31 for 21: Dr. Henry Turkel's book, Post 1: Overview

For the last year, I've wanted to write some posts up going over Dr. Henry Turkel's book, Medical Treatment of Down Syndrome and Genetic Diseases, copyright 1985. From what I know, the book is out of print. I was able to find it used online somewhere several years ago.

It was a great buy and is an extremely interesting book. It's packed full of information and very fascinating to see what he had to work with and through in those early years. It will take several posts to go over the details in this book, so I will do that over a few weeks, Lord willing. I have 5 posts "written" on a few pieces of paper right now (and there will likely be a few more than that), so I have to put them all up here on the blog.

For those who don't know who Dr. Turkel is, here's just a snippet of background info:

Dr. Henry Turkel was a doctor in the 1950's and earlier who treated patients with Down syndrome and other genetic conditions with nutritional supplements, diet and medications.

On Page 1 of the book, Dr. Linus Pauling writes,

There is an increasingly great and increasingly convincing body of evidence that the use of vitamins, minerals, and other orthomolecular substances in the proper amounts, the amounts leading to optimum health and to the best treatment of disease, has great value in the control of infectious diseases, cancer, heart disease and genetic diseases. there seems, however, to be a bias against these substances on the part of the medical profession and of nutritionists. The result is that there is opposition to orthomolecular medicine.

The work of Dr. Henry Turkel provides a striking example of the way in which this opposition operates to the detriment of the health and well being of a large number of people. Dr. Turkel has developed, over a period of decades, a treatment of mentally retarded children with the use of vitamins, minerals, cerebral stimulants, and other substances. He has gathered together a convincing body of clinical observations showing that the genetic condition of mental retardation need not be accepted as inevitably leading to permanent defect and inability of the individual to function in normal society. Dr. Turkel has indeed provided new hope for the mentally retarded and for members of their families, hope that a great improvement in functioning can be achieved.

This is a good overview of what Dr. Turkel's book goes over. It covers everything from the beginning of his development of the U Series, specific cases of Dr. Turkel's patients, his attempt to get his U Series FDA approved, and the success of patients on the U Series with DS both in the US and abroad.

Dr. Turkel earned his medical degree in 1936 and went into private practice. He also perfected biopsy instruments before the second world war. The instruments called the Turkel Trephine Instruments as well as the Turkel Needle. All of which were used routinely in World War II. He was also appointed consultant for the Surgeon General  in 1952.

A boy named Peter was who started Turkel's research into Down Syndrome. Peter's father inquired about possible treatment for his son. Dr. Turkel knew nothing about Down Syndrome, but he had studied how nutrition can help other genetic conditions.

When Dr. Turkel first started working with Peter and his other early patients with DS, it was not known what caused DS. As he states in his book on page 5,

When I first treated Peter, maternal exhaustion, low thyroid, depleted ovarian function, and similar deficiencies were proposed as the cause of the disease.

So, what Dr. Turkel did was,

Instead of considering the underlying cause of Down syndrome, I looked at the anomalies and realized that many of them were similar to those diagnostic of genetic diseases that I had already treated. I immediately considered the possibility of medical/nutritional therapy. I dispensed the three units of the "U" Series simultaneously, adding a broad spectrum of vitamins and minerals in pharmocological dosages, as well as enzymes, to correct the physical retardations that I attributed to malnutrition caused by the accumulations.

Peter is who brought Dr. Turkel into the realm of patients with DS and mental retardation, as Turkel writes on page 6,

Peter improved and news about the "U" Series spread. With few exceptions, since the 1950's, I have restricted my practice to the treatment of patients with Down syndrome and other diseases associated with mental retardation.

This finishes the first post about Dr. Turkel's book. I will leave you waiting for the next post to find out what comes next :).



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31 for 21: History of Targeted Nutritional Intervetion

I've decided to start to go over Dr. Henry Turkel's book which he wrote in the 1980's. Dr. Turkel was one of the first doctors to use nutritional supplementation in people with DS. The first post covering his book is scheduled to post tomorrow. But, before that, I thought it would be helpful to share an article which is in our book that goes over the history of Targeted Nutritional Intervention (TNI).

The History of Targeted Nutritional Intervention
By Qadoshyah Fish

Henry Turkel

The idea of giving vitamin supplements to individuals with Down syndrome has been around for many years.  It started in the 1950’s with Dr. Henry Turkel’s work¹. The effects and all that the extra chromosome did were not yet known at that time.  Therefore, Dr. Turkel’s work was, in a way, working in the dark.  It was not until 1974 that researchers began to realize what genes were on the 21st chromosome. It was not until a few years later that it was discovered some of these genes were actually being over-expressed in patients with Down syndrome and therefore causing some or all of the problems associated with Down syndrome. This would not be fully realized until years later when the Human Genome Project was done in the 1990’s.  In the 1970’s and years prior, it was thought that the genes from the extra chromosome were “turned-off” and played no role once the person was born, as can be seen in this quote from Dr. Turkel’s book,

The medical consensus that there were no metabolic imbalances in Down syndrome was so deeply entrenched that as recently as 1977, some medical students were still being taught that the extra genes encode structural defects before birth and then “turn off” (Expert’s testimony in Superior Court, Los Angeles, California #C 88260). (Medical Treatment of Down Syndrome and Genetic Diseases by Henry Turkel, M.A., M.D., Ilse Nusbaum, M.A. Copyright 1985. Page 172)

Dr. Turkel’s supplement was called the “U Series.”  It was a protocol with a variety of vitamins, minerals, drugs and many other nutrients to be taken throughout the day. Because Dr. Turkel’s work was without all the medical research that we have today, the doses of vitamins and nutrients that were given patients were very large “mega doses” of nutrients. His protocol was conceived after the father of a boy with Down syndrome approached Dr. Turkel in 1940 about a “possible treatment for his son.” Dr. Turkel’s “U Series” helped this child and therefore word spread about the “U Series.” In the 1950’s Dr. Turkel restricted his practice, with a few exceptions, to only patients with Down syndrome and other forms of mental retardation.  Dr. Turkel saw many improvements in the patients in which he used the “U Series.”

In 1959, Dr. Turkel applied for a “New Drug Approval” for his “U Series” from the Food and Drug Administration, but they denied Dr. Turkel’s appeal for approval. It was denied because the FDA did not consider the newly discovered implications of the extra genes on the extra chromosome 21 and therefore “concluded that since the ‘U’ Series could not remove the chromosome, it could not help the patients.” (ibid, page 209).  The FDA stopped Dr. Turkel from interstate distributing of the “U Series”, but he was legally able to sell the “U Series” within the state of Michigan.

Dr. Jerome Lejeune, who discovered the cause of Down syndrome, Trisomy 21, was also using vitamin and nutritional supplements with his patients with Down syndrome during the 1960’s. He was not using the “U Series,” but he was using some of the same vitamins and nutrients that were in the “U Series.”

Jack Warner

Dr. Jack Warner started his private practice in the early 1960’s². A few years after beginning his practice, Dr. Warner saw his first patient with Down syndrome.  It was then that Dr. Warner started extensively researching Down syndrome.  In 1984 his research led him to meeting Dr. Turkel. Dr. Warner was  impressed with the good results that he saw with the “U Series” that he started referring many of his patients to Dr. Turkel.  After constant research and continuing to see the beneficial effects from the “U Series” it led Dr. Warner to several other doctors and biochemists from the Linus Pauling Institute. This gave new knowledge and showed the increased benefits and effectiveness of certain nutrients from new research which led Dr. Warner to design the High Achievement Potential Capsules (HAP Caps) to be used with patients with Down syndrome.

HAP Caps were formulated in an FDA laboratory and received FDA approval in 1986. Unfortunately Dr. Warner’s research and HAP Caps have “fallen by the wayside” since his death in 2004.

Nutrichem’s MSB Plus

In 1982 Kent Macleod met the mother of a child that was severely brain damaged and had seizures³. He was able to treat this child with certain vitamins and it helped him tremendously, stopping his seizures. This mother began to research how nutritional supplements may benefit her son and found the work of Dr. Henry Turkel.  She asked Macleod to look at the research and findings of Dr. Turkel. She set a meeting up with Macleod and some mothers of children with Down syndrome to discuss the work and claim of Dr. Turkel. At this meeting, Macleod told the parents that if he were to consider this treatment, he would change Dr. Turkel’s formula.  Therefore, Macleod started to develop the first MSB Plus formula. Macleod’s work with children with Down syndrome continued to grow slowly over the years by word of mouth as parents told other parents the health benefits.

In the early 1990’s, Macleod was contacted by a mother, Dixie Lawrence, who’s adopted daughter had Down syndrome. Dixie asked Macleod if he would consider customizing the MSB formula based on her daughter’s blood work results.  At this time there was research and work being done in France by Dr. Marie Peeters-Ney and Dr. Jerome Lejeune on amino acid deficiencies being linked to certain genes on the 21st chromosome. After hearing the positive reports by parents who had been giving their children MSB Plus for the past 10 years and seeing the research done in France, Macleod was convinced to work with Dixie on a customized formula for her daughter.  Interest in Nutrichem’s MSB Plus grew tremendously after Dixie aired on the Day One program in 1995.

Today Nutrichem still provides their MSB Plus formula to thousands of families all over the world. 

International Nutrition’s Nutrivene-D

Nutrivene-D was originally developed by Dixie Lawrence Tafoya for her daughter with Down syndrome in the early 1990’s⁴. Dixie learned of Dr. Turkel “U Series” and was able to find Dr. Turkel in Israel where he had retired.  Dr. Turkel informed Dixie that he was not seeing patients anymore and that he had left his “U Series” to a pediatrician, Dr. Jack Warner, in the U.S.⁵. Dr. Warner greatly altered the “U Series” formula, which would now be known as the HAP Caps. Dixie decided to pursue this further and therefore she and 30 other families met with Dr. Warner.  The HAP Caps did not have much impact on Dixie’s daughter.  By this time research had been published that showed metabolic differences in patients with Down syndrome.  Using this research, input from numerous scientists and her daughter’s blood and urine analyses, Dixie started to develop her own TNI formula. Dixie “fine tuned” the formula by looking at the specific abnormalities measured in her daughter’s blood and urine testing.  

The scientists who were initially involved by researching abstracts and articles which documented metabolic and nutrient concerns in Down syndrome also helped reference the TNI formula to the U.S. RDA for safety.
Today, the Nutrivene-D formula still uses scientists and doctors to make updates and improve their formula based on current research and studies which are done. Certain nutrients may be added or changed, as new research emerges. The Nutrivene-D formula is used by thousands of families throughout the world.

Conclusion

Since the calm beginnings in the 1950’s and Dr. Turkel’s approach with “mega-doses” of nutrients, to where we are at currently with Nutrivene-D, it has been a long path and will continue to be an ever changing path as new research emerges. Dr. Turkel started with a good idea, but thanks to new research, and much work to scientists, parents, and doctors, we can now safely give children with Down syndrome a formula which is “targeted” to meet their specific metabolic and nutrient needs. 

1)    Medical Treatment of Down Syndrome and Genetic Diseases by Henry Turkel, M.A., M.D., Ilse Nusbaum, M.A. Copyright 1985
2)    Warner House Clinic History. http://www.warnerhouse.com/
3)    Down Syndrome and Vitamin Therapy, Unlocking the Secrets of Improved Health, Behaviour and Intelligence by Kent Macleod. Printed October 2003
4)    A Circle of Friends II by Aunt Gini Mullaly & Deborah Saxton-Bolt. Copyright 2000.
5)    Smart Drugs & Down’s Syndrome by Steven Wm. Fowkes & Ward Dean, M.D. February 14, 1994 issue of Smart Drug News. [v2n10]




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31 for 21: Gluten-Free Chocolate Chip Pancake Muffins

I haven't put very many gluten-free recipes up as of late. So, I think it's well over-due for some.

Here's a yummy breakfast (or snack-time) muffin that we made a few days ago. They aren't overly sweet, but they are yummy.

I found the recipe via Kevin&Amanda.com who did a guest blog post on another blog. The original recipe is for miniature cupcakes, but I decided to change it up some. The original recipe is also not gluten free, but you can see it here. One of the big variations I did to the recipe besides making it gluten-free, was not using the maple syrup, simply because we didn't have any. I bet these would turn out really good if there was maple syrup or even maple extract in them. I simply used a lot of vanilla extract in the recipe.

So, here goes:

Gluten-Free Chocolate Chip Pancake Muffins

Yield: 27 muffins, 12 miniature muffins

Ingredients:
1 cup butter (softened) or lard
1 cup brown sugar
3 cups rice flour
2 teaspoons baking powder
1/2 teaspoon salt
1 1/2 tablespoons vanilla extract
2/3 cup milk
4 eggs
1 cup chocolate chips

Directions:
1. Preheat oven to 350 degrees.
2. Cream the butter and sugar on medium speed until well combined. Add the vanilla, eggs and milk, beating well after each addition.
3. In a separate bowl, whisk together the flour, baking powder and salt.
4. Add in the flour mixture, stirring just until it's combined.
5. Add the chocolate chips.

6. Bake at 350 for 12-18 minutes (8-10 for the mini muffins).

Enjoy!

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31 for 21: Special Olympics Figure Skater Lauren Miller

I originally saw this video on the blog, Life With My Special K's. But, I thought I would share it here, as this young lady with DS does an amazing job figuring skating at Special Olympics.

2011 Special Olympics Skating Expo - Lauren Miller has Down Syndrome and is 13 years old. She has been skating since she was 6 years old. Lauren is also Global Messenger for Special Olympics Illinois.





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31 for 21: Blueberry

I mentioned in a post a few weeks ago that we would be supplementing extra Blueberry. So, I thought I'd share some articles from Life Extension which goes over the benefits of Blueberry.

We use Swanson Vitamins Greenfoods Blueberry Extract.

I will paste one overview article from LEF here and link to a few others.

Blueberries: Colorful Protection for a Healthier Heart, Sharper Brain, and Cancer Defense

Blueberries: The World's Healthiest Food

Report: Blueberries

Maintaining Youthful Cognitive Function with Blueberries

By Laurie Barclay, MD

Published scientific studies show that blueberries are packed with nutrients that not only improve cognitive function and delay neurological decline but also protect delicate brain structures against oxidative damage.

Rich in powerful polyphenol compounds, blueberries have been shown to uniquely protect the brain against noxious influences such as free radicals, radiation, inflammation, and excitotoxicity. Furthermore, blueberries may even reverse age-related deficits in cognitive and motor function. Scientists have noted that blueberry compounds are readily absorbed into the bloodstream, then cross into the brain where they influence regions involved in memory and motor function—suggesting therapeutic roles against Parkinson’s and Alzheimer’s.

In this report, we speak with some of the scientists at the forefront of this exciting area of research.
Blueberries: A Nutritional Powerhouse

Modern science has made much progress in discovering the benefits of specific compounds found in fruits and vegetables, such as vitamin C and resveratrol. Nutrient-dense “superplants” go a step further and are packed with complex blends of phytonutrients that work together to promote optimal health.
Blueberries: A Nutritional Powerhouse

One such “superfruit” is the blueberry, which contains a powerhouse of nutrients that may defend the body against the ravages of aging and disease. Blueberries are rich in polyphenols, of which some of the most beneficial are a class of flavonoids called anthocyanins, which give the berry its intense blue color.1 These remarkable compounds as well as proanthocyanidins, flavonols, and tannins, which are also found in blueberries, act not only as antioxidants,2 but have been shown in the laboratory to fight inflammation as well.

This dual effect gives anthocyanins the potential to fight cancer,3-6 cardiovascular disease,5 inflammation,7 and aging and degeneration of nerve cells.8,9

Oxidative stress and inflammation are thought to be common culprits not only in aging itself, but also in cardiovascular disease, Alzheimer’s disease, and other neurodegenerative diseases plaguing our graying population. Population studies suggest that consuming a diet high in antioxidants, such as those found in fruits and vegetables, may forestall the onset of Alzheimer’s disease and other dementias.10,11 Polyphenolic compounds found in blueberries can decrease the age-enhanced vulnerability to oxidative stress and inflammation. Compared with other fruits and vegetables, blueberries are among the highest in antioxidant capacity, or in their ability to scavenge harmful free radicals, as measured by the oxygen radical absorbance capacity (ORAC) test.12 Similarly, wild blueberries outpace other fruits such as cranberry, apple, and grapes in the cellular antioxidant activity assay, a newly developed, next-generation technology that measures antioxidant effects within the cells themselves.13
Alzheimer’s disease

Despite the undisputed advances made possible through a variety of drugs available to combat various diseases, drugs have powerful effects, some beneficial, some potentially harmful. The potential risks must be considered when prescribing or taking medications, especially for chronic diseases of aging in which treatment may be needed over the long term.

On the other hand, fruits and vegetables that are naturally found in our diet can be safely processed by the body without concern for possible side effects. Appropriate intervention with blueberries and their extracts may promote health and combat disease—without the risk of adverse complications common with powerful drugs.

A wealth of studies published in 2007 reveal that blueberries do just that. Animal studies have shown that pterostilbene, an active ingredient in blueberries, may specifically help to prevent colon cancer.14 Another constituent of blueberries—tannins—can kill disease-causing bacteria,15 while blueberry phenolics have a beneficial effect on bacteria in the colon, thereby reducing gastrointestinal inflammation.16 Further up-to-the-minute research shows that the antioxidant power of blueberries promotes eye health and protects against chromosomal damage,9 while anthocyanins found in berries may also improve the function of brain cells, with corresponding behavioral improvements.8
Blueberry Extract Protects Brain Cells From Injury

In an exciting study published recently, the National Institute of Aging looked at the effect of a blueberry-enriched diet in protection from brain injury in rats. 17 Young rats received a diet containing 2% blueberry extract, or a control diet, for at least eight weeks. Some of the rats were then given injections of kainic acid, a noxious chemical producing oxidative stress and overexcitability of nerve cells, into the hippocampus, a brain region involved in memory and learning.

Rats that received kainic acid injections clearly had impaired learning performance compared with control rats. However, those rats that had received the blueberry-supplemented diet before kainic acid injection had much less impairment than those that received the control diet. Even more amazingly, microscopic examination of brain tissue confirmed that rats receiving the control diet and kainic acid injections had significantly greater loss of brain cells than rats pretreated with the blueberry-supplemented diet.
Blueberry Extract Protects Brain Cells From Injury

Donald K. Ingram, PhD, from the Nutritional Neuroscience and Aging Laboratory, Pennington Biomedical Research Center, Louisiana State University System in Baton Rouge, who collaborated with the National Institute of Aging on this study told Life Extension, “Beyond the demonstrated antioxidant activity, blueberries appear to stimulate stress responses that protect cells [from] a great variety of injuries.” He added, “Evidence that blueberries could be helpful to the aging brain is derived from a variety of carefully conducted rodent studies showing improved performance of aged animals in behavioral tasks, as well as increased protection against various forms of brain injury relevant to human neurodegenerative disease.”

Dr. Ingram’s group took their findings one step further. They found that serum from the blood of rats fed the blueberry-enriched diet actually protected cells grown in the laboratory from death induced by hydrogen peroxide, a potent oxidative stressor that generates many free radicals. The researchers concluded that blueberry supplementation may protect against neurodegeneration and cognitive impairment caused by excitotoxicity and oxidative stress.17

“Given the epidemiological evidence that diets high in fruit and vegetable content, particularly those of dark color [may help protect against oxidative stress], consumption of blueberries could be highly recommended as part of a healthy diet,” Dr. Ingram said. “There is a great need now for systematic clinical trials to confirm the beneficial effects of blueberry consumption on a number of important health measures, including behavioral function as well as risk factors for age-related disease, such as cardiovascular disease and diabetes.”

Blueberry Extract May Prevent Age-Related Brain Impairment

The potential health benefits of eating blueberries and similar fruits, and the scientific evidence supporting this potential, were also highlighted recently at the 2nd International Symposium on Berry Health Benefits, held in June 2007 at Oregon State University in Corvallis.

One of the main presenters at this symposium was James A. Joseph, head of the Neuroscience Laboratory of the USDA-ARS Human Nutrition Research Center on Aging at Tufts University in Boston, MA.
Blueberry Extract May Prevent Age-Related Brain Impairment

His group sought to confirm whether blueberry supplementation promotes communication between nerve cells, and so theoretically reduces the risk of cognitive and motor impairments associated with aging. Using an animal model, Dr. Joseph’s group studied the effects of a blueberry-supplemented diet on movement and memory problems related to aging, as well as on the underlying chemical and physical changes in the brain.8

“We fed rats a diet containing blueberries, strawberries, or spinach (the equivalent of you eating a large spinach salad, or a cup of blueberries, or about a pint of strawberries) for eight months, beginning at about 19 months of age, at which time they’re starting to show signs of aging in cognitive and motor function,” Dr. Joseph told Life Extension. “We showed that these animals did better than the ones that were maintained on non-supplemented diets.”

Compared with the rats that received the control diet, the aging rats that received supplemented diets were much less likely to develop impairments in water maze performance and on other tests of memory, learning, and coordination, such as balancing on a narrow or spinning rod. What was even more exciting was that when aged rats that already had impairments on these tests were given blueberry extract, their performance improved or even returned to normal!8

“The blueberries were pretty good at blocking some of the effects of the oxidative stressors; in other words, they were fairly good scavengers of free radicals, [and] we also started looking at other mechanisms, and other potential benefits that they might have,” Dr. Joseph said. “We showed that neurogenesis—the growth of new neurons—is increased in these animals, which goes along with the behavioral improvements that we saw.”

Increased levels of a neuronal chemical known as extracellular signal-regulated kinase (ERK), which protects nerve cells, gave further proof of neurogenesis in the blueberry-supplemented animals. In fact, ERK has been shown to be crucial for a variety of memory tasks, making it uniquely poised to change the neuronal and behavioral effects of aging.

Not only is blueberry supplementation associated with growth of new nerve cells,18 but existing nerve cells are better able to communicate with one another through a process known as signal transduction. Levels of enzymes involved in signal transduction, such as GTPase and protective mitogen-activated protein (MAP) kinases, actually increased in the blueberry-supplemented animals.

This led the researchers to suggest that “nutritional interventions with high antioxidant fruits, such as berryfruits, may prove to be a valuable asset in strengthening the brain against the ravages of time and retard or prevent the development of age-related neurodegenerative diseases.”8

Not surprisingly, researchers in Dr. Joseph’s laboratory have confirmed that anthocyanins in blueberries are able to cross the blood-brain barrier of supplemented animals and localize in various brain regions important for learning and memory.19 Using mouse microglial cells (cells that nourish, protect, and enhance the function of brain cells) they also studied the mechanisms by which anthocyanins protect nerve cells and enhance their function.20

“The anthocyanins were localized in the brain, and the more different ones that were localized in the brain, the better the cognitive behavior was,” Dr. Joseph said. “We know that they are very good antioxidants, and very good anti-inflammatories. What we know from our work in mouse microglial cells is that these polyphenols can inhibit the stress pathways at several points involved in the inflammatory pathways, with reductions in inflammatory cytokines.”

This research suggests that blueberries produce antioxidant and anti-inflammatory effects by directly changing oxidative and inflammatory stress-signaling pathways. In the laboratory, blueberry extract prevented harmful biochemical changes associated with exposing microglia to an inflammatory substance.20
Blueberry Extract Protects Specific Brain Region From Injury

“In Alzheimer’s disease and in Parkinson’s disease, it’s postulated that these microglia become very overactivated and start to destroy the cells, functioning deleteriously instead of being beneficial to the brain,” Dr. Joseph explained. “When that happens, they can’t be activated and used for other purposes.”

Although injury and stress ordinarily activate the microglia to release substances that will protect nerve cells, pathological activation of microglia may aggravate the progressive damage associated not only with Alzheimer’s disease and Parkinson’s disease, but also with stroke, multiple sclerosis, and human immunodeficiency virus (HIV)- or AIDS-associated dementia.20,21

An interesting model system to study Alzheimer’s disease is the transgenic mouse that is genetically engineered to have variations in amyloid precursor protein (APP) and presenilin-1 (PS1), proteins that are important in producing the brain pathology characteristic of Alzheimer’s disease. Because of the APP mutation, transgenic mice have increased amounts of amyloid-beta, a protein fragment that makes up the “neuritic plaque,” which is the hallmark of this disorder. When transgenic mice were maintained on a blueberry-supplemented diet, the levels of two neuroprotective chemicals, extracellular signal-regulated kinase and protein kinase C, which are involved in learning and memory, were found to be increased.

Transgenic mice fed the blueberry-supplemented diet were also better able to navigate a maze than their counterparts fed a control diet, even though both groups of animals developed brain plaques. In transgenic mice, blueberry supplements appeared to enhance signaling at the level of the kinases, thereby increasing the sensitivity of brain receptors in the striatum that are involved in memory.8,22

Blueberry extract also reduced stress signaling caused by exposing brain cells from the hippocampus to the neurochemical dopamine or to amyloid-beta, the protein that accumulates in the brains of patients with Alzheimer’s disease.23

Blueberry Extract Protects Specific Brain Region From Injury

In collaboration with NASA at Brookhaven National Laboratory, Dr. Joseph’s group is studying a model system to help understand the injurious effects of radiation on the brain. Young rats exposed to about 150 rads of heavy particle radiation, of the type that astronauts are exposed to on long-term space flights, develop impairments in motor and cognitive function similar to those seen with aging.8,24

“If we pretreat these animals for eight weeks with a diet containing blueberries or strawberries, we find that we can block the effects of the radiation,” Dr. Joseph said. “What’s interesting is that on some behaviors, the strawberries work better, and, on other behaviors, the blueberries work better.”

Specifically, the proanthocyanins in blueberries seem to be drawn to the striatum, a brain structure controlling movement as well as certain memory tasks. The striatum is also one of the brain regions most affected by Parkinson’s disease.

In terms of whether there are actual brain regions where these polyphenols may have receptors, Dr. Joseph said, “If you think about it for a moment, why not—there are opioid receptors in the brain, caffeine receptors, and [marijuana] receptors. We haven’t isolated them yet, but we’re trying to tease out these mechanisms and see which may have the most effect as far as producing the beneficial properties of blueberries.”

If the proanthocyanins in blueberries have specific benefits within the striatum, it seems reasonable to assume that blueberry extract might nurture the predominant population of nerve cells located in the striatum, namely, neurons containing the neurotransmitter known as dopamine. Depletion of dopamine from the striatum is the biochemical basis underlying the rigidity, stiffness, and tremor seen in Parkinson’s disease.

In a rat model of Parkinson’s disease and its treatment,25 dopamine was depleted from the striatum, into which embryonic nerve cells containing dopamine were transplanted. Compared with control rats fed standard lab chow, those fed a diet containing 2% blueberry extract had significantly greater survival of transplanted nerve cells. These nerve cells also functioned well, as seen by better balance on a rotating rod test in the rats given blueberry extract than the controls.

“These findings provide support for the potential of dietary phytochemicals as an easily administered and well-tolerated therapy that can be used to improve the effectiveness of dopamine neuron replacement,” the authors wrote.25

What You Need to Know: Blueberries

    Compounds in blueberries known as flavonoids, especially the anthocyanins, have antioxidant and anti-inflammatory properties, giving them great potential to fight aging, Alzheimer’s disease, and other chronic ailments.

    Blueberries appear to protect cells from a wide range of injuries by exerting potent antioxidant and anti-inflammatory effects to directly change oxidative and inflammatory stress-signaling pathways.

    In animal studies, a blueberry-enriched diet has been shown to protect against loss of brain cells seen with different types of brain injury and aging, as well as against associated impairments in memory, learning, and coordination.

    Blueberry supplementation is also associated with growth of new nerve cells, and with better communication between existing nerve cells through the process known as signal transduction.

    Anthocyanins in blueberries enter the brains of supplemented animals, where they lodge in the striatum, a specific area controlling certain types of memory and motor function. The striatum is also predominantly involved in Parkinson’s disease.

    Population studies in humans suggest that diets high in fruit and vegetables—particularly those of dark color, such as blueberries—may protect against oxidative stress, Alzheimer’s disease, and other chronic conditions.

    Experts interviewed by Life Extension highly recommend consumption of blueberries as part of a healthy lifestyle program.

Human Studies With Blueberries

In human volunteers, studies have shown that polyphenols and antioxidants in blueberry juice are easily absorbed and result in increased blood levels.26

Testing blood samples of these volunteers showed that drinking a blueberry-apple juice cocktail for four weeks resulted in 20% protection against chemical damage to the DNA in white blood cells. Individuals with certain genetic variations were more likely than others to show this protective effect.

In other research, it is known that antioxidant capacity in the blood normally decreases after a heavy meal because metabolizing the food increases free radicals. However, studies in healthy volunteers have shown that eating blueberries increases the level of antioxidant capacity in the blood. Eating high-antioxidant foods, such as blueberries, with each meal as part of a healthy diet is therefore a tasty antidote to prevent periods of oxidative stress that ordinarily follow eating.12
Blueberries For Life

“If I told you to take a certain drug, or to have a certain procedure, without knowing whether or not it’s been tested fully in people and found not to be harmful, I’d be very remiss in doing that, but I have no trouble recommending that someone eat berries or add foods with a lot of antioxidants to their diet,” Dr. Joseph concluded. “There is a lot of data out there which suggests that people who eat a diet high in fruits and vegetables are less likely to develop some of the diseases that occur in aging. It’s like your mother said: eat your fruits and veggies—they’re good for you.” •

If you have any questions on the scientific content of this article, please call a Life Extension Health Advisor at 1-800-226-2370.
References

1. Nicoue EE, Savard S, Belkacemi K. Anthocyanins in wild blueberries of Quebec: extraction and identification. J Agric Food Chem. 2007 Jul 11;55(14):5626-35.

2. Srivastava A, Akoh CC, Fischer J, Krewer G. Effect of anthocyanin fractions from selected cultivars of Georgia-grown blueberries on apoptosis and phase II enzymes. J Agric Food Chem. 2007 Apr 18;55(8):3180-5.

3. Boivin D, Blanchette M, Barrette S, Moghrabi A, Beliveau R. Inhibition of cancer cell proliferation and suppression of TNF-induced activation of NFkappaB by edible berry juice. Anticancer Res. 2007 Mar;27(2):937-48.

4. Huang C, Zhang D, Li J, Tong Q, Stoner GD. Differential inhibition of UV-induced activation of NF kappa B and AP-1 by extracts from black raspberries, strawberries, and blueberries. Nutr Cancer. 2007;58(2):205-12.

5. Neto CC. Cranberry and blueberry: evidence for protective effects against cancer and vascular diseases. Mol Nutr Food Res. 2007 Jun;51(6):652-64.

6. Seeram NP, Adams LS, Zhang Y, et al. Blackberry, black raspberry, blueberry, cranberry, red raspberry, and strawberry extracts inhibit growth and stimulate apoptosis of human cancer cells in vitro. J Agric Food Chem. 2006 Dec 13;54(25):9329-39.

7. Torri E, Lemos M, Caliari V, et al. Anti-inflammatory and antinociceptive properties of blueberry extract (Vaccinium corymbosum). J Pharm Pharmacol. 2007 Apr;59(4):591-6.

8. Joseph JA, Shukitt-Hale B, Lau FC. Fruit polyphenols and their effects on neuronal signaling and behavior in senescence. Ann NY Acad Sci. 2007 Apr;1100:470-85.

9. Zafra-Stone S, Yasmin T, Bagchi M, et al. Berry anthocyanins as novel antioxidants in human health and disease prevention. Mol Nutr Food Res. 2007 Jun;51(6):675-83.

10. Dai Q, Borenstein AR, Wu Y, Jackson JC, Larson EB. Fruit and vegetable juices and Alzheimer’s disease: the Kame Project. Am J Med. 2006 Sep;119(9):751-9.

11. Lau FC, Shukitt-Hale B, Joseph JA. Nutritional intervention in brain aging: reducing the effects of inflammation and oxidative stress. Subcell Biochem. 2007;42:299-318.

12. Prior RL, Gu L, Wu X, et al. Plasma antioxidant capacity changes following a meal as a measure of the ability of a food to alter in vivo antioxidant status. J Am Coll Nutr. 2007 Apr;26(2):170-81.

13. Wolfe KL, Liu RH. Cellular antioxidant activity (CAA) assay for assessing antioxidants, foods, and dietary supplements. J Agric Food Chem. 2007 Oct 31;55(22):8896-907.

14. Suh N, Paul S, Hao X, et al. Pterostilbene, an active constituent of blueberries, suppresses aberrant crypt foci formation in the azoxymethane-induced colon carcinogenesis model in rats. Clin Cancer Res. 2007 Jan 1;13(1):350-5.

15. Heinonen M. Antioxidant activity and antimicrobial effect of berry phenolics—a Finnish perspective. Mol Nutr Food Res. 2007 Jun;51(6):684-91.

16. Russell WR, Labat A, Scobbie L, Duncan SH. Availability of blueberry phenolics for microbial metabolism in the colon and the potential inflammatory implications. Mol Nutr Food Res. 2007 Jun;51(6):726-31.

17. Duffy KB, Spangler EL, Devan BD, et al. A blueberry-enriched diet provides cellular protection against oxidative stress and reduces a kainate-induced learning impairment in rats. Neurobiol Aging. 2007 May 22; [Epub ahead of print].

18. Casadesus G, Shukitt-Hale B, Stellwagen HM, et al. Modulation of hippocampal plasticity and cognitive behavior by short-term blueberry supplementation in aged rats. Nutr Neurosci. 2004 Oct-Dec;7(5-6):309-16.

19. Andres-Lacueva C, Shukitt-Hale B, Galli RL, Jauregui O, Lamuela-Raventos RM, Joseph JA. Anthocyanins in aged blueberry-fed rats are found centrally and may enhance memory. Nutr Neurosci. 2005 Apr;8(2):111-20.

20. Lau FC, Bielinski DF, Joseph JA. Inhibitory effects of blueberry extract on the production of inflammatory mediators in lipopolysaccharide-activated BV2 microglia. J Neurosci Res. 2007 Apr;85(5):1010-7.

21. McGeer PL, McGeer EG. Inflammation and neurodegeneration in Parkinson’s disease. Parkinsonism Relat Disord. 2004 May;10 Suppl 1:S3-S7.

22. Joseph JA, Denisova NA, Arendash G, et al. Blueberry supplementation enhances signaling and prevents behavioral deficits in an Alzheimer disease model. Nutr Neurosci. 2003 Jun;6(3):153-62.

23. Joseph JA, Carey A, Brewer GJ, Lau FC, Fisher DR. Dopamine and Abeta-induced stress signaling and decrements in Ca2+ buffering in primary neonatal hippocampal cells are antagonized by blueberry extract. J Alzheimers Dis. 2007 Jul;11(4):433-46.

24. Shukitt-Hale B, Carey AN, Jenkins D, Rabin BM, Joseph JA. Beneficial effects of fruit extracts on neuronal function and behavior in a rodent model of accelerated aging. Neurobiol Aging. 2007 Aug;28(8):1187-94.

25. McGuire SO, Sortwell CE, Shukitt-Hale B, et al. Dietary supplementation with blueberry extract improves survival of transplanted dopamine neurons. Nutr Neurosci. 2006 Oct;9(5-6):251-8.

26. Wilms LC, Boots AW, de Boer VC, et al. Impact of multiple genetic polymorphisms on effects of a 4-week blueberry juice intervention on ex vivo induced lymphocytic DNA damage in human volunteers. Carcinogenesis. 2007 Aug;28(8):1800-6.




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31 for 21: Wordless Wednesday...Gluten Free Goodies

If you're looking for yummy gluten free recipes, check out my sister's blog!

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31 for 21: Glutathione

Side note: There was a mis-link on the post from yesterday regarding the Down Syndrome awareness shirts. The correct link is on that post, but you can also order the shirts from here.

There was some recent discussion on the Einstein Syndrome list (I know I mention this list frequently, but it's such a beneficial list!) about Glutathione (GSH) and if it's beneficial or not.

Bottom line: Yes, it's very beneficial!

But, I'll get to more detailed information here :).

L-Glutathione is an amino acid, which is a tripeptide (made up from 3 other amino acids). It's also a potent antioxidant and helps with many different functions in the body.

One of the best articles I have ever read on Glutathione and it's many mechanisms is Glutathione: Systemic Protection Against Oxidative & Free Radical Damage, which you can view as a full text here.

Glutathione is essential in the body's antioxidant system. As one quote from the above study says,

Antioxidants are the body's premier resource for protection against the diverse free radical and other oxidative stressors to which it invariably becomes exposed. the antioxidant defense system is sophisticated and adaptive, and GSH is a central constituent of this system

 Another interesting quote,

The consequences of sustained GSH depletion are grim. As cellular GSH is depleted, first individual cells die in those areas most affected [my note: we have lots of cell death already going on in DS]. Then zones of tissue damage begin to appear; those tissues with the highest content of polyunsaturated lipids and/or the most meager antioxidant defenses are generally the most vulnerable. Localized free-radical damage [my note: which is an issue in DS, due to low antioxidant levels & high oxidative stress] spreads across the tissue in an ever-widening, self-propagating wave. If this spreading wave of tissue degeneration is to be halted, the antioxidant defenses must be augmented.

Because Glutathione is low in people with DS and because it plays such a vital role in the immune system, it's important for us to try to help raise the levels of Glutathione in the body. Nutrivene-D does have Glutathione in it.

But, there is one tricky thing with GSH.

It's not very easily absorbed, although it can be absorbed. The best form of GSH is Reduced L-Glutathione. There are also some other forms of GSH called Lipsomal GSH, sublingual GSH and I believe there is also a Glutathione patch that people in the Autism community use. All of the above forms are supposed to be absorbed pretty well.

Methylcobalamin B12 also has been shown to help raise Glutathione levels in a study done by Jill James.

Someone may wonder about using N-Acetyl-Cysteine (NAC) to raise Glutathione levels. If you do much research, you will see this mentioned when talking about ways to raise Glutathione. From the research I have done, NAC should not be used in Down Syndrome. It has been shown to increase oxidative stress in people with DS and it also appears that it can cause leaky gut. Neither of which are needed in anyone, let alone someone with DS who is already struggling with increased oxidative stress and possibly gut issues.

Finally, one more interesting note about Glutathione from the above study,

Many pharmaceutical products are oxidants capable of depleting GSH [my note: Glutathione] from the liver, kidneys, heart, and other tissues. The popular over-the-counter drug acetaminophen [my note: active ingredient in Tylenol] is a potent oxidant. It depletes GSH from the cells of the liver [my note: which is where GSH is made & stored], and by so doing renders the liver more vulnerable to toxic damage.

Some may say it doesn't really matter if a drug such as Tylenol is used, if it's used in moderation. If you are comfortable giving your child Tylenol at various times, that's fine. It may be necessary at some times. We do not give Tylenol to O because of the concern that it would deplete already low Glutathione levels. There's more info on GSH and the Acetaminophen issue here.

*Don't forget to enter the book giveaway, which ends on November 2nd!*

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31 for 21: Shirts & Bumper Stickers

Several years ago, I think it's been 5 years or so, I made up a few Down Syndrome Awareness shirts and bumper stickers. Several of us have these shirts. I particularly like to wear the "My brother has Down Syndrome. He wasn't terminated. He's loved" shirt.

I don't know that I've ever shared these on the blog, but thought I would now!

A few of the shirts are pictured below. They are available in My Son, My Daughter, My Brother, My Sister, My Cousin, My Friend, My Grandson, My Granddaughter, My Niece & My Nephew.

The shirts can all be ordered from here.

 

A few of the bumper stickers can be seen here as well. The rest can be seen over here, where they can also be ordered.

 

 

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31 for 21: Zinc

As you saw with the my brother's vitamin protocol which I shared last week, he gets extra zinc every morning.

He takes Zinc in his Nutrivene-D, but ever since he was a one year old, he has been deficient in zinc. This is commonly seen in people with Down syndrome (I will share an article below), due to the overexpression of the Cu/Zn Superoxide Dismutase gene on the third 21st chromosome. So, we have been supplementing with 25-30mg/day extra of Zinc since that time. If we keep him on that dosage of extra zinc, he never gets TOO much zinc (it can be tested via blood work - with a zinc free needle!) and he is not deficient anymore. If we go any lower - 15 mg/day - then he becomes deficient again.

We typically use Nutricology Zinc Citrate or Swanson Zinc Citrate. Another really good form of zinc to use is Opti-Zinc (that's not a brand, it's a form of zinc).

Thiel R.J., Fowkes S.W. Can cognitive deterioration associated with Down syndrome be reduced? Medical Hypotheses, 2005; 64(3):524-532 (full text can be viewed here)

Abstract

Individuals with Down syndrome have signs of possible brain damage prior to birth. In addition to slowed and reduced mental development, they are much more likely to have cognitive deterioration and develop dementia at an earlier age than individuals without Down syndrome. Some of the cognitive impairments are likely due to post-natal hydrogen peroxide-mediated oxidative stress caused by overexpression of the superoxide dismutase (SOD-1) gene, which is located on the triplicated 21 st chromosome and known to be 50% overexpressed. However, some of this disability may also be due to early accumulation of advanced protein glycation end-products, which may play an adverse role in prenatal and postnatal brain development. This paper suggests that essential nutrients such as folate, vitamin B6, vitamin C, vitamin E, selenium, and zinc, as well as alpha-lipoic acid and carnosine may possibly be partially preventive. Acetyl-L-carnitine, aminoguanidine, cysteine, and N-acetylcysteine are also discussed, but have possible safety concerns for this population. This paper hypothesizes that nutritional factors begun prenatally, in early infancy, or later may prevent or delay the onset of dementia in the Down syndrome population. Further examination of this data may provide insights into nutritional, metabolic and pharmacological treatments for dementias of many kinds. As the Down syndrome population may be the largest identifiable group at increased risk for developing dementia, clinical research to verify the possible validity of the prophylactic use of anti-glycation nutrients should be performed. Such research might also help those with glycation complications associated with diabetes or Alzheimer’s.

Oral zinc supplementation in Down's syndrome subjects decreased infections and normalized some humoral and cellular immune parameters.

Abstract

The effect of 4 months of oral zinc supplementation on immune functions in non-institutionalized young female and male Down's syndrome (DS) subjects was studied. Along with plasma levels of zinc, the immune parameters, measured before and after zinc treatment, were plasma levels of thymulin, the percentage and the absolute number of circulating white blood cells, total lymphocytes, lymphocyte subpopulations, the mitogen-induced lymphocyte proliferation, the production of interleukin-2, and the activity of stimulated granulocytes. Some immune parameters were significantly influenced by zinc treatment. In particular, a normalization of thymulin and zinc plasma levels were found in these subjects after zinc supplementation. At the end of the clinical trial, in vitro lymphocyte proliferation and polymorphonuclear activity also increased and reached normal values. Zinc administration exerted a positive clinical effect in these children, since a reduced incidence of infections was found.

The Role of Zinc in Down’s Syndrome (view the full text here)

Summary

This paper considers a single nutrient, zinc, and its place in supporting people with Down’s syndrome. The importance of zinc is suggested by the many disease states found in DS that have also been observed in subjects with zinc deficiency. These include diabetes mellitus, dwarfism, hypogonadism, atherosclerosis, vitamin A deficiency night blindness, cirrhosis of the liver, myeloid leukaemia (Milunsky, 1970), and hyperthyroidism and hypothyroidism (Napolitano et al, 1990). Fabris et al (1993) cite the importance of zinc in the homeostatic networks found to be altered in DS, namely nervous, neuroendocrine and immune, and their interrelationship, plus a reduced turnover of this mineral, leading to the hypothesis that zinc deficiency could be implicated in at least some of the DS phenotype.

“Zinc forms part of the composition of at least 160 different enzymes. Indeed, zinc is the most widely used mineral in enzymes” (Graham and Odent, 1986).

It is vital for protein, essential fatty acid and carbohydrate metabolism, and for DNA synthesis, and can be used to detoxify lead and mercury (ibid.). The body only has a small pool of biologically available zinc, and a rapid turnover, meaning that deficiency signs appear very quickly (Passwater and Cranton, 1983).

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31 for 21: Thoughts On Loss Of Neurons

A few weeks ago, there was some discussion on the Einstein-Syndrome list regarding statements made by the Changing Minds Foundation regarding the loss of neurons.

Because of this quote (namely the bolded portion) from the CMF website,

"Problem: Loss of neurons in the hippocampus:  Down syndrome loses 50% of their neuronal structure by 6 months old. This is an insurmountable problem.

The University Of Maryland School Of Medicine treated Down syndrome mice with prozac for 24 days (2006). It increased neurogenesis (the formation of new nerves) to a normal level.  This is like increasing the hardware on your computer. It allows you to run more complicated software. In fetuses with Down syndrome, neurons fail to show normal dendritic development, yielding a "tree in winter" appearance. This developmental failure is thought to result in mental retardation.""

I did some researching and wrote up a response to this, which I thought I would share below. From what I recall, CMF did change some of the wording on their site to make sure there was no confusion.

I am not a CMF protocol expert by any means, but I thought I would share what I could find in doing some researching on this.

This study, "Neurogenesis impairment and increased cell death reduce total neuron number in the hippocampal region of fetuses with Down syndrome" can be seen in full text here: http://bit.ly/ok9kuN. If anyone would like a PDF of the full text, just let me know, as I have it downloaded and can email it.

A quote from the abstract: "Results show reduced neuron number in the DS hippocampal region and suggest that this defect is caused by disruption of neurogenesis and apoptosis, two fundamental processes underlying brain building."

While I don't understand all of the terminology in this study, here are a few interesting quotes:

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"In all structures, however, DS fetuses had a significantly smaller number of neurons compared with controls (Figure 6D)."

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"Comparison of the density of apoptotic cells, evaluated with either method, in control and DS fetuses showed that DS fetuses had a larger density of apoptotic cells both in the granule cell layer (Figure 8B,E) and in the ventricular zone of the hippocampus and PHG (Figure 8C,H) compared with control fetuses."

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"The current study in DS fetuses demonstrates for the first time a severe hypocellularity in all areas forming the fetal hippocampal region and that neurogenesis impairment underlies this defect.

These findings allow us to trace back to early developmental stages the hippocampal hypotrophy of the adult DS brain. This precocious atrophy may explain the early impairment of hippocampus-related memory functions observed in children with DS (7, 50)."

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"Although hypocellularity in the DS brain was previously documented in several studies, it was not known whether this defect was caused by a neurodegenerative processes or to decreased neuron production. With our investigations we demonstrate for the first time that in DS subjects neurogenesis is severely impaired during early phases of brain development. The ensemble of current and previous (10) data suggests that neurogenesis impairment may be a generalized feature of the DS brain and underlie the widespread brain hypotrophy that characterizes DS subjects starting from infancy."

Some of my thoughts: I can't find a study which says there is a 50% loss of neuronal structure by 6 months old either. I just did quite a bit of searching, although I'm sure I could've missed it if I didn't search for the right thing ;). I'd be glad to see it if it's there. Anyone have the reference for that?

From research I have done over the years, I know there is lack of neurogenesis (which some of the above quotes show) and increased apoptosis (programmed cell death) that starts from before the child is born. The above study also shows that there is a marked difference in the number of neurons babies with Down syndrome have. If the child starts out with 35%-55% less neurons than a non-T21 child (the above study mentioned those numbers in certain measurements/areas), then where is the idea of a 50% loss by the time the child is 6 months old? 

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