Friday, December 28, 2007

New ACOG guidelines: Invasive prenatal testing should be offered to all pregnant women


This makes me want to get our book finished all the more and sooner! Doctors and many others need to be educated about Down syndrome.

The ACOG put new guidelines out in January/February of 2006 that recommended all pregnant women be screened for Down syndrome. 90% of babies who are prenatally diagnosed with Down syndrome are aborted. That statistic is disgusting! It seems as if the ACOG is trying to "rid the world" of people with Down syndrome. It's terrible that these babies are aborted because of a chromosomal abnormality, which they had nothing to do with. God is the one who made them with that extra chromosome. Our society has warped views that they have to have "the perfect child." But, what's also terrible is that the amniocentesis and the CVS screenings are not even accurate. They have a lot of false negatives and false positives.


New ACOG guidelines: Invasive prenatal testing should be offered to all pregnant women.

From Obstetrics & Gynecology, Volume 110, No. 6, December 2007, page 1459 (ACOG membership or $20 payment required for articles.)

Heralding a change in standard obstetric practice, the American College of Obstetricians and Gynecologists has recommended that pregnant women of all ages – not just women aged 35 and over — should be offered invasive prenatal diagnostic testing such as amniocentesis and chorionic villus sampling to detect possible genetic abnormalities in their fetuses.

The recommendation, published in a practice bulletin in the December issue of the organization’s journal Obstetrics & Gynecology, dramatically expands women’s access to prenatal diagnosis, effectively making all prenatal tests and screens available to all of the 6 million American women who get pregnant each year. It will establish a new standard of care, and change expectations for insurance coverage and legal liability involving pregnancy.

Until now, obstetricians have usually offered invasive testing just to women at or above age 35 at delivery. The age threshold was chosen because at that age the risk of miscarriage as a result of the testing was roughly equal to the risk of having a child with Down syndrome, the most common genetic abnormality occurring in live births. In addition, the medical community balanced the cost of offering the testing against their calculation of the cost savings associated with preventing the birth of an infant with Down syndrome.

This past January, ACOG expanded the scope of prenatal testing by recommending for the first time that all pregnant women regardless of age be offered prenatal screening, a process in which a woman’s blood is used to calculate the risk that her fetus has an abnormality.

The December ACOG bulletin will open prenatal testing access wider still. The current bulletin does not explain why the professional organization has now dramatically expanded access to prenatal testing twice within a year. Researchers have maintained that universal access to prenatal testing will allow women to make their own informed decisions regarding their pregnancies and minimize disparities in access to health care.

The changes come at a time when growing numbers of medical malpractice lawsuits are pushing insurance costs for obstetricians and gynecologists to record highs, resulting in a situation that ACOG has called a “medical liability crisis.”

In a statement posted on the group’s website last year, ACOG executive vice president Ralph W. Hale said the rising tide of lawsuits was caused not by a high rate of medical wrongdoing but by unreasonable public expectations. “Ob-gyns are vulnerable because they practice in a high-risk field, and all too often, doctors are held liable for less than perfect outcomes,” he said.

ACOG’s current recommendation seems to thrust the 49,000-member professional organization deeper into the cultural debate over public attitudes toward abortion, particularly about where to draw the line between preventing disability and accepting human diversity.

The National Down Syndrome Congress (NDSC) last January condemned ACOG’s recommendation for universally offered prenatal screening, saying it conveyed “tacit approval for terminating pregnancies where the fetus has Down syndrome.” Studies say that approximately 9 out of 10 pregnancies in the U.S. in which Down syndrome is diagnosed end in abortion.

The NDSC also cited research noting that many doctors are not adequately prepared to deliver a diagnosis of Down syndrome, and often use negative language and out-of-date information.

Down syndrome, which results when a person has three copies of the 21st chromosome instead of the usual pair, is longest known and most common genetic birth defect, as well as the most common cause of intellectual disability. Approximately 250,000-350,000 Americans have Down syndrome, which occurs once in every 733 to 1,000 births, according to the NDSC and the National Down Syndrome Society.

Advocacy groups and parents say gains in health care and education have brought about markedly improved outcomes for these individuals over the past two decades, with many people with Down syndrome now completing high school, holding jobs and living semi-independently. But parents say these gains have not been adequately documented and are poorly understood within the obstetrics community.

In an apparent nod to the NDSC’s criticism, ACOG included in its December practice bulletin for the first time the recommendation that prospective parents who receive a diagnosis of a fetal disorder should be provided with “detailed information, if known, about the natural history of individuals” with the disorder.

ACOG also noted that “it may be very helpful” to refer prospective parents to advocacy groups such as the NDSC or the NDSS.

The bulletin does not, however, offer any recommendations for collecting or distributing information to doctors about the lives of people with Down syndrome or other chromosomal abnormalities, nor for training its 49,000 members in delivering and interpreting prenatal test information. A study published in ACOG’s journal last year found that 45 percent of obstetricians rated their training about prenatal testing as “barely adequate or nonexistent.”

As a result of the new ACOG bulletin, each pregnant woman will now need to decide which is greater: her fear of a chromosomal abnormality, or her fear that invasive testing could harm her fetus. The ACOG bulletin estimates that the risk of miscarriage as a result of the invasive tests is “as low as” one in 300-500, and “may be even lower with experienced individuals or centers.” Other estimates say that approximately one in every 200 women who undergoes invasive testing will miscarry her pregnancy.

The risk of a fetus with a chromosomal abnormality varies with the mother’s age. According to ACOG data, the lowest recorded risk goes to 19-year-olds, with a risk of 1 in 555, and the highest goes to a 49-year-old, with a risk of 1 in 6.

The financial impact of the new ACOG bulletin is not known, but could extend above the billion-dollar mark. Amniocentesis and chorionic villus sampling (CVS), the invasive tests, are both more expensive and more accurate than the maternal blood test screens. The consumer cost of each amniocentesis is more than $1,000. Chorionic villus sampling costs between $600 and $1200. More invasive tests would also call for an increase in costs for training, facilities and equipment.

Amniocentesis and CVS each involve removing and examining material from inside the uterus during pregnancy with a long needle or plastic tube to check for chromosomal differences.

The maternal blood-test screens do not deliver definitive results but only report the odds that a particular fetus may have an abnormality. They also carry a significant risk of both false positives and false negatives.

In a tacit acknowledgment of the ongoing abortion debate, the bulletin notes that “Prenatal diagnosis is not performed solely for assistance in the decision of pregnancy termination. It can provide useful information for the physician and the patient.”

The practice bulletin listed the recommendation for offering invasive diagnostic testing to all pregnant women as a “Level C” recommendation, one that is “based primarily on consensus and expert opinion.” This is the lowest rank used in justifying ACOG recommendations.

Higher rankings that may be used for ACOG recommendations are “Level A” (”based on good and consistent scientific evidence”) and “Level B” (”based on limited or inconsistent scientific evidence.”)

Thursday, December 13, 2007

Diet & Nutrition Study

DSRF is doing a new study:

Nutritional Interventions in Children wtih Down's syndrome (NICDS study)
"Can nutritional intervention prevent or reduce the risks of associated diseases and illnesses in Down's syndrome?"

For more information on the study, here's a link ~
http://www.dsrf.co.uk/2007ResearchStudy/dietandnutrition.html

"
The aim of this study is to see if nutritional interventions can help to prevent or reduce the risks that children with Down's Syndrome are exposed to in terms of illnesses such as type 2 diabetes, vascular disease, obesity, leukaemia and early onset dementia. Much is known about the ways in which nutrition and lifestyle can be modified to prevent, or at least reduce the risk of these disorders."

Monday, December 3, 2007

Website for Book - Down Syndrome: What You CAN Do

As some may know, my mother and I are in the process of writing a book about Down syndrome. The title is going to be "Down Syndrome: What You CAN Do." I put a website up with information about the book. The link is:

Like Any Other Boy

I wrote this and submitted it to the Band of Angels site for the brothers & sisters column on the site by Harper Kidder.

~~~~~~~

Like Any Other Boy

I’m the oldest of 11 children. One of my 4 brothers is 2 ½ years old. He also happens to have a twin sister, who is 5 minutes younger than him.

My brother is like any other little boy. He likes to play with cars. He likes to run and play outside. When he hears that one of the kids is going outside, he always asks to have his shoes put on and to go outside with them. He chases his twin sister around. He really enjoys playing ball. When all the other kids play pass the ball, he is right there with them passing the ball. He even likes to play with baby dolls with his twin sister!

One of his favorite things to do is dance! He dances all the time and is so cute. He has some of the cutest little jigs and rhythm. Often times the whole family will be watching him dance because it’s such a blast watching him. One of the best times when it comes to dancing was at this past Thanksgiving at our friend’s house. All of us (including our friends who were there) were in a big circle and each person was taking their turn doing a dance in the middle while everyone followed them. It finally came to where everyone had done it, so we asked my bother to come in the middle and dance. He did it perfectly!

I guess I should mention now that my brother has Down syndrome. When my brother was born his diagnosis was news to us. But, contrary to the “he can’t” and “he won’t” statements that we were told back on that February day 2 ½ years ago, my brother has exceeded and shown that those statements were wrong. He is just a part of our family; one of the kids. He can do a lot.

One thing about him is that he is so loving, so happy almost all the time and so much fun. He puts a smile on our faces! We are thankful that God has shown great mercy on him and us and made him excel way beyond what we were told.

- Qadoshyah

19 yr. old sister to boy(DS)/girl twins - February. 05

Friday, November 30, 2007

Another Chapter

Another update in regards to the book - we have made another chapter in the book which is going to be about "What They Can Do." It'll be stories written by people with DS or by a family member who have had great success. We have the story of Christopher Scott, who starred in the movie, "My Brother."

Zoom! Babies learn to ride robots at UD

Zoom! Babies learn to ride robots at UD

(More pictures can be seen at: http://www.udel.edu/research/media/babiesrobotsgallery.html)

Researchers at the University of Delaware are providing safe mobility to children with special needs who are unable to fully explore the world on their own through the development of kid-sized robots that infants can drive using joysticks.

The work is important because much of infant development, both of the brain and behavior, emerges from the thousands of experiences each day that arise as babies independently move and explore their world.

The robot, UD1, is designed with smart technology to address safety issues so infants can be a part of the real world environment, and in this way uses technology to meet human need.


Babies driving robots. It sounds like the theme of a cartoon series but it is actually the focus of important and innovative research being conducted at the University of Delaware that could have significant repercussions for the cognitive development of infants with special needs.

UD1Two UD researchers – James C. (Cole) Galloway, associate professor of physical therapy, and Sunil Agrawal, professor of mechanical engineering – have outfitted kid-size robots to provide mobility to children who are unable to fully explore the world on their own.

The work is important because much of infant development, both of the brain and behavior, emerges from the thousands of experiences each day that arise as babies independently move and explore their world. This is the concept of “embodied development,” Galloway said.

Infants with Down Syndrome, cerebral palsy, autism and other disorders can have mobility limitations that disconnect them from the ongoing exploration that their peers enjoy.

“If these infants were adults, therapists would have options of assistive technology such as power wheelchairs,” Galloway said. “Currently, children with significant mobility impairments are not offered power mobility until they are 5-6 years of age, or older. This delay in mobility is particularly disturbing when you consider the rapid brain development during infancy. Their actions, feelings and thinking all shape their own brain’s development. Babies literally build their own brains through their exploration and learning in the complex world.”

When a baby starts crawling and walking, everything changes for everyone involved. “Now consider the negative impact of a half decade of immobility for an infant with already delayed development,” Galloway said. “When a baby doesn’t crawl or walk, everything also changes. Immobility changes the infant, and the family. Given the need, you would think that the barriers to providing power mobility must be insurmountable. In fact, the primary barrier is safety.” Therapists and parents fear a young child in a power wheelchair might mistakenly go the wrong way, end up in a roadway and get hit by a car.

“This is, of course, understandable, and is the same fear that every parent with a newly walking infant faces. It is the solution to the safety problem that is the real barrier. The current clinical practice is to avoid power mobility until the child can follow adult commands,” Galloway said. “Your parents didn’t wait until you followed their every command before they let you walk – they held your hand, they required you to stay near them, and alerted you to obstacles in your way. This is the way infants learn real world navigation, and it is exactly these safety features that are being built into our mobile robot.”

“Our first prototype, affectionately called UD1, was designed with smart technology that addresses each of these safety issues so that infants have the opportunity to be a part of the real world environment,” Agrawal said.

UD1The tiny robot is ringed with sensors that can determine the obstacle-free roaming space, and will either allow infants to bump obstacles or will take control from the infant and drive around the obstacle itself. The next prototype, UD2, will build on the current technology to provide additional control to a parent, teacher or other supervising adult.

“In this way, we can bind technology and human need together to remove barriers for movement in the environment,” Agrawal said.

Galloway said no one had ever tried using robots with babies – early experiments show that seven-month-olds can learn to operate the simple joystick controls – and he is passionate about the possible benefits to children with special needs of even younger ages.

“Infants with limited mobility play in one location while their peers or siblings go off on distant adventures all over the room or playground,” Galloway said. “With the robot, they become the center of attention because their classmates want to try it. We predict that this increased social interaction alone will provide an important boost in their cognitive development.”

The idea sprang from a parking lot conversation in which Agrawal approached Galloway, who he knew worked with babies with special needs, and said he might have developed something of interest. Agrawal is a robotics expert who had been developing a fleet of small, rounded robots that could work as a unit through a wireless network.

Galloway knew of Agrawal’s successes with rehabilitation robotics for adults but admitted to being anti-robot for pediatric rehabilitation at first. Galloway was convinced otherwise within minutes of his first visit to Agrawal’s laboratory. “When I saw his little robots, it was easy to envision a baby driving one,” he said. “We knew from our previous work that newly reaching infants could use a joystick to control a distant toy. This and other research strongly suggests that very young infants can be trained in real world navigation. It was a special feeling to see a potential solution to a really serious healthcare gap for young kids. There was and still is a special tingle when we think of the not so distant future. “

Thus, UD1 was born. The researchers took their robot to the UD Early Learning Center, which has a wide range of infants, a gymnasium for initial training on the robot and a varied outdoor landscape to use as a test track.

“It was a relief when we saw that the children quickly grasped the use of the joystick,” Agrawal said. “If they had just sat there or cried, it would have been back to the drawing board. But over time we have seen them gradually increase their time with the robot and the amount of distance they cover.”

The project will now move on to a second generation with more than one robot. The goal is to place multiple mobile robots with special needs infants in communities throughout Delaware and to gather data to analyze how they are used and what the children learn so that the research team can continue to make modifications.

Both note that Delaware, with its mix of urban, rural and suburban communities, is a model state for a clinical project such as this. “For a real world mobility device to emerge, we have to build it for exploring the real world experienced by infants and their families, and then rigorously study its performance in that world,” Galloway said.

Both said the project will significantly expand understanding of young infants’ learning capacity and provide a model for tracking the development of real world exploration with laboratory quality data.

They believe the training, robot design and new technology derived from the project will provide the foundation for the first generation of safe, smart vehicles for infants born with mobility impairments. They want the UD1 product to be light enough for moms to stow in a car trunk, and robust enough for babies to use in the home, yard and playground, and maybe even the beach.

This interdisciplinary project is bringing together students and researchers from fields that have had little or no interaction: engineering, early childhood education and pediatric therapy.

“The research, educational and health care impact is hard to overestimate, given the critical nature of early development, the relatively short time to prepare special needs infants to enter mainstream education and the complete lack of power mobility early in life,” Galloway said. “This project has so many positives, and is of interest to so many in the community. We are encouraging everyone interested in special needs infants to get involved – from parents to policy makers. We are thinking locally and globally at the same time.”

He added, “Although there are special needs kids in every community, you have never seen a special needs child driving themselves down Main Street in Newark, and neither has anyone else in any community anywhere. They, and often their families, are hidden citizens. We predict that very soon that will change in Newark, and then across Delaware, and then who knows. But time is of the essence because there is a baby being born right now who could use this today. That is the race we are in, so back to work.”

Agrawal, who directs the UD robotics laboratory, received his doctorate in mechanical engineering in 1990 from Stanford University, where he was a research assistant in the university's robotics laboratory. He taught and conducted research at Ohio University from 1990 until 1996, when he joined the UD faculty. He received his bachelor's degree from the Indian Institute of Technology in Kanpur and his master's degree from Ohio State University.

Galloway, who directs the UD Infant Motor Behavior Laboratory, received his doctorate in physiological sciences from the University of Arizona in 1998 and joined the UD faculty in 2000. He received bachelor’s degrees in exercise science and biology from the University of Southern Mississippi in 1987 and in physical therapy from Virginia Commonwealth University in 1989.

Providing important technical support to the project is Ji-Chul Ryu, a doctoral candidate in the Department of Mechanical Engineering with expertise in the planning and control of mobile robots.

The UD Early Learning Center is a focal point for interdisciplinary research on early learning and development, prevention, intervention and education. It provides exemplary infant, toddler, preschool and kindergarten care to a diverse population of approximately 180 children, specifically targeting children with risk factors including poverty, foster care and disabilities. The ELC is accredited by the National Association for the Education of Young Children, a recognition awarded to only 5-7 percent of all child care centers nationwide. The center, which is part of the College of Human Services, Education and Public Policy, received the Governor’s Award of Excellence in Early Care and Education in 2006.

Natural Strategies for Preventing Hearing Loss

I wonder if this would apply at all to people with DS who have hearing loss? I know much of hearing loss in DS is due to fluid in the ears, etc. But, still, this is interesting.

Natural Strategies for Preventing Hearing Loss

Alarmingly, nearly half of all baby boomers today suffer from some degree of hearing loss. While its onset can be almost imperceptible, the end result is an impaired ability to interact with the world that significantly detracts from quality of life.

For more than 20 years, leading otolaryngologist Dr. Michael Seidman has been searching for the underlying causes of age-related hearing loss and for natural strategies to prevent and even reverse this debilitating condition. His remarkable research and clinical experience shows that it is now possible to slow the progression—and sometimes even reverse hearing loss—using an integrative approach that includes optimal nutritional and lifestyle choices.

In the following excerpt from Save Your Hearing Now (Warner Wellness, 2006), Dr. Seidman reveals the intimate link between aging andhearing loss, and how you can implement a program today to protect your hearing against the ravages of aging.

After treating hundreds of patients suffering from hearing loss— and seeing the devastating effects it had on their lives—I decided to look for a natural solution. Knowing that antioxidants counteract the damage caused by free radicals, I thought there might be a way to use those same safe, natural substances to protect and/or restore hearing.

But first, the fact that there was a link between free-radical damage and hearing loss had to be established.

So the first study my colleagues and I conducted was designed to find out if there was a connection between damaged hearing in humans and the common hearing loss seen with aging. To measure free-radical damage, scientists can look for certain “markers,” chemical or cellular signposts that indicate change within a cell. In humans, one of these markers is known as the common aging deletion.

It is a sign of both advancing years and free-radical damage to the DNA of tiny organelles within each cell known as mitochondria.

From previous research in our lab and by others, we knew four things:

  1. Common aging deletions accumulate as we grow older.

  2. Blood flow to the cochlea, home to the nerve endings that make hearing possible, decreases as we age.1

  3. At the same time, our hearing apparatus becomes less sensitive.2,3

  4. As we age, our bodies produce more free radicals and fewer of the antioxidants that protect our hearing from free-radical damage.4

To test the theory that aging damages hearing and common aging deletions are a sign of that damage, we examined the temporal bones (those found at the sides and base of the skull) of thirty-four individuals, seventeen with normal hearing and seventeen who had age-related hearing loss. Temporal bones house the cochlea, the snail-shell-shaped organ responsible for hearing, and this is why we focused on that particular area. We found the common aging deletion in fourteen of the seventeen individuals with hearing loss and in eight of those with normal hearing.

Why didn’t the deletion appear in all seventeen of those with hearing loss? And why did it appear in bones of people whose hearing was fine? At least two reasons: The common aging deletion is only one type of hearing loss. It could be that other deletions contribute to hearing loss, too. In addition, there are four different types of age-related hearing loss.

The common aging deletion may not be responsible for all four. At any rate, this study provided us with enough evidence to conclude that the common aging deletion is associated with aging and hearing loss.5

Supporting the First Findings

The link between aging and hearing loss was underscored by our next study. It involved a number of rats, which were divided into four age groups: young, mid-young, mid-old, and old. We tested the sensitivity of rats’ hearing and examined their DNA for the common aging deletion, to determine if there was an association between the two.

We found that, like humans, rats tend to have higher levels of the common aging deletion as they grow older, and they have an increased tendency to develop hearing loss as well.6

Now we had established that the aging process resulted in an increase in common aging deletions, which weakened the mitochondria and damaged hearing. But could the damage be slowed, prevented, or possibly even repaired with supplements of naturally occurring antioxidants?

That’s the question we set out to answer with two additional studies. In one clinical trial, we followed animals from approximately several months old to the day they died. One group received a calorie-restricted diet, shown to reduce free-radical production, reduce mitochondrial damage, and to increase life span.

For purposes of comparison, a placebo-controlled group was allowed to eat freely. Other groups were treated with antioxidants, including vitamins E and C, and the hormone melatonin. With this study, we demonstrated that free radicals and damage to the mitochondria that occurs with aging leads to presbycusis, the medical term given to agerelated hearing loss.

Furthermore, we were able to demonstrate that dietary moderation and specific nutrients reduce the progression of age-related hearing loss, and we concluded that it is likely that a combination therapy would provide a synergistic protective effect on presbycusis and possibly on aging as well.7

But even more dramatic results occurred in our next clinical trial. In this study, we used twenty-one two-year-old rats, senior citizens in the rodent world, and divided them into three groups of seven each.

For six weeks, one group was given ALC (acetyl-L-carnitine), the second was given ALA (alpha-lipoic acid), and the third group, used as a control, received a placebo (sugar pill).

When we tallied the results, it was clear that hearing in the control (placebo) group had deteriorated at a rate typical for animals of that age. But that didn’t happen with either group of supplemented animals. Instead, we discovered the ALA and ALC did something pretty amazing. The supplemented rats not only avoided hearing loss, but their hearing actually improved. In other words, supplements didn’t just stop age-related hearing loss—they reversed it!8

During the study, the control group lost anywhere from 3 to 7 dB of hearing, while the ones treated with ALC or ALA had a 7 to 10 dB improvement in their hearing, with the greatest improvements occurring after six months of treatment. While the ALA was more effective for protecting hearing at low frequencies, ALC did better at higher frequencies. We demonstrated that taking both supplements is the best way to protect against hearing damage in general.

Of all the research I’ve done, I consider this study the most important. It clearly demonstrates that hearing loss can be prevented—and even reversed—by simply taking a combination of antioxidants that includes ALA and ALC. Both these substances have been popular in Europe for some time, and are widely considered nontoxic, very effective in treating hearing loss, and also capable of providing overall antiaging and wellness benefits.

But there is another reason this study stands out. Medical research is full of surprises. Sometimes what makes perfect sense on paper just doesn’t work in the lab. Other times we are literally astonished by the unanticipated benefits. That’s what happened in this particular study. Along with improved hearing in the supplemented animals, we found a much lower level of common aging deletions in the mitochondria all throughout the body.

The supplements actually reduced the amount of free-radical damage everywhere, creating an antiaging effect that improved hearing and carried over to other cells throughout the body. In other words, we had proven that age-related hearing loss can be reversed in mammals, with allnatural, side-effect-free substances.

Although this research was groundbreaking at the time, other scientists have since shown that ALA, ALC, and various other substances, including the antioxidant coenzyme Q10 (CoQ10) and glutathione, provide substantial protection for the mitochondria and thereby support healthy hearing.

How Aging Affects Hearing

Age-related hearing loss affects approximately one-third of all people aged sixty-five and older. Technically known as presbyacusia or presbycusis, age-related hearing loss is due to the changes that occur in the body as we grow older. Circulatory disorders, for example, which limit the flow of blood throughout the body, as well as to the brain and auditory system, are common in later years.

There are any number of reasons why circulation slows down as we grow older, among them heart disease, hardening of the arteries, diabetes, and sedentary lifestyles.

My research and that of many colleagues clearly show that the same things that protect us from the damage done by passing years also prevent damage to our hearing. In order to understand how hearing can be saved by slowing the clock, let’s take a look at the aging process and what happens in the body, especially the auditory system, as time passes.

Aging Begins in the Cells

During a normal lifetime, our cells divide anywhere from twenty to thirty times. This ongoing process of cellular expansion turns a child into an adult, and then cell division slows. Ultimately, because of inherent limits, our cells are no longer able to divide.

So although we continue to need new cells, later in life our bodies are not as efficient as they once were at producing them. The result: Disease or malfunctions occur because faulty cells are not replaced with fully functional versions.

In addition to the inherent limitations on new cell production, other factors are thought to play a role in aging. There are several different theories about the process, including the free-radical or mitochondrial clock theory, dysdifferentiation theory, and the telomerase theory. Thus far, the free-radical theory hasthe widest acceptance.

The Enemy: Free Radicals

In simplest terms, a free radical is an unstable molecule or cluster of molecules that is missing an electron. Like mini-atomic bombs, free radicals damage or destroy cells they come in contact with.

Free radicals are by-products of everything from eating to living in a world filled with toxic chemicals and pollution. In other words, they are unavoidable.

Although some free radicals are actually beneficial, others damage healthy cells. Free radicals can cause errors in genetic “messages” by altering DNA (deoxyribonucleic acid, the “blueprint” that governs cell growth).

This can, among other things, lead to a reduced blood supply to organs such as the inner ear and brain, thereby damaging hearing. When one of these loose cannon free-radical molecules binds with a healthy cell, it wreaks havoc on the cell’s ability to function. Mother Nature did not leave us completely defenseless, though.

Our bodies produce enzymes known as antioxidants—such as superoxide dismutase (SOD), catalase, and glutathione peroxidase—to counteract the damage. We can also obtain antioxidants from certain foods and supplements.

But if inadequate production or a poor diet results in a shortage of antioxidants, cellular damage may not be repaired, and sooner or later, we become ill. There have been many studies documenting that free radicals are responsible for more than a hundred human diseases, including Alzheimer’s, cancer, heart attacks, strokes, and arthritis, as well as aging.

Even though free radicals are microscopic and exist for far less time than it takes to blink an eye, they are capable of doing considerable damage simply because of their sheer numbers.

According to research at Emory University, each human cell receives approximately ten thousand free-radical hits each day. Further calculations have shown that this equals 7 trillion (7,000,000,000,000!) insults per second throughout our bodies.9

Certainly, 7 trillion is a staggering number, but the body counteracts this assault with its own arsenal of antioxidant enzymes. Unfortunately, there is a significant decline in these enzymes as we grow older. In fact, we now know that by the time the average person reaches the late twenties, production of these detoxifying enzymes has declined dramatically.

Based on the findings of scientists studying free radicals and human health, the best approach to slowing aging is one that provides the body with plenty of antioxidant ammunition against free radicals.

That means increasing intake of antioxidants, something that can be done in part with the proper diet or, more effectively, by taking supplements.

The Mighty Mitochondria

To measure free-radical damage, scientists can look for certain “markers,” chemical or cellular signposts that indicate change within a cell. In humans, one of these markers is known as the common aging deletion.

It is a sign of both advancing years and free-radical damage to the DNA of tiny organelles within each cell known as mitochondria. About 98 percent of our body’s energy is produced in mitochondria, so they are often described as the cells’ powerhouses. A number of studies have shown that the functions of the mitochondria decrease with age, leading some experts to speculate that this may be why many people feel less energetic as they grow older.

The hardworking mitochondria also serve as the cells’ “gatekeepers,” with the power to determine whether a cell lives or dies, so it’s doubly important to keep the mitochondria healthy.10

The mitochondria have their own DNA, which is completely separate from the DNA found in the cells. When free radicals ravage the cellular DNA, it can be repaired, but the mitochondria’s cannot. The mitochondria can be weakened or may even die, creating a slowdown in many essential processes. Even an incredibly small mutation in the mitochondrial DNA can dramatically slow energy production.

In fact, the drop in mitochondrial activity is the basis of the free radical or mitochondrial clock theory of aging. According to this theory, the aging body increases its production of free radicals, which damage the body’s tissues and subcellular elements, such as the mitochondria.

When we see the common aging deletion in mitochondria, we know the cells’ little energy factories aren’t fully functioning.

Full article at: www.lef.org/magazine/mag2007/nov2007_report_hearingloss_01.htm

Thursday, November 29, 2007

The Castle

What a sweet story this is ~

The Castle

He was born at the wrong time to the right woman. 67 years ago Richard
was born with Down Syndrome, his mother was informed moments after his
birth that he was a defective child and should be sent to the 'Castle'.
She decided then and there that no child of her's would grow up in
Lennox Castle, the hospital for disabled children in her area. Doctors,
unnerved at her determination to keep her child, young Richard, informed
her that because he had Down Syndrome he would die young that his
'fourth birthday' would be his last.

She loved that baby.

Loved him.

When his first birthday approached the family began to wonder about the
celebrations. It was decided then and there that Richard's first
birthday would go uncelebrated, there would be no party, no cards, no
gifts. This was not a result of grief, of denial, of shame. Richard's
mom decided that if he didn't have a first birthday - he could never
have a last one. If he didn't turn one, then he wouldn't turn two, if he
didn't turn two he wouldn't turn three, and if he didn't turn three then
he'd not celebrate his last - the fourth. Instead, family celebrations
intensified. Christmas and Easter and all the rest became huge family
celebrations. More than ever before the family pulled together.
Celebrated every life together.

Richard never knew a birthday party.

He never turned one.

His neices and nephews, his great neices and nephews, never even knew
how old their uncle was. Richard was hospitalized only once in his life.
His family filled his room, many stayed with him through the nights,
through the days, caring for him in shifts. Nurses had to constantly ask
people to move and give them room to work. Though very ill, Richard
pulled through ... as if his family had lassooed his soul and pulled it
back from heaven's shore.

It was then that one of the boys took a look at the plastic wristband
the hospital had placed around Richard's wrist to see how old his uncle
was, no one knew. Because he'd never had a first birthday.

Richard died three years ago. Calculations showed that he'd lived for 64
years. He lived loved. He lived part of a family that celebrated
belonging to him. There were "Richard" traditions, at every family
wedding, after the dance between bride and groom, Richard took the floor
with the bride. With every new home or apartment, Richard was the first
overnight guest.

At his funeral, the whole family decided to walk behind the casket. They
wanted not to be in cars hidden from view. They wanted to walk, publicly
proclaiming their membership in Richard's family. This boy who was to be
sent to the castle, lived his life a king. This boy who was to die at 4
had a mother that stole birthdays away and gave celebration to every
day. This boy who was to be hidden died - and 5 generations of his
family walked behind his coffin.

Crying.

***

I am in Falkirk, just about to start a day's long lecture, and my host
Helen, is telling me the story of her husband's uncle Richard. I begged
her to let me write his story here on my blog. She graciously gave me
permission.

Thank you Helen, for a wonderful day with the staff there at Falkirk.
And for the gift of Richard's story.


From: http://davehingsburger.blogspot.com/2007/11/castle.html


Tuesday, November 27, 2007

How Little Gabriel Survived by Fighting

While this doesn't have much to do with particularly DS, this is an article written by Dr. Mostert (I put another article he wrote about abortion & DS up in October).

This article shows how God is totally in control!

How Little Gabriel Survived by Fighting

by Mark R. Mostert

Recently, the London Daily Mail ran photos of the beautiful seven month old Jones twins. Dressed in similar outfits, (right down to their blue socks) their smiling, curious faces are crowned by shocks or red hair.

Rebecca Jones knew at ten weeks that she was pregnant with twin boys. “When they told us” the Mail reported, she and her husband Mark “were over the moon." As the pregnancy progressed, the happy parents picked out names: Gabriel and Ieuan.

Life was good.

Ten weeks later, however, something wasn’t right. A routine check-up brought news no expectant parents want to hear. Gabriel was only half his brother’s size and his heart was three times larger than normal. The doctors said that such a condition meant that Gabriel would likely die before he was born—a heart attack, or perhaps of a stroke. They also told the parents that should Gabriel make it into the world he would not survive for long.

The news got worse. If Gabriel died in utero, Ieuan’s life was also in jeopardy. The doctors advised “that it would be better to end Gabriel's suffering sooner rather than later.” Rebecca and Mark were being asked to make the unbearable a reality: "We had to decide whether to end his life and let his brother live, or risk them both."

They had some help in making their decision. The Joneses were advised, it seems, that it “would be kinder to let him die in the womb with his brother by his side than to die alone after being born.” This was enough to convince Rebecca: "That made my mind up for me. I wanted the best thing for him."

Everything neatly rationalized, the doctors promptly went work. First, they tried to cut Gabriel’s umbilical cord to end his blood supply. It didn’t work – the umbilical cord was too thick. The doctors then divided the placenta so that when Gabriel died, Ieuan would survive. "I put my hands on my stomach, thinking of Gabriel“ Rebecca said. “It was devastating. I had said my goodbyes."

But Gabriel lived on. The following morning his mother could feel him “kicking madly.” Not only had he survived two deliberate medical attempts to end his life, but over the next few weeks he gained weight and his enlarged heart began to return to its normal size.

Gabriel (1lb 15oz) and Ieuan (3lb 8oz) were born by caesarian section at 31 weeks. Now, the Mail’s photos show Ieuan tipping the scales at 15lb, and the almost disposed of Gabriel at 12lb 6oz.

Gabriel, according to his mother, “is always laughing.” "Doctors tried to break their bond in the womb, but they just proved it couldn't be broken."

At first glance, Gabriel’s story is a heartwarming one. Consider the headline: We're twinseparable! Happy with his brother, the boy who refused to die.

One would reasonably expect a story about the resilience of the human spirit: perhaps an unborn child facing some dire medical emergency with the help of courageous family and skilled physicians; of a roller coaster where doctors never give up trying to keep the child alive, beating back challenge after medical challenge. They use every medical intervention in their considerable arsenal because they believe life is precious and that doing everything possible to save an unborn child is a moral and professional imperative.

In this case, however, such a scenario is a lie.

Increasingly, as in Gabriel’s story, we treat unborn children with serious medical disabilities as threats to their unborn siblings, their families, and even their communities. It’s getting more difficult not to believe that many in medicine think that some entire groups of unborn children with disabilities are expendable. That’s one reason why we dispose of most children with Down Syndrome in-utero. Perhaps, as with Gabriel, killing unborn children with heart defects are next. Why not unborn children with cystic fibrosis, spina bifida, or those genetically likely to have blue eyes? Why not by gender? Why not destroy certain ethnic groups?

What really happened was that Gabriel survived in spite of his parent’s permission for him to die (after some serious prompting by the doctors, no doubt) and in spite of his doctors, who were trying to kill him. Gabriel’s physicians were deliberate and tenacious in wanting him dead: When one method didn’t work, they tried another. When he didn’t die, they marveled at this little boy holding out against their sophisticated plotting. That’s why his doctors nicked named Gabriel “Rocky.”

The underdog, facing incredible odds, willing to give his all, fought back. But that’s where the Ricky analogy ends. Gabriel couldn’t match his adversaries pound for pound, move for move, scalpel for scalpel.

But fight he did, blind to his enemies, unable to anticipate the direction of incoming blows in a lethal dance bereft of rules or referee.

But fight he did, as mightily as his little limbs would allow.

Mark R. Mostert, Ph.D is the director of the Institute for the Study of Disability and Bioethics at Regent University.

http://www.theconservativevoice.com/article/29476.html

Sunday, November 11, 2007

One more thing

One more thing I forgot to add in our "Book Update" post was about pictures!

If anyone would be willing to share pictures of their child in our book, that would be very appreciated too. We are looking for pictures to include throughout the book and also on the cover.


Thursday, November 8, 2007

What we mix my brother's vitamins in

Someone emailed and asked what it was that we used to mix my brother's vitamins in. I realized I didn't have it anywhere on the site or blog, so thought I'd put up what I wrote to this person:

~~~

We mix my brother's vits in Fruit spread most of the time. Sometimes it's a mix of fruit spread and coconut flavored coconut oil. We use Crofter's Organic Fruit Spread. We typically use Raspberry. The link for Crofter's is www.croftersorganic.com.

Wednesday, November 7, 2007

Book Update


We are making alot of progress on our book, yet we also have alot to do on it still!

The foreword is being written by Karen Gaffney (who recently swam across lake Tahoe!). The introduction is being written by Dr. Lawrence Leichtman. We've emailed Dr. Mostert (I posted an article he wrote on abortion a couple months back) to ask if he would be wiling to write an article on diagnosis and how doctors need to be informed.

We also have articles from alot of other individuals (including Sujeet Desai's mother) who gave us their permission to use their articles. We are waiting to hear from Pat Winders to see if I can include an article she wrote on PT in DS. I spoke to her on the phone a few weeks ago and she had contacted the editor of the journal that her paper was published in to get permission to let us use her article.

We are still looking for stories of anyone who would be interested in writing their stories - regarding their child's heart defect and the surgery, breastfeeding experience, birth/diagnosis experience, and whatever it may be.

~~ Qadoshyah

Special Needs Feeders

While I was working on the breastfeeding section in our book, I came across the link below that has several different "Special Needs Feeders" for babies that need help with feeding. We had to use the SNS with my brother when he was little. I thought I'd post the link up incase anyone was interested in it.


http://www.medela.com/NewFiles/specialtyfdg.html

Too Many Babies Take Anti-Reflux Drugs

http://children.webmd.com/news/20071105/too-many-babies-take-anti-reflux-drugs

Too Many Babies Take Anti-Reflux Drugs

Study Shows Some Infants Get Treated for GERD Unnecessarily
By Salynn Boyles
WebMD Medical News
Reviewed by Louise Chang, MD

Nov. 5, 2007 -- Too many babies who don't need anti-reflux drugs are being treated with them for normal spitting up and vomiting, new research suggests.

When 44 infants with persistent regurgitation were evaluated for gastroesophageal reflux disease (GERD), only eight met the accepted diagnostic criteria for the condition, even though all but two were already on anti-reflux medications.

Pediatric gastroenterologist Vikram Khoshoo, MD, PhD, says a dramatic increase in referrals for regurgitation issues over the past few years prompted the study, which appears in the November issue of the journal Pediatrics.

"Parents have come to view normal spitting up as a medical condition that requires treatment. But in many cases it is more of a laundry issue than a medical issue," he tells WebMD. "We are replacing Tide and Febreze with Prevacid and Zantac."

Babies and GERD Medication

The prescribing of anti-reflux drugs to infants with presumed GERD has skyrocketed in recent years, with one study showing a sevenfold increase in the use of one class of commonly prescribed acid-reducing medicines used by infants between 1999 and 2004.

This dramatic rise in usage has occurred despite the fact that almost no research has been done on the safety of anti-reflux drugs in children younger than age 1, Eric Hassall, MD, of Vancouver's British Columbia Children's Hospital, tells WebMD.

Hassall says the newer generation of anti-reflux drugs, known as proton pump inhibitors (PPI), has revolutionized the treatment of serious reflux in children, leading to a tenfold drop in surgeries for the condition at his hospital.

But he adds that there is no question that the drugs are prescribed too often for use in babies.

"We know that up to 70% of otherwise completely healthy babies spit up up to four times a day," he says. "As they reach the 7- or 8-month mark this rate drops. And by the time they start walking, less than 5% are still spitting up."

He says parents and pediatricians increasingly label normal vomiting as reflux disease, especially if the baby is also irritable.

Constipation, formula protein allergies, and exposure to cigarette smoke are much more common causes of irritability, as is colic, which generally resolves around age 3 months, he says.

"If you remove these exposures, at least 25% of babies will get better within a few weeks," he says. "They may continue to spit up, but they will be much happier."

He adds that the long-term safety of treating infants with powerful acid-suppressing drugs remains unknown.

While studies have shown the drugs to be generally safe in older children with reflux disease, there is also a suggestion that their long-term use may increase vulnerability to pneumonia and gastric disease.

Reflux Red Flags

Khoshoo says babies who spit up frequently should be evaluated for reflux disease if they are not gaining weight normally, if they have recurrent respiratory symptoms or wheezing, and if they are constantly irritable.

Forceful vomiting is another red flag that should not be ignored.

"If a baby is gaining weight and generally happy, the chances are very good that they have uncomplicated reflux that does not need drug treatment," he says.

When the babies in Khoshoo's study who did not have clinically relevant reflux were taken off anti-reflux drugs, most did not experience an increase in symptoms.

There are things parents can do to minimize normal spitting up. The Children's Digestive Health and Nutrition Foundation has these recommendations:

  • Avoid overfeeding. Don't feed the baby again immediately after he spits up. Instead, wait until the next scheduled feeding.
  • If a baby is formula fed, thickening the formula with rice cereal may help. But Khoshoo cautions that doing this without reducing formula volume will result in overfeeding, which could make the problem worse. He says a baby normally given 6 ounces of formula during a feeding should be fed 4 ounces of formula thickened with 4 tablespoons of cereal.
  • Avoid exposure to cigarette smoke.
  • Keep an infant upright for at least 30 minutes after feeding.

Khoshoo also recommends putting babies to sleep on their backs at a 30 to 45 degree angle "to let gravity work for you."

Thursday, November 1, 2007

Brain Tour

I thought this Brain Tour was interesting. I found it on the Alzheimer's Association website.

http://www.alz.org/alzheimers_disease_4719.asp

Wednesday, October 31, 2007

Bit more info. . .

Here's a link that has a bit more info about the research grant at DSRTF ~ http://dsrtf.org/news-103007.htm

Tuesday, October 30, 2007

KKI DS Clinic Research

I was at Kennedy Krieger Institute's DS clinic site and saw this DS research announcment and thought I'd pass it along, incase someone was interested - http://www.kennedykrieger.org/pdf/programs/ds_flier_07.pdf

DSRTF Grants Research Funds to Dr. Roger Reeves

DSRTF Grants $250,000 to Dr. Roger Reeves at Johns Hopkins School of Medicine

DSRTF announces funding for a major new research program led by Dr. Roger Reeves at Johns Hopkins School of Medicine. Dr. Roger Reeves’ recent research discovered that a certain area of the brain, the cerebellum, is underdeveloped in a Down syndrome mouse model, analogous to observations in individuals with Down syndrome. These studies by Dr. Reeves and his colleagues further led to the identification of a potential drug that essentially normalizes the development of the cerebellum in the mouse model.

This new grant from DSRTF significantly extends Dr. Reeves’ research, and includes addressing two critical next questions:

  1. Does the potential drug also correct a deficit in the development of the nerve cells in the hippocampus, a brain area involved in learning and memory?
  2. Does the potential drug produce positive and measurable effects on learning and memory in a Down syndrome mouse model?

“The DSRTF award allows us to pursue our preliminary observations immediately without the now considerable delay that’s usually associated with obtaining federal funding,” says Dr. Reeves. “With a decrease of nearly 70 percent- from $42 to $13 million- in the amount of Down syndrome research dollars from the National Institutes of Health in the last few years the role of groups like DSRTF has become critical to continued progress in the effort to help 350,000 Americans with Down syndrome.”

This new grant adds a third novel potential therapeutic target to the DSRTF-supported research portfolio, which also includes two additional recently discovered potential therapeutic targets currently under investigation at Stanford University School of Medicine. DSRTF’s Scientific Advisory Board unanimously agreed that the new research is intriguing and closely aligns with DSRTF’s mission of accelerating research that will lead to a treatment to improve learning and memory in individuals with Down syndrome.

Thursday, October 25, 2007

Turmeric is needed at a young age!

The abstract below shows that they detected Abeta levels in the spinal fluid of children with DS at a very young age (8 mths, being the youngest one they tested!). This shows all the more reason to supplement accordingly to deal with the bad effects of the APP gene triplication - it is causing problems very early on. Turmeric helps break-up Abeta plaques and tangles (in the brain - part of the AD pathogenesis). We supplement my brother with Turmeric. He gets it in his NTV-D and we also give him some extra at times (although I think we will be more consistent now, especially after doing some of this reading).


Increase in beta-Amyloid Levels in Cerebrospinal Fluid of Children with Down

Syndrome.

Background: Individuals with Down syndrome (DS) invariably develop
Alzheimer's disease (AD) during their life span. It is therefore of
importance to study young DS patients when trying to elucidate early events
in AD pathogenesis. Aim: To investigate how levels of different amyloid-beta
(Abeta) peptides, as well as tau and phosphorylated tau, in cerebrospinal
fluid (CSF) from children with DS change over time. The first CSF sample was
taken at 8 months and the following two samples at 20-40 and 54 months of
age. Results: Individual levels of the Abeta peptides, as well as total
Abeta levels in CSF increased over time when measured with Western blot. Tau
in CSF decreased whereas there was no change in levels of phosphorylated tau
over time. Conclusion: The increasing levels of Abeta in CSF during early
childhood of DS patients observed in this study are probably due to the
trisomy of the Abeta precursor APP, which leads to an overproduction of
Abeta. Despite the increased CSF concentrations of Abeta, there were no
signs of an AD-indicating tau pattern in CSF, since the levels of total tau
decreased and phosphorylated tau remained unchanged. This observation
further strengthens the theory of Abeta pathology

Wednesday, October 24, 2007

Turmeric helping AD again!

I read about the following abstract in LEF's newest magazine. I thought it was pretty interesting. Basically it is saying that by giving these people with AD curcuminoids (the active ingredient in Turmeric) that it increased the absorption of amyloid-beta (which is a good thing). AB creates plaques and tangles in the brain and that is part of the problem in AD. The curcuminoids helped strengthen the immune system of these people to be able to deal with the AB.
Curcuminoids enhance amyloid-β uptake by macrophages of Alzheimer's disease patients

Laura Zhang A1, Milan Fiala A1, John Cashman A2, James Sayre A3, Araceli Espinosa A4, Michelle Mahanian A1, Justin Zaghi A1, Vladimir Badmaev A5, Michael C. Graves A6, George Bernard A4 A7, Mark Rosenthal A1

Abstract:

Treatment of Alzheimer's disease (AD) is difficult due to ignorance of its pathogenesis. AD patients have defects in phagocytosis of amyloid-β (1-42) (Aβ) in vitro by the innate immune cells, monocyte/macrophages and in clearance of Aβ plaques [5]. The natural product curcuminoids enhanced brain clearance of Aβ in animal models. We, therefore, treated macrophages of six AD patients and 3 controls by curcuminoids in vitro and measured Aβ uptake using fluorescence and confocal microscopy. At baseline, the intensity of Aβ uptake by AD macrophages was significantly lower in comparison to control macrophages and involved surface binding but no intracellular uptake. After treatment of macrophages with curcuminoids, Aβ uptake by macrophages of three of the six AD patients was significantly (P<0.001>

Wednesday, October 17, 2007

Love & Learning in the News

http://www.freep.com/apps/pbcs.dll/article?AID=/20071016/NEWS02/710160395/1004

Daughter's disability serves as motivation for this family
October 16, 2007

BY BEN SCHMITT

FREE PRESS STAFF WRITER

Nearly 23 years ago, a doctor stared at a happy couple with a newborn daughter and told them she'd probably never read.

But instead of taking the news with tears and defeat, Joe and Susan Kotlinski looked at their baby girl, Maria, diagnosed with Down syndrome, and decided to turn the prognosis into motivation.

Today, Maria Kotlinski not only reads, she volunteers at a hospital and child care center, takes jazz dance classes and plays the piano.
Working out of their living room in Dearborn, the Kotlinski family has developed a reading system targeting special needs children, particularly those with Down syndrome and autism. Their company, Love and Learning, has touched 6,800 families worldwide.

"We were faced with a challenge that changed our life completely," said Joe Kotlinski, a 53-year-old Ford retiree who worked on the automaker's technical hotline.

They use instructional books and computer programs, but their most successful approach has been with DVDs.

"We know the average child watches 5,000 hours of TV before first grade," Joe Kotlinski said. "We use TV in a very constructive way."

The key to the Kotlinski family's success is repetition and starting early with children.

"The first thing we do with parents is congratulate them on their newborn, because what you get in hospitals and the perception of your child can be scary," Joe Kotlinski said. "Then we tell them about Maria -- she was reading a thousand words by age 5. That opens their mind."

But the most important message for these parents is immediacy: "We tell them to start now. Don't expect the school system to be able to teach your children to read."

The videos focus on simplification. The words on the screen appear by themselves: black words with a white background. The next frame shows an image of the words. The first kit, for example, teaches the alphabet and about 24 words.

And the lessons are intentionally short: only 2 to 4 minutes a day.

"We try to stimulate the child to try and imitate sounds and play around with sounds," Susan Kotlinski said. "Those sounds are the building blocks of spoken words."

One of their satisfied customers is Wayne County Medical Examiner Carl Schmidt, whose 3-year-old son, Lawrence, has Down syndrome.

"They provide the tools to help parents make that commitment, which I think is their most significant achievement," Schmidt said. "When you have a child with a disability, you become aware of the many misconceptions regarding particular ones, even among the medical community."

Schmidt said his first meeting with Maria Kotlinski surprised him.

"I was taken aback by the clarity of her diction and enunciation," he said. "Although it's obvious that her parent's efforts had much to do with it, their systematic way of approaching language instruction also played an important role."

Maria has a close relationship with her parents and younger sister, Lea, 21. They joke about Maria's piano playing, her dancing classes and proudly sit back as she describes her job duties as a volunteer at Cotter Early Childhood Center in Dearborn.

"I interact with the children," Maria said. "I play with them. I help them with their work and I keep them safe."

Joe Kotlinski still marvels at this foray into the world of educating kids with special needs.

"It's really turned into a wonderful opportunity to help people," he said. "The word 'miraculous' is appropriate. But it's not just for Maria. It's there for a lot of children."

Tuesday, October 16, 2007

Blood Test Could ID Alzheimer's Patients

http://www.cbsnews.com/stories/2007/10/15/health/main3368895.shtml

Blood Test Could ID Alzheimer's Patients

Researchers at Stanford University say they have developed a potentially pathbreaking blood test that could help to identify patients with Alzheimer's disease.

According to a paper published in the online edition of the British journal Nature Medicine, preliminary studies by a team of scientists led by a Stanford neurology professor show the test is yielding promising results in predicting which patients with mild memory loss are at high risk of developing Alzheimer's disease.

In a study of 259 blood samples, the test identified early markers for Alzheimer's with 90 percent accuracy, reports CBS News correspondent John Blackstone.

Today only an autopsy can establish for sure that a patient had Alzheimer's. Brain scans and spinal taps are helpful but they're not certain.

There is still plenty of lab work to be done, more rigorous research before it's proven a simple blood test can diagnose Alzheimer's, but those working on the test are hopeful it can be approved for use by 2009, adds Blackstone.

Currently, an early Alzheimer's diagnosis requires complex brain scans. Spinal fluid can also reveal the disease but that can be a difficult and painful test.

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