(HealthDay News) -- A once-promising pathway for research into preventing and treating Alzheimer's disease may have been derailed by a surprise chemical finding, researchers report.
Scientists in laboratories around the world have been investigating drug candidates called amyloid inhibitors, which many experts believed could keep proteins such as amyloid-beta from sticking together in brain tissue.
This type of "sticky" protein plaque build-up is a hallmark of Alzheimer's disease. It also characterizes brain illnesses such as Huntington's disease and "mad cow" disease.
But the new study, published Jan. 27 in the journal Nature Chemical Biology, may sound an unexpected death knell for amyloid inhibitor research.
In the study, a team of chemists at the University of California, San Francisco, found that these candidate drugs form large, unwieldy clumps themselves, rendering them useless as targeted therapy against amyloid in the brain.
High-tech research in the lab is revealing that typical amyloid inhibitors "seem to act not in the way people expect them to and want them to," explained study senior author Brian Shoichet, professor of pharmaceutical chemistry at UCSF.
Once these drugs aggregate into clumps, "they no longer have the right pharmacology, they won't cross the [brain's] membrane barriers, and they inhibit everything -- any protein will bind with them," he said.
In other words, the drugs lose their ability to migrate to the brain to fight amyloid plaque. They also give up their targeted specificity against amyloid, Shoichet said. "They end up inhibiting everything -- any protein that sees them will be sequestered by them," he said. This molecular clumping process is largely inevitable, Shoichet added.
His advice to neuroscientists investigating these agents as potential Alzheimer's therapies: "They should stop."
Another expert agreed.
David Lynn is a Howard Hughes Institute investigator and professor of biological chemistry at Emory University in Atlanta. "I think that Brian's paper argues that [scientists] have been missing the boat here," he said. "It's not clear that you are ever going to get the concentrations that you need of these agents at the right site to be able to have any therapeutic intervention."
On the level of basic chemistry, attacking Alzheimer's and other protein-clumping diseases by preventing amyloid from concentrating has "always been a long shot," Lynn said. That's because amyloid proteins are incredibly "sticky," chemically speaking.
"To find things that will competitively stick and stop them from assembling is theoretically hard to imagine," Lynn said. It was thought that individual molecules of amyloid inhibitors might do so, but the new finding -- that the molecules inevitably bind together in a more impractical mass -- renders them therapeutically useless.
But other avenues of Alzheimer's research remain promising, Lynn said.
"There are certainly other strategies that have potential," he noted, including antibody-focused strategies aimed at eliminating plaques, or treatments focused on easing the downstream effects of amyloid buildup.
Both scientists stressed that it's still not certain whether protein plaques even cause Alzheimer's and other brain diseases, or whether they are merely byproducts of the disease process. "That's really another open area of research," Shoichet said.
"The problem with these diseases is that it is such a moving target," Lynn said. "And so, different people are looking at different things."
More information
There's much more on Alzheimer's disease at the Alzheimer's Association.
Showing posts with label Alzheimer's-Disease. Show all posts
Showing posts with label Alzheimer's-Disease. Show all posts
Wednesday, January 30, 2008
Tuesday, December 11, 2007
Hypertension Linked to Risk of Mild Cognitive Impairment
(HealthDay News) -- High blood pressure may be associated with increased risk for mild cognitive impairment, says a study by researchers at the Columbia University Medical Center in New York City.
Mild cognitive impairment, which causes learning and thinking difficulties, has "attracted increasing interest during the past years, particularly as a means of identifying the early stages of Alzheimer's disease as a target for treatment and prevention," the study authors wrote.
They followed 918 Medicare recipients aged 65 and older (average age 76.3) who were assessed every 18 months for an average of 4.7 years. None of the participants had mild cognitive impairment at the start of the study, but 334 of them developed the condition during the study period.
Of those, 160 developed amnestic mild cognitive impairment (which involves low scores on memory portions of neuropsychological tests), and 174 developed non-amnestic mild cognitive impairment. Hypertension was associated with an increased risk of all types of mild cognitive impairment, especially non-amnestic mild cognitive impairment, the researchers said.
The findings are published in the December issue of the Archives of Neurology.
"The mechanism by which blood pressure affects the risk of cognitive impairment or dementia remains unclear. Hypertension may cause cognitive impairment through cerebrovascular disease. Hypertension is a risk factor for subcortical white matter lesions found commonly in Alzheimer's disease. Hypertension may also contribute to a blood-brain barrier dysfunction, which has been suggested to be involved in the cause of Alzheimer's disease.
Other possible explanations for the association are shared risk factors," including the formation of cell-damaging compounds known as free radicals, the study authors wrote.
"Our findings support the hypothesis that hypertension increases the risk of incident mild cognitive impairment, especially non-amnestic mild cognitive impairment," the researchers concluded. "Preventing and treating hypertension may have an important impact in lowering the risk of cognitive impairment."
More information
The Alzheimer's Association has more about mild cognitive impairment.
Mild cognitive impairment, which causes learning and thinking difficulties, has "attracted increasing interest during the past years, particularly as a means of identifying the early stages of Alzheimer's disease as a target for treatment and prevention," the study authors wrote.
They followed 918 Medicare recipients aged 65 and older (average age 76.3) who were assessed every 18 months for an average of 4.7 years. None of the participants had mild cognitive impairment at the start of the study, but 334 of them developed the condition during the study period.
Of those, 160 developed amnestic mild cognitive impairment (which involves low scores on memory portions of neuropsychological tests), and 174 developed non-amnestic mild cognitive impairment. Hypertension was associated with an increased risk of all types of mild cognitive impairment, especially non-amnestic mild cognitive impairment, the researchers said.
The findings are published in the December issue of the Archives of Neurology.
"The mechanism by which blood pressure affects the risk of cognitive impairment or dementia remains unclear. Hypertension may cause cognitive impairment through cerebrovascular disease. Hypertension is a risk factor for subcortical white matter lesions found commonly in Alzheimer's disease. Hypertension may also contribute to a blood-brain barrier dysfunction, which has been suggested to be involved in the cause of Alzheimer's disease.
Other possible explanations for the association are shared risk factors," including the formation of cell-damaging compounds known as free radicals, the study authors wrote.
"Our findings support the hypothesis that hypertension increases the risk of incident mild cognitive impairment, especially non-amnestic mild cognitive impairment," the researchers concluded. "Preventing and treating hypertension may have an important impact in lowering the risk of cognitive impairment."
More information
The Alzheimer's Association has more about mild cognitive impairment.
Tuesday, August 28, 2007
Food for the Aging Mind
Agricultural Research
08-27-07
Originally Published:20070801.
Scientists know that certain nutrients and other key chemical compounds are essential to human brain function. Serious deficiencies in some of these, such as vitamin B12 and iron, can lead to impaired cognitive function due to neurological, or nerve fiber, complications.
Cognition can be defined as the ability to use simple-to-complex information to meet the challenges of daily living.
So, could careful attention to diet help protect the aging brain from problems with nerve cell signals involved in memory and cognition? A clear-cut answer could greatly affect the 77 million baby boomers who are now facing retirement. Their independence, quality of life, and even economic status will largely be defined by their ability to traffic information signals as they age.
In researching the nutrition-brain connection, new technologies are being used, such as those that take images of the brain or actually count individual brain cells. Behavioral tests that measure motor and cognitive skills-or lack thereof-are also providing insights. Yet the science of nutrition and brain function is relatively new and evolving.
Agricultural Research Service scientists at several locations nationwide are contributing to a growing body of research that explores the effect of diet and nutrition on the brain and its function across the lifespan.
Boosting Neuronal Function
The brain's billions of neurons "talk" to one another through chemical neurotransmitters that convey signals through neural pathways. These chemical transporters- which include norepinephrine, serotonin, and dopamine-are key to signal movement.
Although people naturally lose brain cells throughout their lives, the process of neuronal death does not necessarily accelerate with aging. "There is a lot of individual difference," says ARS neuroscientist James Joseph. "Loss of mental agility may be less due to loss of brain cells than to the cells' failure to communicate effectively."
Joseph heads the Neuroscience Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University in Boston. There, researchers are looking at the beneficial effects of certain dietary plant compounds to learn how they affect brain function.
"Vitamins and minerals in plant foods provide protective antioxidants," says Joseph. "But fruits, vegetables, nuts, seeds, and grains contain thousands of other types of compounds that contribute significantly to the overall dietary intake of antioxidants.
"A partial measure of the antioxidant effect is called 'ORAC,' for Oxygen Radical Absorbance Capacity. ORAC scores are now showing up in charts and on some food and beverage packages. They may be helpful in choosing foods to include in your diet."
Perhaps there is no better place in which to gauge the power of antioxidants than between the minute connections of the nerve cells.
Bucking Long-Held Dogma
Eight years ago, Joseph and colleagues began publishing a series of studies, done in rodents, that shed light on the relationship between various diets and the mechanisms behind cognitive losses in specific neighborhoods of the aging brain.
Many in the series are groundbreaking in that they challenge the long-accepted belief that the central nervous system, which includes the brain, is not capable of regenerating itself. Other published studies in the series echo similar findings based on primate and human brain research at the Salk Institute for Biological Studies, San Diego, California. Scientists there, using new technologies, disputed the notion that the brain does not make new neurons-a process called "neurogenesis"-into old age: It does, but at a much slower rate.
One of the first of Joseph's studies, published in the Journal of Neuroscience, showed a protective effect of consuming antioxidants. Study rats were fed-from adulthood to middle age-vitamin E, strawberry extracts, or spinach extracts, all with similar ORAC values. Animals receiving the high-antioxidant diets did not experience the age-related cognitive performance losses seen in control rats fed standard chow.
A later study, also published in the Journal of Neuroscience, showed a reversal of functional loss among rats on special diets. Each of three groups of rats, equivalent in age to 63-year-old humans, was fed a different high-antioxidant extract. A control group was fed standard chow.
After 8 weeks-equivalent to about 10 years in humans-the rats' performance levels were measured.
The rats fed the spinach, strawberry, or blueberry extracts effectively reversed age-related deficits in neuronal and cognitive function. In addition, the blueberryfed group far outperformed their peers while traversing a rotating rod to test balance and coordination.
"Despite their status as 'senior citizens,' those rats showed remarkable stamina on neuromotor function tests," says psychologist and coauthor Barbara Shukitt-Hale, also with the Neuroscience Laboratory.
Examination of the brain tissue of those blueberry-fed rats showed much higher levels of dopamine than were found in the other groups. Dopamine has many functions within the brain. In particular, it can affect the way the brain controls movements.
"We suspected that the combined antioxidant potency of compounds in blueberry extract may have reduced inflammatory compounds in the brains of these older animals," says Joseph.
"Inflammation ordinarily contributes to neuronal and behavioral shortfalls during aging."
Tests have since shown that blueberry compounds cross the blood-brain barrier and localize in rodent brain tissue.
Hard News: Brain Plaques
Later, the lab's researchers published an Alzheimer's disease model study in Nutritional Neuroscience. They studied mice that carried a genetic mutation for promoting increased amounts of amyloid beta, a protein fragment found within the telltale neuritic plaque, or "hardening of the brain," seen in Alzheimer's disease.
Although the exact cause of Alzheimer's is not completely understood, experts have recently identified one mechanism involving the insufficient breakdown and recycling of amyloid protein in the brain. That mechanism is both genetic and physiological. In those individuals, normally harmless amyloid protein turns into fragments of amyloid beta, which build up as plaque in the brain rather than being escorted into cellular recycling. That action leads to cell death and weakened neuronal communication.
In the mouse study, beginning at age 4 months-early adulthood-half the brainplaqued group was fed a diet that included blueberry extract for 8 months. The other half was fed standard rat chow and so was a control group of mice that didn't carry the amyloid-plaque mutation.
At 12 months-early middle age-all groups were tested for their performance in a maze.
The brain-plaqued mice that were fed the blueberry extract performed as well as the healthy control mice and performed much better than their brain-plaqued peers fed standard chow.
A look at the plaqued brains of both the blueberry-fed and chow-fed mice after death revealed no difference in the number of brain plaques in either group. "Amyloid-beta-induced plaques are only one aspect of Alzheimer's disease," says Joseph. "But the fact that we saw a dietinduced behavioral difference, despite a similarity in plaque density in both these animal groups, is significant."
The team found increased activity of a family of enzymes called "kinases" in the brains of the amyloid-plaqued mice that were fed blueberry extract. Two kinases found in particular, ERK and PKC, are important in mediating cognitive function, such as converting short-term memory to long-term.
"These kinase molecules are involved in signaling pathways for learning and memory," says Joseph. "It could be that the increased kinase activity within the plaque-ridden brains of the blueberry-fed mice enhanced the signaling in certain receptors."
Brain Cells Are Born
Another HNRCA rat study looked at the aged brain's ability to change physiologically- a condition scientists refer to as "neuronal plasticity." In addition to cell division and differentiation, or "mission assignment," brain tissue undergoes many other changes throughout aging.
For example, a newborn sprouts billions of nerve cells while soaking up information from the environment. But lower levels of synapse growth continue in waves throughout the lifespan.
Littleused synapses are eliminated, while others are strengthened in a neuronal pruning process, of sorts.
Repair mechanisms involve neural immune cells, called "microglia," that seek to heal and protect injured brain tissue; enzymes that regulate safe chemical levels; and genes that are expressed in response to inflammation.
The neuronal-plasticity study investigated the physiological link between nutrition and the memory-control hippocampal area of the aged brain. That region, in the center of the brain, is essential for what's called "working" or "short-term" memory. It receives and processes data, and then, if needed, passes it on for storage.
Neurogenesis also plays a role in the formation of new memories. The capacity of the hippocampus to produce new neurons is thought to be greatly diminished during aging. But this study suggested that old rats fed blueberry extracts for a short time had increased neurogenesis in the dentate gyrus area of their brain's hippocampus. The dentate gyrus is one of the few regions of the brain where neurogenesis occurs.
"We found changes in the proliferation of neurons in blueberry-fed rats," said Gemma Casadesus, formerly a graduate student with the Neuroscience Laboratory and now with Case Western Reserve University. In maze tests, blueberry-fed aged lab rats showed improvement in cognition over chow-fed peers. "There was an association between the proliferation of neuronal precursor cells and better performance of spatial memory," she says.
The researchers don't yet know whether the cognitive improvements seen in the aged blueberry-fed rats translate to humans. "But it's an important step in learning about the brain's ability to rescue itself from age-associated declines in physiological function," Casadesus says.
Can You Hear Me Now?
Neurons that can't get their messages through signaling pathways are like cell phones that can't get their signals through to other cell phones. Why does this happen?
As the brain matures, cell division becomes largely restricted to specific regions of the brain, and brain cells tend to become more vulnerable to two partners in crime: oxidative stress and inflammation.
In the body, free radicals-weakened atoms formed during activities of daily living-are missing an electron and want to bond with neighboring biomolecules to stabilize. The problem is that unless neutralized, free radicals cause cellular damage known as "oxidative stress."
Cellular antioxidant defense systems counterbalance these rogue molecules, but they're not 100 percent effective-particularly as the body and brain mature. And the brain is thought to be especially vulnerable to oxidative stress.
"Weighing just 3 pounds, the brain accounts for only 2 percent of the body's total mass, yet it uses up to half of the body's total oxygen consumed during mental activity," says Joseph.
"Phytochemicals, together with essential nutrients in foods, provide a health-benefits cocktail of sorts. It is feasible that continued research in this area will point to dietary regimens that are effective in boosting neuronal function."
Inflammation is thought to be stoked by the overactivation of microglia-the neural immune cells mentioned earlier.
Microglia are usually dormant, but they migrate to the site of any brain injury. These sentries make up about 20 percent of the cell population in certain regions of the brain.
While seeking to protect and repair tissue, microglia cells produce and send out molecular stress signals, some by way of defensive cytokines, as a bugle call to other cells. Those signals begin a cascade of reactions, including the activation of genes that express proteins and other stress chemicals to help clear away cellular debris.
Microglial activation by amyloid beta is thought to be a key event in the progression of Alzheimer's disease. "When microglia are stuck in an always-on loop in response to plaque buildup in the brain, they become problematic in and of themselves," says Joseph.
This year, Francis Lau, a molecular biologist in the Neuroscience Laboratory, published a study that investigated whether blueberry extracts could have a preventive effect on inflammatory signals coming from activated microglia cells.
Microglial activation is considered the hallmark of inflammation in the central nervous system. For this study, Lau used a rodent microglial cell line that has previously served as a model to study plaqueinduced microglial activation.
Lau exposed groups of those test cells to various levels of blueberry extracts. He then challenged the cells with oxidative stress by exposing them to a toxin-lipopolysaccharide- that triggers secretion of inflammatory chemicals.
Neuroinflammation has been linked to the expression of genes that spew two inflammatory enzymes, iNOS and COX-2, and two cytokines, IL-1b and TNF-a.
Lau used real-time PCR (polymerase chain reaction) to find and measure expression of genes that produce iNOS and COX-2 in the stress-induced cell cultures. He found that the blueberry treatment significantly reduced that expression.
The blueberry extract also markedly lessened secretion of the two inflammatory cytokines. In fact, says Lau, "In cells exposed to the highest blueberry extract concentration, the amount of TNF-a cytokine found was next to nothing- essentially identical to that found in the control cells."
Looking to the Future
The food industry is now using a range of new and existing product ingredients to gain entrance into the emerging brainhealth market. Some are producing food labels that list ORAC values-for example, for use on containers of polyphenol-rich fruit juices and teas. So far, however, there has been no review conducted by the U.S. Food and Drug Administration on health benefits from eating berries.
Future studies at HNRCA will ideally include use of new diagnostic tools as well as human clinical trials. Neuroimaging equipment, for example, could be used to monitor the influence of various dietary factors on development of plaque within the human brain. Such studies aim to find the best dietary regimens to help adults preserve their mental capabilities while aging.-By Rosalie Marion Bliss, ARS.
This research is part of Human Nutrition, an ARS national program (#107) described on the World Wide Web at www. nps.ars.usda.gov.
James A. Joseph is with the USDA-ARS Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111; phone (617) 556-3178, fax (617) 556-3222, e-mail jim.joseph@ ars.usda.gov.
08-27-07
Originally Published:20070801.
Scientists know that certain nutrients and other key chemical compounds are essential to human brain function. Serious deficiencies in some of these, such as vitamin B12 and iron, can lead to impaired cognitive function due to neurological, or nerve fiber, complications.
Cognition can be defined as the ability to use simple-to-complex information to meet the challenges of daily living.
So, could careful attention to diet help protect the aging brain from problems with nerve cell signals involved in memory and cognition? A clear-cut answer could greatly affect the 77 million baby boomers who are now facing retirement. Their independence, quality of life, and even economic status will largely be defined by their ability to traffic information signals as they age.
In researching the nutrition-brain connection, new technologies are being used, such as those that take images of the brain or actually count individual brain cells. Behavioral tests that measure motor and cognitive skills-or lack thereof-are also providing insights. Yet the science of nutrition and brain function is relatively new and evolving.
Agricultural Research Service scientists at several locations nationwide are contributing to a growing body of research that explores the effect of diet and nutrition on the brain and its function across the lifespan.
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Boosting Neuronal Function
The brain's billions of neurons "talk" to one another through chemical neurotransmitters that convey signals through neural pathways. These chemical transporters- which include norepinephrine, serotonin, and dopamine-are key to signal movement.
Although people naturally lose brain cells throughout their lives, the process of neuronal death does not necessarily accelerate with aging. "There is a lot of individual difference," says ARS neuroscientist James Joseph. "Loss of mental agility may be less due to loss of brain cells than to the cells' failure to communicate effectively."
Joseph heads the Neuroscience Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University in Boston. There, researchers are looking at the beneficial effects of certain dietary plant compounds to learn how they affect brain function.
"Vitamins and minerals in plant foods provide protective antioxidants," says Joseph. "But fruits, vegetables, nuts, seeds, and grains contain thousands of other types of compounds that contribute significantly to the overall dietary intake of antioxidants.
"A partial measure of the antioxidant effect is called 'ORAC,' for Oxygen Radical Absorbance Capacity. ORAC scores are now showing up in charts and on some food and beverage packages. They may be helpful in choosing foods to include in your diet."
Perhaps there is no better place in which to gauge the power of antioxidants than between the minute connections of the nerve cells.
Bucking Long-Held Dogma
Eight years ago, Joseph and colleagues began publishing a series of studies, done in rodents, that shed light on the relationship between various diets and the mechanisms behind cognitive losses in specific neighborhoods of the aging brain.
Many in the series are groundbreaking in that they challenge the long-accepted belief that the central nervous system, which includes the brain, is not capable of regenerating itself. Other published studies in the series echo similar findings based on primate and human brain research at the Salk Institute for Biological Studies, San Diego, California. Scientists there, using new technologies, disputed the notion that the brain does not make new neurons-a process called "neurogenesis"-into old age: It does, but at a much slower rate.
One of the first of Joseph's studies, published in the Journal of Neuroscience, showed a protective effect of consuming antioxidants. Study rats were fed-from adulthood to middle age-vitamin E, strawberry extracts, or spinach extracts, all with similar ORAC values. Animals receiving the high-antioxidant diets did not experience the age-related cognitive performance losses seen in control rats fed standard chow.
A later study, also published in the Journal of Neuroscience, showed a reversal of functional loss among rats on special diets. Each of three groups of rats, equivalent in age to 63-year-old humans, was fed a different high-antioxidant extract. A control group was fed standard chow.
After 8 weeks-equivalent to about 10 years in humans-the rats' performance levels were measured.
The rats fed the spinach, strawberry, or blueberry extracts effectively reversed age-related deficits in neuronal and cognitive function. In addition, the blueberryfed group far outperformed their peers while traversing a rotating rod to test balance and coordination.
"Despite their status as 'senior citizens,' those rats showed remarkable stamina on neuromotor function tests," says psychologist and coauthor Barbara Shukitt-Hale, also with the Neuroscience Laboratory.
Examination of the brain tissue of those blueberry-fed rats showed much higher levels of dopamine than were found in the other groups. Dopamine has many functions within the brain. In particular, it can affect the way the brain controls movements.
"We suspected that the combined antioxidant potency of compounds in blueberry extract may have reduced inflammatory compounds in the brains of these older animals," says Joseph.
"Inflammation ordinarily contributes to neuronal and behavioral shortfalls during aging."
Tests have since shown that blueberry compounds cross the blood-brain barrier and localize in rodent brain tissue.
Hard News: Brain Plaques
Later, the lab's researchers published an Alzheimer's disease model study in Nutritional Neuroscience. They studied mice that carried a genetic mutation for promoting increased amounts of amyloid beta, a protein fragment found within the telltale neuritic plaque, or "hardening of the brain," seen in Alzheimer's disease.
Although the exact cause of Alzheimer's is not completely understood, experts have recently identified one mechanism involving the insufficient breakdown and recycling of amyloid protein in the brain. That mechanism is both genetic and physiological. In those individuals, normally harmless amyloid protein turns into fragments of amyloid beta, which build up as plaque in the brain rather than being escorted into cellular recycling. That action leads to cell death and weakened neuronal communication.
In the mouse study, beginning at age 4 months-early adulthood-half the brainplaqued group was fed a diet that included blueberry extract for 8 months. The other half was fed standard rat chow and so was a control group of mice that didn't carry the amyloid-plaque mutation.
At 12 months-early middle age-all groups were tested for their performance in a maze.
The brain-plaqued mice that were fed the blueberry extract performed as well as the healthy control mice and performed much better than their brain-plaqued peers fed standard chow.
A look at the plaqued brains of both the blueberry-fed and chow-fed mice after death revealed no difference in the number of brain plaques in either group. "Amyloid-beta-induced plaques are only one aspect of Alzheimer's disease," says Joseph. "But the fact that we saw a dietinduced behavioral difference, despite a similarity in plaque density in both these animal groups, is significant."
The team found increased activity of a family of enzymes called "kinases" in the brains of the amyloid-plaqued mice that were fed blueberry extract. Two kinases found in particular, ERK and PKC, are important in mediating cognitive function, such as converting short-term memory to long-term.
"These kinase molecules are involved in signaling pathways for learning and memory," says Joseph. "It could be that the increased kinase activity within the plaque-ridden brains of the blueberry-fed mice enhanced the signaling in certain receptors."
Brain Cells Are Born
Another HNRCA rat study looked at the aged brain's ability to change physiologically- a condition scientists refer to as "neuronal plasticity." In addition to cell division and differentiation, or "mission assignment," brain tissue undergoes many other changes throughout aging.
For example, a newborn sprouts billions of nerve cells while soaking up information from the environment. But lower levels of synapse growth continue in waves throughout the lifespan.
Littleused synapses are eliminated, while others are strengthened in a neuronal pruning process, of sorts.
Repair mechanisms involve neural immune cells, called "microglia," that seek to heal and protect injured brain tissue; enzymes that regulate safe chemical levels; and genes that are expressed in response to inflammation.
The neuronal-plasticity study investigated the physiological link between nutrition and the memory-control hippocampal area of the aged brain. That region, in the center of the brain, is essential for what's called "working" or "short-term" memory. It receives and processes data, and then, if needed, passes it on for storage.
Neurogenesis also plays a role in the formation of new memories. The capacity of the hippocampus to produce new neurons is thought to be greatly diminished during aging. But this study suggested that old rats fed blueberry extracts for a short time had increased neurogenesis in the dentate gyrus area of their brain's hippocampus. The dentate gyrus is one of the few regions of the brain where neurogenesis occurs.
"We found changes in the proliferation of neurons in blueberry-fed rats," said Gemma Casadesus, formerly a graduate student with the Neuroscience Laboratory and now with Case Western Reserve University. In maze tests, blueberry-fed aged lab rats showed improvement in cognition over chow-fed peers. "There was an association between the proliferation of neuronal precursor cells and better performance of spatial memory," she says.
The researchers don't yet know whether the cognitive improvements seen in the aged blueberry-fed rats translate to humans. "But it's an important step in learning about the brain's ability to rescue itself from age-associated declines in physiological function," Casadesus says.
Can You Hear Me Now?
Neurons that can't get their messages through signaling pathways are like cell phones that can't get their signals through to other cell phones. Why does this happen?
As the brain matures, cell division becomes largely restricted to specific regions of the brain, and brain cells tend to become more vulnerable to two partners in crime: oxidative stress and inflammation.
In the body, free radicals-weakened atoms formed during activities of daily living-are missing an electron and want to bond with neighboring biomolecules to stabilize. The problem is that unless neutralized, free radicals cause cellular damage known as "oxidative stress."
Cellular antioxidant defense systems counterbalance these rogue molecules, but they're not 100 percent effective-particularly as the body and brain mature. And the brain is thought to be especially vulnerable to oxidative stress.
"Weighing just 3 pounds, the brain accounts for only 2 percent of the body's total mass, yet it uses up to half of the body's total oxygen consumed during mental activity," says Joseph.
"Phytochemicals, together with essential nutrients in foods, provide a health-benefits cocktail of sorts. It is feasible that continued research in this area will point to dietary regimens that are effective in boosting neuronal function."
Inflammation is thought to be stoked by the overactivation of microglia-the neural immune cells mentioned earlier.
Microglia are usually dormant, but they migrate to the site of any brain injury. These sentries make up about 20 percent of the cell population in certain regions of the brain.
While seeking to protect and repair tissue, microglia cells produce and send out molecular stress signals, some by way of defensive cytokines, as a bugle call to other cells. Those signals begin a cascade of reactions, including the activation of genes that express proteins and other stress chemicals to help clear away cellular debris.
Microglial activation by amyloid beta is thought to be a key event in the progression of Alzheimer's disease. "When microglia are stuck in an always-on loop in response to plaque buildup in the brain, they become problematic in and of themselves," says Joseph.
This year, Francis Lau, a molecular biologist in the Neuroscience Laboratory, published a study that investigated whether blueberry extracts could have a preventive effect on inflammatory signals coming from activated microglia cells.
Microglial activation is considered the hallmark of inflammation in the central nervous system. For this study, Lau used a rodent microglial cell line that has previously served as a model to study plaqueinduced microglial activation.
Lau exposed groups of those test cells to various levels of blueberry extracts. He then challenged the cells with oxidative stress by exposing them to a toxin-lipopolysaccharide- that triggers secretion of inflammatory chemicals.
Neuroinflammation has been linked to the expression of genes that spew two inflammatory enzymes, iNOS and COX-2, and two cytokines, IL-1b and TNF-a.
Lau used real-time PCR (polymerase chain reaction) to find and measure expression of genes that produce iNOS and COX-2 in the stress-induced cell cultures. He found that the blueberry treatment significantly reduced that expression.
The blueberry extract also markedly lessened secretion of the two inflammatory cytokines. In fact, says Lau, "In cells exposed to the highest blueberry extract concentration, the amount of TNF-a cytokine found was next to nothing- essentially identical to that found in the control cells."
Looking to the Future
The food industry is now using a range of new and existing product ingredients to gain entrance into the emerging brainhealth market. Some are producing food labels that list ORAC values-for example, for use on containers of polyphenol-rich fruit juices and teas. So far, however, there has been no review conducted by the U.S. Food and Drug Administration on health benefits from eating berries.
Future studies at HNRCA will ideally include use of new diagnostic tools as well as human clinical trials. Neuroimaging equipment, for example, could be used to monitor the influence of various dietary factors on development of plaque within the human brain. Such studies aim to find the best dietary regimens to help adults preserve their mental capabilities while aging.-By Rosalie Marion Bliss, ARS.
This research is part of Human Nutrition, an ARS national program (#107) described on the World Wide Web at www. nps.ars.usda.gov.
James A. Joseph is with the USDA-ARS Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111; phone (617) 556-3178, fax (617) 556-3222, e-mail jim.joseph@ ars.usda.gov.
Sunday, July 29, 2007
Blood Pressure Drop During Bypass Might Impair Thinking
(HealthDay News) -- Patients who experience a blood pressure drop during bypass surgery may be at increased risk for a short-term dip in their cognitive abilities.
Researchers at the Johns Hopkins University School of Medicine in Baltimore studied 15 patients, aged 57 to 81, who were given cognitive tests before and then three to five days after they had coronary artery bypass graft (CABG) surgery.
All the patients had a decrease in mean arterial pressure (MAP) during surgery compared with their MAP before surgery. MAP provides doctors with an estimate of the blood pressure in various organs in the body.
The study found that patients whose MAP decreased by 27 millimeters of mercury or more had an average decrease of 1.4 points (out of a maximum of 30 points) on a standard cognitive test. Patients with a MAP decrease of less than 27 millimeters of mercury increased their scores by an average of one point.
Patients with a high MAP before their surgery were more likely to score lower on the cognitive test after their surgery.
The researchers also used MRI to examine the brains of 13 of the patients. They found that patients whose MAP decreased by more than 27 millimeters of mercury were 2.7 times more likely to show evidence of acute stroke.
The study was published online this week in the Archives of Neurology and is expected to be published in the August print issue.
The preliminary data from this small study suggests "that a substantial decrease in MAP from a patient's baseline may be a risk factor for short-term cognitive dysfunction," the study authors wrote. "This may be in part because of an increased risk for radiographic stroke."
Further studies are needed, the researchers said.
More information
The Alzheimer's Association has more about mild cognitive impairment.
Researchers at the Johns Hopkins University School of Medicine in Baltimore studied 15 patients, aged 57 to 81, who were given cognitive tests before and then three to five days after they had coronary artery bypass graft (CABG) surgery.
All the patients had a decrease in mean arterial pressure (MAP) during surgery compared with their MAP before surgery. MAP provides doctors with an estimate of the blood pressure in various organs in the body.
The study found that patients whose MAP decreased by 27 millimeters of mercury or more had an average decrease of 1.4 points (out of a maximum of 30 points) on a standard cognitive test. Patients with a MAP decrease of less than 27 millimeters of mercury increased their scores by an average of one point.
Patients with a high MAP before their surgery were more likely to score lower on the cognitive test after their surgery.
The researchers also used MRI to examine the brains of 13 of the patients. They found that patients whose MAP decreased by more than 27 millimeters of mercury were 2.7 times more likely to show evidence of acute stroke.
The study was published online this week in the Archives of Neurology and is expected to be published in the August print issue.
The preliminary data from this small study suggests "that a substantial decrease in MAP from a patient's baseline may be a risk factor for short-term cognitive dysfunction," the study authors wrote. "This may be in part because of an increased risk for radiographic stroke."
Further studies are needed, the researchers said.
More information
The Alzheimer's Association has more about mild cognitive impairment.
Friday, November 17, 2006
Certain Fatty Acid May Cut Dementia Risk
(HealthDay News) -- Adding further weight to the theory that fish may be brain food, new research found that people with diets rich in fish have a significantly lower risk of dementia and Alzheimer's disease.
The key appears to be docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid that appears to affect dementia risk and to be important for the proper functioning of the central nervous system.
"If you have a high level of DHA, a fatty acid found in fish, it reduced your risk of dementia by about half," said study lead researcher Dr. Ernst J. Schaefer, senior scientist and director of the Lipid Metabolism Laboratory at the Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University in Boston.
It's known that omega-3 fatty acids protect the heart and the circulatory system. "Just as fish is good for your heart, it's probably good for your brain as well," Schaefer said.
Fatty fish like mackerel, lake trout, herring, sardines, albacore tuna and salmon are high in DHA.
The study findings are published in the November issue of the Archives of Neurology.
In the study, Schaefer and his colleagues collected data on DHA levels and dementia in 899 men and women who were part of the Framingham Heart Study. Over nine years of follow-up, 99 people developed dementia, including 71 with Alzheimer's disease.
The researchers found that people with the highest blood levels of DHA had a 47 percent lower risk of developing dementia and a 39 percent lower risk of developing Alzheimer's, compared with those with lower DHA levels.
Levels of DHA in the blood vary by how much the liver converts alpha-linolenic acid, an essential fatty acid, to DHA and also by the amount of DHA in the diet, the researchers noted.
People with the highest blood levels of DHA said they ate an average of two to three servings of fish a week. People with lower DHA levels ate substantially less fish, the researchers reported.
Schaefer thinks the same benefit can be realized by taking fish-oil supplements. "Everything that we know suggests that supplements would be as effective as eating fish," he said. "Since low fish intake appears to be a risk factor for developing dementia, either eat more fish or use one or two fish oil capsules a day."
However, Schaefer added that a randomized clinical trial is still needed to see if DHA really protects the brain from dementia.
Martha Clare Morris is an epidemiologist at Rush University Medical Center in Chicago and author of an accompanying editorial in the journal. "This is the first study to link blood levels of DHA to protection against Alzheimer's disease," she said, adding that recent animal studies have shown that DHA reduces amyloid plaques -- a hallmark of Alzheimer's -- in the brain and also improves memory.
"There is a lot of animal and biochemical evidence to support what this new study shows," Morris said.
But, she said, she's not sure there is enough data to suggest the value of fish oil supplements. "It looks like the protective benefits from omega-3 fatty acids are at a very low level. There is very little evidence that you get better protection from higher intake," she said. "Whether fish oil supplements are protective is yet to be seen."
Another expert thinks clinical trials are needed to see if DHA really protects against Alzheimer's.
"This shows in a prospective study that DHA is the only plasma lipid to cut the risk for developing dementia a decade or more later," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System and associate director of the Alzheimer's Disease Research Center at UCLA's David Geffen School of Medicine.
This apparent protection is associated with eating fish, Cole said. "Other studies have pointed to fish intake as protective but have been far less clear that the omega-3 fatty acids in fish were the factor associated with risk reduction," he said. "This matters because if it is the fat, you could take fish oil supplements and avoid mercury contamination issues."
More information
The Alzheimer's Association can tell you more about Alzheimer's disease.
The key appears to be docosahexaenoic acid (DHA), an omega-3 polyunsaturated fatty acid that appears to affect dementia risk and to be important for the proper functioning of the central nervous system.
"If you have a high level of DHA, a fatty acid found in fish, it reduced your risk of dementia by about half," said study lead researcher Dr. Ernst J. Schaefer, senior scientist and director of the Lipid Metabolism Laboratory at the Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University in Boston.
It's known that omega-3 fatty acids protect the heart and the circulatory system. "Just as fish is good for your heart, it's probably good for your brain as well," Schaefer said.
Fatty fish like mackerel, lake trout, herring, sardines, albacore tuna and salmon are high in DHA.
The study findings are published in the November issue of the Archives of Neurology.
In the study, Schaefer and his colleagues collected data on DHA levels and dementia in 899 men and women who were part of the Framingham Heart Study. Over nine years of follow-up, 99 people developed dementia, including 71 with Alzheimer's disease.
The researchers found that people with the highest blood levels of DHA had a 47 percent lower risk of developing dementia and a 39 percent lower risk of developing Alzheimer's, compared with those with lower DHA levels.
Levels of DHA in the blood vary by how much the liver converts alpha-linolenic acid, an essential fatty acid, to DHA and also by the amount of DHA in the diet, the researchers noted.
People with the highest blood levels of DHA said they ate an average of two to three servings of fish a week. People with lower DHA levels ate substantially less fish, the researchers reported.
Schaefer thinks the same benefit can be realized by taking fish-oil supplements. "Everything that we know suggests that supplements would be as effective as eating fish," he said. "Since low fish intake appears to be a risk factor for developing dementia, either eat more fish or use one or two fish oil capsules a day."
However, Schaefer added that a randomized clinical trial is still needed to see if DHA really protects the brain from dementia.
Martha Clare Morris is an epidemiologist at Rush University Medical Center in Chicago and author of an accompanying editorial in the journal. "This is the first study to link blood levels of DHA to protection against Alzheimer's disease," she said, adding that recent animal studies have shown that DHA reduces amyloid plaques -- a hallmark of Alzheimer's -- in the brain and also improves memory.
"There is a lot of animal and biochemical evidence to support what this new study shows," Morris said.
But, she said, she's not sure there is enough data to suggest the value of fish oil supplements. "It looks like the protective benefits from omega-3 fatty acids are at a very low level. There is very little evidence that you get better protection from higher intake," she said. "Whether fish oil supplements are protective is yet to be seen."
Another expert thinks clinical trials are needed to see if DHA really protects against Alzheimer's.
"This shows in a prospective study that DHA is the only plasma lipid to cut the risk for developing dementia a decade or more later," said Greg M. Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System and associate director of the Alzheimer's Disease Research Center at UCLA's David Geffen School of Medicine.
This apparent protection is associated with eating fish, Cole said. "Other studies have pointed to fish intake as protective but have been far less clear that the omega-3 fatty acids in fish were the factor associated with risk reduction," he said. "This matters because if it is the fat, you could take fish oil supplements and avoid mercury contamination issues."
More information
The Alzheimer's Association can tell you more about Alzheimer's disease.
Monday, November 13, 2006
Hydergine: Desire Better Brain-Power?
Q: Hydergine: Desire Better Brain-Power? What do you think of hydergine to boost mental powers?
A: Hydergine has been touted for some time as a "smart" drug for use in enhancing mental abilities and improving intelligence.
It has been around for more than 20 years and is marketed today as a nonspecific cerebral stimulant and prescribed to help relieve symptoms of age-related mental decline. Hydergine has been studied but found ineffective for the treatment of Alzheimer's disease.
Originally developed for the treatment of hypertension, hydergine didn't really help lower blood pressure and is no longer used for that purpose. However, some people who took it soon after its introduction noticed improvements in memory and mood, which they associated with use of the drug. At first, these changes were attributed to increased blood flow to the brain, but later research suggested that hydergine improved brain cell metabolism.
Today, hydergine is FDA approved only for the treatment of people over the age of 60 who show signs of mental decline. I'm told it is more widely used in Europe, and I understand that some in the anti-aging community advocate taking more than the 3 mg daily dose recommended by the FDA.
Frankly, I wouldn't bother. I tried hydergine myself some years ago to see what it could do, but I detected no benefits. While the drug seems safe enough, I don't see the point of using it - especially since it's expensive. I'm unconvinced that it makes good on the promises made for it by its Internet promoters.
Andrew Weil, M.D.
A: Hydergine has been touted for some time as a "smart" drug for use in enhancing mental abilities and improving intelligence.
It has been around for more than 20 years and is marketed today as a nonspecific cerebral stimulant and prescribed to help relieve symptoms of age-related mental decline. Hydergine has been studied but found ineffective for the treatment of Alzheimer's disease.
Originally developed for the treatment of hypertension, hydergine didn't really help lower blood pressure and is no longer used for that purpose. However, some people who took it soon after its introduction noticed improvements in memory and mood, which they associated with use of the drug. At first, these changes were attributed to increased blood flow to the brain, but later research suggested that hydergine improved brain cell metabolism.
Today, hydergine is FDA approved only for the treatment of people over the age of 60 who show signs of mental decline. I'm told it is more widely used in Europe, and I understand that some in the anti-aging community advocate taking more than the 3 mg daily dose recommended by the FDA.
Frankly, I wouldn't bother. I tried hydergine myself some years ago to see what it could do, but I detected no benefits. While the drug seems safe enough, I don't see the point of using it - especially since it's expensive. I'm unconvinced that it makes good on the promises made for it by its Internet promoters.
Andrew Weil, M.D.
Folic Acid to Boost Memory?
Q: Folic Acid to Boost Memory?Is it true that folic acid can prevent Alzheimer's disease? I heard that it improves memory.
A: New findings do suggest that folic acid may slow the declines in memory that can occur with age. Dutch researchers recently presented compelling evidence from a three-year study that included 818 adults between the ages of 50 and 70, none of whom were having any memory problems.
During the study, the participants took either a placebo or 800 mg folic acid (twice the amount recommended for women of childbearing age to protect against birth defects).
Results showed that those who took the folic acid had memory scores equal to people five and a half years younger. The folic acid group in the study also did better in information processing and muscle skills. The study was conducted by researchers at Wageningen University in the Netherlands and reported at the Alzheimer's Association International Conference on Dementia Prevention.
A: New findings do suggest that folic acid may slow the declines in memory that can occur with age. Dutch researchers recently presented compelling evidence from a three-year study that included 818 adults between the ages of 50 and 70, none of whom were having any memory problems.
During the study, the participants took either a placebo or 800 mg folic acid (twice the amount recommended for women of childbearing age to protect against birth defects).
Results showed that those who took the folic acid had memory scores equal to people five and a half years younger. The folic acid group in the study also did better in information processing and muscle skills. The study was conducted by researchers at Wageningen University in the Netherlands and reported at the Alzheimer's Association International Conference on Dementia Prevention.
Saturday, October 14, 2006
Aricept Use Expanded to Severe Alzheimer's Dementia
(HealthDay News) -- Aricept (donepezil hydrochloride) has been approved by the U.S. Food and Drug Administration to treat severe dementia associated with Alzheimer's disease.With its approval a decade ago for mild-to-moderate Alzheimer's dementia, Aricept becomes the first sanctioned drug to treat all forms of the memory-robbing disease, the FDA said in a statement.
The latest approval followed clinical testing in Sweden and Japan involving more than 500 people with severe Alzheimer's. Compared to those taking a placebo, participants on Aricept performed better on tests of cognitive functions including memory, language and orientation, the FDA said.
Aricept is manufactured by Eisai Inc. of Teaneck, N.J.
More information
You can learn more about Alzheimer's from the U.S. National Institute on Aging.
Saturday, September 16, 2006
Commentary on Nutritional Treatment
from Willam Walsh, Ph.D., Senior Scientist, Pfeiffer Treatment Center http://www.hriptc.org/(The following information is taken from Dr. William Walsh's discussion on Safe Harbor's "Integrative Psychiatry" email list for professionals.
To preserve Dr. Walsh's wealth of information, we have posted his comments here, with the notation of added commentary [with the date] as discussion goes on.)
SAMe
SAMe is very promising for undermethylated persons and a bad idea for those who suffer from a genetic tendency for overmethylation. I don't particularly like the "allopathic" method you referred to which is simply trial & error. SAMe can do great harm if given to the wrong person.
I hate going to funerals. (17 Dec, 2002)The mechanisms of action of SAMe and TMG are quite different. Most of our methyl groups come from dietary methionine. The methionine is converted to SAMe in a reaction with magnesium, ATP, methionine-adenosyl-transferase, and water. SAMe is a relatively unstable carrier of methyl groups and is the primary source of methyl for most reactions in the body.
Once the methyl group has been donated, the residual molecule is s-adenosyl-homocysteine which converts to homocysteine. TMG (betaine) is a biochemical which can donate a methyl group to homocysteine, thus converting it back to methionine.
The TMG route is secondary to the 5-methyl-tetrahydrofolate/B-12 reaction which the primary route for restoring methionine. Methionine and SAMe supplements directly introduce new methyl groups into the body.
TMG can provide a methyl group only to the extent that there is insufficient folate/B-12 to do the job. In some persons, the methylation effect of TMG is very minimal. In addition, persons who are undermethylated have a SAM cycle which is "spinning very slowly", much like a superhighway with little traffic.
The answer for them is NOT to more efficiently convert the small amount of homocysteine to methionine (using TMG), but rather to directly introduce more methionine or SAMe into the body. A small percentage of persons with sufficient dietary methionine cannot efficiently produce SAMe --- These persons need supplemental SAMe, and not methionine or TMG and are the exception to the rule. In most other cases, methionine supplements alone are sufficient.
TMG is a great way to treat individuals with dangerously high homocysteine levels. TMG can be very useful in augmenting methionine therapy along with B-6/P-5-P , serine, etc. The challenge is to supply enough methyl groups to help the patient, without creating dangerously high levels of homocysteine. Use of TMG is an "insurance policy" against this happening. (Jan 22, 2003)
A quick way to test for need for methylation therapy is to carry out a cautious trial of SAMe.
Within a week or two you should have your answer. If she clearly is improving on the SAMs (which is frightfully expensive)..... you can get usually the same benefits (albeit more slowly) using methionine plus calcium, magnesium, and B-6. This should be side-effect free unless (a) the methylation is begun too abruptly or (b) the patient has a rare genetic enzyme disorder which disrupts the SAM cycle. We've found that direct methylation is usually more successful than tinkering with the SAM cycle. The primary way humans receive most of their methyl groups is from dietary methionine. It's often hard to improve on Mother Nature. (Jan 20, 2003)
SAMe is likely to cause great worsening of symptoms, including mania, if given to an OVER-methylated person. The incidence of overmethylation in our patient database of 1,500 bipolar cases is about 18%. Bipolar disorder is not a single condition, but a collection of very different biochemical disorders under the same umbrella diagnosis. SAMe works great for truly undermethylated patients, but all hell breaks out if given to someone who is overloaded (genetically) with methyl groups. The right way to do this is to (a) first determine the person's innate methylation tendency & then (b) act accordingly. (Jan 31, 2003)
Schizophrenia
Severe wheat gluten intolerance can cause classic symptoms of schizophrenia, and amounts to about 4% of all schizophrenia diagnoses in the U.S. These persons usually become quite normal when placed on a gluten-free diet.I've done medical histories for more than 2,000 persons diagnosed with schizophrenia and have always been struck by the high frequency of schizophrenia in other relatives. Interestingly, the schizophrenia would often skip a generation.
NIMH data suggests that the overall incidence of schizophrenia in the USA is between 1% and 4%, depending on the definitions. However, the incidence of schizophrenia for children who have a schizophrenic parent is about 16%. This number doesn't change much for children of schizophrenics adopted at birth. I don't think there is "a schizophrenia gene", partly because this is a garbage term which encompasses several completely different conditions.
There are a number of biochemical ingredients which predispose to each phenotype of SZ..... these may be either genetic or acquired. However, I'm absolutely certain there is a genetic component in most cases.
Carl Pfeiffer was the first to develop meaningful chemical classifications of schizophrenia (and separate treatments for each phenotype). Carl Pfeiffer of Princeton, N.J. saw more than 20,000 schizophrenics in his lifetime. He found that 90% of all SZ patients could be classified into 3 large groups, with completely different etiologies & treatment approaches. These he termed "histapenia", "histadelia", and "pyroluria". The remaining 10% fit into several splinter groups.
One of the splinter groups was gluten intolerance, which represents 4% (1 case in 25). This is a rare form of schizophrenia, but if you've got it, it's everything!Multiple food & chemical sensitivities are also associated with histapenia (low histamine, overmethylation), the largest of all SZ groups, amounting to about 48% of all cases.
For this group, SZ symptoms often worsen if exposed to the offending substances, & nice improvements often occur if they are identified & avoided. However, the food sensitivities usually disappear after about 1 year of aggressive Folate/B-12/B-3 treatment, which is the primary route to a normal life for these patients.
We've known for more than 20 years that the metallothionein protein system does not perform well in most ADHD patients. About 68% of them exhibit very poor control of Cu & Zn, based on lab data from more than 6,000 patients diagnosed with ADD/ADHD. Autism is different in that about 90% of patients exhibit Cu/Zn imbalances that are generally much more severe than in ADHD.For several months, we have extended our metallothionein-promotion protocol to ADHD, behavior, depression, and schizophrenic patients who exhibit Cu/Zn imbalance.
The informal results so far are very encouraging. However, we've not yet done a formal outcome study for these populations, and thus have no statistics yet.We are considering applying MT-Promotion to Alzheimers & Parkinsons patients in the near future. Both disorders involve serious oxidative stress and abnormal trace metal levels. In addition, recent research has revealed a striking metallothionein deficiency in the brains of Alzheimers patients. (Feb 25, 2003)I've evaluated more than 3,500 patients with a diagnosis of bipolar or schizophrenia. The predominance of auditory hallucinations, serious self abuse, aggressiveness, inability to continue school, and social isolation...... all point in the direction of classic "paranoid schizophrenia", although many of these patients are labeled "bipolar disorder with psychotic features". Most severely mentally ill persons with a history of exceptional artistic or musical talent test as overmethylated. The biochemical recipe for these patients usually consists of (1) overmethylation, (2) low folate levels, and (3) elevated blood copper levels. All three of these chemical imbalances impact dopamine and norepinephrine in the brain, and together can cause rather extraordinary abnormalities in these important neurotransmitters. In my opinion, the key to successful treatment is biochemical treatment to overcome these chemical imbalances...... fortunately this can be accomplished using aggressive therapy with nutrients to normalize the chemical factors.Most mental breakdowns are triggered by severe stress, but the underlying cause is genetic and involves brain chemistry. Many persons self-medicate with alcohol, marijuana, or other illegal drugs in a desperate attempt to feel better. Many patients and their families erroneously believe that the EtOH or drug experiences were the underlying cause of the condition. They are wrong! This adult-onset condition will strike eventually in most cases, even if substance abuse never occurs.Traditional medicine can provide medication support which can usually eliminate (temporarily) most/all psychosis symptoms. However, these patients are usually plagued by drug side effects and are a mere shadow of their original selves. Common side effects are (a) fatigue, (b) inability to focus/concentrate for more than a few minutes, (c) change in personality, (d) massive weight gain, etc. The most popular drugs for these patients are Zyprexa, Seroquil, Risperdal, Geodon, and Clozaril..... the so-called atypical antipsychotics. Since most patients hate these medications, poor compliance is a major problem.I've seen many young schizophrenics and bipolar patients achieve complete recoveries through biochemical (nutrient) therapy. This rarely occurs with traditional medication therapy. (May 12, 2003)Some of schizophrenics who spontaneously get better are those who experience a toxic psychosis. I have a friend who had a toxic psychosis after an accidental overdose of a medication during childbirth. For 6 hours she was a full blown paranoid schizophrenic..... No symptoms in the following 20 years. Also, schizophrenia comes in mild, moderate, and severe versions. Many persons with a very mild genetic tendency for SZ can experience an environmental insult which pushes them into a temporary mental illness. Most will become quite ok with or without therapy.The real problem is the millions of SZ persons who have moderate to severe SZ which does not go away easily. (May 27, 2003)
Taurine
Yes, I've read a few articles and a book that talked about Taurine's slow metabolism and tendency to build up over time. Because of this, I've believed that high doses of Taurine (1,000 to 2,000 mg/day) are ok in the beginning..... but that the dosages need to be reduced within 2 weeks to about 400 to 500 mg/day..... to achieve the same effect.I believe that Taurine is especially effective for (1) combating seizure tendency and (2) reducing liver stress in processing fats. There have been several reports of intolerances and side effects from use of Taurine, and I feel that indiscriminant high doses are unwise.About 12 months ago, there was a fad among several alternative practitioners in which high doses of Taurine were given to every autistic patient. One of the reasons given was "to assist the liver cope with stresses associated with toxic metal overload". This seems to be a poor reason, since Taurine's action in the liver appears to be limited to fat metabolism, and most autistics are slender malabsorbers with low lipid levels. (June 24, 2003)
Womb Trauma
There is an exquisite and fragile biological/biochemical process during gestation in which short, dense immature brain cells are pruned, grow into fully-developed brain cells, and then (remarkably) experience growth inhibition to complete the process. The molecular biology of this process is becoming very well defined, and it is clear that many environmental events can hinder or disrupt early brain development. The primary culprits are oxidative stress, teratological chemicals, and infections. The least appreciated of these harmful factors is oxidative stress which can deplete key proteins and enzymes required for normal brain development.Environmental harm to a developing fetus can result from (a) biochemical inadequacies of the mother, and (b) external environmental insults. We're all familiar with birth defects that can result from Thalidomide, Thorazine, Prolixin, Haldol, and other psychiatric medications. Also the dangers of mercury, lead, and other toxics are well established, and we know that a mother's improper diet (e.g. inadequate folic acid) can be harmful. Although lower on the radar screen, fetal oxidative stresses can be equally devastating.What I'm leading up to.... is the scientific fact that serious emotional or physical stresses experienced by the mother can impair early brain development, especially if the mother is not biochemically intact. For example high emotional stresses or physical trauma to the mother will weaken the activity of metallothionein (MT) and glutathione (GSH) proteins, andincrease oxidative stress in the brain. MT-1 and MT-2 are directly involved in growth of immature brain cells. MT-3 is a key protein required for pruning and growth inhibition. These proteins also have the job of defending against oxidative stress in the brain and are consumed in the process. Maternal emotional stresses and psychic traumae deplete the embryonic brain of MT proteins and can compromise brain development.Womb trauma is real and the concept of "a cry so deep" is not psycho-babble guesswork. Rather, it is solidly supported by scientific fields such as embryology and molecular biology. (Aug 1, 2003)If fetal or early infant traumae have resulted in a brain that hasn't completely matured..... therapies to promote MT and GSH appear very promising..... especially in tandem withbehavioral therapies which stimulate the development of new brain cells.If the net result of the traumae is biochemical or neurotransmitter differences, then biochemical therapy aimed at normalizing brain chemistry would be indicated.If the traumae resulted in diminished ability to tolerate environmental toxins (for example an incompetent blood-brain barrier), then avoidance of such toxins would be an important aspect of treatment.If the traumae resulted in an innate inability to cope with emotional stresses, then counseling or other psychological services could be very beneficial.If the traumae resulted in a brain that is structurally different, this may represent "brain damage" that may be refractory to all treatments. (Aug 1, 2003)
Zinc
There have been several recent published articles which indicate that zinc and zinc metallothionein proteins (1) tend to prevent brain strokes, (2) tend to assist brain recovery after strokes, and (3) that deficiency of Zn or Zn-MT is associated with increased stroke likelihood. An occasional test for plasma Zn could help identify the proper dosage. Most adults can safely start with 25 to 50 mg/day of Zn. Without indication of B-6 deficiency, it might be a good idea to limit pyridoxine hydrochloride (usual form of B-6) to about 200 mg/day. B-6 is very helpful in enhancing the utilization of Zn.After use of these nutrients with thousands of persons, I'm not aware of a single case of harm. However, it is a good idea to introduce zinc gradually & to take Zn during the PM only. (June 3, 2003
Every 5 years or so, the zinc experts of the world convene for a symposium in which they share new advances in Zn technogy & research..... It's usually headed up by the eminent Prof. Prasad.One of the topics is laboratory testing to indicate an individual's Zn status. They consider about 10 different methods including packed cells, taste tests, etc...... The last two symposia resulted in the consensus that none of the testing options is wonderful, but that the best of the commercially available tests is plasma zinc. Taste tests didn't make the top three methods.However the Zn experts also stated that the most definitive determination of zinc depletion is the presence of symptoms of Zn depletion which disappear after Zn supplementation.My organization has evaluated the Zn status of 18,000 patients and we've tried all of these methods. Our standard protocol involves plasma Zn, being careful to use acid-etched, trace-metal-free tubes.We find that virtually all treatment-naive ASD persons are very Zn depleted and overloaded in "free" (unbound by ceruloplasmin) copper. Our patient population for ASD is 2,800. Our database of 5,600 ADHD patients indicates that about 75% are depleted in Zn. The remaining 25% have problems associated with pyrrole disorders, methylation disorders, EFA disorders, toxic overloads, etc. (July 22, 2003)
The high level of zinc depletion in ASD appears to stem from a genetic weakness in the metallothionein protein system.Cu/Zn ratios in hair are very helpful in ADHD and behavior disorders..... but far less useful in ASD, depression, and schizophrenia. Tracking plasma Zn, serum Cu and serum ceruloplasmin levels can be very helpful in guiding dosages aimed at normalizing Zn.
Management of Zn & Cu levels is a challenging problem in ASD. Sometimes rather extraordinary Zn dosages are required to normalize blood Zn levels.Virtually all ASD persons are Zn depleted., but not all exhibit an elevated Cu/Zn ratio. A minority of ASD patients exhibit normal or low Cu levels in serum, but have vastly inadequate levles of ceruloplasmin. Thus, the level of "unbound" Cu can be very high, even though all standard measures of Cu appear to be low. Some of these patients seem to have a mild version of Wilson's Disesase. (July 24, 2003)
Friday, September 15, 2006
Bacopa: A Better Memory Booster?
Bacopa: A Better Memory Booster?
Q: What you can tell me about bacopa? I first read about it as a treatment for memory problems. Do you know anything about its effectiveness in treating memory problems or what the recommended dosage should be?
A: Bacopa (Bacopa monnieri) is an herb native to India that has been used traditionally in Ayurvedic medicine to enhance memory, learning and concentration and also to treat anxiety, heart problems, digestive disorders, asthma, and bronchitis. Most of the research on bacopa has been in animals, but a few small studies on humans have also been done.
The single study I've been able to find on bacopa's effect on memory was a small, double-blind, placebo-controlled 12-week trial conducted in Australia with 46 volunteers between the ages of 18 and 60, divided into two groups.
The volunteers in one group were given 300 milligrams of bacopa daily, and the others received a placebo. Prior to the study, the researchers tested all the volunteers to assess their verbal learning abilities, memory and speed of information processing. The tests were repeated five and 12 weeks after the study began. The researchers noted a significant improvement among the volunteers in the bacopa group compared to those in the placebo group.
A review article of some 38 scientific studies of bacopa was published in the March, 2004, issue of the journal Alternative Medicine Review, and noted two small studies that demonstrated an improvement in cognitive function in children as a result of taking bacopa.
A single small-scale human study also found a decrease in anxiety symptoms among patients treated with bacopa.
Bacopa is now being widely promoted as a treatment for memory problems, but I would recommend more proven protective strategies. Keep your mind active by reading newspapers and books, doing crossword puzzles, playing musical instruments, participating in ongoing education, and learning a new language. As far as supplements to enhance memory are concerned, the ones listed below have been studied more thoroughly than bacopa:
Ginkgo biloba. This well-studied botanical remedy increases blood flow to the head, has a reputation as a memory-enhancing agent and may slow the progression of dementia in early onset Alzheimer's disease. You probably won't notice any effects for six to eight weeks. (Look for products standardized to 24 percent ginkgo flavone glycosides and 6 percent terpene lactones; the dose is 60 to 120 milligrams twice a day with food.) Ginkgo has low toxicity, although it may cause mild stomach irritation.
Acetyl-L-carnitine (also called ALC or ALCAR) is an amino acid derivative. Human clinical studies of this compound are currently underway, and the early evidence from animal trials is encouraging. Many people take ALC as a cognitive enhancer. The dose is 500-1,000 milligrams twice a day on an empty stomach. It is nontoxic, but this is an expensive regimen.
Phosphatidyl serine, or PS. A naturally occurring lipid that is a component of cell membranes, PS is considered a brain-cell nutrient. Human studies have reported positive effects on memory and concentration; PS may improve cognitive function in normal adults and may help reverse age-related cognitive decline. The supplement form, derived from soybeans, is readily available, but fairly expensive. The starting dose is 100 milligrams two or three times a day; if this produces positive benefits after a month or more, it may be possible to go on a lower maintenance dose. It is nontoxic.
Andrew Weil, M.D.–
Author of:
Eight Weeks to Optimum Health
Spontaneous Healing
The Natural Mind
The Marriage of the Sun and Moon
Health and Healing
Natural Health, Natural Medicine
From Chocolate to Morphine (with Winifred Rosen)
Q: What you can tell me about bacopa? I first read about it as a treatment for memory problems. Do you know anything about its effectiveness in treating memory problems or what the recommended dosage should be?
A: Bacopa (Bacopa monnieri) is an herb native to India that has been used traditionally in Ayurvedic medicine to enhance memory, learning and concentration and also to treat anxiety, heart problems, digestive disorders, asthma, and bronchitis. Most of the research on bacopa has been in animals, but a few small studies on humans have also been done.
The single study I've been able to find on bacopa's effect on memory was a small, double-blind, placebo-controlled 12-week trial conducted in Australia with 46 volunteers between the ages of 18 and 60, divided into two groups.
The volunteers in one group were given 300 milligrams of bacopa daily, and the others received a placebo. Prior to the study, the researchers tested all the volunteers to assess their verbal learning abilities, memory and speed of information processing. The tests were repeated five and 12 weeks after the study began. The researchers noted a significant improvement among the volunteers in the bacopa group compared to those in the placebo group.
A review article of some 38 scientific studies of bacopa was published in the March, 2004, issue of the journal Alternative Medicine Review, and noted two small studies that demonstrated an improvement in cognitive function in children as a result of taking bacopa.
A single small-scale human study also found a decrease in anxiety symptoms among patients treated with bacopa.
Bacopa is now being widely promoted as a treatment for memory problems, but I would recommend more proven protective strategies. Keep your mind active by reading newspapers and books, doing crossword puzzles, playing musical instruments, participating in ongoing education, and learning a new language. As far as supplements to enhance memory are concerned, the ones listed below have been studied more thoroughly than bacopa:
Ginkgo biloba. This well-studied botanical remedy increases blood flow to the head, has a reputation as a memory-enhancing agent and may slow the progression of dementia in early onset Alzheimer's disease. You probably won't notice any effects for six to eight weeks. (Look for products standardized to 24 percent ginkgo flavone glycosides and 6 percent terpene lactones; the dose is 60 to 120 milligrams twice a day with food.) Ginkgo has low toxicity, although it may cause mild stomach irritation.
Acetyl-L-carnitine (also called ALC or ALCAR) is an amino acid derivative. Human clinical studies of this compound are currently underway, and the early evidence from animal trials is encouraging. Many people take ALC as a cognitive enhancer. The dose is 500-1,000 milligrams twice a day on an empty stomach. It is nontoxic, but this is an expensive regimen.
Phosphatidyl serine, or PS. A naturally occurring lipid that is a component of cell membranes, PS is considered a brain-cell nutrient. Human studies have reported positive effects on memory and concentration; PS may improve cognitive function in normal adults and may help reverse age-related cognitive decline. The supplement form, derived from soybeans, is readily available, but fairly expensive. The starting dose is 100 milligrams two or three times a day; if this produces positive benefits after a month or more, it may be possible to go on a lower maintenance dose. It is nontoxic.
Andrew Weil, M.D.–
Author of:
Eight Weeks to Optimum Health
Spontaneous Healing
The Natural Mind
The Marriage of the Sun and Moon
Health and Healing
Natural Health, Natural Medicine
From Chocolate to Morphine (with Winifred Rosen)
Thursday, September 14, 2006
B-Vitamins Won't Prevent Alzheimer's
(HealthDay News) -- Using B vitamins to lower levels of the blood protein homocysteine does not ward off Alzheimer's disease, at least not in older people with high homocysteine levels, according to new research.
The findings come as a disappointment after previous work had suggested a link between Alzheimer's and elevated concentrations of the amino acid.
"There is no short-term benefit of homocysteine lowering with B-vitamins on cognitive performance in healthy older people with high homocysteine," confirmed Murray Skeaff, co-author of the study published in the June 29 issue of the New England Journal of Medicine and associate professor of human nutrition at the University of Otago in Dunedin, New Zealand.
But the issue is not dead, yet.
"We would love to see something as simple and relatively non-toxic as a vitamin intervention that would prevent dementia and/or Alzheimer's," said William Thies, vice president of medical and scientific relations at the Alzheimer's Association in Chicago. "This trial probably has an inadequate number of people and too short a time period to show an effect. This particular trial will not end the discussion," he said.
Previous observational studies had shown higher homocysteine levels in Alzheimer's patients. Also, among older adults, higher homocysteine levels were correlated with poorer performance on cognitive tests.
About 4.5 million people in the United States suffer from dementia, the association said, and many more experience some form of cognitive impairment.
The authors of this study wanted to see if lowering homocysteine levels had any impact on cognitive function in older adults.
The two-year study involved 276 healthy participants, age 65 or older, who had blood homocysteine levels above a certain threshold.
Participants were given a daily supplement containing 1,000 micrograms of folate, 500 micrograms of vitamin B12 and 10 milligrams of B6. Cognitive testing was done at the beginning of the study as well as after one and two years of treatment.
Folates are B-vitamin nutrients found in foods such as bananas and oranges, leafy green vegetables, asparagus, broccoli, liver, and many types of beans and peas.
Although homocysteine levels did become lower in the vitamin group, the researchers detected no significant differences in scores of mental functioning.
"We used a range of tests to assess specific aspects of cognition and found no evidence of better cognition in those who took vitamins," Skeaff said. "If dementia is at the extreme of the continuum of cognitive decline, then, according to the 'homocysteine hypothesis,' we might have expected better cognitive performance in the vitamins group. This did not happen. If there was a hint of anything -- the emphasis is on hint -- it was lower cognitive scores in the vitamins group" he said.
"This study puts a chink in [the hypothesis'] armor, because we did not find even a hint of better cognition in those who took the vitamins," Skeaff said, concluding, "Population-based screening for high homocysteine concentrations or treatment with high-dose B-vitamins to improve cognitive performance cannot be advocated, based on current evidence."
But to truly understand the effect of lowering homocysteine on dementia, much larger and longer trials would be needed, Thies said. Such trials are invariably expensive.
One interesting aside to the current study is that it did manage to demonstrably lower homocysteine levels, even in the United States, where foods like bread are already folate-enriched.
"That's always been one of the questions about doing a trial like this: Is there enough folic acid supplementation around the world now that it makes homocysteine lowering difficult to achieve in a 'real' population?" Thies asked. "They've shown they can do that, but obviously, it has virtually no effect on any of the cognitive markers," he said.
The U.S. Department of Agriculture began requiring that all grain products be fortified with folic acid in 1998. The supplement is key in helping prevent neural tube defects such as spina bifida in newborns.
There has been concern, however, that such fortification may not be safe for older people with vitamin B12 deficiency.
More information
For much more on Alzheimer's disease, visit the Alzheimer's Association.
The findings come as a disappointment after previous work had suggested a link between Alzheimer's and elevated concentrations of the amino acid.
"There is no short-term benefit of homocysteine lowering with B-vitamins on cognitive performance in healthy older people with high homocysteine," confirmed Murray Skeaff, co-author of the study published in the June 29 issue of the New England Journal of Medicine and associate professor of human nutrition at the University of Otago in Dunedin, New Zealand.
But the issue is not dead, yet.
"We would love to see something as simple and relatively non-toxic as a vitamin intervention that would prevent dementia and/or Alzheimer's," said William Thies, vice president of medical and scientific relations at the Alzheimer's Association in Chicago. "This trial probably has an inadequate number of people and too short a time period to show an effect. This particular trial will not end the discussion," he said.
Previous observational studies had shown higher homocysteine levels in Alzheimer's patients. Also, among older adults, higher homocysteine levels were correlated with poorer performance on cognitive tests.
About 4.5 million people in the United States suffer from dementia, the association said, and many more experience some form of cognitive impairment.
The authors of this study wanted to see if lowering homocysteine levels had any impact on cognitive function in older adults.
The two-year study involved 276 healthy participants, age 65 or older, who had blood homocysteine levels above a certain threshold.
Participants were given a daily supplement containing 1,000 micrograms of folate, 500 micrograms of vitamin B12 and 10 milligrams of B6. Cognitive testing was done at the beginning of the study as well as after one and two years of treatment.
Folates are B-vitamin nutrients found in foods such as bananas and oranges, leafy green vegetables, asparagus, broccoli, liver, and many types of beans and peas.
Although homocysteine levels did become lower in the vitamin group, the researchers detected no significant differences in scores of mental functioning.
"We used a range of tests to assess specific aspects of cognition and found no evidence of better cognition in those who took vitamins," Skeaff said. "If dementia is at the extreme of the continuum of cognitive decline, then, according to the 'homocysteine hypothesis,' we might have expected better cognitive performance in the vitamins group. This did not happen. If there was a hint of anything -- the emphasis is on hint -- it was lower cognitive scores in the vitamins group" he said.
"This study puts a chink in [the hypothesis'] armor, because we did not find even a hint of better cognition in those who took the vitamins," Skeaff said, concluding, "Population-based screening for high homocysteine concentrations or treatment with high-dose B-vitamins to improve cognitive performance cannot be advocated, based on current evidence."
But to truly understand the effect of lowering homocysteine on dementia, much larger and longer trials would be needed, Thies said. Such trials are invariably expensive.
One interesting aside to the current study is that it did manage to demonstrably lower homocysteine levels, even in the United States, where foods like bread are already folate-enriched.
"That's always been one of the questions about doing a trial like this: Is there enough folic acid supplementation around the world now that it makes homocysteine lowering difficult to achieve in a 'real' population?" Thies asked. "They've shown they can do that, but obviously, it has virtually no effect on any of the cognitive markers," he said.
The U.S. Department of Agriculture began requiring that all grain products be fortified with folic acid in 1998. The supplement is key in helping prevent neural tube defects such as spina bifida in newborns.
There has been concern, however, that such fortification may not be safe for older people with vitamin B12 deficiency.
More information
For much more on Alzheimer's disease, visit the Alzheimer's Association.
Thursday, August 31, 2006
Stroke May Trigger Memory Trouble
(HealthDay News) -- Stroke may harm memory without necessarily causing dementia or other cognitive impairment, researchers report.
Columbia University researchers in New York performed an initial assessment of nearly 1,300 people, averaging just over 76 years of age, with no cognitive impairment or dementia. The evaluations were done between January 1992 and December 1994, and the study volunteers were then re-examined at 18-month intervals until November 1999.
Close to 8 percent of the study participants had a history of stroke. While all the participants experienced some memory decline over the course of the study, the decline was more rapid in people who had a history of stroke, the researchers reported in the April issue of the journal Archives of Neurology.
The association between stroke and memory decline was strongest in men and in people with a type of gene called apoE4 allele, which has long been linked to Alzheimer's disease. The study also identified a decline in abstract/visuospatial abilities among men and people without the apoE4 variant who also had a history of stroke.
"The mechanisms by which stroke increases the risk of cognitive decline are not clear," the study authors wrote.
They suggested that stroke may cause memory problems by damaging or destroying certain areas of the brain or by triggering the deposit of materials that form brain plaques associated with Alzheimer's disease.
"It is also possible that the occurrence of stroke adds cognitive deficits in persons with subclinical Alzheimer's disease that brings them over the diagnostic threshold and that stroke does not have a direct specific effect on Alzheimer's disease," the authors noted.
More information
The American Academy of Family Physicians has more about memory and age.
Columbia University researchers in New York performed an initial assessment of nearly 1,300 people, averaging just over 76 years of age, with no cognitive impairment or dementia. The evaluations were done between January 1992 and December 1994, and the study volunteers were then re-examined at 18-month intervals until November 1999.
Close to 8 percent of the study participants had a history of stroke. While all the participants experienced some memory decline over the course of the study, the decline was more rapid in people who had a history of stroke, the researchers reported in the April issue of the journal Archives of Neurology.
The association between stroke and memory decline was strongest in men and in people with a type of gene called apoE4 allele, which has long been linked to Alzheimer's disease. The study also identified a decline in abstract/visuospatial abilities among men and people without the apoE4 variant who also had a history of stroke.
"The mechanisms by which stroke increases the risk of cognitive decline are not clear," the study authors wrote.
They suggested that stroke may cause memory problems by damaging or destroying certain areas of the brain or by triggering the deposit of materials that form brain plaques associated with Alzheimer's disease.
"It is also possible that the occurrence of stroke adds cognitive deficits in persons with subclinical Alzheimer's disease that brings them over the diagnostic threshold and that stroke does not have a direct specific effect on Alzheimer's disease," the authors noted.
More information
The American Academy of Family Physicians has more about memory and age.
Doctors Should Heed Patients' Memory Complaints
(HealthDay News) -- Patients who complain that they are having trouble remembering things -- especially when they are at a genetic risk for Alzheimer's disease -- may be at higher risk for cognitive decline, a new study shows.
"There's a lot of confusion about memory complaints, and whether they should be taken seriously or not," study author Dr. Linda Ercoli, an assistant clinical professor at the University of California's Semel Institute for Neuroscience and Human Behavior in Los Angeles, said in a prepared statement.
"The study is one of the first to show an association between memory complaints and underlying brain function decline, and although not every complaint will lead to Alzheimer's disease, it's important to listen when patients talk about their memory concerns," Ercoli said.
The findings appear in the April issue of the Archives of General Psychiatry.
The two-year study included 30 adults, aged 50 to 82, with memory complaints. At the start and end of the study, the participants' brain function was assessed using positron emission tomography (PET), which measures brain activity by revealing how much glucose is metabolized by the brain as fuel.
Among all the participants, greater frequency of memory complaints was associated with global brain decline, which appears to be part of the normal aging process, the study authors said.
However, people with APOE-4, a gene associated with Alzheimer's disease, who made more use of memory-compensation strategies (for example, lists and calendars) showed a greater decline in the temporal regions of the brain compared to those without APOE-4. The temporal regions are involved with memory functions.
"These findings may eventually help us identify which patients may benefit from clinical monitoring and early interventions to prevent or delay the onset of Alzheimer's disease," principal investigator Dr. Gary Small, professor at the Semel Institute, said in a prepared statement.
More information
The U.S. National Institute on Aging has more about forgetfulness.
"There's a lot of confusion about memory complaints, and whether they should be taken seriously or not," study author Dr. Linda Ercoli, an assistant clinical professor at the University of California's Semel Institute for Neuroscience and Human Behavior in Los Angeles, said in a prepared statement.
"The study is one of the first to show an association between memory complaints and underlying brain function decline, and although not every complaint will lead to Alzheimer's disease, it's important to listen when patients talk about their memory concerns," Ercoli said.
The findings appear in the April issue of the Archives of General Psychiatry.
The two-year study included 30 adults, aged 50 to 82, with memory complaints. At the start and end of the study, the participants' brain function was assessed using positron emission tomography (PET), which measures brain activity by revealing how much glucose is metabolized by the brain as fuel.
Among all the participants, greater frequency of memory complaints was associated with global brain decline, which appears to be part of the normal aging process, the study authors said.
However, people with APOE-4, a gene associated with Alzheimer's disease, who made more use of memory-compensation strategies (for example, lists and calendars) showed a greater decline in the temporal regions of the brain compared to those without APOE-4. The temporal regions are involved with memory functions.
"These findings may eventually help us identify which patients may benefit from clinical monitoring and early interventions to prevent or delay the onset of Alzheimer's disease," principal investigator Dr. Gary Small, professor at the Semel Institute, said in a prepared statement.
More information
The U.S. National Institute on Aging has more about forgetfulness.
Sunday, August 27, 2006
Urine Testing for Alzheimer's Disease
Two new tests for Alzheimer’s disease have received attention lately, both of which use urine samples to detect biochemical markers associated with this condition. The tests have slightly different purposes. The first, which is currently being marketed, is a diagnostic aid, while the other test, still in development, could be useful as a predictor of Alzheimer’s disease.
A major advantage of these tests is that they are non-invasive, requiring just a urine sample from the patient, unlike other testing methods used to help diagnose this disease, such as a spinal tap to collect cerebrospinal fluid for analysis of beta amyloid precursor and Tau proteins (see Tau/Aß42 Test).
Alzheimer’s disease is a fatal neurological disease that is fairly common in the U.S., primarily among the elderly, and causes cognitive impairment, including memory loss. It is a difficult disease to diagnose; currently, definite diagnoses can only be made through an analysis of brain tissue during an autopsy or brain biopsy. However, there is a new test that can aid in diagnosing and monitoring patients who are living with this disease.
It uses a first-morning urine sample and detects the level of a brain protein called neural thread protein (NTP). Studies have shown that elevation of this biochemical marker is associated with disease severity and progression. In helping to identify Alzheimer’s disease early on, this test will allow patients to receive available therapies when they can be most effective and before irreversible damage occurs.
It will probably be most useful as a confirmatory test in the diagnosis of Alzheimer’s, used in combination with other relevant medical data and physicians’ clinical assessment of patients’ symptoms.
The other test detects the biomarker isoprostane 8,12-iso-iPf2ª-VI, which is indicative of brain oxidative damage and is elevated in the spinal fluid, blood, and urine of patients with mild cognitive impairment (MCI), believed to be a precursor to Alzheimer’s disease. Researchers are hopeful that using a simple urine test for this biomarker among patients with MCI will help to identify those who are at increased risk for Alzheimer’s disease.
This would allow time to intervene with therapies that may slow the brain damage and cognitive decline that accompanies Alzheimer’s disease. Studies are ongoing and development of the urine test continues, with a product likely to be available for clinical use within two years.
A major advantage of these tests is that they are non-invasive, requiring just a urine sample from the patient, unlike other testing methods used to help diagnose this disease, such as a spinal tap to collect cerebrospinal fluid for analysis of beta amyloid precursor and Tau proteins (see Tau/Aß42 Test).
Alzheimer’s disease is a fatal neurological disease that is fairly common in the U.S., primarily among the elderly, and causes cognitive impairment, including memory loss. It is a difficult disease to diagnose; currently, definite diagnoses can only be made through an analysis of brain tissue during an autopsy or brain biopsy. However, there is a new test that can aid in diagnosing and monitoring patients who are living with this disease.
It uses a first-morning urine sample and detects the level of a brain protein called neural thread protein (NTP). Studies have shown that elevation of this biochemical marker is associated with disease severity and progression. In helping to identify Alzheimer’s disease early on, this test will allow patients to receive available therapies when they can be most effective and before irreversible damage occurs.
It will probably be most useful as a confirmatory test in the diagnosis of Alzheimer’s, used in combination with other relevant medical data and physicians’ clinical assessment of patients’ symptoms.
The other test detects the biomarker isoprostane 8,12-iso-iPf2ª-VI, which is indicative of brain oxidative damage and is elevated in the spinal fluid, blood, and urine of patients with mild cognitive impairment (MCI), believed to be a precursor to Alzheimer’s disease. Researchers are hopeful that using a simple urine test for this biomarker among patients with MCI will help to identify those who are at increased risk for Alzheimer’s disease.
This would allow time to intervene with therapies that may slow the brain damage and cognitive decline that accompanies Alzheimer’s disease. Studies are ongoing and development of the urine test continues, with a product likely to be available for clinical use within two years.
Wednesday, August 09, 2006
Answers At Last!: To Avoid Pandemic Pandemonium, Read Infection Protection: Pandemic Your Personal Survival Handbook for Today's New Infectious Dise
Infection Protection: Pandemic
by Ronald Klatz, M.D., D.O. and Robert Goldman, M.D., Ph.D., D.O., FAASPISBN 0-9668937-8-6Copyright © 2006; 176 pages, softcover
A4M American Academy of Anti-Aging Medicine, US $27.95
JUNE 30, 2006 Chicago , IL USA Historians estimate that, at one point, over half of the 1.6 billion people in the world in 1918 were infected with the Spanish Flu.
Millions of young, healthy adults fell ill to the disease and died from the suffocation it caused. Experts now estimate that approximately 80 to 100 million people perished worldwide. Not only reducing the global population by one-sixteenth, the 1918 flu pandemic caused brain damage in many of its survivors. The 1918 flu pandemic caused the largest one-year decline in the average lifespan in the United States in modern history, slashing it by a full twelve years.
Sometimes referred to as " America 's forgotten pandemic," the 1918 flu pandemic continues to haunt medical experts and scientists around the globe. We are on the verge of experiencing another worldwide infectious disease outbreak, this time perhaps caused by the bird flu virus known as H5N1.
In a worst-case scenario:
• Worldwide, the United Nations estimates that from 5 to 150 million people may die should an H5N1 pandemic occur. The World Health Organization projects from 2 million to 7.4 million deaths, which it concedes is a "relatively conservative estimate" for purposes of providing a plausible planning target. The World Bank cites sources suggesting that a more virulent form (similar to the 1918-1919 strain) of pandemic flu may kill as many as 180–260 million in a worst-case scenario.
• In preparing its Implementation Plan for the National Strategy for Pandemic Influenza, the U.S. federal government assumes that 30% of the population
100 million
would be infected, and that as many as 1.9 million would die
greater than the total deaths caused in a single year by heart disease, cancers, strokes, chronic pulmonary disease, AIDS, and Alzheimer's disease combined. One disease model projects that if the U.S. population (standing at 295 million at the time of the projection) is exposed to the H5N1 flu strain, 33% would be infected (97.3 million) with a resulting death rate of 0.58% (5.6 million deaths)
more than twice the number of deaths from all the ten leading causes of death combined. So far, however, H5N1 has been 57% lethal in humans, meaning that in the very-worst case, possibly upwards of 50 million Americans may die.
In the best-case scenario: An H5N1 pandemic strikes but is no more lethal than seasonal influenza. Be mindful, however, that even this scenario has a sizeable death toll
200,000 to 1.5 million deaths worldwide and 36,000 in the U.S. alone. That's the "good news."
Infectious disease experts agree that it's not "if" bird flu will enter the United States , but "when." The resulting H5N1 pandemic will cripple the US economy, halting most commerce for a period of 12 to 24 months and bankrupting the federal government and most American citizens.
The pandemic will also cause grave panic among the nation's residents, as sources of food, medicine, and the necessities of daily living will ultimately become unavailable. Presently, there is little effective, unified worldwide or national leadership in the arena of discovering real prevention and/or treatment protocols for H5N1. Consequently, it is up to each of us as individuals, to mount our own personal preparedness and protection program.
Infection Protection: Pandemic provides an introductory backdrop of information about influenza in-general and bird flu in-specific, and the current
and potentially fatal future
ramifications of the H5N1 virus.
Readers are then provided a set of Top Ten Preventive Strategies that aim to help optimize the performance of an individual's immune system, as well as enhance an individual's overall immune resistance to a wide variety of infectious diseases. Some of the specific tips offered in Infection Protection: Pandemic include:
• The simplest, cheapest ways to ward off pathogens from invading the body
• The "Immunity Desk Reference," offering 70+ natural, non-toxic approaches to immune enhancement, and highlighting the Top Ten Immune Enhancers
• Inexpensive yet critical ways to boost an individual's resistance to infectious disease by using readily available materials from the supermarket and drug store
• Do-it-yourself barriers and personal safety practices
• No-cost ways to minimize the germ load on the body
• How to safely handle food (particularly, chicken and eggs) in the kitchen
• How to travel smartly and safely given today's infectious disease threats
• The latest news on anti-viral medications, including novel uses of existing Rxs
• Checklists for individuals and families to be properly prepared in advance of a pandemic
Infection Protection: Pandemic was written by Ronald Klatz, M.D., D.O., and Dr. Robert Goldman, M.D., Ph.D., D.O., FAASP.
Dr. Klatz is a long-time scientific pioneer and innovator. As the originator of the the term "anti-aging" and regarded as the movement's first physician and chief champion, Dr. Klatz serves as President of the American Academy of Anti-Aging Medicine (A4M; http://www.worldhealth.net/ ), the world's leading non-profit organization dedicated to advancing research and clinical pursuits that enhance the quality, and extend the quantity, of the human lifespan.
In an Online Extra to the BusinessWeek March 2006 issue, the magazine refers to Dr. Klatz as the "Guru of anti-aging" and is hailed as a " leading light in the anti-aging medical movement." Dr. Klatz is considered a futurist in the field of advanced biotechnology, having overseen a patent portfolio of over 100 scientific patents and with more than 32 medical/health book titles in print. Dr. Goldman, physician, research scientist, and surgeon, serves as Chairman of the A4M, as well as Chairman of the International Medical Commission, which oversees sports medicine programs in over 170 nations.
Drs. Klatz and Goldman wrote Infection Protection: Pandemic because succumbing to infectious disease can dramatically
and negatively
impact how long and how well each of us lives.
The physician authors of Infection Protection: Pandemic remind readers of a recent upward trend in deaths due to respiratory diseases. In the U.S. , influenza and pneumonia are now the 7 th leading cause of death (responsible for 2.7% of all deaths in the nation), and chronic lower respiratory diseases are now are the 4 th leading cause of death (5.1% of all U.S. deaths). All totaled these diseases kill more than 190,000 Americans each year. A direct threat to how long and well you live, respiratory diseases are largely avoidable and preventable.
To write Infection Protection: Pandemic , Drs. Klatz and Goldman distilled thousands of pages of information, from unbiased expert sources including the United Nations, the World Health Organization, the U.S. Department of Health & Human Services, the U.S. Centers for Disease Control and Prevention, the U.S. Food and Drug Administration, and the U.S. White House. This book is your single source of the essential personal knowledge you need to survive the H5N1 threat
and the many other emerging and re-emerging infectious disease threats that plague our modern world.
Infection Protection: Pandemic will be available to the general public 10 July 2006 .
It can be ordered by calling the American Academy of Anti-Aging Medicine
(A4M) at tel. (773) 528-4333 or by visiting the A4M's Online Bookstore at http://www.worldhealth.net/ .
>> ORDER THIS BOOK ON-LINE
by Ronald Klatz, M.D., D.O. and Robert Goldman, M.D., Ph.D., D.O., FAASPISBN 0-9668937-8-6Copyright © 2006; 176 pages, softcover
A4M American Academy of Anti-Aging Medicine, US $27.95
JUNE 30, 2006 Chicago , IL USA Historians estimate that, at one point, over half of the 1.6 billion people in the world in 1918 were infected with the Spanish Flu.
Millions of young, healthy adults fell ill to the disease and died from the suffocation it caused. Experts now estimate that approximately 80 to 100 million people perished worldwide. Not only reducing the global population by one-sixteenth, the 1918 flu pandemic caused brain damage in many of its survivors. The 1918 flu pandemic caused the largest one-year decline in the average lifespan in the United States in modern history, slashing it by a full twelve years.
Sometimes referred to as " America 's forgotten pandemic," the 1918 flu pandemic continues to haunt medical experts and scientists around the globe. We are on the verge of experiencing another worldwide infectious disease outbreak, this time perhaps caused by the bird flu virus known as H5N1.
In a worst-case scenario:
• Worldwide, the United Nations estimates that from 5 to 150 million people may die should an H5N1 pandemic occur. The World Health Organization projects from 2 million to 7.4 million deaths, which it concedes is a "relatively conservative estimate" for purposes of providing a plausible planning target. The World Bank cites sources suggesting that a more virulent form (similar to the 1918-1919 strain) of pandemic flu may kill as many as 180–260 million in a worst-case scenario.
• In preparing its Implementation Plan for the National Strategy for Pandemic Influenza, the U.S. federal government assumes that 30% of the population
100 million
would be infected, and that as many as 1.9 million would die
greater than the total deaths caused in a single year by heart disease, cancers, strokes, chronic pulmonary disease, AIDS, and Alzheimer's disease combined. One disease model projects that if the U.S. population (standing at 295 million at the time of the projection) is exposed to the H5N1 flu strain, 33% would be infected (97.3 million) with a resulting death rate of 0.58% (5.6 million deaths)
more than twice the number of deaths from all the ten leading causes of death combined. So far, however, H5N1 has been 57% lethal in humans, meaning that in the very-worst case, possibly upwards of 50 million Americans may die.
In the best-case scenario: An H5N1 pandemic strikes but is no more lethal than seasonal influenza. Be mindful, however, that even this scenario has a sizeable death toll
200,000 to 1.5 million deaths worldwide and 36,000 in the U.S. alone. That's the "good news."
Infectious disease experts agree that it's not "if" bird flu will enter the United States , but "when." The resulting H5N1 pandemic will cripple the US economy, halting most commerce for a period of 12 to 24 months and bankrupting the federal government and most American citizens.
The pandemic will also cause grave panic among the nation's residents, as sources of food, medicine, and the necessities of daily living will ultimately become unavailable. Presently, there is little effective, unified worldwide or national leadership in the arena of discovering real prevention and/or treatment protocols for H5N1. Consequently, it is up to each of us as individuals, to mount our own personal preparedness and protection program.
Infection Protection: Pandemic provides an introductory backdrop of information about influenza in-general and bird flu in-specific, and the current
and potentially fatal future
ramifications of the H5N1 virus.
Readers are then provided a set of Top Ten Preventive Strategies that aim to help optimize the performance of an individual's immune system, as well as enhance an individual's overall immune resistance to a wide variety of infectious diseases. Some of the specific tips offered in Infection Protection: Pandemic include:
• The simplest, cheapest ways to ward off pathogens from invading the body
• The "Immunity Desk Reference," offering 70+ natural, non-toxic approaches to immune enhancement, and highlighting the Top Ten Immune Enhancers
• Inexpensive yet critical ways to boost an individual's resistance to infectious disease by using readily available materials from the supermarket and drug store
• Do-it-yourself barriers and personal safety practices
• No-cost ways to minimize the germ load on the body
• How to safely handle food (particularly, chicken and eggs) in the kitchen
• How to travel smartly and safely given today's infectious disease threats
• The latest news on anti-viral medications, including novel uses of existing Rxs
• Checklists for individuals and families to be properly prepared in advance of a pandemic
Infection Protection: Pandemic was written by Ronald Klatz, M.D., D.O., and Dr. Robert Goldman, M.D., Ph.D., D.O., FAASP.
Dr. Klatz is a long-time scientific pioneer and innovator. As the originator of the the term "anti-aging" and regarded as the movement's first physician and chief champion, Dr. Klatz serves as President of the American Academy of Anti-Aging Medicine (A4M; http://www.worldhealth.net/ ), the world's leading non-profit organization dedicated to advancing research and clinical pursuits that enhance the quality, and extend the quantity, of the human lifespan.
In an Online Extra to the BusinessWeek March 2006 issue, the magazine refers to Dr. Klatz as the "Guru of anti-aging" and is hailed as a " leading light in the anti-aging medical movement." Dr. Klatz is considered a futurist in the field of advanced biotechnology, having overseen a patent portfolio of over 100 scientific patents and with more than 32 medical/health book titles in print. Dr. Goldman, physician, research scientist, and surgeon, serves as Chairman of the A4M, as well as Chairman of the International Medical Commission, which oversees sports medicine programs in over 170 nations.
Drs. Klatz and Goldman wrote Infection Protection: Pandemic because succumbing to infectious disease can dramatically
and negatively
impact how long and how well each of us lives.
The physician authors of Infection Protection: Pandemic remind readers of a recent upward trend in deaths due to respiratory diseases. In the U.S. , influenza and pneumonia are now the 7 th leading cause of death (responsible for 2.7% of all deaths in the nation), and chronic lower respiratory diseases are now are the 4 th leading cause of death (5.1% of all U.S. deaths). All totaled these diseases kill more than 190,000 Americans each year. A direct threat to how long and well you live, respiratory diseases are largely avoidable and preventable.
To write Infection Protection: Pandemic , Drs. Klatz and Goldman distilled thousands of pages of information, from unbiased expert sources including the United Nations, the World Health Organization, the U.S. Department of Health & Human Services, the U.S. Centers for Disease Control and Prevention, the U.S. Food and Drug Administration, and the U.S. White House. This book is your single source of the essential personal knowledge you need to survive the H5N1 threat
and the many other emerging and re-emerging infectious disease threats that plague our modern world.
Infection Protection: Pandemic will be available to the general public 10 July 2006 .
It can be ordered by calling the American Academy of Anti-Aging Medicine
(A4M) at tel. (773) 528-4333 or by visiting the A4M's Online Bookstore at http://www.worldhealth.net/ .
>> ORDER THIS BOOK ON-LINE
Monday, July 31, 2006
Dr. Andrew Weil: Living longer, better
Friday, January 13, 2006; Posted: 10:52 a.m. EST (15:52 GMT)Programming note: CNN's Heidi Collins profiles health expert Dr. Andrew Weil on "Anderson Cooper 360°," 10 p.m. ET Friday.
(CNN) -- Dr. Andrew Weil is arguably America's foremost practitioner of alternative medicine, or as he likes to call it, integrative medicine.
CNN correspondent Heidi Collins sat down with Dr. Weil recently to discuss his new book, "Healthy Aging."
Here is an edited version of their discussion.
COLLINS: Can you make me live longer?
WEIL: I don't know. Possibly by reducing your risks of the age-related diseases, especially cardiovascular disease. But, my emphasis is not on life extension. It's on healthy aging. So, I'm trying to keep you healthy as long as possible.
COLLINS: So, what is the key to longevity?
WEIL: I think the key to longevity is delaying the onset and reducing the risk of age-related disease. Age-related disease are these big categories of illness that become more common after age 60 and that account for a great deal of premature death and disability. So, the big ones are cardiovascular disease, cancer, Alzheimer's disease and its relative. So, I think the emphasis is on preventing those, showing you how to reduce the risk or delay the onset. And if you came to me as a patient, I would look at your family history, personal history to see where your greatest risks were. And then I would concentrate the preventive efforts in those areas.
COLLINS: So, I mean, this isn't all that complicated?
WEIL: I don't think it's all that complicated. It just means doing some work, though. It means doing some homework and then learning the information that you need then applying it. And it's applying it really in all areas of your lifestyle. It means looking at how you eat, how you use dietary supplements, how you exercise, how you handle stress, how you sleep, how you rest, how you deal with your mind. You know, you really need to work in all those areas to ensure healthy aging.
COLLINS: So, if I breathe, if I put flowers in my house, if I get massaged by love, if I have spiritual health, if I walk, dance, golf, and couple other things, I am going to feel better longer?
WEIL: Yes, probably. But, if you ...
COLLINS: I forgot eat fruits and vegetables.
WEIL: Correct. But, if you are smoking also, I probably can't do much for you. And if you're not paying attention to weight and not paying attention to your cholesterol and not paying attention to other medical risks that you may have, you know, you can put all the flowers you want in your house and it's not gonna help. So, you know, we have to attend to that part of you as well.
COLLINS: What's the bottom line with stress? How do we learn to maintain nonstress?
WEIL: There's lots of ways of doing that. Everything from doing yoga to listening to relaxing music to getting massaged. My favorite techniques are breathing methods because they're so cost efficient and time efficient. And these mostly come from the yoga tradition. But, they're simple. I mean, there's a relaxing breath that I teach that takes all of two minutes a day to practice that has a remarkable effects if you do it regularly over time.
COLLINS: How much of being healthy and living longer is really up to the individual?
WEIL: Well, I think most of it's up to the individual. You know, a lot of people ask me how much is genetics and how much is environment and lifestyle? I think it's always both. My way of thinking of this is that we're all dealt a certain hand of genetic cards, some good, some bad. But, it's up to us how we play them.
COLLINS: Okay. So, we'll keep this one simple. But if you were to give me the sort of outline to walk away with today, diet-wise.
WEIL: Eat fewer foods of animal origin; more fruits and vegetables; more plant-based protein from soy foods, for example. Make sure you've got omega-3 fatty acids in your diet, either from oily fish, or fish oil supplements. Try to reduce consumption of quick-digesting carbohydrate foods, which are the ones made from any kind of flour, sugar, high fructose corn syrup.
And try to eat more of the slower-digesting carbohydrate foods, which are beans, whole grains, packed grains, winter squashes, sweet potatoes. Really learn the differences between good fats and bad fats. Use olive oil as a main cooking oil. Include nuts, seeds, avocados, in your diet.
Take a good multivitamin, multimineral supplement. Add things to the diet, like green tea and dark chocolate and red wine, in moderation, if you want their antioxidant effects.
COLLINS: Should we have dogs?
WEIL: I can't imagine life without dogs. It doesn't have to be dogs. There's very interesting medical research showing that people who have pets recover faster from illness. They get out of the hospital faster if they have surgery. So I think there's a lot of benefits to being involved with, you know, other things than yourself.
COLLINS: Anything else?
WEIL: Well, I think aside from eating right, you want to maintain physical activity throughout life. And that doesn't mean you have to run marathons, or go to aerobics classes. Walking is a perfectly good physical activity if you do enough of it regularly enough. You want to learn some method of stress management. You know, as I said, I like breathing exercises. But, you know, anything you can do. You want to really try to identify negative thought patterns that lead to negative behavior, and see how you can change them.
I think you want to keep your mind active, whether that's by learning another language, or changing your computer operating system frequently. You want to stay connected and involved with life. I think you really want to try to focus on the positive attributes that come with aging, as well as the negative ones.
Andrew Weil, M.D.
–Author of:
Eight Weeks to Optimum Health
Spontaneous Healing
The Natural Mind
The Marriage of the Sun and Moon
Health and Healing
Natural Health, Natural Medicine
From Chocolate to Morphine (with Winifred Rosen)
Wednesday, July 19, 2006
Weight Loss May Yield Alzheimer's Clues
MONDAY, July 17 (HealthDay News) -- Gradual weight loss can precede dementia and begin as early as 10 years prior to memory loss, concludes a Mayo Clinic study involving women with and without dementia.
The findings may provide clues to the origins of dementia, say the researchers, who were expected to present the findings Sunday at the International Conference on Alzheimer's Disease and Related Disorders, in Madrid, Spain.
The Mayo team compared the long-term medical records of 560 people diagnosed with the onset of dementia between 1990 and 1994. These patients were compared to a group of patients who did not have dementia.
Both groups averaged about the same weight -- 140 pounds -- at the beginning of the study. Women who did not develop dementia maintained that weight over the next 30 years.
In contrast, "The women who later developed dementia started off at the same weight as those who didn't develop dementia, but their weight drifted downward to 136 pounds 10 years before symptom onset and 128 pounds at symptom onset," Dr. David Knopman, lead researcher and neurologist, said in a prepared statement.
He and his colleagues said it's unclear what caused the weight loss in the women who later developed dementia, but they have some theories.
"The weight loss findings raise scientific questions about the cause or causes of the weight loss. This points to changes in the brain that develop years before the actual memory loss. We think that there are several possible explanations," Knopman said.
"The women might have less initiative and lose interest in eating, they might develop a duller sense of taste and smell, or they might experience an earlier sense of satiety (feeling full). Also, because, we didn't observe the anticipatory weight loss in men, the weight loss could have something specific to do with postmenopausal hormonal changes," he said.
Pinpointing the brain mechanisms that influence weight loss in women who develop dementia may help researchers better understand how it develops, Knopman said.
More information
The American Medical Association has more about dementia.
The findings may provide clues to the origins of dementia, say the researchers, who were expected to present the findings Sunday at the International Conference on Alzheimer's Disease and Related Disorders, in Madrid, Spain.
The Mayo team compared the long-term medical records of 560 people diagnosed with the onset of dementia between 1990 and 1994. These patients were compared to a group of patients who did not have dementia.
Both groups averaged about the same weight -- 140 pounds -- at the beginning of the study. Women who did not develop dementia maintained that weight over the next 30 years.
In contrast, "The women who later developed dementia started off at the same weight as those who didn't develop dementia, but their weight drifted downward to 136 pounds 10 years before symptom onset and 128 pounds at symptom onset," Dr. David Knopman, lead researcher and neurologist, said in a prepared statement.
He and his colleagues said it's unclear what caused the weight loss in the women who later developed dementia, but they have some theories.
"The weight loss findings raise scientific questions about the cause or causes of the weight loss. This points to changes in the brain that develop years before the actual memory loss. We think that there are several possible explanations," Knopman said.
"The women might have less initiative and lose interest in eating, they might develop a duller sense of taste and smell, or they might experience an earlier sense of satiety (feeling full). Also, because, we didn't observe the anticipatory weight loss in men, the weight loss could have something specific to do with postmenopausal hormonal changes," he said.
Pinpointing the brain mechanisms that influence weight loss in women who develop dementia may help researchers better understand how it develops, Knopman said.
More information
The American Medical Association has more about dementia.
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Health Tip: How to Reduce Wandering in Alzheimer's Patients
(HealthDay News) -- Wandering is a common but dangerous symptom of Alzheimer's disease -- a degenerative disease of the brain that affects memory and cognition.
Alzheimer's patients may suddenly walk off and become lost, frightened and confused about where they are, and many do not even know where they are trying to go. Since many of these people can't identify themselves or where they live, wandering in unconfined and unsecured areas can be very dangerous.
Disorientation, medication, stress, fear or anxiety, and restlessness may all cause an Alzheimer's patient to wander.
To keep patients safe and minimize wandering, the Alzheimer's Association of Los Angeles offers these suggestions:
Make sure the patient is always comfortable and doesn't need to use the restroom and isn't hungry or thirsty.
Try to make sure he receives regular exercise and activity to reduce restlessness and boredom. If he is still capable, let the patient help with daily chores like laundry or light cooking or housekeeping.
Tell the person often that you are there to help him, and make sure he understands he doesn't need to be anywhere but right where he is.
Keep the environment quiet and relaxing -- avoid noise and confusion that may frighten the patient into trying to scamper away.
If possible, keep doors locked and secured to prevent wandering into the street and getting lost.
Devise a plan of action in the event the patient does become lost -- keep current information on hand, like height and weight, and a recent photograph. Also, keep a list of places where the person has wandered previously, or places he used to frequent that he may be trying to find.
Alzheimer's patients may suddenly walk off and become lost, frightened and confused about where they are, and many do not even know where they are trying to go. Since many of these people can't identify themselves or where they live, wandering in unconfined and unsecured areas can be very dangerous.
Disorientation, medication, stress, fear or anxiety, and restlessness may all cause an Alzheimer's patient to wander.
To keep patients safe and minimize wandering, the Alzheimer's Association of Los Angeles offers these suggestions:
Make sure the patient is always comfortable and doesn't need to use the restroom and isn't hungry or thirsty.
Try to make sure he receives regular exercise and activity to reduce restlessness and boredom. If he is still capable, let the patient help with daily chores like laundry or light cooking or housekeeping.
Tell the person often that you are there to help him, and make sure he understands he doesn't need to be anywhere but right where he is.
Keep the environment quiet and relaxing -- avoid noise and confusion that may frighten the patient into trying to scamper away.
If possible, keep doors locked and secured to prevent wandering into the street and getting lost.
Devise a plan of action in the event the patient does become lost -- keep current information on hand, like height and weight, and a recent photograph. Also, keep a list of places where the person has wandered previously, or places he used to frequent that he may be trying to find.
Saturday, May 27, 2006
New Focus on Nutrition and Health?
New Focus on Nutrition and Health?
Provided by: DrWeil.com
Q: I notice that you're having another Nutrition and Health Conference. What kinds of issues are you going to be discussing this time? Is it only for medical professionals or can members of the public attend? -- Theresa
A: The 2005 Nutrition and Health Conference is scheduled for March 6-9 here in Tucson. I'm very excited about the program we've planned, which will cover a wide range of nutrition and health-related topics, both in the sessions designed for health professionals (including students) and the media and during our Public Forum on "Food, Politics and Society," which will launch the conference on Sunday, March 6 and is open to everyone.
During the forum, we'll deal with such topical issues as "The Optimal Diet" (a subject that I'll discuss), as well as "Micronutrients and the Role of Dietary Supplements" to be reviewed by Bruce Ames, Ph.D., senior scientist at Children's Hospital, Oakland Research Institute and a professor at the Graduate School in Molecular and Cell Biology at the University of California at Berkeley. Others speaking at the Public Forum include Dan Glickman, former U.S. Secretary of Agriculture, who will focus on our national agricultural policy and its effect on U.S. nutrition and Walter Willett, MD, professor of Epidemiology, Nutrition and Medicine at the Harvard School of Public Health, who will discuss obesity, diabetes and the food industry.
The sessions for health professionals will focus on such subjects as nutritional science and the Mediterranean diet, the benefits of a low glycemic-index diet, the challenge to health professionals of the growing epidemic of childhood obesity, and the latest findings on vegetarian nutrition. In separate sessions throughout the three-day conference we'll also discuss the latest research on nutrition for patients with a number of different health problems including arthritis, allergic diseases, attention deficit disorder, osteoporosis, diabetes, Alzheimer's disease as well as nutritional strategies for prevention of breast and prostate cancer and to prevent or minimize the degenerative diseases of aging.
Other sessions will cover what we know about antioxidants, low-carb and fad diets, and whether or not the way you eat really can reduce your risk of cancer. The conference is presented by the Program in Integrative Medicine here at the University of Arizona and sponsored by the Richard and Hinda Rosenthal Center for Complementary and Alternative Medicine at Columbia University's College of Physicians & Surgeons.
An integral part of the conference is the opportunity to sample various high quality organic foods, from fruits and vegetables to soy foods, teas, chocolate, and cheeses as well as learn from nutrition-minded chefs who will be demonstrating their talents. Rather than eating bagels and donuts, as they do at most medical conferences, attendees can eat well and experience how delicious healthy food can be.
You're welcome to attend the public forum, and there's still time for health professionals and the media to sign up for the conference. I expect that we'll have some important insights on nutrition and health to share on this site and elsewhere after the conference.
Andrew Weil, M.D. –Author of:
Eight Weeks to Optimum Health
Spontaneous Healing
The Natural Mind
The Marriage of the Sun and Moon
Health and Healing
Natural Health, Natural Medicine
From Chocolate to Morphine (with Winifred Rosen)
Provided by: DrWeil.com
Q: I notice that you're having another Nutrition and Health Conference. What kinds of issues are you going to be discussing this time? Is it only for medical professionals or can members of the public attend? -- Theresa
A: The 2005 Nutrition and Health Conference is scheduled for March 6-9 here in Tucson. I'm very excited about the program we've planned, which will cover a wide range of nutrition and health-related topics, both in the sessions designed for health professionals (including students) and the media and during our Public Forum on "Food, Politics and Society," which will launch the conference on Sunday, March 6 and is open to everyone.
During the forum, we'll deal with such topical issues as "The Optimal Diet" (a subject that I'll discuss), as well as "Micronutrients and the Role of Dietary Supplements" to be reviewed by Bruce Ames, Ph.D., senior scientist at Children's Hospital, Oakland Research Institute and a professor at the Graduate School in Molecular and Cell Biology at the University of California at Berkeley. Others speaking at the Public Forum include Dan Glickman, former U.S. Secretary of Agriculture, who will focus on our national agricultural policy and its effect on U.S. nutrition and Walter Willett, MD, professor of Epidemiology, Nutrition and Medicine at the Harvard School of Public Health, who will discuss obesity, diabetes and the food industry.
The sessions for health professionals will focus on such subjects as nutritional science and the Mediterranean diet, the benefits of a low glycemic-index diet, the challenge to health professionals of the growing epidemic of childhood obesity, and the latest findings on vegetarian nutrition. In separate sessions throughout the three-day conference we'll also discuss the latest research on nutrition for patients with a number of different health problems including arthritis, allergic diseases, attention deficit disorder, osteoporosis, diabetes, Alzheimer's disease as well as nutritional strategies for prevention of breast and prostate cancer and to prevent or minimize the degenerative diseases of aging.
Other sessions will cover what we know about antioxidants, low-carb and fad diets, and whether or not the way you eat really can reduce your risk of cancer. The conference is presented by the Program in Integrative Medicine here at the University of Arizona and sponsored by the Richard and Hinda Rosenthal Center for Complementary and Alternative Medicine at Columbia University's College of Physicians & Surgeons.
An integral part of the conference is the opportunity to sample various high quality organic foods, from fruits and vegetables to soy foods, teas, chocolate, and cheeses as well as learn from nutrition-minded chefs who will be demonstrating their talents. Rather than eating bagels and donuts, as they do at most medical conferences, attendees can eat well and experience how delicious healthy food can be.
You're welcome to attend the public forum, and there's still time for health professionals and the media to sign up for the conference. I expect that we'll have some important insights on nutrition and health to share on this site and elsewhere after the conference.
Andrew Weil, M.D. –Author of:
Eight Weeks to Optimum Health
Spontaneous Healing
The Natural Mind
The Marriage of the Sun and Moon
Health and Healing
Natural Health, Natural Medicine
From Chocolate to Morphine (with Winifred Rosen)
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