zealander with a
Retinal dystrophy being involved, to a varying degree, in medical and
scientific research that ultimately leads to treatments. While we don't at
this stage know how the database will look and precisely how the data will be
gathered, my advice to you is to stay tuned to find out what you will need to
do.
The need has never been more critical than now for patient databases with
large numbers of files. Clinical researchers will require significant numbers
of patients with specific genotypes and phenotypes in order to carry out
trials that present results that are statistically reliable and valid.
6 Address by Dr Marion Maw, Chair of the Retina NZ Scientific
& Medical Advisory Board (SMAB), to their Annual General Meeting
held in Christchurch in September, 2004
It is a pleasure to again attend the annual general meeting of Retina New Zealand.
A few weeks ago the XIth International Symposium on
Retinal Degenerations was held in Perth,
Australia.
Post doctoral fellow Dr Shubiao Wu and myself
attended in our capacity as researchers while Auckland
ophthalmologists Drs Dianne Sharp and Rachel Barnes attended on behalf of the
Scientific and Medical Advisory Board of Retina New Zealand.
It was the first time Shubiao and Rachel had
attended this biennial meeting and about ten years since Dianne had
participated.
I would like to tell you about a couple of conference highlights. Firstly Dr
Paul Sieving, who is currently Director of the National Eye Institute in the USA, gave a
lecture on our past and present understanding of X linked retinoschisis.
Later Dr Laurie Molday gave a talk on gene therapy
in a mouse model for this disorder. The disorder involves splitting apart of
the retinal cell layers. In retinal detachment, the splitting of layers
occurs between the neural retina and the retinal pigment epithelial cells.
But in retinoschisis, the splitting occurs between
layers within the neural retina itself. I was fascinated to learn that a
technique called ocular coherence tomography enables researchers to see this
phenomenon in the intact eye. This means that there will be a non invasive
method to follow the progress of patients, and perhaps the response to
potential treatments. Initial gene therapy studies have been very encouraging
and it seems that the therapy may even be able to provide a degree of rescue
to retinas in which the gene therapy was initiated after the disease
processes had already begun. Reversal of an ERG abnormality was observed
suggesting that there was functional rescue of light signalling
pathways within the retina.
During discussion, it was suggested that this condition might be one of the
first retinal disorders in which gene therapy will be attempted in human
patients. X linked retinoschisis is a more common
condition than RPE65 related retinal degeneration: the condition in which
gene therapy has been applied to the Briard dog
model. Probably there are only a few hundred RPE65 patients in the entire USA.
Another interesting talk concerned identification of a gene for a protein
called rod derived cone viability factor. It has been known for some time
that if the rods in a retina die, then the cone photoreceptors will
eventually also die. By contrast, if the cone photoreceptors die, then the
rod photoreceptors can survive. Various experiments have suggested that rod
photoreceptors release one or more substances that are required for cone
survival. If the rods die, then the substance is absent and so the cone
photoreceptors die too. If it is not possible to prevent the rod
photoreceptors from dying, it might still be very useful to artificially
provide the remaining cone photoreceptors with these substances. Accordingly,
it is exciting that one such substance has now been identified. No doubt
there will now be a lot of follow up work to investigate how this substance
works and to see if it is a useful supplement in retinal degeneration models.
Prof Dryja gave a plenary lecture on the genetics
of RP and allied diseases. He talked about the progress to date and gaps that
remain. He estimated that about 50% of the autosomal
dominant genes remain to be identified, and that 80 90% of X linked RP cases
involve the RPGR gene. To date, none of the recessive RP genes has been
responsible for a major percentage of cases. Any such major gene would
probably have been found by now. This suggests that many more recessive RP
genes, each perhaps responsible for less than 1 2% of the cases, may remain
to be found.
There was a session on the importance of glucose metabolism, oxygen and light
in retinal degenerations. The healthy retina has a high metabolic rate and
uses a lot of glucose and oxygen. At night glucose levels decrease and light
detection sensitivity of the retina also decreases, especially in the macular
region. Similarly over medicated diabetics or marathon runners may also
experience a transient loss of central vision. A Dr Robert Barlow and
colleagues reported on their studies of a GE mouse in which the glucogon receptor gene had been knocked out. This line of
mice is chronically hypoglycaemic, i.e. has low
blood sugar levels and by 12 months of age, these mice became retinal
degenerate.
In another talk Professor Jonathon Stone, who leads an Australian research
team, talked about the role of oxygen. Remember that the healthy retina uses
a lot of oxygen. In the degenerate retina, the dying cells use less oxygen
and retinal oxygen levels rise. Prof Stone suspects that these higher oxygen
levels are toxic and lead to further cell death. Interestingly enough,
apparently patients with RP and diabetes rarely get diabetic retinopathy. My
impression is that this may be because of the role of low oxygen levels in
stimulating abnormal blood vessel growth in the retina of a diabetic person.
Finally someone from Peter Humphries group gave a talk about the use of a RNAi based mutation
independent approach to dominant RP. RNAi is a
relatively new and very impressive way of switching OFF a gene by destroying
the RNA messages from the gene. These RNA messages are used as the
instructions for production of the corresponding protein. For example, a
large number of different mutations in the rhodopsin
gene are each capable of causing RP. The approach of Prof Humphries group was
to use RNAi to destroy all rhodopsin
RNA, ie from both the healthy and the damaged
copies of the rhodopsin gene. Meanwhile an
artificial rhodopsin gene that had been engineered
to be resistant to RNAi, was being introduced to ensure that healthy rhodopsin would be made. This approach avoids the
challenge of trying to turn off the damaged gene without turning off the
healthy gene as well.
4 Two Otago Medical Students
carry out Retinal Research
This summer two medical students will contribute to a long term research programme to understand an inherited retinal disorder
that affects a large New
Zealand whanau.
Both students will be supervised by Dr Shubiao Wu
and Dr Marion Maw, Biochemistry Department, University of Otago.
Abdulmnaem (Monier) Alshoarb, a third year medical student at Otago
University has been
awarded The SA and GJ Ombler Charitable Trust
Summer Scholarship. His topic is "A mouse model for inherited blindness:
characterisation of an antibody for detection of
the causative protein". Monier will be testing
the specificity of a newly generated antibody to a protein called Cacna1f. In
humans, damage to the CACNA1F gene causes the inherited retinal disorder X
linked incomplete congenital stationary night blindness. If time permits, Monier will also determine the labelling
pattern in mouse retina of a commercially available antibody to the closely
related protein Cacna1d.
The same laboratory will host Moana Wyllie, a
second year medical student at Otago University.
His topic is "Detection of ZENK, a gene implicated in short sightedness,
in mouse retina". Individuals affected by inherited retinal disorders
often develop long or short sightedness. In the healthy eye, the retina is
able to determine whether images are in plus or minus defocus and to modulate
eye growth so that the plane of focus and the retina will coincide. The
molecular basis of the mechanism that ensures axial eye length is appropriate
for the refractive power of the lens and cornea remains to be determined.
Expression of the ZENK gene in specific retinal cells has been implicated in
several animal models. Moana will carry out initial
studies to detect ZENK gene activity in mouse retina. He will be supported by
a Summer Studentship in Maori Health Research from the Health Research Council
of New Zealand.
New Clues to Hereditary Blinding Disease (RP) Found
Dartmouth Medical
School researchers have
discovered a critical role for
zinc in RP. The amount of zinc, a trace metal naturally absorbed by the
body, can determine whether a key protein for vision functions normally or
misfolds. An inability to successfully bind zinc to
rhodopsin, a light
receptor in the eye, can trigger RP, a degenerative disease that leaves many
patients legally blind by the age of 40.
The research, appearing as the "Paper of the Week" in the August 20
issue
of the Journal of Biological Chemistry (JBC), is the first confirmation
that zinc is present and plays a significant role in the normal folding and
functions of rhodopsin, and if defective, leads to
retinal degeneration.
If there is not enough zinc in the body or if there is a mutation in the
zinc binding site, the protein rhodopsin will misfold and break down,
triggering cell death, degeneration of the retina and eventually blindness.
Zinc has a strong presence in the body, the average
person has 2.3 grams
of zinc, making it the second most prevalent trace metal behind iron.
For more information contact : < DMS.Communications@dartmouth.edu >
5 Treatments
Macugen on track for FDA approval
From the Macular Degeneration Partnership, 23 September 2004
The first of the long awaited antiangiogenic drugs
for wet macular degeneration has cleared the final hurdle for FDA approval
and may be available for patients in a few months. Macugen
was given "fast track" status to allow the review to take place in
the shortest time possible. A final decision is expected December 17. If the
drug is approved, it may reach the market in the United States as early as January
2005. Regulatory filings have also been submitted to market the drug in
Europe and Canada.
The drug was developed by Eye Tech Pharmaceuticals and will be distributed by
Pfizer Inc.
Macugen is injected directly into the eye and works
to halt the growth of the problematic blood vessels in wet macular degeneration.
It has been shown to slow the vision loss but does not result in improved
vision. There were some safety concerns early in the research, but these have
been satisfactorily addressed.
So far, they have 54 weeks of follow up after the treatment. At that point,
70% of Macugen patients had lost fewer than three
lines of vision, while 55% of placebo patients lost that much vision. Since
wet AMD is a progressive disease, anything that will slow that progression is
of interest. Part of the good news about this drug is that it appears to be
effective for all types of wet macular degeneration.
One of the potential uses of Macugen will be in
combination with other treatments, like photodynamic therapy (PDT). A patient
might receive PDT to seal off the blood vessels that are already leaking, and
then an injection of Macugen to stop the blood
vessels from growing. This "one two" punch could potentially save
vision for many AMD patients.
Other antiangiogenic drugs are under development
and we can expect to hear more about them in the coming year. Next month the
results of the Phase III clinical trial for RETAANE will be announced by Alcon Laboratories. The Macular Degeneration Partnership
will be reporting on that news from the American Academy
of Ophthalmology Annual Conference.
For further information go to < www.amd.org >
Results of Age-related Eye Disease Study (AREDS)
25 October 2004
The report on the AREDS (Age related Eye Disease) Study on Nutrition &
Dietary supplements was released on 25 October at the American Academy of
Ophthalmology Conference.
VITAMIN SUPPLEMENT, AMD AND CATARACTS
On October 12, 2001, the National Eye Institute released the long awaited
results of the AREDS (Age Related Eye Disease Study), designed to look at the
effect of vitamin supplementation on AMD and cataracts. This multi year
research project involved almost 5,000 individuals 55 80 years old. They were
divided into four groups according to their eye condition (no AMD, early AMD,
intermediate AMD, advanced AMD). In each group,
participants were randomly selected to receive daily tablets of either zinc
alone, antioxidants alone, a combination of zinc and antioxidants, or a
placebo (so called sugar pill). About 90% of the participants remained in the
study for five years.
The Encouraging Results
For people at high risk of developing advanced stages of AMD, use of the
combination of antioxidants and zinc supplements reduced that risk by 25%.
For this same group, the risk of vision loss itself was reduced by 19%. Study
participants who had either no AMD or early AMD did not derive any apparent
benefit from the supplements. The vitamins also did not appear to have an
effect on the development of cataracts.
The Supplement
The combined antioxidant/zinc supplement used in the study contained:
* Vitamin C 500 milligrams
* Vitamin E 400 IU
* Beta Carotene 15 milligrams
* Zinc (as zinc oxide) 80 milligrams
* Copper (as cupric oxide) 2 milligrams
It is important to remember several things about supplements. You should talk
to your doctor before embarking on any program of supplementation, especially
if you have other medical conditions. Frederick Ferris, M.D., director of
clinical research at the NEI and chairman of the AREDS stated, "For
example, beta carotene has been shown to increase the risk of lung cancer
among smokers," he said. "These people may want to discuss with
their primary care doctor the best combination of supplements for them. With
any supplements containing zinc, it is important to add appropriate amounts
of copper to the diet to prevent copper deficiency." At the time of the
study, lutein was not as widely recognized as a
critical antioxidant for the eyes. It was not tested in this study, but has
been shown to be important. Your diet should include at least five servings
of fruits and vegetables a day to provide a balance of nutrients and
antioxidants. Taking a vitamin supplement does not mean you shouldn't eat
properly as well!
The Take Home Message
The best news is for people who already have intermediate or advanced AMD,
since this population had the greatest response to the supplements. According
to Paul A. Sieving, M.D., Ph.D., director of the American National Institute
of Health NEI, "This is an exciting discovery because, for people at
high risk for developing advanced AMD, these dietary supplements are the
first effective treatment to slow the progression of the disease. The
supplements are not a cure for AMD, nor will they restore vision already lost
from the disease. But they will play a key role in helping people at high
risk for developing AMD keep their vision."
Dr Ferris also noted that almost two thirds of the people in the study chose
to take a daily multivitamin in addition to the assigned treatment. He notes
that, "The AREDS also showed that, even with a daily multivitamin,
people at high risk for developing advanced AMD can lower the risk of vision
loss by adding a dietary supplement with the same high levels of antioxidants
and zinc used in the study."
Bausch & Lomb, who provided the vitamins for the study, is already
marketing a new eye formula based on these results. Other vitamin companies
are sure to follow. You can also buy separate components of the supplement,
like zinc, but be sure to check with your doctor before you do to make sure
you are buying the right amount of each component.
For further information and answers to frequently asked questions take this
to your doctor and ask him/her to check it out by going to
:
http://www.amd.org/site/PageServer?pagename=AREDS
Coping
7 READY
ANYTHING EASILY JUST POINT
From Premier Assistive Technology, 22 October 2004
Premier Assistive Technology unveiled its latest product at the Closing the
Gap Conference in Minneapolis, Minnesota, its new Talking Pointer. The
Talking Pointer has been integrated into the Universal Reader and Universal
Reader Plus products. The Talking Pointer will start to ship on November
1, 2004.
What makes this "talking pointer" technology so remarkable is its
ability
to read almost anything on the screen. The user has the ability to control
how much or how little it reads. One of the most common barriers to
getting individuals to use assistive technology has often been the
complexity of products themselves. Many software companies just keep
adding more features to existing products in an effort to make them better,
but in reality they make the products more difficult to use, hence, they
often end up on the shelf collecting dust. It generally takes a user less
than five minutes to start using it proficiently. Just use your mouse,
point at anything on the screen and it reads it to you. This ease of use
makes it appealing to ALL age groups. It can be used by anyone from second
graders who can't read yet to a retired individual who has trouble reading.
You can now make the web come alive with voice. Just point at a link and
it will be read to you. Read a paragraph simply by pointing at it! Even
icons, field headings, virtually ANYTHING that you can point to with your
cursor on the screen can be read to you! In addition to the Talking
Pointer, the Universal Reader can be used to read documents, emails and
web pages. The words are highlighted as they are being read back to you.
It has a full set of options that let you pick a voice, reading speed, font
size and even foreground and background colors.
The Universal Reader suggested retail price is only US$39.95 and Universal
Reader Plus (with scanning) sells for US$79.95.
For More Information Contact:
Ken Grisham CEO, Premier Assistive Technology
Email: < info@readingmadeeasy.com >
URL: < www.readingmadeeasy.com >
EDITOR's NOTE : It is relatively cheap for a
product that reads a screen aloud. If any member has checked this out, how
about writing a letter to the Editor
and let us all know what you think of it and if it's really as good as it
sounds.
8 People
Tim Prendergast - A Golden Paralympic
Tim Prendergast, who we featured in our last newsletter is now settling down
to work again as the Wellington Recreation Adviser of the RNZFB after having
a month's holiday overseas with his Partner Lisa before returning home after
the Athens Paralympics.
Unfortunately he lost a shoe not long after the start of the 1500 metres track race, which cost him a medal in that event.
But on the last day he clinched a Gold medal for New Zealand, timing everything
perfectly to allow him to surge ahead of his rivals at the finish.
Photograph: Caption. Tim Prendergast after receiving his Gold Medal for
winning the 800 metres track race in Athens at the
Paralympics.
Tim said that he wishes to thank all those people who sent him messages of
support, which inspired him to win.
Congratulations Tim, we are all proud of you.
9 Profile of Mary Dobbie
By Camille Guy
Thirty years ago Mary Dobbie retired at Piha, a small settlement out on Auckland's rugged west coast. Hers had been
a busy and stimulating life. After completing a diploma in journalism at Auckland University in the 1930s and at the
urging of friend Robin Hyde, Mary had accepted a job as lady editor on the
weekly, the New Zealand Observer.
When printer Bob Lowry wandered into the offices one day and invited her to a
meal with him and wife Irene, Mary was to find herself meeting all the left
wingers of the time. For a while Mary herself belonged to the New Zealand
Communist Party.
Photograph: Caption Mary Dobbie had a busy
retirement mapped out but coping with sight loss is proving a challenge.
An early marriage had resulted in a daughter, and later Mary and husband Pat Dobbie, a radio announcer, had a further four daughters. Over
the years Mary became caught up in social issues such as nutrition, family
planning and the parent centre movement. Still an active member of the
Historical Society, Mary has contributed to film documentaries and histories
of these movements.
During the war Mary and Irene Lowry and their children shared a large rented
house in Cornwall
Park. Once their
husbands returned from war service the two couples used to throw regular
Saturday night parties. These were a social highlight for many Aucklanders and visitors to the house included such
literary luminaries as Sargeson, Fairburn and
Curnow.
In her sixties, Mary was able to satisfy her longing to live where there was
a more rural aspect by making the move to Piha. It
was not long before Mary's habits of journalism resurfaced and in 1982 she
established the Piha Community News, a quarterly
publication which continues to this day.
Mary has never been a driver, and by her late eighties the walk up the steep
hill from the Piha store was getting tougher. Bowing
to her family's concerns Mary made the move back to the city, relocating her
computer and cartons of papers with a view to now writing a memoir of her
life for her family.
But shortly afterwards Mary made a long postponed visit to the optometrist to
see about new glasses. She had not needed reading glasses until in her mid
sixties. So it was a shock to find herself referred
to an ophthalmologist for investigation of wet macular degeneration.
This sight loss and Mary's increasing inability to read was a serious blow.
One of her first acts on moving to an inland home not buffeted by coastal
winds was to establish a flower and vegetable garden. Now she found herself
pulling up carefully nurtured plants rather than weeds.
While Mary did have the advantage of good touch typing and familiarity with a
computer, osteoporosis began to affect her fingers and typing has become
impossible.
Now 91, Mary continues to live independently in her One Tree Hill unit, with
its sunny terrace overlooking her garden. She is surrounded by books, not
just the yellow plastic cased ones from the RNZFB library, but newly
published histories and poetry collections. She intends to attend all three
of the book launches she is invited to this month.
What is helping Mary most through this trying phase of life is her family and
friends. Several volunteers read to her regularly, allowing her to read books
that the Foundation is unlikely to record.
I ask Mary how she is coping with the new constraints on her life. "I
don't think I've really come to grips with it. I put off doing the things I
know I should do, I should tidy my place up, move
the furniture around a bit. Somehow I think, oh well maybe tomorrow. "
That is a feeling only too familiar to the recently blind. Until more of us
are computer literate and can access the equipment and software we need after
sight loss, then adaptation will never be easy. But watching Mary Dobbie go about her still active and stimulating life is
indeed an inspiration.
Branch News
Auckland Branch
From Camille Guy
About 30 members and several Foundation staff attended a meeting held at the
RNZFB on Sunday afternoon, 31st October. Besides the two Auckland executive members, Camille Guy and
Fraser Alexander, Kaye Newton and Elizabeth East were also able to attend.
Auckland Ophthalmologist Dr Rachel Barnes spoke on recent research on
diagnosis and treatment of retinal disorders and answered questions.
Afternoon tea was served and members mingled. Two new members were recruited.
Letter
FROM : Don Jeffery, Learning Design Centre
Open Polytechnic of NZ, Lower Hutt
Email: Don.Jeffery@openpolytechnic.ac.nz
First may I say how much I enjoy reading the articles in the Retina News and
the clear structure of the journal.
Now to the reason for my letter. Three years ago I was diagnosed with a
melanoma on the choroid of my right eye. I had
radiation therapy at Christchurch
Hospital with a radio
active plaque attached to the back of my eye for 5 1/2 days. It was a
relatively painless procedure and the long term prognosis is good but there
has been some deterioration in the vision from my right eye due to the tumour being close to the optic nerve.
I would be interested in sharing my experiences and supporting data with
other people who have had a similar eye affliction, with the aim of setting
up a support group. I can be contacted at 38 Settlement Road, Te Horo, RD1 Otaki, phone 06 364
2419.
Notice
National Deafblind Camp for all ages in March 2005
If you have both vision and hearing loss, you are welcome to attend the camp
being held near Tongariro National
Park from March 18 21, 2005.
For more information contact:
Richelle Frantz, RNZFB Deafblind
Services, Email:
< rfrantz@rnzfb.org.nz > or
Phone: 0274 372 685 or 03 375 4302.
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