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A shocking new study finds that glyphosate, the active ingredient in Roundup herbicide, “…may be the most biologically disruptive chemical in our environment,” capable of contributing to a wide range of fatal human diseases.
Alzheimer’s disease is sure making the health news rounds lately. What’s promising about this scary illness is how much we are able to help shield our minds from it. A brand new health breakthrough proposes that coffee could help older adults avoid dementia.
Here’s some health news about a natural remedy for those of you who want to boost your mental health: scientists have discovered that creatine could protect the brain. Creatine is a substance in your body the main job of which has to do with energy production. About 95% of your body’s creatine is stored in your muscles. For this reason, creatine is a favorite supplement for athletes and bodybuilders Continue reading →
Scientists have made remarkable advances in medicine during the past century, finding treatments for everything from strep throat to Parkinson’s disease. Even vanity causes aren’t beyond the reach of drug companies, which offer solutions to even our most embarrassing physical shortcomings. Continue reading →
When Dr. Avram Hershko, 74, a biochemist at the Technion-Israel Institute of Technology in Haifa and a winner of the 2004 Nobel Prize in Chemistry, was recently asked to name the most important fact of his life, he answered: “That I love my six grandchildren. For two, three days every week, I take them to dance class, sport and school. I am completely in their lives.” Continue reading →
Although the best diets contain a large amount of vegetarian, raw foods, several commonly eaten foods have remarkably robust health benefits. Even if your busy life makes it hard to eat right, simply adding chocolate, coffee and orange juice to your menus can offer a distinct boost to your well-being.
I’ve heard and laughed at the health claims for chocolate over the years. The chocolate you buy and eat has been processed and formulated with refined sugar. However, even though many of the potent antioxidant flavonoids in raw cacao (the original source of chocolate) are depleted, the processed chocolate you buy still shows clear health benefits.
The August 2011 British Medical Journal includes a meta-analysis of randomized controlled trials and observational studies with a total of 114,009 participants that demonstrated a 37 percent reduction in cardiovascular disease and a 29 percent reduction in stroke for people who consumed the highest levels of chocolate compared to those who consumed the least.1Continue reading →
One bad apple is all it takes to spoil the barrel. And one misfolded protein may be all that’s necessary to corrupt other proteins, forming large aggregations linked to several incurable neurodegenerative diseases such as Huntington’s, Parkinson’s and Alzheimer’s.
Stanford biology Professor Ron Kopito has shown that the mutant, misfolded protein responsible for Huntington’s disease can move from cell to cell, recruiting normal proteins and forming aggregations in each cell it visits.
Knowing that this protein spends part of its time outside cells “opens up the possibility for therapeutics,” he said. Kopito studies how such misfolded proteins get across a cell’s membrane and into its cytoplasm, where they can interact with normal proteins. He is also investigating how these proteins move between neuronal cells.
The ability of these proteins to move from one cell to another could explain the way Huntington’s disease spreads through the brain after starting in a specific region. Similar mechanisms may be involved in the progress of Parkinson’s and Alzheimer’s through the brain.
Kopito discussed his research at the annual meeting of the American Association for the Advancement of Science in Washington, D.C.
Not all bad
Not all misfolded proteins are bad. The dogma used to be that all our proteins formed neat, well-folded structures, packed together in complexes with a large number of other proteins, Kopito said. But over the past 20 years, researchers have found that as much as 30 percent of our proteins never fold into stable structures. And even ordered proteins appear to have some disordered parts.
Disordered proteins are important for normal cellular functions. Unlike regular proteins, they only interact with one partner at a time. But they are much more dynamic, capable of several quick interactions with many different proteins. This makes them ideal for a lot of the standard communication that happens within a cell for its normal functioning, Kopito said.
But if some of our proteins are always disordered, how do our cells tell which proteins need to be properly folded, and which don’t? “It’s a big mystery,” said Kopito, and one that he’s studying. This question has implications for how people develop neurodegenerative diseases, all of which appear to be age-related.
Huntington’s disease is caused by a specific mutated protein. But the body makes this mutant protein all your life, so why do you get the disease in later adulthood? Kopito said it’s because the body’s protective mechanisms stop doing their job as we get older. He said his lab hopes to determine what these mechanisms are.
A bad influence
But it’s clear what happens when these mechanisms stop working – misfolded proteins start recruiting normal versions of the same protein and form large aggregations. The presence of these aggregations in neurons has been closely linked with several neurodegenerative diseases.
Kopito found that the mutant protein associated with Huntington’s disease can leave one cell and enter another one, stirring up trouble in each new cell as it progresses down the line. The spread of the misfolded protein may explain how Huntington’s progresses through the brain.
This disease, like Parkinson’s and Alzheimer’s, starts in one area of the brain and spreads to the rest of it. This is also similar to the spread of prions, the self-replicating proteins implicated in mad cow disease and, in humans, Creutzfeldt-Jakob disease. As the misfolded protein reaches more parts of the brain, it could be responsible for the progressive worsening of these diseases.
Now that we know that these misfolded proteins spend part of their time outside of cells, traveling from one cell to another, new drugs could target them there, Kopito said. This could help prevent or at least block the progression of these diseases.
Kopito is currently working to figure out how misfolded proteins get past cell membranes into cells in the first place. It is only once in the cell’s cytoplasm that these proteins can recruit others. So these studies could help find ways to keep these mischief-makers away from the normal proteins.
He is also collaborating with biology professor Liqun Luo to track these proteins between cells in the well-mapped fruit fly nervous system. In the future, Kopito said he hopes to link his cell biology work to disease pathology in order to understand the role misfolded proteins play in human disease.
“Man is but a worm” was the title of a famous caricature of Darwin’s ideas in Victorian England. Now, 120 years later, a molecular analysis of mysterious marine creatures unexpectedly reveals our cousins as worms, indeed.
An international team of researchers, including a neuroscientist from the University of Florida, has produced more evidence that people have a close evolutionary connection with tiny, flatworm-like organisms scientifically known as “Acoelomorphs.”
The research in the Thursday (Feb. 10) issue of Nature offers insights into brain development and human diseases, possibly shedding light on animal models used to study development of nerve cells and complex neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
“It was like looking under a rock and finding something unexpected,” said Leonid L. Moroz, Ph.D., a professor in the department of neuroscience with the UF College of Medicine. “We’ve known there were very unusual twists in the evolution of the complex brains, but this suggests the independent evolution of complex brains in our lineage versus invertebrates, for example, in lineages leading to the octopus or the honeybee.”
The latest research indicates that of the five animal phyla, the highest classification in our evolutionary neighborhood, four contain worms. But none are anatomically simpler than “acoels,” which have no brains or centralized nervous systems. Less than a few millimeters in size, acoels are little more than tiny bags of cells that breathe through their skin and digest food by surrounding it.
Comparing extensive genome-wide data, mitochondrial genes and tiny signaling nucleic acids called microRNAs, the researchers hailing from six countries determined a strong possibility that acoels and their kin are “sisters” to another peculiar type of marine worm from northern seas, called Xenoturbella.
From there, like playing “Six Degrees of Kevin Bacon,” the branches continue to humans.
“If you looked at one of these creatures you would say, ‘what is all of this excitement about a worm?’” said Richard G. Northcutt, Ph.D., a professor of neurosciences at Scripps Institution of Oceanography, who was not involved in the study. “These are tiny animals that have almost no anatomy, which presents very little for scientists to compare them with. But through genetics, if the analysis is correct – and time will tell if it is – the study has taken a very bothersome group that scientists are not sure what to do with and says it is related to vertebrates, ourselves and echinoderms (such as starfish).
“The significance of the research is it gives us a better understanding of how animals are related and, by inference, a better understanding of the history of the animals leading to humans,” Northcutt said.
Scientists used high-throughput computational tools to reconstruct deep evolutionary relationships, apparently confirming suspicions that three lineages of marine worms and vertebrates are part of a common evolutionary line called “deuterostomes,” which share a common ancestor.
“The early evolution of lineages leading to vertebrates, sea stars and acorn worms is much more complex than most people expect because it involves not just gene gain, but enormous gene loss,” said Moroz, who is affiliated with the Whitney Laboratory for Marine Bioscience and UF’s McKnight Brain Institute. “An alternative, yet unlikely, scenario would be that our common ancestor had a central nervous system, and then just lost it, still remaining a free living organism.
Understanding the complex cellular rearrangements and the origin of animal innovations, such as the brain, is critically important for understanding human development and disease, Moroz said.
“We need to be able to interpret molecular events in the medical field,” he said. “Is what’s happening in different lineages of neuronal and stem cells, for example, completely new, or is it reflecting something that is in the arrays of ancestral toolkits preserved over more than 550 million years of our evolutionary history? Working with models of human disease, you really need to be sure.”
Research shows that Velvet bean, a natural source of L-Dopa, improves the symptoms of Parkinson’s disease. This herb has been used in Ayurvedic medicine for centuries.
Mucuna pruriens, or Velvet bean, is an ancient herb that has received much attention in recent years because of its effectiveness in treating Parkinson’s disease, a debilitating neurological condition that affects millions, particularly with advancing age. Velvet bean’s active chemical ingredient is a natural form of dopamine, making it very specific for Parkinson’s disease, as well as for any disorder caused by insufficient levels of this critical neurotransmitter. Research has shown that when natural dopamine is chemically removed from the herb, Velvet bean is still effective against the symptoms of Parkinson’s disease, indicating that the herb possesses multiple anti-Parkinsonian properties.
Velvet bean has been used as part of the traditional herbal treatment for Parkinson’s disease in Ayurvedic medicine for centuries. Empirical evidence gathered over this time strongly suggests that this treatment stops the progress of the disease by helping to regenerate the nervous system and arresting damage caused by free radicals. Herbal treatment has not been shown to reverse Parkinson’s disease, however.
Velvet Bean as an Herbal Alternative to L-Dopa
Due to the high concentration of naturally-occuring L-dopa in Velvet bean seeds, it has been studied intensively for its potential use in slowing the progress of Parkinson‘s, which is characterized by progressive degeneration of dopaminergic neurons in specific areas in the brain. Dopamine does not cross the blood-brain barrier and therefore cannot be used directly as a treatment. However, L-dopa does gain access to the brain-where it is converted to dopamine.
In a clinical trial, the effects of Velvet bean were compared with standard doses of L-dopa in Parkinson’s patients. For this study, eight Parkinson‘s patients were treated with a short duration L-dopa response and completed a randomized, controlled, double blind crossover trial. Compared with standard treatment, the velvet bean preparation proved to have a significantly faster effect. The average onset was approximately 22% faster with a dose of 30 g of Velvet bean extract than that of the standard drug treatment.
Further Research on Velvet Bean and Parkinson’s Disease Symptoms
In a second clinical study, the efficacy of a traditional Ayurvedic treatment including Velvet bean was studied in 18 clinically diagnosed Parkinson’s disease patients. Patients whose herbal therapy was accompanied by traditional Ayurvedic cleansing experienced significant improvements in their Parkinson’s disease symptoms, particularly in motor activities. These patients showed reductions in tremors, radykinesia, stiffness and cramps as compared to patients receiving herbal therapy alone.
This research indicates that the naturally-occurring L-dopa contained in Velvet bean may offer advantages over conventional L-dopa preparations in the long-term management of Parkinson’s disease. The necessity of combining such treatment with whole-body cleansing, such as that traditionally administered in Ayurveda, significantly enhances the effectiveness of the herbal treatment.
NEW YORK – Excessive intake of Vitamin A can have a negative effect on the human body, a new study says.
The research shows that Vitamin A plays a crucial role in energy production within cells but too much or too little of it can harm the system.
This is particularly important as combinations of foods, drinks, creams, and nutritional supplements containing added Vitamin A make an overdose more possible than ever before.
“Our work illuminates the value and potential harm of Vitamin A use in cosmetic creams and nutritional supplements,” said study co-author UlrichHammerling of Sloan-Kettering Institute for Cancer Research, New York.
“Although Vitamin A deficiency is not very common in our society, over-use of this vitamin could cause significant disregulation of energy production impacting cell growth and cell death.”
Though Vitamin A for nutrition and foetal development is well-known, it has been unclear why Vitamin A deficiencies and overdoses cause such widespread and profound harm to our organs, until now.
The discovery by Hammerling and colleagues explains why these effects occur, while also providing insight into Vitamin A’s anti-cancer effects, says a Sloan-Kettering release.
The scientists used cultures from both human and mice cells containing specific genetic modifications of the chemical pathways involved in mitochondrial (which powers the cell) energy production.
These findings were published in the FASEB Journal.
URMC Study Links Vitamin D, Race, And Cardiac Deaths
ROCHESTER – Vitamin D deficiency may contribute to a higher number of heart and stroke-related deaths among black Americans compared to whites, according to a University of Rochester Medical Center study.
The journal Annals of Family Medicine is publishing the study in the January-February edition, which goes online Jan. 11, 2010.
Researchers sought to understand the well-documented disparity between blacks and whites in cardiovascular deaths. They turned to vitamin D because growing evidence links low serum levels of D to many serious illnesses including diabetes, hypertension, kidney and heart disease.
Lead author KevinFiscella, M.D., said a complex host of genetic and lifestyle factors among blacks may explain why this population group has lower vitamin D levels across the lifespan than other races.
People get vitamin D through their diets, sun exposure, and oral supplements. Genetic factors common to blacks sometimes preclude vitamin D absorption, such as a higher incidence of lactose intolerance, which can eliminate vitamin-D fortified milk from the diet, and darker skin pigment that significantly reduces vitamin D synthesis.
“Therefore, our study suggests that the next step would be to intervene to boost vitamin D levels safely, with supplements,” said Fiscella, a national expert on disparities in health care and a professor of Family Medicine and Community and Preventive Medicine at URMC.
With funding through the National Heart Lung and Blood Institute, Fiscella and colleagues studied a sample of more than 15,000 American adults. The data included measurements of blood levels of vitamin D and death rates due to cardiovascular disease. Researchers also looked at other factors that contribute to heart health, such as body mass index, smoking status and levels of C-reactive protein.
Overall, the analysis showed that, as expected, a vitamin D deficiency was associated with higher rates of death among all people in the sample. In fact, those adults with the worst deficiency had a 40 percent higher risk of death from cardiac illness. This suggests that vitamin D may be a modifiable, independent risk factor for heart disease, Fiscella said.
Most striking, however, was that when researchers adjusted the statistics to look at race, blacks had a 38 percent higher risk of death than whites. As vitamin D levels rose, however, the risk of death was reduced. The same was true when researchers analyzed the effect of poverty on cardiovascular death rates among blacks, which suggests that vitamin D deficiency and poverty each exert separate risk factors, the study said.
A review article published in September 2009 in The American Journal of Medicine, noted that Vitamin D deficiency is a worldwide health problem. In the U.S., inadequate Vitamin D has been reported in about 36 percent of otherwise healthy young adults and about 57 percent of general medicine hospitalized patients.
Vitamin D is metabolized in the liver and converted to 25 hydroxyvitamin D or 25(OH) D, the form used to determine a person’s status through a blood test. Deficiency is usually defined by levels of less than 20 nanograms per milliliter; 30 ng/ml is viewed as sufficient. The mean blood level in the study sample was 29.5 ng/ml.
Most of the body’s tissues and cells have vitamin D receptors, making it a potent regulator of cell activity and growth. A deficiency contributes to inflammation associated with heart disease, many cancers and poor bone health.
Fiscella cautions, however, that not all observational studies of vitamin deficiency are borne out by subsequent clinical trials. For example, previous observational studies of vitamin E and beta-carotene that were associated with poor heart health did not hold up in later clinical studies. The need to further assess the vitamin D connection to heart disease is convincing, however, particularly among blacks, he added.
Other at-risk people include the obese and the elderly, (particularly housebound or nursing home residents), because vitamin D levels decline with age. And although more sun exposure can boost levels of D, skin cancer is also an increasing risk to many people. Therefore, medical authorities usually recommend increased dietary intake and/or supplementation as the best way to correct a deficiency.
Neurogenesis (birth of neurons) is the process by which neurons are generated. Most active during pre-natal development, neurogenesis is responsible for populating the growing brain.
New neurons are continually born throughout adulthood in predominantly two regions of the brain:
Many of the newborn cells die shortly after they are born, but a number of them become functionally integrated into the surrounding brain tissue.
Adult neurogenesis is a recent example of a long-held scientific theory being overturned, with the first evidence of mammalian neurogenesis presented in 1992. Early neuroanatomists, including Santiago Ramon y Cajal, considered the nervous system fixed and incapable of regeneration. For many years afterward, only a handful of biologists (including JosephAltman, ShirleyBayer, and MichaelKaplan) considered adult neurogenesis a possibility.
In 1983, with the characterization of neurogenesis in birds and the use of confocal microscopy, the possibility of mammalian neurogenesis became more apparent, but it was not until the early 1990s that hippocampal neurogenesis was demonstrated in non-human primates and humans. More recently, neurogenesis in the cerebellum of adult rabbits has also been characterized. Further, some authors (particularly ElizabethGould) have suggested that adult neurogenesis may also occur in regions within the brain not generally associated with neurogenesis including the neocortex. However, others have questioned the scientific evidence of these findings arguing that the new cells may be of glial origin.
The functional relevance of adult neurogenesis is uncertain but there is some evidence that hippocampal adult neurogenesis is important for learning and memory. Multiple mechanisms for the relationship between increased neurogenesis and improved cognition have been suggested, including computational theories to demonstrate that new neurons increase memory capacity reduce interference between memories or add information about time to memories.
Experiments aimed at ablating neurogenesis have proven inconclusive, but several studies have proposed neurogenic-dependence in some types of learning. and others seeing no effect. Studies have demonstrated that the act of learning itself is associated with increased neuronal survival. However, the overall findings that adult neurogenesis is important for any kind of learning are equivocal.
Adult-born neurons appear to have a role in the regulation of stress. Studies have linked neurogenesis to the beneficial actions of specific antidepressants, suggesting a connection between decreased hippocampal neurogenesis and depression. In a subsequent paper, scientists demonstrated that the behavioral benefits of antidepressant administration in mice is reversed when neurogenesis is prevented with x-irradiation techniques. In fact, new-born neurons are more excitable than older neurons due to a differential expression of GABA receptors. A plausible model, therefore, is that these neurons augment the role of the hippocampus in the negative feedback mechanism of the HPA-axis (physiological stress) and perhaps in inhibiting the amygdala (the region of brain responsible for fearful responses to stimuli).[vague] This is consistent with numerous findings linking stress-relieving activities (learning, exposure to a new yet benign environment, and exercise) to increased levels of neurogenesis, as well as the observation that animals exposed to physiological stress (cortisol) or psychological stress (e.g. isolation) show markedly decreased levels of new-born neurons.
Some studies have hypothesized that learning and memory are linked to depression, and that neurogenesis may promote neuroplasticity. One study proposes that mood may be regulated, at a base level, by plasticity, and thus not chemistry. Accordingly, the effects of antidepressant treatment would only be secondary to change in plasticity.
Effect of sleep reduction and stress levels on neurogenesis
One study has linked lack of sleep to a reduction in rodent hippocampal neurogenesis. The proposed mechanism for the observed decrease was increased levels of glucocorticoids. It was shown that two weeks of sleep deprivation acted as a neurogenesis-inhibitor, which was reversed after return of normal sleep and even shifted to a temporary increase in normal cell proliferation.
Neurogenesis and Parkinson’s disease
Parkinson’s disease is a neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the nigrostriatal projection. Transplantation of fetal dopaminergic precursor cells has paved the way for the possibility of a cell replacement therapy that could ameliorate clinical symptoms in affected patients. Recent years have provided evidence for the existence of neural stem cells with the potential to produce new neurons, particularly of a dopaminergic phenotype, in the adult mammalian brain. Experimental depletion of dopamine in rodents decreases precursor cell proliferation in both the subependymal zone and the subgranular zone. Proliferation is restored completely by a selective agonist of D2-like (D2L) receptors.] Neural stem cells have been identified in the neurogenic brain regions, where neurogenesis is constitutively ongoing, but also in the non-neurogenic zones, such as the midbrain and the striatum, where neurogenesis is not thought to occur under normal physiological conditions.
A detailed understanding of the factors governing adult neural stem cells in vivo may ultimately lead to elegant cell therapies for neurodegenerative disorders such as Parkinson’s disease by mobilizing autologous endogenous neural stem cells to replace degenerated neurons.
Neurogenesis and Exercise
Scientists have shown that physical activity in the form of voluntary exercise results in an increase in the number of newborn neurons in the hippocampus of aging mice. The same study demonstrates an enhancement in learning of the “runner” (physically active) mice . While the association between exercise-mediated neurogenesis and enhancement of learning remains unclear, this study clearly demonstrates the benefits of physical activity and could have strong implications in the fields of aging and/or Alzheimer’s disease.
Regulation of Neurogenesis
Many factors may affect the rate of hippocampal neurogenesis. Exercise and an enriched environment have been shown to promote the survival of neurons and successful integration newborn cells into the existing hippocampus. Another factor is central nervous system injury since neurogenesis occurs after cerebral ischemia, epileptic seizures, and bacterial meningitis. On the other hand, conditions such as chronic stress and aging can result in a decreased neuronal proliferation.
Adult neural stem cells
Neural stem cells (NSCs) are the self-renewing, multipotent cells that generate the main phenotypes of the nervous system. In 1992, Reynolds and Weiss were the first to isolate neural progenitor and stem cells from the striatal tissue, including the subventricular zone — one of the neurogenic areas — of adult mice brain tissue. Since then, neural progenitor and stem cells have been isolated from various areas of the adult brain, including non-neurogenic areas, such as the spinal cord, and from various species including human.
Epidermal growth factor (EGF) and fibroblast growth factor (FGF) are mitogens that promote neural progenitor and stem cell growth in vitro, though other factors synthesized by the neural progenitor and stem cell populations are also required for optimal growth. It is hypothesized that neurogenesis in the adult brain originates from NSCs. The origin and identity of NSCs in the adult brain remain to be defined.
Neural stem cells are routinely studied in vitro using a method referred to as the Neurosphere Assay (or Neurosphere culture system), first developed by Reynolds and Weiss. While the Neurosphere Assay has been the method of choice for isolation, expansion and even the enumeration of neural stem and progenitor cells, several recent publications have highlighted some of the limitations of the neurosphere culture system as a method for determining neural stem cell frequencies.[vague] In collaboration with Reynolds, STEMCELL Technologies has developed a collagen-based assay, called the Neural Colony-Forming Cell (NCFC) Assay, for the quantification of neural stem cells. Importantly, this assay allows discrimination between neural stem and progenitor cells.
Other names: All-heal, Amantilla, Setwall, Setewale, Capon’s Tail, Valeriana officinalis
Valerian is a plant native to Europe and Asia. It grows to up to four feet high and has trumpet-shaped flowers. The roots are used medicinally. Although the fresh root is relatively odorless, the dried root has a strong odor that many find unpleasant.
Valerian is believed to have been used since at least the time of ancient Greece and Rome. It was used as a folk remedy for a variety of conditions such as sleeping problems, digestive complaints, nervousness, trembling, tension headaches and heart palpitations. Valerian’s popularity waned with the introduction of prescription sleep medication.
There is no consensus on what the active constituents of valerian are. It’s possible that valerian’s activity may result from a combination of compounds rather than any one. Valerian appears to increase the body’s available supply of the neurotransmitter gamma aminobutyric acid (GABA), possibly by increasing its production, decreasing its absorption or slowing its breakdown.
Valerian can be found in capsule, tea, tablet or liquid extract forms in most health food stores, some drugstores and online.
Why Do People Use Valerian?
The use of valerian is supported by some evidence from clinical studies. The problem with many of the studies, however, is they’ve generally been small, used different amounts of valerian for varying lengths of time, or had problems with the study design, making it impossible to form a conclusion about the effectiveness of valerian.
Valerian appears to be less effective than prescription sleep medication. One possible advantage of valerian, however, is that it may not have as much of a “hangover” effect on mental or physical functioning the following day. Also, people taking sleeping pills sometimes have a temporary worsening of insomnia when they are discontinued, an effect that hasn’t been reported with valerian.
Valerian is also used for anxiety, although there’s insufficient evidence that it’s effective.
Side Effects and Safety Concerns
Pregnant or nursing women and children should not use valerian.
People taking medications for insomnia or anxiety, such as benzodiazepines, should not combine these medications with valerian.
Side effects of valerian may include headache, dizziness, itchiness, upset stomach, drowsiness during the daytime, dry mouth and vivid.dreams.
Rarely, liver damage has been associated with the use of valerian. It’s not certain whether the cause of the liver damage was due to valerian itself or to contaminants in the product. Until we know more, people should use valerian only under the supervision of a qualified health care practitioner and those with liver disease should avoid it. Although liver damage doesn’t always produce noticeable symptoms, if excessive tiredness, intense itching, nausea, vomiting, diarrhea, pain or discomfort in the upper right side of the abdomen, or a yellowing of the whites of the eyes or skin occurs, see your doctor immediately.
Valerian may cause excessive sleepiness or daytime drowsiness if combined with other drugs that cause drowsiness, such as the benzodiazepines Ativan (lorazepam) or Valium (diazepam), some antidepressants, narcotics such as codeine, and barbituates such as phenobarbitol, or with over-the-counter sleep and cold products containing diphenhydramine and doxylamine.
It may also cause excessive sleepiness if taken with herbs thought to have a sedative effect, such as hops, catnip and kava.
Valerian is broken down in the liver. Theoretically, it could interfere with the effectiveness of medications that are broken down by the same liver enzymes, such as:
allergy medications like Allegra (fexofenadine)
cholesterol medication such as Mevacor (lovastatin)
antifungal drugs such as Sporanox (itraconazole) and Nizoral (ketoconazole)
cancer medications such as Camptosar (irinotecan), Etopophos, Vepesid (etoposide), Gleevec (STI571), Taxol (paclitaxel), Velbe (vinblastine) or Oncovin (vincristine)
WASHINGTON – In a large-scale clinical trial in US and Canada, researchers at Rush University Medical Center are trying to find out if an over-the-counter vitamin-like substance, in high doses, can slow the progression of Parkinson’s disease.
The substance being tested, called coenzyme Q10, is produced naturally in the body and is an important link in the chain of chemical reactions that produce energy in mitochondria, the “powerhouses” of cells.
The enzyme is also a potent antioxidant – a chemical that “mops up” potentially harmful chemicals generated during normal metabolism.
“At present, the very best therapies we have for Parkinson’s can only mask the symptoms – they do not alter the underlying disease. Finding a treatment that can slow the degenerative course of Parkinsons’s is the holy grail of Parkinson’s research,” said neurologist Dr.KatieKompoliti, a specialist in movement disorders.
Many past studies have shown that Parkinson’s patients have impaired mitochondrial function and low levels of coenzyme Q10.
Moreover, laboratory research has demonstrated that coenzyme Q10 can protect the area of the brain damaged in Parkinson’s.
The Phase III clinical trial, a large, randomized study with a control group, follows an earlier investigation that tested several doses of coenzyme Q10 in a small group of patients with early-stage Parkinson’s disease.
The highest dose, 1,200 mg, appeared promising-over the course of 16 months, patients taking this dose experienced significantly less decline than other patients in motor (movement) function and ability to carry out activities of daily living, such as feeding or dressing themselves.
In the present trial, 600 patients will be enrolled at 60 centers in the U.S. and Canada.
Two dosages of coenzyme Q10 are being tested,1,200 mg and 2,400 mg, delivered in maple nut-flavored chewable wafers that also contain vitamin E.
Participants in the study will be evaluated periodically over 16 months for symptoms of Parkinson’s disease, including tremor, stiffness of the limbs and trunk, impaired balance and coordination, and slowing of movements.
They will also be assessed for ability to perform daily activities, overall quality of life, and need to take medications to alleviate symptoms.
HELSINKI- Scientists from University of Helsinki Institute of Biotechnology have identified a novel therapeutic target for Parkinson’s disease.
Lead researcher Professor Raimo K. Tuominen and colleagues have identified a growth factor that can be used to halt the progress of damage brought on by a nerve poison, and possibly restore the function of damaged cells.
The team is investigating two new nerve growth factors. MANF (mesencephalic astrocyte-derived neurotrophic factor) and CDNF.
MANF is released from glial cells in the midbrain and is a member of the same growth factor family as CDNF.
The team found that in the experimental PD model, MANF and CDNF injections into the brain prevented dopamine nerve destruction caused by nerve poison and to some extent even restored the function of damaged cells in rats.
This suggests that MANF spreads more readily in brain tissue than other known growth factors.
This may be a highly significant finding in respect to the development of growth factor therapy for PD.