E-NUMBER Listings --FOOD ADDITIVES and CHEMICALS---Current EU approved additives and their E Numbers
ScienceDaily (June 24, 2010) — Why is it that only some drug users become addicts? [U1]This is the question that has been addressed by the teams of Pier Vincenzo Piazza and Olivier Manzoni, at the Neurocentre Magendie in Bordeaux (Inserm unit 862). These researchers have just discovered that the transition to addiction could result from a persistent impairment of synaptic plasticity in a key structure of the brain. This is the first demonstration that a correlation exists between synaptic plasticity and the transition to addiction.----The results from the teams at Neurocentre Magendie call into question the hitherto held idea that addiction results from pathological cerebral modifications which develop gradually with drug usage. Their results show that addiction may, instead, come from a form of anaplasticity, i.e. from incapacity of addicted individuals to counteract the pathological modifications caused by the drug to all users.---This research is published in the journal Science on 25 June 2010.--The voluntary consumption of drugs is a behaviour found in many species of animal. However, it had long been considered that addiction, defined as compulsive and pathological drug consumption, is a behaviour specific to the human species and its social structure. In 2004, the team of Pier Vincenzo Piazza showed that the behaviours which define addiction in humans, also appear in some rats which will self administer cocaine*. Addiction exhibits astonishing similarities in men and rodents, in particular the fact that only a small number of consumers (humans or rodents) develop a drug addiction. The study of drug dependent behaviour in this mammal model thus opened the way to the study of the biology of addiction.---Now, the teams of Pier Vincenzo Piazza and Olivier Manzoni are reporting discovery of the first known biological mechanisms for the transition from regular but controlled drug taking to a genuine addiction to cocaine, characterised by a loss of control over drug consumption.---Chronic exposure to drugs causes many modifications to the physiology of the brain. Which of these modifications is responsible for the development of an addiction? This is the question the researchers wanted to answer in order to target possible therapeutic approaches to a disorder for which treatments are cruelly lacking.---The addiction model developed in Bordeaux provides a unique tool to answer this question. Thus it allows comparing animals who took identical quantities of drugs, but of which only few become addicted. By comparing addict and non-addict animals at various time points during their history of drug taking, the teams of Pier Vincenzo Piazza and Olivier Manzoni have demonstrated that the animals which developed an addiction to cocaine exhibit a permanent loss of the capacity to produce a form of plasticity known as long term depression (or LTD). LTD refers to the ability of the synapses (the region of communication between neurons) to reduce their activity under the effect of certain stimulations. It plays a major role in the ability to develop new memory traces and, consequently, to demonstrate flexible behaviour.----After short term usage of cocaine, LTD is not modified. However, after a longer use, a significant LTD deficit appears in all users. Without this form of plasticity, which allows new learning to occur, behaviour with regard to the drug becomes more and more rigid, opening the door to development of a compulsive consumption. The brain of the majority of users is able to produce the biological adaptations which allow to counteract the effects of the drug and to recover a normal LTD. By contrast, the anaplasticity (or lack of plasticity) exhibited by the addicts leaves them without defences and hence the LTD deficit provoked by the drug becomes chronic. This permanent absence of synaptic plasticity would explain why drug seeking behaviour becomes resistant to environmental constraints (difficulty in procuring the substance, adverse consequences of taking the drug on health, social life, etc.) and consequently more and more compulsive. Gradually, control of the taking of the drug is lost and addiction appears.---For Pier-Vincenzo Piazza and his collaborators, these discoveries also have important implications for developing new treatment of addiction. "We are probably not going to find new therapies by trying to understand the modifications caused by a drug in the brains of drug addicts," explain the researchers, "since their brain is anaplastic." For the authors, "The results of this work show that it is in the brain of the non-addicted users that we will probably find the key to a true addiction therapy. Indeed," the authors estimate, "understanding the biological mechanisms which enable adaptation to the drug and which help the user to maintain a controlled consumption could provide us with the tools to combat the anaplastic state that leads to addiction."----Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by INSERM (Institut national de la santé et de la recherche médicale), via EurekAlert!, a service of AAAS.---Journal Reference:Fernando Kasanetz, Véronique Deroche-Gamonet, Nadège Berson, Eric Balado, Mathieu Lafourcade, Olivier Manzoni, and Pier Vincenzo Piazza. Transition to Addiction is Associated with a Persistent Impairment in Synaptic Plasticity. Science, June 24, 2010 DOI: 10.1126/science.1187801
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ScienceDaily (Mar. 2, 2007) — The function of an enzyme in the brain -- strongly linked to a number of major brain diseases such as Alzheimer's, schizophrenia and bi-polar disorder -- has been identified for the first time by researchers at the University of Bristol, UK.---These findings, published today in Neuron, will help in the understanding of how memories are laid down and what goes wrong in these disorders.----The research showed how controlling the activity of glycogen synthase kinase-3 (GSK3) might prevent a memory being erased by improving the strength of connections between neurons in the brain, thus allowing better consolidation of new information.---Professor Collingridge from the University of Bristol said: "While GSK3 has previously been implicated in major neurological disorders, until now its role in normal neuronal function has been largely unknown. Our new understanding will help pharmaceutical companies develop drugs to inhibit it when things go wrong."---Professor Graham Collingridge and his team, with colleagues from the University of British Columbia, revealed that the activity of GSK3 facilitates a form of 'cross-talk' between the two major forms of synaptic plasticity in the brain.---Synaptic plasticity is the strength of a connection between neurons and forms the basis of learning and memory. ---Story Source--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Bristol, via EurekAlert!, a service of AAAS.
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‘Natural’ has become a word consumers like to see on food product packages, while ‘clean label’ is an industry term to describe an E-number-free ingredients list. But exact definitions depend on who you are talking to, and what additive you are taking about. --At the beginning of July any food products sold in the EU that still contain the so-called Southampton colours that were implicated in a study on hyperactivity in children will have to carry a warning label. ---This has accelerated the drive towards using ‘natural colours’. The Natural Food Colours Association (NatCol) has a list classifying colours according to whether they occur in nature and are naturally-sourced, occur in nature but can be synthetically manufactured, or do not occur in nature and are manufactured synthetically, but these are not legal definitions. ---Both colours that are naturally sourced and synthetically manufactured are attributed an E-number which has to be used on product packaging in the EU – but consumers may not be aware that no all E-numbers are artificial. A way to avoid having to use an E-number coloured is to use a colouring foodstuff, that is, ingredients that used in their natural food form to lend their colour to the formulation, without any purification having taken place. --Food companies tend to couch references to colourings carefully. For instance, a manufacturer may declare their products contain ‘no artificial colourings’, but they may still have colours that do exist naturally but which tend to be synthetically produced when used on an industrial scale. ---Natural taste ---The new EU regulation has brought some clarity to what natural means in a flavour context. ---It does away with the distinction between ‘nature identical’ and ‘synthetic’ flavourings, meaning that all non-natural flavourings will simply be called ‘flavouring substances’. ---Meanwhile, natural flavourings can be labelled in one of four ways, depending on their precise make up: ‘natural flavouring’; ‘natural flavouring substances’; ‘natural (eg) strawberry flavouring’; and ‘natural (eg) strawberry flavouring with other natural flavours’. ---For named natural flavours – for instance, ‘natural strawberry flavour’ - 95 per cent of the flavour must come from the named source. ---However when natural flavours are used with other named flavours – for example ‘natural strawberry with other natural flavourings’; those ‘other natural flavourings’ would not be strawberry derived. ----The clean label question ---As for clean label, Julie Scott, regulatory manager EMEA at National Starch Innovation believes the lack of a regulatory definition has created “confusion and discrepancies”. ---NSFI has recently offered its definition to the market. It says a clean label: is free from chemical additives; has a simple ingredient listing (without ingredients that sound chemical or artificial); and is minimally processed using traditional techniques that are understood by consumers and not perceived as being artificial. ---According to Clean Eating magazine, ‘clean eating’ means consuming food that is in its most natural state, or as close to it as possible. ---Leatherhead Food International defines clean label as: “Seeking natural alternatives to food additives as, when these are listed on labels as the named ingredients rather than by E-number, it gives the food product a ‘clean label’ declaration”.
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‘No-additives’, and ‘no-preservatives’ are the most popular clean label claims with consumers, while ‘natural’ struggles because of over-use and lack of definition, according to research.
National Starch commissioned research on consumer understanding of clean label terms in the UK, Germany and the US in 2007, and followed it up in 2010 in Germany and France. The study involved holding a series of moderated focus groups with consumers who were the main shoppers in their households, and the aim was to see not only how attitudes to clean label terms have changed but also to understand language-specific terms. ---Mike Croghan, global director wholesome ingredients at National Starch Food Innovation told FoodNavigator.com: “No additives or preservatives, whether you like it or not, that’s what consumer want.” --He added that natural would be more powerful, but it is still subject to some misunderstanding. “If it were better defined, it would grow stronger,” he said. ---Non-legal guidelines on use of the term ‘natural’ do exist in the UK and France, but with the exception of flavours there is no Europe-wide directive defining the term. ---Moreover, consumers have seen ‘natural’ used as an adverb and an adjective so often that there is some scepticism. They also expect consistency between the front and the pack of a pack. For example, if there is natural imagery on the front, such as a picture of a farm, but on the back there are e-numbers listed, consumers will be mistrustful. ---They may also make a judgement based on perceived level of processing or the food’s packaging, rather than just the ingredients list, asking: “Is it really that natural? It’s in a can”. --Natural or clean label? --Clean label is a term intended for industry use rather than consumer-use. Importantly, natural and clean label are not necessarily the same thing. Clean label embraces organic, but organic and natural are not interchangeable terms. Moreover, there are some natural additives and they may or may not be accepted as clean label. ---National Starch has drawn up its own definition of ‘clean label’: Free from chemical additives; simple ingredient listing (without ingredients that sound chemical or artificial); minimally processed using traditional techniques that are understood by consumers and not perceived as being artificial.. ---No compromise, no chemistry ---Croghan said he has observed a growth in clean label eating in the last three years. “It was strong in 2007, now it’s not just a trend but the way consumers expect and increasingly demand foods to be”. At the same time, however, they are unwilling to compromise on aspects such as taste. --National Starch has also drawn up lists of ingredients that are well-accepted by consumers, including starches, flour and bran. Maltodextrin, lecithin and guar gum are borderline ingredients, while e-numbers, anything chemically-modified, monodiglycerides, and other chemically sounding names may be best replaced. ---Xanthan gum is an interesting case, Croghan said: “Anything that begins with an x sounds like chemistry. It is not necessarily the most natural ingredient anyway, but the name doesn’t do it any favours”.
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Children prefer the taste of foods branded with images of popular cartoon characters and choose those foods more often than unbranded ones, according to research from Yale’s Rudd Center for Food Policy and Obesity. ---The researchers presented a group of 40 four- to six-year-old children with three different snacks – graham crackers, gummy fruit snacks and carrots – each in two different packages. Half the packages were branded with popular cartoon characters Dora the Explorer, Shrek, and Scooby Doo while the other half were unbranded. They found that children were significantly more likely to choose the cartoon-branded products over the unbranded ones – and to prefer the taste of the branded food. ---In addition, the researchers found that the effect was weaker for carrots than it was for gummy fruit snacks and graham crackers. ----Lead author Christina Roberto wrote: “Our results provide evidence that licensed characters can influence children’s eating habits negatively by increasing positive taste perceptions and preferences for junk food. Given that 13 percent of marketing expenditures targeting youths are spent on character licensing and other forms of cross-promotion, our findings suggest that the use of licensed characters on junk food packaging should be restricted.” -----Childhood obesity is at record levels, with 32 percent of US children and adolescents overweight or obese, according to statistics from the Centers for Disease Control and Prevention. --The researchers highlighted that the increase in childhood obesity – which has more than tripled since the 1970s – has coincided with increased marketing of products to children. Food and beverage companies spend more than $1.6bn a year on marketing products to younger consumers, according to Federal Trade Commission figures. ----“Rather than advocating the use of licensed characters in the marketing of healthy foods, these findings suggest a need for regulation to curtail the use of licensed characters in the marketing of low-nutrient, high-energy foods,” the researchers wrote. ------Despite finding no statistically significant preference for the taste of character-branded carrots, children were much more likely to choose all three foods if they were labeled with a cartoon character. A range of 72.5 percent to 87.5 percent of children selected the character-associated carrots, gummy fruit snacks, and graham crackers. ---Source: Pediatrics --Published online ahead of print ---“Influence of Licensed Characters on Children's Taste and Snack Preferences” ---Authors: Christina Roberto, Jenny Baik, Jennifer Harris and Kelly Brownell
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Li W, Wu JX, Tu YY.--Department of Tea Science, Zhejiang--University, Hangzhou 310029, China.
Tea polyphenols have been shown to have anticancer activity in many studies. In the present study, we investigated effects of theaflavin-3-3'-digallate (TF(3)), one of the major theaflavin monomers in black tea, in combination with ascorbic acid (AA), a reducing agent, and (-)-epigallocatechin-3-gallate (EGCG), the main polyphenol presented in green tea, in combination with AA on cellular viability and cell cycles of the human lung adenocarcinoma SPC-A-1 cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay showed that the 50% inhibition concentrations (IC(50)) of TF(3), EGCG, and AA on SPC-A-1 cells were 4.78, 4.90, and 30.62 micromol/L, respectively. The inhibitory rates of TF(3) combined with AA (TF(3)+AA) and EGCG combined with AA (EGCG+AA) at a molar ratio of 1:6 on SPC-A-1 cells were 54.4% and 45.5%, respectively. Flow cytometry analysis showed that TF(3)+AA and EGCG+AA obviously increased the cell population in the G(0)/G(1) phase of the SPC-A-1 cell cycle from 53.9% to 62.8% and 60.0%, respectively. TF(3)-treated cells exhibited 65.3% of the G(0)/G(1) phase at the concentration of its IC(50). Therefore, TF(3)+AA and EGCG+AA had synergistic inhibition effects on the proliferation of SPC-A-1 cells, and significantly held SPC-A-1 cells in G(0)/G(1) phase. The results suggest that the combination of TF(3) with AA or EGCG with AA enhances their anticancer activity
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ScienceDaily (June 18, 2010) — Conventional drugs used in the treatment of liver diseases inevitably have side effects. An increasing number of natural substances have been studied to explore if they have protective effects on the liver. Blueberries have unique effects on human retinal, brain and tumor cells, but reports about the effects of blueberries on liver diseases are lacking.-A research article to be published on June 7, 2010 in the World Journal of Gastroenterology addresses this question. The research team led by Ming-Liang Cheng, MD, from Department of Infectious Diseases, Guiyang Medical College, Guiyang, presented some data from their research on the effectiveness of blueberries on liver fibrosis induced in laboratory animals.---Their study showed that blueberries could reduce liver indices, serum levels of hyaluronic acid and alanine aminotransferase, and increase levels of superoxide dismutase and decrease levels of malondialdehyde in liver homogenates compared with the model group. Meanwhile, the stage of hepatic fibrosis was significantly weakened. Blueberries increased the activity of glutathione-S-transferase in liver homogenates and the expression of Nrf2 and Nqo1 compared with the normal group, but there was no significant difference compared with the model group.----The authors suggest that blueberry consumption is beneficial for hepatic diseases (including fibrosis).---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by World Journal of Gastroenterology, via EurekAlert!, a service of AAAS.---Journal Reference:---Wang YP, Cheng ML, Zhang BF, Mu M, Wu J. Effects of blueberry on hepatic fibrosis and transcription factor Nrf2 in rats. World J Gastroenterol, 2010; 16 (21): 2657-2663 DOI: http://www.wjgnet.com/1007-9327/full/v16/i21/2657.htm
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ScienceDaily (June 17, 2010) — Researchers at the Stanford University School of Medicine have identified a new group of proteins involved in determining the life span of laboratory roundworms. Blocking the expression of one member of the group can extend the worm's life span by up to 30 percent. Because the proteins work in the worms' reproductive systems, the research represents yet another intriguing link between longevity and fertility.---In particular, the researchers showed that the proteins are involved in epigenetics -- a phenomenon in which chemical modifications to DNA and the proteins around it affect how it is packaged and expressed in a cell. Although an organism can't change the DNA sequence of the genes it has inherited, epigenetic changes allow it to silence or tweak their expression in response to environmental or other external cues.---"We've shown here that an epigenetic change can affect the life span of an organism," said Anne Brunet, PhD, assistant professor of genetics, "but only within the context of an intact reproductive system." Brunet is the senior author of the study, which will be published online June 16 in Nature.---Roundworms, also known as Caenorhabditis elegans, are a popular laboratory animal. They are easy to care for, and their approximately four-week life span makes them good models for longevity studies. For technical reasons, though, most longevity researchers have conducted their experiments on sterile worms.--Brunet and graduate student Eric Greer wanted to explore the effect of epigenetic changes on longevity. But they wondered if using fertile worms might be more appropriate for their studies. After all, other studies of the worms have suggested that fertility is at least indirectly linked to longevity.--Greer, who is the lead author of the study, used a technique called RNA interference in fertile worms to methodically block the expression -- one by one -- of genes known to affect a cell's epigenetic status. He identified a number of genes that, when inhibited, caused the worms to live up to 30 percent longer than normal.---The gene with the most pronounced effect, Ash-2, makes a protein that functions as a methyltransferase -- meaning it works together with other proteins to add a chemical tag called a methyl group to a component of a cell's DNA packaging machinery, which is known as a histone. The presence or absence of this tag affects whether the DNA remains wound up tightly like thread on a spool, or unfurls to allow its genes to be expressed.---Inhibiting Ash-2 activity reduces the number of methyl tags on the histone, which keeps the DNA inaccessible and somehow extends the animal's life by as much as 30 percent. Conversely, the researchers found, blocking the expression of a protein called Rbr-2 taxed with removing the tag -- a demethylase -- shortened the worm's life span by about 15 to 25 percent. Worms in which the expression of both proteins were blocked had slightly shortened lives.---Clearly the levels of methylation on that particular spot on the histone are important to longevity. But why? And how are they calibrated?---The researchers found that Ash-2 is highly expressed in the germline, or reproductive cells, as well as in newly formed eggs. These cells also had high levels of the methyl tag. When Greer blocked the expression of Ash-2 in worms that lacked normal reproductive cells, he found that this no longer extended worm life span, suggesting that an intact germline is necessary for Ash-2 to regulate longevity.---Further investigation showed that Ash-2 activity affects the expression of several genes specific to germline cells, including a group previously shown to affect adult life span. Blocking Ash-2 expression only in germline cells, but not in the rest of the worm's body, still extended its life span, as did expressing excess amounts of the tag-removal protein Rbr-2 in the germline. Finally, another series of experiments showed that the presence of mature eggs is required for Ash-2 knockdown to have an effect.---"We still don't know exactly how this works mechanistically," said Brunet, "but we've shown that the presence of the germline is absolutely essential for this longevity extension to happen."----In the future the researchers plan to monitor the methylation status of the histone during the animal's life span. Because epigenetic changes are reversible, it's likely they'll see a natural ebb and flow as the worm ages. They'd also like to examine the effect of environmental situations known to affect longevity, such as calorie restriction, on the tagged histone.---"Aging is a very plastic process," said Brunet, who cautioned that it's possible that Ash-2 also works elsewhere in the worm. "This tagging doesn't affect reproduction directly, but it somehow talks to the rest of the body to affect the whole organism." Perhaps, they speculate, the genes activated by the loss of Ash-2 work together with other factors produced by mature eggs to lengthen the animal's life.---"It makes a sort of sense that the reproductive system would be involved in life span, since that is really the only 'immortal' part of an organism," said Brunet. "In that context, the body is just the mortal envelope."---In addition to Greer and Brunet, other Stanford researchers involved in the study include assistant professor Or Gozani, PhD; postdoctoral scholars Travis Maures, PhD, Erin Green, PhD, and Geraldine Maro, PhD; graduate students Dena Leeman, Shuo Han and Max Banko; and undergraduate student Anna Hauswirth. The research was supported by the National Institutes of Health, the Human Frontier Science Program and a Searle Scholar Award.---- Story Source: --The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Stanford University Medical Center. The original article was written by Krista Conger. --Journal Reference Eric L. Greer, Travis J. Maures, Anna G. Hauswirth, Erin M. Green, Dena S. Leeman, Géraldine S. Maro, Shuo Han, Max R. Banko, Or Gozani & Anne Brunet. Members of the H3K4 trimethylation complex regulate lifespan in a germline-dependent manner in C. elegans. Nature, June 16, 2010 DOI: 10.1038/nature09195
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ScienceDaily (Nov. 5, 2009) — If worms are any indication, all the sugar in your diet could spell much more than obesity and type 2 diabetes. Researchers reporting in the November issue of Cell Metabolism, a Cell Press publication, say it might also be taking years off your life.--By adding just a small amount of glucose to C. elegans usual fare of straight bacteria, they found the worms lose about 20 percent of their usual life span. They trace the effect to insulin signals, which can block other life-extending molecular players.---Although the findings are in worms, Cynthia Kenyon of the University of California, San Francisco, says there are known to be many similarities between worms and people in the insulin signaling pathways. (As an aside, Kenyon says she read up on low-carb diets and changed her eating habits immediately -- cutting out essentially all starches and desserts -- after making the initial discovery in worms. The discovery was made several years ago, but had not been reported in a peer-reviewed journal until now.)----"In the early 90s, we discovered mutations that could double the normal life span of worms," Kenyon said. Those mutations effected insulin signals. Specifically, a mutation in a gene known as daf-2 slowed aging and doubled life span. That longer life depended on another "FOXO transcription factor" called DAF-16 and the heat shock factor HSF-1.---Now, the researchers show that those same players are also involved in numbering the days of worms who are fed on glucose. In fact, glucose makes no difference to the life span of worms that lack DAF-16 or HSF-1, they show. Glucose also completely prevents the life-extending benefits that would otherwise come with mutations in the daf-2 gene.---Ultimately, worms fed a steady diet containing glucose show a reduction in aquaporin channels that transport glycerol, one of the ingredients in the process by which the body produces its own glucose. "If there is not enough glucose, the body makes it with glycerol," Kenyon explained. That glycerol has to first get where it needs to go, which it does via the aquaporin channels.----Further studies are needed to see if these same effects of sugar can be seen in mice, or even people. But there is reason to think they may.---"Although we do not fully understand the mechanism by which glucose shortens the life span of C. elegans, the fact that the two mammalian aquaporin glycerol-transporting channels are downregulated by insulin raises the possibility that glucose may have a life-span-shortening effect in humans, and, conversely, that a diet with a low glycemic index may extend human life span," the researchers write. Kenyon also points to recent studies that have linked particular FOXO variants to longevity in several human populations, making the pathway the first with clear effects on human aging.----She says the findings may also have implications for drugs now in development for the treatment of diabetes, which are meant to block glucose production by inhibiting glycerol channels. The new findings "raise a flag" that glycerol channels might be doing something else, she says, and that drugs designed to block them might have a downside.---The researchers include Seung-Jae Lee, University of California, San Francisco, CA, Pohang University of Science and Technology, Pohang, Kyungbuk, South Korea; Coleen T. Murphy, University of California, San Francisco, CA; and Cynthia Kenyon, University of California, San Francisco, CA.-- Story Source--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Cell Press, via EurekAlert!, a service of AAAS.
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ScienceDaily (Oct. 6, 2007) — A new study in Cell Metabolism reveals that worms live to an older age when they are unable to process the simple sugar glucose. Glucose is a primary source of energy for the body and can be found in all major dietary carbohydrates as a component of starches and other forms of sugar, including sucrose (table sugar) and lactose. ---"In the US and Europe, added sugar accounts for 15 to 20 percent of daily calories, and the breakdown of that sugar always generates glucose," said Michael Ristow of the University of Jena in Germany and the German Institute of Human Nutrition Potsdam-Rehbrücke. If the findings in worms hold for humans, it "suggests that, in healthy people, glucose may have negative effects on life span." The findings may also cast some doubt on the prevailing treatments for type 2 diabetes, all of which are aimed at lowering blood levels of glucose by increasing the amount of sugar taken up by body tissues, Ristow said. --What's more, Ristow's group further demonstrated in their report that antioxidants and vitamins given to the worms erased the life-extending benefits of sugar deprivation, raising questions about the widespread use of antioxidant supplements, according to the researchers. In westernized countries, glucose represents a key dietary component since the most commonly ingested sugar, sucrose, contains equal amounts of glucose and fructose, the researchers noted. Nevertheless, it is a matter of debate whether glucose and other carbohydrates have a relevant effect on disease burden and mortality in humans, they said.---To begin to address the issue in the current study, the researchers exposed the nematode Caenorhabditis elegans to a chemical that blocked the worms' ability to process glucose, producing a metabolic state the researchers said resembles that of dietary glucose restriction. That treatment extended the worms' life span up to 20 percent, Ristow reported, noting that the observed gain extrapolated to humans would mean an additional 15 years of life.---Unable to depend on glucose for energy, the long-lived worms ramped up the activity of cellular powerhouses known as mitochondria to fuel their bodies, Ristow said. That mitochondrial activity led to the increased production of reactive oxygen species, sometimes referred to as free radicals. In turn, the worms' defenses against "oxidative stress" increased, the researchers found. ---Free radicals are usually considered harmful, Ristow said, and scientists have generally thought that exposure to them would shorten life span. The new findings suggest that, at least in some cases, the opposite may be true.---Indeed, even when the researchers returned the worms to their normal environment, allowing them to again use glucose for energy, the worms' increased defenses and longevity persisted, Ristow said. In contrast, treatment with antioxidant vitamins prevented the oxidative stress and the defenses against it, eliminating the life-boosting effects. Ristow called the result "scary" because it means that, rather than being protective, antioxidant pills may actually leave the body more vulnerable by thwarting those natural defenses.---Ristow doesn't recommend that people toss out their multivitamins just yet, however, cautioning that his findings were made in worms. He also noted that antioxidant-rich foods, including fruits and vegetables, contain thousands of substances--many of which have yet to be identified. While scientists don't yet know what all those ingredients do, it's clear that such natural foods support "healthy pathways," Ristow said.---The researchers include Tim J. Schulz of the Department of Human Nutrition, Institute of Nutrition, University of Jena in Jena and the German Institute of Human Nutrition Potsdam-Rehbrücke in Nuthetal; Kim Zarse of the Department of Human Nutrition, Institute of Nutrition, University of Jena in Jena; Anja Voigt of the Department of Human Nutrition, Institute of Nutrition, University of Jena in Jena and the German Institute of Human Nutrition Potsdam-Rehbrücke in Nuthetal; Nadine Urban and Marc Birringer of the Department of Human Nutrition, Institute of Nutrition, University of Jena in Jena; and Michael Ristow of the Department of Human Nutrition, Institute of Nutrition, University of Jena in Jena and the German Institute of Human Nutrition Potsdam-Rehbrücke in Nuthetal.----This work was supported in part by the Deutsche Forschungsgemeinschaft (Bonn) and the Wilhelm Sander Stiftung (Munich).---Reference: Schulz et al.: "Glucose Restriction Extends Caenorhabditis elegans Life Span by Inducing Mitochondrial Respiration and Increasing Oxidative Stress." Publishing in Cell Metabolism 6, 280--293, October 2007. DOI 10.1016/j.cmet.2007.08.011 Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Cell Press, via EurekAlert!, a service of AAAS.
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ScienceDaily (Mar. 9, 2009) — We know that lifespan can be extended in animals by restricting calories such as sugar intake. Now, according to a study published in the journal PLoS Genetics, Université de Montréal scientists have discovered that it's not sugar itself that is important in this process but the ability of cells to sense its presence.---Aging is a complex phenomenon and the mechanisms underlying aging are yet to be explained. What researchers do know is that there is a clear relationship between aging and calorie intake. For example, mice fed with half the calories they usually eat can live 40 percent longer. How does this work?--As part of the PLoS Genetics study, Université de Montréal Biochemistry Professor Luis Rokeach and his student Antoine Roux discovered to their surprise that if they removed the gene for a glucose sensor from yeast cells, they lived just as long as those living on a glucose-restricted diet. In short, the fate of these cells doesn't depend on what they eat but what they think they're eating.--There are two obvious aspects of calorie intake: tasting and digestion. By the time nutrients get to our cells there is an analogous process: sensors on the surface of the cell detect the presence of, for example, the sugar glucose and molecules inside the cell break down the glucose, converting it to energy. Of these processes, it is widely thought that the by-products of broken down sugars are the culprits in aging. The study by Rokeach and Roux suggests otherwise.---To understand aging, Rokeach and Roux in collaboration with Université de Montréal Biochemistry Professors Pascal Chartrand and Gerardo Ferbeyre used yeast as a model organism. At a basic level, yeast cells are surprisingly similar and age much like human cells, as well as being easy to study.--The research team found that the lifespan of yeast cells increased when glucose was decreased from their diet. They then asked whether the increase in lifespan was due to cells decreasing their ability to produce energy or to the decrease in signal to the cells by the glucose sensor.The scientists found that cells unable to consume glucose as energy source are still sensitive to the pro-aging effects of glucose. Conversely, obliterating the sensor that measures the levels of glucose significantly increased lifespan.---"Thanks to this study, the link between the rise in age-related diseases and the over-consumption of sugar in today's diet is clearer. Our research opens a door to new therapeutic strategies for fighting age-related diseases," says Professor Rokeach.----Professor Rokeach's research is supported by the Canadian Institutes of Health Research and by the National Science and Engineering Research Council. Professor Ferbeyre's and Professor Chartrand's research are funded by the Canadian Institutes of Health Research.---Story Source--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Montreal, via EurekAlert!, a service of AAAS.---Journal Reference--Antoine E. Roux, Alexandre Leroux, Manal A. Alaamery, Charles S. Hoffman, Pascal Chartrand, Gerardo Ferbeyre, Luis A. Rokeach. Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast. PLoS Genetics, 2009; 5 (3): e1000408 DOI: 10.1371/journal.pgen.1000408
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ScienceDaily (May 13, 2009) — Cell biologists have found a more filling substitute for caloric restriction in extending the life span of simple organisms.--In a study published May 8 in the open-access journal PLoS Genetics, researchers from the University of Southern California Andrus Gerontology Center show that yeast cells maintained on a glycerol diet live twice as long as normal -- as long as yeast cells on a severe caloric-restriction diet. They are also more resistant to cell damage.---Many studies have shown that caloric restriction can extend the life span of a variety of laboratory animals. Caloric restriction is also known to cause major improvements in a number of markers for cardiovascular diseases in humans. This study is the first to propose that "dietary substitution" can replace "dietary restriction" in a living species.---"If you add glycerol, or restrict caloric intake, you obtain the same effect," said senior author Valter Longo. "It's as good as calorie restriction, yet cells can take it up and utilize it to generate energy or for the synthesis of cellular components."---Longo and colleagues Min Wei and Paola Fabrizio introduced a glycerol diet after discovering that genetically engineered long-lived yeast cells that survive up to 5-fold longer than normal have increased levels of the genes that produce glycerol. In fact, they convert virtually all the glucose and ethanol into glycerol. Notably, these cells have a reduced activity in the TOR1/SCH9 pathway, which is also believed to extend life span in organisms ranging from worms to mice.---When the researchers blocked the genes that produce glycerol, the cells lost most of their life span advantage. However, Longo and colleagues believe that the "glucose to glycerol" switch represents only a component of the protective systems required for the extended survival. The current study indicates that glycerol biosynthesis is an important process in the metabolic switch that allows this simple organism to activate its protective systems and live longer.----"This is a fundamental observation in a very simple system," Longo said, "that at least introduces the possibility that you don't have to be calorie-restricted to achieve some of the remarkable protective effects of the hypocaloric diet observed in many organisms, including humans. It may be sufficient to substitute the carbon source and possibly other macronutrients with nutrients that do not promote the "pro-aging" changes induced by sugars."---Funding for the study came from the American Federation for Aging Research and the National Institute on Aging (NIH).---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Public Library of Science, via EurekAlert!, a service of AAAS.---Journal Reference:--Wei M, Fabrizio P, Madia F, Hu J, Ge H, et al. Tor1/Sch9-Regulated Carbon Source Substitution Is as Effective as Calorie Restriction in Life Span Extension. PLoS Genetics, 2009; 5(5): e1000467 DOI: 10.1371/journal.pgen.1000467
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[U1]This also applies to Prescription Drugs---if you get on them then there is a use for them for a limited time and not an indefinite period---if it is prolonged use then there is a forced addiction being done through the Doctor who is using this to addict and prosper at the expense of the addict
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New Zealand’s Prime Minister: Climate Change bill a “load of rubbish” and “hoax”
Sleep Seems to Fuel Energy Surge in Rats' Brains
ScienceDaily (June 30, 2010) — UK scientists show for the first time that high doses of caffeine directly increase muscle power and endurance during relatively low-intensity activities.---New research shows increased muscle performance in sub-maximal activities, which in humans can range from everyday activities to running a marathon.--With no current regulations in place, the scientists from Coventry University believe their findings may have implications for the use of caffeine in sport to improve performance.---The scientists present their work at the Society for Experimental Biology Annual Meeting in Prague.---"A very high dosage of caffeine, most likely achieved via tablets, powder or a concentrated liquid, is feasible and might prove attractive to a number of athletes wishing to improve their athletic performance," explains lead researcher, Dr Rob James.----"A small increase in performance via caffeine could mean the difference between a gold medal in the Olympics and an also-ran," he added.---Caffeine is not currently listed by the World Anti-Doping Agency (WADA) as a banned substance at any concentration in blood or urine samples. Before 2004 WADA did set a specific level over which athletes could be banned, but this restriction was removed.---Muscle activity is divided into maximal, where the muscles are pushed to full capacity such as in sprinting or weight lifting, and sub-maximal, which covers all other activities.---A member of the team, Jason Tallis, tested the effect of caffeine on both the power output and endurance of soleus muscles (lower leg muscle) in mice, under both maximal and sub-maximal activities.---He found that a caffeine dosage of 70 µM enhanced power output by ~6% during both types of activity. This effect in humans is likely to be very similar, according to the researchers.---"70 μM caffeine concentration is the absolute maximum that can normally achieved in the blood plasma of a human, however concentrations of 20-50 μM are not unusual in people with high caffeine intakes,"---explains Dr James.---Resultant caffeine in blood plasma (70μM maximum) may act at receptors on skeletal muscle causing enhanced force production. Scientists already know that ingestion of caffeine can increase athletic --performance by stimulating the central nervous system.---Additionally, 70μM caffeine treatment increased endurance during sub-maximal activity, but significantly reduced endurance during maximal activity.
Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Society for Experimental Biology, via EurekAlert!, a service of AAAS
Recipe—take coffee and beet powder and combo this as a beverage
What you will do is dry up beets and turn into a powder by either juicing the beet and saving the left over and dehydrating this by either dehydrator –stove---or air dry or sun---Then take the dried stuff and pulverize this or powder this and then use ½ a teaspoon with your cup of coffee---Orrr you can take a caffeine pill and add it to your beet juice---beet powder or beet capsules you have made—this will also have other effect on the body---anti cancer properties---blood enhancing properties---antioxidant properties---so it has a multi faceted effect
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New Zealand’s Prime Minister: Climate Change bill a “load of rubbish” and “hoax”
Via Andrew Bolt [2] in email, some surprising revelations about New Zealand’s Prime minister and his previous opinion of the ETS. It appears he has done a complete about face from his very strong opinions of 2005.---The Prime Minister of New Zealand, John Key [3], (shown above) has just introduced the world’s first Emissions Trading Scheme (ETS) today for new Zealand. It is not going over well with voters [4]. ---This is the same man who, when in opposition, described anthropogenic climate change as a hoax on the 10th may, 2005.---See Hansard debates at:
EXCERPTS:
JOHN KEY (National—Helensville) : “I rise on behalf of the National Party to give the good news to the people of New Zealand—that is, the Climate Change Response Amendment Bill is a load of rubbish and the National Party will not be supporting it, for very, very good reasons indeed.”---“Yet here we are down in New Zealand, a very little country with about 0.2 percent of the world’s emissions, putting a self-imposed straitjacket on our businesses, and waving a huge flag that says: “Foreign investment, don’t come anywhere near us. Australia is over there—the West Island. Go over there to pour your dollars in.” To the Chinese we are saying: “Come in and buy as much coal as you like from our West Coast. We’ll sell it to you and you can burn it without a carbon charge—but, by the way, to those back here in Aotearoa New Zealand we will be slapping on a carbon charge and you won’t be able to operate.”[U1] “This is a complete and utter hoax, if I may say so. The impact of the Kyoto Protocol, even if one believes in global warming—and I am somewhat suspicious of it—is that we will see billions and billions of dollars poured into fixing something that we are not even sure is a problem. Even if it is a problem, it will be delayed for about 6 years. Then it will hit the world in 2096 instead of 2102, or something like that. It will not work.”
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Meanwhile, carbon trading in the USA flatlines [7].
URLs in this post:
[1] Watts Up With That?: http://wattsupwiththat.com/2010/07/01/new-zealands-prime-minister-climate-change-response-a-load-of-rubbish/
[2] Andrew Bolt: http://blogs.news.com.au/heraldsun/andrewbolt/
[3] John Key: http://www.johnkey.co.nz/pages/bio.html
[4] not going over well with voters: http://www.reuters.com/article/idUSSGE65S00S20100701
[5] Image: http://infowars-shop.stores.yahoo.net/post4rioffe.html
[6] http://www.parliament.nz/en-NZ/PB/Debates/Debates/3/2/8/47HansD_20050510_00001115-Climate-Change-Response-Amendment-Bill-First.htm: http://www.parliament.nz/en-NZ/PB/Debates/Debates/3/2/8/47HansD_20050510_00001115-Climate-Change-Response-Amendment-Bill-First.htm
[7] carbon trading in the USA flatlines: http://wattsupwiththat.com/2010/06/30/new-zealand-begins-emissions-trading-scheme-meanwhile-the-gorepachauri-chicago-climate-exchange-is-flatlining/
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ScienceDaily (Mar. 22, 2006) — Amid reports that a drug used to treat Parkinson's disease has caused some patients to become addicted to gambling and sex, University of Pittsburgh researchers have published a study that sheds light on what may have gone wrong. ---In the current issue of Proceedings of the National Academy of Sciences, Pitt professor of neuroscience, psychiatry, and psychology Anthony Grace and Pitt neuroscience research associate Daniel Lodge suggest a new mechanism for how the brain's reward system works. ---The main actor in the reward system is a chemical called dopamine. When you smell, touch, hear, see, or taste a pleasurable stimulus, the dopamine neurons in your brain start firing in bursts. So-called "burst firing" is how the brain signals reward and modulates goal-directed behavior. But just how the stimulus you perceive causes neurons to switch into or out of this mode has been a mystery. ---Using anesthetized rats, Lodge and Grace found that one area in the brain stem, known as the laterodorsal tegmental nucleus, is critical to normal dopamine function. ---"We've found, for the first time, the brain area that acts as the gate, telling neurons either to go into this communication mode or to stop communicating," says Grace. "All the other parts of the brain that talk to the dopamine neurons can only do it when this area puts them into the communication mode." ---As a result, disruption in that area may play a major role in dopamine-related brain function, both in normal behaviors and psychiatric disorders. --The brain area identified by the Pitt researchers is regulated by the "planning" part of the brain, the prefrontal cortex (PFC), thereby providing a powerful indirect means for the PFC to affect the activity of dopamine neurons. Such a link could explain how changes in the PFC, seen in disorders like schizophrenia and drug addiction, disrupt the signaling of dopamine neurons. ---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Pittsburgh, via EurekAlert!, a service of AAAS
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ScienceDaily (June 30, 2010) — Babies born to women who do not consume enough folic acid (sometimes referred to as folate or vitamin B9) are at high risk of developing neural tube defects (i.e., defects in the development of the spinal cord or brain). This is the reason underlying the recommendation that women who are pregnant take a folic acid supplement.---A team of researchers, led by Bermans Iskandar, at the University of Wisconsin, Madison, has now generated data in rodents suggesting that folic acid might also help promote healing in injured brain and spinal cord.---Specifically, the team was able to uncover a molecular pathway by which folate can promote nerve cell regeneration following injury in rodents.---In an accompanying commentary, Matthias Endres and Golo Kronenberg, at Charité -- Universitätsmedizin Berlin, Germany, discuss how these data, together with the safety and simplicity of folate supplementation, provide a rationale for testing whether folate supplementation is beneficial for patients with spinal cord and brain trauma.---The research appears in the Journal of Clinical Investigation.---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Journal of Clinical Investigation, via EurekAlert!, a service of AAAS.---Journal References:---bermans J. Iskandar, Elias Rizk, Brenton Meier, Nithya Hariharan, Teodoro Bottiglieri, Richard H. Finnell, David F. Jarrard, Ruma V. Banerjee, J.h. Pate Skene, Aaron Nelson, Nirav Patel, Carmen Gherasim, Kathleen Simon, Thomas D. Cook and Kirk J. Hogan. Folate regulation of axonal regeneration in the rodent central nervous system through DNA methylation. Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI40000----golo Kronenberg, and Matthias Endres. Neuronal injury: folate to the rescue? Journal of Clinical Investigation, 2010; DOI: 10.1172/JCI40764
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Sleep Seems to Fuel Energy Surge in Rats' Brains
Regions needed to function during waking hours got a boost during shuteye, study says ---Brain energy may replenish itself during sleep, a new study suggests. Experiments with rats revealed that during the initial stages of sleep there is a dramatic increase in cellular energy levels in brain regions that are active during waking hours. The findings suggest that this energy boost reinvigorates brain processes that are required for normal functioning while awake.---The study appears in the June 30 issue of the journal Neuroscience.---While it's known that a good night's sleep helps restore body and mind, it's been difficult to pinpoint the actual biological processes that occur during sleep, researchers at the Boston VA Healthcare System and Harvard Medical School said in a news release from the journal.---For this study, researchers measured levels of adenosine triphosphate (ATP) -- the energy currency of cells -- in rats. During non-REM sleep, there was an overall decrease in brain activity but an increase in ATP levels in four key brain regions normally active during wakefulness.---When the rats were awake, ATP levels were steady. When the rats were made to stay awake three to six hours past their normal sleep times, ATP didn't increase.---The findings suggest that a certain amount of sleep is necessary for an ATP surge, which may power restorative processes in the brain, the researchers said.---The research was supported in part by the Department of Veterans Affairs and the National Institute of Mental Health.--SOURCE: Society for Neuroscience, June 29, 2010, news release.
Here are some things to get the ATP up so even if your sleep is in disarray you can still elevate this to get brain activity up and running---as well as body functioning better
Lipoic Acid increases the production of ATP within Muscles.
Vitamin B3 is involved in the production of ATP.---start of with 100 mgs ( this will cause a slight flush---but has been used successfully in the healing or regulating of Bi Polar issues
Vitamin B5 is an essential cofactor for the production of ATP (due to its incorporation into ATP's precursor - Acetyl Coenzyme A).—Taking B5 in the morning at 500-1000mgs with tyrosine 500 mgs may actually increase mood and act as a normal antidepressant not to mention a better brain and body activity increase
Vitamin C facilitates the production of endogenous ATP. When combo’d with B5 it triggers B5 to increase a whole host of support for the system including ATP production
Creatine will do this as well---Use 3-5 grams of creatine with acetyl L carnitine 500-1000mgs in a glass of water---add baking soda and ascorbic acid ( 2 000mgs) stir and drink as soon as it fizzes---then head to bed in about 15 min or less—While sleeping this will be absorbed and will increase ATP production so for those of you who are lethargic or having an immune response to some health dysfunction this can assist in the recovery
Ginger increases the production of ATP by the Heart
Golden Root enhances the production of ATP via the process of oxidative phosphorylation.
Magnesium is required for the production of ATP (Magnesium is responsible for transferring the Phosphorus molecule to ATP).
ATP contains three Phosphorus groups
Inosine enhances the production of ATP in the body (including the Heart).---You can get this from Beets—making a good beet juice and adding creatine ( 3-5 grams )with it should see an elevated level of endurance
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New Source Discovered for Generation of Nerve Cells in Brain--- Things that increase GABA
The importance of dietary supplements in preventative healthcare has once more been highlighted to US health policy staffers, just weeks after the government announced more funds for the prevention of chronic diseases.
At a Congressional briefing held on Capitol Hill last week, members of Congress and nutrition experts stressed that as part of a healthy diet and lifestyle, supplements can help maintain the health of Americans and reduce healthcare costs. ---The briefing was one in a series or meetings organized by the Congressional Dietary Supplement Caucus. Made up of Members of Congress, the caucus was set up in 2006 in cooperation with two leading trade groups – Council for Responsible Nutrition (CRN) and Natural Products Association (NPA). ---“These meetings increase our visibility on the Hill,” said Steve Mister, president and CEO of CRN. “So much of what happens in Congress is based on relationships, so it’s important to have that continuous dialogue, which can help counter some of the misconceptions about supplements.” ---“For some of the Congressional staffers, all they know about dietary supplements is what they read in the papers. These caucus briefings expose them to the real dietary supplement industry, and they come to recognize CRN and NPA as credible sources of information on supplements,” he told NutraIngredients-USA.com.
Funds for disease prevention
Last month, the US Department of Health and Human Services (HHS) announced it had earmarked $250m for investment in the prevention of chronic diseases as part of the Prevention and Public Health Fund. ---According to HHS, chronic diseases such as these are responsible for 7 of 10 deaths each year among Americans, and account for 75 percent of the nation’s health spending. “Many Americans engage in behaviors such as tobacco use, poor diet, physical inactivity, and alcohol abuse, which harm their health,” it said. ---The $250m investment under this new fund is designed to tackle some of the underlying causes of chronic disease. It will be channelled into initiatives on a federal, state and community level to help prevent obesity and improve fitness. It will also be used to support the existing public health infrastructure, to develop research and tracking and to expand public health training initiatives.
Supplements: A bi-partisan issue
The Dietary Supplement Caucus is made up of both Republican and Democratic congressional members, which Mister says is important in demonstrating how issues relating to dietary supplements are bi-partisan. “Unlike so many other issues, this is an area where people can work together,” said Mister. --In last week’s meeting, co-chair of the DSC, Rep. Jared Polis (D-Colo.), described as a “champion” of the supplement industry, told attendees that “supplements used properly help prevent disease and promote good health as part of an overall healthy lifestyle”, adding that “scientific evidence strongly suggests that the use of daily dietary supplements would be an effective way to address nutritional gaps” in deficient populations. ---Another speaker was registered dietician and president of Nutrition Housecall David Grotto. He said a healthy diet and lifestyle, along with appropriate dietary supplements, can “really make a difference in helping to mitigate” health problems, such as heart disease. He added that people have “lost touch” with the purpose of food and that most people are not meeting the Dietary Guidelines. “We don’t always necessarily eat the best every day of the week, so it does make sense to include some responsible dietary supplements along with that,” he said. [U2]
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The Federal Trade Commission will not be granted extra authority to police healthy foods and supplements marketing – among other powers – after a provision that would have done just that was removed from a Bill designed to reform Wall Street practices. ---Industry was concerned the Bill would hand the FTC rights to quash marketing and bring it into conflict with rights established in the 1994 Dietary Supplements and Health Education Act (DSHEA), and lobbied hard against the provision. They stated such a provision was not only unnecessary but had no place in a Bill that was primarily about another topic – financial reform. --“This is a great victory, but the war isn’t over,” said John Gay, Natural Products Association executive director and chief executive officer. “Those forces on Capitol Hill that want to over-regulate us are still out there, planning their next move. We need to remain vigilant.” Detrimental ---Mike Greene, senior director of government relations at the Council for Responsible Nutrition (CRN), emphasized industry’s role in having the provision removed. ---“This demonstrates the importance of maintaining credibility on the Hill, something which is a key priority for CRN,” he said. “We believe we’ve done a very good job of educating legislators as to why this was a bad provision.” ----“This provision would have been detrimental for industry, but as importantly, detrimental for consumers as it would have given FTC free-reign to rewrite its advertising regulations at the expense of consumers being unable to get complete information about a host of consumers products, from dietary supplements to toaster ovens. We’re pleased it didn’t make it into the final bill.” ---Greene added: “If FTC still believes it needs more authority, then the proper way to go would be to have a Committee hearing through Energy and Commerce or through the FTC Reauthorization legislation.” ----Industry feared marketing statements on dietary supplements may have required two ‘gold standard’ clinical trials to back them.
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Members of the European Parliament have voted to put back clauses on nutrient profiling into the proposed food information regulation, after Environment Committee members voted to take them out – but it was a close call. ---Nutrient profiles define what products can make claims relating to nutritional content, based on their levels of fat, sugar or salt. The idea is that a product that is exceptionally high in one of these nutrients that should be consumed in moderation, it may not be labelled a ‘low in fat’, say, or ‘low in sugar’. Profiles would also be used in the new health claims regulation, as products exceeding levels of these nutrients would not be able to make positive claims. ---Rapporteur for the Parliament’s Envi committee deleted the requirement for nutrient profiles to be established in her amendments, on which Envi voted in March. ---In a vote following the first hearing at the parliamentary session in Strasbourg yesterday, however, MEPs voted to keep nutrient profiles in. ----A statement from the Parliament said: “By a single vote, MEPs rejected an Environment Committee recommendation to delete nutrient profiles from existing EU nutrition health claims legislation. Considered unscientific by its critics, the system is seen by others as essential to assess health claims.” --Heart health lobby ----The European Heart Network has send a letter to MEPs prior to the vote asking them to reject the removal of nutrient profiles. The network’s director Susanne Løgstrup wrote: ---“Without nutrient profiles, products that are high in fat, sugar or salt may be able to bear claims and this misleads people as to the true nature of the product. Considering the crushing burden of chronic diseases in Europe, it is vital that only products that are overall healthy should be allowed to bear claims. ---“Nutrient profiles play a vital role in guiding people towards the healthier option. The absence of nutrient profiles undermines the provision of proper information on product benefits to consumers.” ---She argues that nutrient profiling is well-recognised in the scientific literature, and many models exist on how to establish them. “They show that nutrient profiling models that are based on both positive and negative nutrients provide a realistic picture of the nutrition quality of a product.”
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ScienceDaily (Aug. 22, 2007) — The research group of Prof. Dr. Magdalena Götz at the Institute of Stem Cell Research of the GSF – National Research Centre for Environment and Health, and the Ludwig Maximilians University, Munich, has achieved an additional step for the potential replacement of damaged brain cells after injury or disease: functional nerve cells can be generated from astroglia, a type of supportive cells in the brain by means of special regulator proteins.---The majority of cells in the human brain are not nerve cells but star-shaped glia cells, the so called “astroglia”. “Glia means “glue”, explains Götz. “As befits their name, until now these cells have been regarded merely as a kind of “putty” keeping the nerve cells together.----A couple of years ago, the research group had been already able to prove that these glia cells function as stem cells during development. This means that they are able to differentiate into functional nerve cells. However, this ability gets lost in later phases of development, so that even after an injury to the adult brain glial cells are unable to generate any more nerve cells.---In order to be able to reverse this development, the team studied what molecular switches are essential for the creation of nerve cells from glial cells during development. These regulator proteins are introduced into glial cells from the postnatal brain, which indeed respond by switching on the expression of neuronal proteins.----In his current work, Dr. Benedikt Berninger, was now able to show that single regulator proteins are quite sufficient to generate new functional nerve cells from glia cells. The transition from glia-to-neuron could be followed live at a time-lapse microscope. It was shown that glia cells need some days for the reprogramming until they take the normal shape of a nerve cell. “These new nerve cells then have also the typical electrical properties of normal nerve cells”, emphasises Berninger. “We could show this by means of electrical recordings”.--- “Our results are very encouraging, because the generation of correctly functional nerve cells from postnatal glia cells is an important step on the way to be able to replace functional nerve cells also after injuries in the brain,” underlines Magdalena Götz.----Reference: Benedikt Berninger, Marcos R. Costa, Ursula Koch, Timm Schroeder, Bernd Sutor, Benedikt Grothe, and Magdalena Götz: “Functional Properties of Neurons Derived from In Vitro Reprogrammed Postnatal Astroglia” J. Neurosci. 2007 27: 8654-8664; doi:10.1523/JNEUROSCI.1615-07.2007---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by GSF - National Research Center for Environment and Health.
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ScienceDaily (Nov. 29, 2009) — The generation of new nerve cells in the brain is regulated by a peptide known as C3a, which directly affects the stem cells' maturation into nerve cells and is also important for the migration of new nerve cells through the brain tissue, reveals new research from the Sahlgrenska Academy published in the journal Stem Cells.---Although the research has been carried out using mice and cultured cells, it could lead to a new medicine for human beings, which could be given to patients who have had a stroke or other disorders that damage or destroy the nerve cells. "Our research findings show that it could be possible to use molecules that are similar to the peptide C3a to boost the formation of nerve cells and stimulate the replacement of nerve cells lost due to injury or illness," says senior lecturer Marcela Pekna who headed the research group at theSahlgrenska Academy.---The peptide C3a is generated through the activation of the complement system, a group of proteins in the blood that is essential for the body's immune defence. "Our research group was the first in the world to show that the complement system also plays an important role in the repair and regeneration of the brain," says Pekna. "This was a surprising discovery that opened up a whole new field of research."
New Nerve Cells---New nerve cells are formed in the brain throughout our lives. The brain's stem cells are formed in the hippocampus and the subventricular zone, an area next to the fluid-filled cavities (lateral ventricles). Stem cells from the subventricular zone mature into nerve cells in the olfactory bulb, but can also migrate out into the brain to replace nerve cells that have been damaged or destroyed. By finding out more about how new nerve cells are formed and what controls their migration, stem cell researchers hope to find new ways of treating stroke, Parkinson's disease and other disorders that result from the nerve cells failing to function as they should.---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Gothenburg.---Journal Reference:---Shinjyo et al. Complement-Derived Anaphylatoxin C3a Regulates In Vitro Differentiation and Migration of Neural Progenitor Cells. Stem Cells, 2009; 27 (11): 2824 DOI: 10.1002/stem.225
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ScienceDaily (Dec. 1, 2009) — The research group of Professor Magdalena Götz of Helmholtz Zentrum München and Ludwig-Maximilians-Universität (LMU) Munich has made a significant advance in understanding regeneration processes in the brain. The researchers discovered progenitor cells which can form new glutamatergic neurons following injury to the cerebral cortex. Particularly in Alzheimer's disease, nerve cell degeneration plays a crucial role. In the future, new therapeutic options may possibly be derived from steering the generation and/or migration mechanism. ---These findings have been published in the current issue of the journal Nature Neuroscience.---Until only a few years ago, neurogenesis -- the process of nerve cell development -- was considered to be impossible in the adult brain. The textbooks asserted that dead nerve cells could not be replaced. Then researchers discovered regions in the forebrain in humans in which new nerve cells can be generated throughout life. These so-called GABAergic cells use gamma-aminobutyric acid (GABA), a neurotransmitter of the central nervous system.----A research team of scientists led by Magdalena Götz, director of the Institute of Stem Cell Research at Helmholtz Zentrum München and chair of the Department of Physiological Genomics of LMU, has now taken a closer look at this brain region in the mouse model. Their findings: Even in the forebrain, there are other nerve cells that are regularly generated -- the so-called glutamatergic nerve cells, which use glutamate as neurotransmitter. The stem cell researchers could prove this by means of a specific transcription factor: Tbr2 is only present in progenitor cells of glutamatergic nerve cells.----The newly generated nerve cells in the adult organism are located in the olfactory bulb, the region of the brain involved in the sense of smell. Nerve cells that use glutamate as a neurotransmitter are also responsible for memory -- storing and retrieving information. In Alzheimer dementia, alterations in the signal transduction pathways of these special cells play a significant role.----Magdalena Götz explained the reason why this finding is so important: "Neural progenitor cells can generate these newly discovered glutamatergic nerve cells for the neighboring cerebral cortex -- for example after brain injury." The research group was able to demonstrate this on the mouse model: There the cells migrated into the damaged neighboring cerebrum tissue and generated mature neurons. Accordingly, progenitor cells could then replace degenerate nerve cells.---"Now it will be interesting to find out whether this process also takes place in humans, particularly in Alzheimer's patients," said Magdalena Götz, "and also whether the process can be kept under control to avoid massive cell death." One therapeutic approach would then be to attempt to stimulate the body's own replacement mechanism.---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Helmholtz Zentrum München - German Research Center for Environmental Health.--Journal Reference:---Brill et al. Adult generation of glutamatergic olfactory bulb interneurons. Nature Neuroscience, 2009; 12 (12): 1524 DOI: 10.1038/nn.2416
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Inositol is a necessary cofactor for many of the functions of GABA.---Vitamin B3 (Niacinamide form) enhances the function of GABA.---Vitamin B6 is an essential cofactor for the conversion of Glutamic Acid to GABA
GABA is a constituent of Reishi Mushrooms-----Saint John’s Wort inhibits the reuptake of GABA (which leads to increased GABA levels and increased GABA activity). This action occurs from the Hyperforin content of Saint John’s Wort. ----Valerian inhibits the breakdown of GABA
ØMake a Tea with Valerian and St johns ( equal parts ) before going to bed ---it may take some time ( 3 weeks or longer) but you will see a deeper level of sleep as well as a better Mood and less anxious and clearer thinking as well
[U1]Sounds like Canada as well—WE will levy UNLAWFUL TAXES on our own Citizens ---but foreign investors can come here and rape the country side with GMO or OIL DRILLING or Mineral Mining without any due responsibility to cleaning up or to Give people in Canada a Fair Profit from these exchanges---what is going on Globally is Criminal---with all the distraction of illegal immigrants—Gov’ts use this distraction to Chem trail us—GE our Foods---Pollute recklessly---And in the end we ( the citizens ) are subsidizing our own death---what they give us Freely ( again paid for through our Taxes) is free and clear access to the medical where they prescribe death and do very little in mitigating the illnesses that are occurring
[U2]This is such an oxymoron---the gov’t should be regulating the food industry to eliminate toxic waste that is being put In our foods—and poisons in the creams and Restricting GE and GMO contamination in the fields---Supplements do help in keeping you healthy and alive and viable longer but if the changes are not made at the foundation ---food and CLEAN FOODS without SOY—CANOLA—MICROWAVE—SUGAR LOADED—MSG –COLOURS –Not to mention additives then telling people they do not eat right is definitely accurate but then again who regulates the industry—they regulate themselves---and that is alarming
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The GM clause to food security
Music Thought To Enhance Intelligence, Mental Health And Immune System
Oxidative stress modulation by Rosmarinus officinalis in CCl4-induced liver cirrhosis
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The GM clause to food security
The US Global Food Security Act of 2009 (S. 384) sponsored by Richard Lugar
(Indiana, Republican), Robert Casey (Pennsylvania, Democrat) and seven other US
-Senators in February 2009 is [1, 2] “A bill to authorize appropriations for
fiscal years 2010 through 2014 to provide assistance to foreign countries to
promote food security, to stimulate rural economies, and to improve emergency
response to food crises, to amend the Foreign Assistance Act of 1961, and for
other purposes.”---However, the proposed amendment to the Foreign Assistance Act
(FAA) of 1961 has proven controversial. It would “include research on
biotechnological advances appropriate to local ecological conditions, including
genetically modified technology.”---The bill is supported by the US land grant
colleges as well as InterAction (American Council for Voluntary International
Action) and its 26 member organizations including WWF, Oxfam, Bread for the
World CARE, Save the Children, and ONE [3]. The bill was passed through the
Senate foreign Relations Committee on 31 March 2009, and the Senate is expected
to vote on it soon in 2010.
Widespread opposition to GM mandate
In April 2010, 140 civil society groups, scientists, and development experts
signed an open letter
to US Senators, urging them to “strip the GM mandate” from the Global Food
Security Act [4].
While the petitioners applaud the bill’s intention to reform aid programmes to
focus on longer-term agricultural development and restructure aid agencies to
better respond to crises, they object to the clause effectively earmarking one
agricultural technology –
genetic modification - for billions of dollars in federal funding.
US$7.7
billion goes with the bill, and no other farming methods or technologies are
mentioned. Not
surprisingly, Monsanto has lobbied the hardest to support the bill.
The US company is the world’s leader in the increasingly concentrated
agricultural biotech industry, which is already subject to an anti-trust inquiry
(see [5] US Farmers Oppose 'Big Ag' in Anti-Trust Hearing, SiS
46
http://www.i-sis.org.uk/US_farmers_oppose_big_ag.php).
Monsanto is likely to benefit most from the new research funding stream, and
to profit from its patented products (both GM seeds and pesticides).--The
petitioning groups represent the anti-hunger, family farms, farm-workers,
consumers and those practicing and supporting sustainable agriculture. The
letter delivered urges the Senate to reject the bill until it is made
technology-neutral, and calls for agricultural research funding to concentrate
on addressing local challenges faced by small-scale farmers, instead of
mandating a specific and narrow technological fix, particularly one with little
prospect of success
and increasingly rejected by countries around the world. “Independent science
tells us that genetically modified (GM) crops have neither increased yield nor
reduced hunger in the world,” said Marcia Ishii-Eiteman, Senior Scientist of
Pesticide Action Network. “The
most credible and comprehensive assessments of agriculture to date say
that if we want to end global poverty and hunger,
we’ll need to focus on increasing the biodiversity and ecological resilience of
small-scale farming systems.”--Mariam Mayet
of the African Center for Biosafety based in South Africa
pointed out that pressure to import GM crops is
wreaking havoc on local economies in Africa.“In
South Africa, we
are now dumping GM corn into other countries, disrupting local markets and
undermining the livelihoods of family farmers there.
As a result, Zimbabwe has
imposed a ban on GM corn imports, and Kenya, which has a bumper crop of GM-free
corn and doesn’t need any
imports, is now grappling with
a massive, illegal and unwanted shipment of 280 000 metric tons of GM corn from
South Africa. A handful of powerful agribusinesses’ obsession with GM is
pitting African countries against each other, with Monsanto and international
grain traders reaping the benefits and ordinary farmers losing out. The last
thing we need from the US is a bill legislating yet more money for GM crops.” “At
the end of the day, the GM mandate has more to do with breaking open markets
for American biotech
corporations than
fighting hunger,”
explained Annie Shattuck of the Institute for Food and Development Policy. “To
get at the root of the global hunger crisis, we need to tackle poverty,
something no technological silver bullet can ever do.”Ben Burkett, President of
National Family Farm Coalition and Mississippi family farmer, added,
“Corporate control over inputs
and the free trade agenda have destroyed the livelihoods of so many farmers at
home and abroad.
That’s why farmers
worldwide are calling for food sovereignty—the right to choose fair and
sustainable farming practices that protect our local food and livelihood
security. This is
what works best for our farms and communities.”
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GM-Spin Meltdown in China
Bt cotton in China is often cited as an example of a successful GM crop. In
fact, its widespread
use has merely replaced the cotton borer with a serious pest that not only
attacks cotton but also many other crops.
Prof. Peter Saunders
The ‘success’ of Bt cotton short lived
Genetically modified (GM) crops not only present serious dangers to health and
the environment (see [1] GM Food Angel or Devil, ISIS report for a succinct
recent summary and references), they have not delivered on their promises.
For all the investment and effort that has gone into developing and pushing them,
it is really only the biotech industry that has profited, especially now that GM
crops are leading to serious problems with herbicide resistant weeds and
secondary insect pests in the USA, the world’s leading GM producer
[2] (GM Crops Facing Meltdown in the USA, SiS 46).-A detailed study on cotton
growers in the US state of Georgia published in 2008 found
that no transgenic technology
system provided greater returns than a non-transgenic system in any year or
location [3, 4]
(Transgenic Cotton Offers No Advantage, SiS 38). The editor of Nature
Biotechnology summed it up [5]: “This journal champions biotech research, so we
are not downbeat on its prospects to, one day, generate products that will heal,
fuel and feed the world. That is, nevertheless, an outrageous act of faith
bordering on the religious.” To support their claim that GM is the way forward,
its supporters often cite the example of what they claim is the success of Bt
cotton in India and China.
Bt cotton is genetically modified to produce a toxin originating from the soil
bacterium Bacillus thuringiensis that kills the cotton bollworm Helicoverpa
armigera. We are
told that yields have greatly increased since Bt cotton was introduced and that
farmers’ profits have correspondingly gone up. Because farmers no longer have to
use pesticides against the bollworm, both their health and the environment have
improved [6].
If Bt cotton really is an example of what GM crops have to offer,
then it is a
warning rather than a promise,
because what actually happened is rather
different. Bt cotton
has been disastrous in India. It has accelerated farm suicides by increasing the
farmers' burden of debt. Crop failures and bad harvests, exorbitant cost of GM
seeds, secondary and new pests, Bt-resistant pests, new diseases, and worst of
all, soils so depleted of nutrients that they considerably reduce the
productivity of subsequent crops planted after Bt cotton is harvested [7,8]
(Farmer Suicides and Bt Cotton Nightmare Unfolding in India, Mealy Bug Plagues
Bt Cotton in India and Pakistan , SiS 45).
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ScienceDaily (June 22, 2006) — A recent volume of the Annals of the New York Academy of Sciences takes a closer look at how music evolved and how we respond to it. Contributors to the volume believe that animals such as birds, dolphins and whales make sounds analogous to music out of a desire to imitate each other. This ability to learn and imitate sounds is a trait necessary to acquire language and scientists feel that many of the sounds animals make may be precursors to human music.--Another study in the volume looks at whether music training can make individuals smarter. Scientists found more grey matter in the auditory cortex of the right hemisphere in musicians compared to nonmusicians. They feel these differences are probably not genetic, but instead due to use and practice.--Listening to classical music, particularly Mozart, has recently been thought to enhance performance on cognitive tests. Contributors to this volume take a closer look at this assertion and their findings indicate that listening to any music that is personally enjoyable has positive effects on cognition. In addition, the use of music to enhance memory is explored and research suggests that musical recitation enhances the coding of information by activating neural networks in a more united and thus more optimal fashion.--Other studies in this volume look at music's positive effects on health and immunity, how music is processed in the brain, the interplay between language and music, and the relationship between our emotions and music.--The Neurosciences and Music II is volume 1060 of the Annals of the New York Academy of Sciences . --Story Source:The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Blackwell Publishing Ltd., via EurekAlert!, a service of AAAS
RECIPE---learn to play any instrument from a harmonica to a guitar to any simple or elaborate instrument---and learn to read music as well
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Compounds in both garlic and onion may increase the bio-accessibility of iron and zinc from cereals seven-fold, according to new data from India.
Consuming garlic or onion with cereals increased the uptake of iron by about 70 percent, and zinc by to 160 percent, according to new results published in the Journal of Agricultural and Food Chemistry that could offer opportunities to tackle two of the globe’s major deficiency concerns. ---“Both garlic and onion were evidenced here to have a promoting influence on the bio-accessibility of iron and zinc from food grains,” state the researchers, led by Krishnapura Srinivasan from the Central Food Technological Research Institute in Mysore, India. ---“This novel information has the potential application in evolving a food-based strategy to improve the bioavailability of trace minerals and hence contributes to the human health benefit,” they added.
Global problems
Iron deficiency is reported to affect about a third of the global population, with two billion people anemic around the world. In addition, zinc deficiency affects 30 per cent of the world’s population. ---The bioavailability of both micronutrients is said to be particularly low from plant foods[U1]. --In attempt to enhance the uptake of these minerals from plant sources, the Mysore-based researchers used a model of the gastrointestinal tract to simulate passage through a human gut. Two cereals – rice and sorghum – and two pulses – chickpea and green gram – were used in their raw and cooked forms, and in the presence of two levels of garlic (0.25 and 0.5 g per 10 g of grain) and onion (1.5 and 3 g per 10 g of grain). ---Results showed that iron and zinc uptakes from both cooked and raw cereals were significantly increased in the presence of both garlic and onion, with increases up to 70 percent recorded. Improvements in the bioaccessibility of zinc were also observed for both spices, with increases in cereals ranging from 10.4 to 159.4 percent, and in pulses from 9.8 to 49.8 percent.
How?
Commenting on the potential mechanism behind the improvements, Srinivasan and co-workers point to the high sulfur content in garlic and onion: Sulfur-containing amino acids like cysteine have previously been shown to boost iron and zinc status in lab animals, they said. --“The information generated in this study on the promotive influence of natural sources of sulfur compounds on mineral bioaccessibility from food grains is novel and has a promising application in evolving a food-based strategy for alleviating deficiencies of these minerals in sections of the population,” concluded the researchers.
Into foods
Fortification of foods with iron poses several challenges, depending on the types of iron used. Using water-soluble iron sulfate or iron gluconate offer the advantages of providing high bioavailability, but the disadvantage of adversely affecting the color of the resultant product. On the other hand, water- insoluble elemental iron or ferric phosphate offer poor bioavailability. Source: Journal of Agricultural and Food Chemistry-Published online ahead of print, doi: 10.1021/jf100716t “Higher Bioaccessibility of Iron and Zinc from Food Grains in the Presence of Garlic and Onion”-Authors: S. Gautam, K. Platel, K. Srinivasan
Recipe
Take the minerals Zinc and Selenium ( iron if you have a deficiency then use beet and wine for this ) add MSM to this---what you will do is take approximately 5-10 grams of MSM and add to it 100-200 mgs of zinc and 1000mcgs-1mg of Selenium in this mix ---now if you are doing the beet and wine then chop up beet and add 1 cup of wine ( add more depending how big the beet is---) blend in a blender either the Zinc+selenium+MSM or MSM + BEET EXTRACT\
When done place in glass and use ½ tsp of the powder mix throughout the day to insure adequate protection and utilization of these mineral---this combo is extremely potent to protect reproductive organs of both men and women from cancers---they offer hormonal regulating and removal of the hormones
Incredibly poten to asssit several organs such as thyroid –Pancrease Heart
Brain –Liver---
You can as well use the Kyolic brands of Garlic
Preferably the formula 108 and 110
Mix these nutrients in a syrup using honey onion or garlic and these nutrients
Take a look at the new vid in regard to making your own syrup
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Oxidative stress modulation by Rosmarinus officinalis in CCl4-induced liver cirrhosis.
Phytother Res. 2010 Apr;24(4):595-601
Authors: Gutiérrez R, Alvarado JL, Presno M, Pérez-Veyna O, Serrano CJ, Yahuaca P
Rosmarinus officinalis (Lamiaceae) possesses antioxidant activity and hepatoprotective effects, and so may provide a possible therapeutic alternative for chronic liver disease. The effect produced by a methanolic extract of Rosmarinus officinalis on CCl(4)-induced liver cirrhosis in rats was investigated using both prevention and reversion models. Over the course of the development of cirrhosis, the increased enzymatic activities of gamma-glutamyl transpeptidase and alanine aminotransferase, and the rise in bilirubin levels caused by CCl(4) administration, were prevented by Rosmarinus officinalis co-administration. When the cirrhosis by oxidative stress was evaluated as an increase on liver lipoperoxidation, total lipid peroxides, nitric oxide in serum, and loss of erythrocyte plasma membrane stability, R. officinalis was shown to prevent such alterations. On cirrhotic animals treated with CCl(4), histological studies showed massive necrosis, periportal inflammation and fibrosis which were modified by R. officinalis. These benefits on experimental cirrhosis suggest a potential therapeutic use for R. officinalis as an alternative for liver cirrhosis.---PMID: 19827016 [PubMed - indexed for MEDLINE]
Recipe Make a Rosemary Tea and combo this with Milk thistle and Sage to assist in the restoration of the Liver---using light doses of the sprigs ( 3 or 4 ) 1 tablespoon of milk thistle ( go up or down as desired or as needed with the measurements ) and with Sage use again 1-3 sprigs—Bring to boil and let boil for 3-5 minutes and then allow to steep---drink several times a day
FMake a coffee and add rosemary to it---the studies done on coffee expres that coffee has a healing or preventing effect against cirrhosis up to 80 % at a dose of 7 cups a day----I would add cardamom to reduce the caffeine and would add rosemary and drink half the dose and go up from there if needed
Add again either 1-2 drops of the essential oil of rosemary---or add 1 tsp to a 2 cup amount ( boil the rosemary in a pot and allow to steep and then add the rosemary tea water in a cup and add coffee to it –NO SUGAR OR SYNTHETIC SWEETNER-OR CREAMS or SYNTHETIC OILS in the coffee or tea
[U1]This is Initially why you are taking vitamins in the First place to offset any deficient nutrient that should be in the foods which are no longer there or have been depleted out through either the harvesting or processing of the foods we eat
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Studies on antioxidant effects of the red grapes seed extract from Vitis vinifera
Antioxidant effects of a grape seed extract in a rat model of diabetes mellitus.
Antioxidant activities of curcumin and combinations of this curcuminoid with other phytochemicals
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NEW YORK (Reuters Health) - "Stealth fiber" increasingly added to processed foods, while not a problem for most, can cause gastrointestinal discomfort for some who may not know they're consuming too much of it, Minnesota researchers warn. The fiber is called "inulin."--"Normal fiber foods like wheat bran and legumes are self-limiting, it's hard to over eat them," Joanne Slavin, a registered dietitian in the department of food science and nutrition at the University of Minnesota at St. Paul, told Reuters Health.---Inulin, she explained, may be in chocolate bars, drinks, and snacks around the house, and "before you know it, you may eat more than you can tolerate and have gastrointestinal issues you wouldn't necessarily associate" with those foods.--Inulin is a carbohydrate fiber that occurs naturally in many foods like bananas, wheat, onions and garlic. Found in high concentrations in chicory root, is can be extracted for industrial use. Unlike more familiar carbohydrates, which are broken down in the small intestines and turned into fuel for the body, inulin passes through the small intestines to the colon where it stimulates the growth of "good bacteria" and is fermented by bacteria. In some people it can cause gas, bloating, flatulence, and diarrhea.---Because of its growing popularity as a food additive, Slavin and her colleagues wanted to assess how much inulin it takes to cause gastrointestinal problems.---They designed a study involving 26 healthy men and women aged 18 to 60. After a night of fasting, once a week for five weeks, participants were fed a breakfast of a bagel with cream cheese and orange juice. The orange juice was mixed with a placebo or with 5- or 10-gram doses of two commonly used inulin products -- native inulin and shorter-chain oligofructose.---After their "fiber challenge," participants were called several times over two days and asked about symptoms such as gas/bloating, nausea, flatulence, stomach cramping, diarrhea, constipation and GI rumbling.---Those that got any dose of inulin generally reported "mild symptoms"; the highest scores in every symptom except constipation were reported by those who got 10 grams of oligofructose. The findings are in line with previous research that found the short-chain "sweet" inulin causes faster fermentation in the gut leading to more gas and gastrointestinal symptoms.---Flatulence was the most common symptom reported by all subjects who got fiber although symptoms were "highly variable" among individuals and many subjects did not experience any, the investigators say. Slavin and colleagues conclude, based on their study, that most healthy people can tolerate up to 10 grams of native inulin and 5 grams of the "sweet" inulin a day.---Food manufacturers, faced with demands to reduce calories, fat, and sodium while increasing fiber and flavor, are increasingly turning to products like inulin. They have discovered they can chemically manipulate the chemical structure of inulin to mimic tastes and textures consumers want in food. "It's like a food manufacturer's nirvana," Slavin said.--Inulin can be found in high fiber breakfast bars, ice creams, and beverages among other processed foods. The label may list inulin, chicory root extract, oligosaccharide, or oligofructose. For example, the Fiber One Chewy Bar with 9 grams of dietary fiber lists chicory root extract as its top ingredient. -Slavin and her colleagues urge continued study of tolerance levels of food additives like inulin because their use is likely to continue to grow and "there is the potential for overuse." The research was funded by Cargill, Inc. a maker of inulin food additives, which provided the product used in the study.- SOURCE: http://link.reuters.com/tur56m Journal of the American Dietetic Association, June 2010
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Acta Physiol Hung. 2010 Jun;97(2):240-6--Authors: MureÅan A, Alb C, Suciu S, Clichici S, Filip A, Login C, Decea N, Mocan T
To estimate the effects of hydroethanolic red grapes seeds extract obtained from Vitis vinifera, Burgund Mare variety, RecaÅ , Romania (BMR) on oxidant-antioxidant ballance, as compared to ascorbic acid, during pregnancy in rats. Thirty Wistar female rats were assigned to three groups (n=10) which were administered by gavage: Group I, 3 x 100 mg/kg body weight saline, Group II - BMR 3 x 30 mg gallic acid equivalents/kg body weight; Group III - vitamin C 3 x 100 mg/kg body weight on days 1, 7 and 14 of pregnancy. On day 21 blood samples were collected. Malon dyaldehyde, lipid peroxides, protein carbonyls, nitric oxide (as oxidative stress parameters) and hydrogen donor ability and total thiol groups (as antioxidant parameters) serum concentrations were measured. Vitamin C significantly enhanced the antioxidant capacity of plasma (hydrogen donor ability, p=0.0001; thiol groups, p=0.0001), as well as nitric oxide levels (p=0.001). The extract increased the plasma antioxidant capacity (hydrogen donor ability, p=0.001; thiol groups p=0.001) and did not elevate the nitric oxide plasma levels in pregnant rats. In conclusion, in the chosen dose, the red grapes seed extract enhanced the plasma antioxidant capacity and did not influence the nitric oxide levels in pregnant rats.---PMID: 20511134 [PubMed - indexed for MEDLINE]
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Antioxidant effects of a grape seed extract in a rat model of diabetes mellitus.
Diab Vasc Dis Res. 2009 Jul;6(3):200-4--Authors: Chis IC, Ungureanu MI, Marton A, Simedrea R, Muresan A, Postescu ID, Decea N
In the present study we investigated the anti-hyperglycaemic and antioxidant effect of grape seed extract, a polyphenolic flavonoid, in normal and streptozotocin-induced diabetic Wistar rats. Adult male Wistar rats were divided into three groups: Group I: non-diabetic control; Group II: diabetic control; Group III: diabetic rats treated with grape seed extract, administered via an intragastric tube (0.6 ml/rat), at a dose of 100 mg/kg for 20 consecutive days after the induction of diabetes mellitus. Diabetes was induced by an i.p. injection with streptozotocin for groups II and III. TheTBARS, carbonylated proteins, were measured in the plasma and in the supernatant of liver homogenisates, and superoxide dismutase and catalase were measured in the haemolysates of RBCs and supernatant of liver homogenisates. The results showed that oral administration of grape seed extract (100 mg/kg/day) reduced the levels of lipid peroxides and carbonylated proteins and improved the antioxidant activity in plasma and hepatic tissue in rats treated with grape seed natural extract as compared with the diabetic control rats. These results suggested that the grape seed extract enhanced the antioxidant defence against reactive oxygen species produced under hyperglycaemic conditions, hence protecting the liver cells.---PMID: 20368212 [PubMed - indexed for MEDLINE]
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Mol Carcinog. 2010 Jul;49(7):641-52--Authors: Velmurugan B, Singh RP, Agarwal R, Agarwal C
Chemoprevention by dietary agents/supplements has emerged as a novel approach to control various malignancies, including colorectal cancer (CRC). This study assessed dietary grape seed extract (GSE) effectiveness in preventing azoxymethane (AOM)-induced aberrant crypt foci (ACF) formation and associated mechanisms in Fischer 344 rats. Six-week-old rats were injected with AOM, and fed control diet or the one supplemented with 0.25% or 0.5% (w/w) GSE in pre- and post-AOM or only post-AOM experimental protocols. At 16 wk of age, rats were sacrificed and colons were evaluated for ACF formation followed by cell proliferation, apoptosis, and molecular analyses by immunohistochemistry. GSE-feeding caused strong chemopreventive efficacy against AOM-induced ACF formation in terms of up to 60% (P < 0.001) reduction in number of ACF and 66% (P < 0.001) reduction in crypt multiplicity. Mechanistic studies showed that GSE-feeding inhibited AOM-induced cell proliferation but enhanced apoptosis in colon including ACF, together with a strong decrease in cyclin D1, COX-2, iNOS, and survivin levels. Additional studies showed that GSE-feeding also decreased AOM-caused increase in beta-catenin and NF-kappaB levels in colon tissues. Compared to control animals, GSE alone treatment did not show any considerable change in these biological and molecular events in colon, and was nontoxic. Together, these findings show the chemopreventive efficacy of GSE against the early steps of colon carcinogenesis in rats via likely targeting of beta-catenin and NF-kappaB signaling, and suggest its potential usefulness for the prevention of human CRC.--PMID: 20564341 [PubMed - indexed for MEDLINE]
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Antioxidant activities of curcumin and combinations of this curcuminoid with other phytochemicals.
Phytother Res. 2010 Apr;24(4):500-2
Authors: Aftab N, Vieira A
Biomedical investigations of curcumin (and curcuminoids) have provided evidence of a wide range of molecular and cellular activities, most related to redox reactions and signal transduction. The main goal of the present study was to compare antioxidant activities of curcumin with those of resveratrol, a polyphenol present in some dietary plants such as Vitis vinifera (L.) and Arachis hypogaea (L.) and many other, non-dietary plants. Combinations of the two were also examined for potential synergism in a heme-enhanced oxidation reaction. Curcumin exhibited antioxidant effects at all time points (1-5 min; 10 microM), e.g., 30.5 +/- 11.9% (SEM) oxidation relative to controls without phytochemicals (p < 0.01) at 3 min, a time chosen for comparisons. The same concentration of resveratrol exhibited about half of curcumin's activity. Curcumin and resveratrol together (5 microM each) resulted in a synergistic antioxidant effect: 15.5 +/- 1.7% greater than an average of individual activities. This synergy was significantly greater (p < 0.05; about 4-fold) than that of curcumin together with the flavonol quercetin. In conclusion, curcumin is a potent antioxidant in a reaction that may be relevant to in vivo toxicity. In relation to two other well-known antioxidants, curcumin shows significantly greater synergism with resveratrol than with quercetin.---PMID: 19927272 [PubMed - indexed for MEDLINE]
Recipe---take a good red wine you enjoy add 1-1/12 cup of wine---add ¼ cup of tumeric---blend at high speed for 10 minutes to heat the wine and tumeric---strain and bottle in glass and use 1 tablespoon 3 times a day or as needed
ORR—You can buy resveratrol powder and add equal parts to the tumeric powder and add Aloe Vera to this---you would use 1-cup of aloe vera juice an blend til fused ---if you want to maintain the solution so it does not separate add ¼ tsp of xanthium gum---use ½ ounce dose 1- 3 times a day or as needed
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---- Window Farming Click on link to take you to another page where there is another """recipe""--Window Farming
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Researchers have engineered aluminum-tolerant crops.
Much of the world's cropland contains aluminum that stunts crops. But a new study has found a way to make plants grow tall in spite of the metal's toxic effects. The discovery, by plant biologists at the University of California, Riverside, suggests that genetic engineering could boost yields from fields that today are not ideal for growing crops.---Aluminum is common in soils--it's a major component of clay--but only in acidic soils does the metal form an ion that can dissolve into liquids and that's toxic to plants. Acidic soils make up as much as half the world's croplands, however, and aluminum toxicity is the main factor holding back crop growth in nearly 20 percent of the world's arable soils, including large areas of the United States east of the Mississippi River and northwestern Europe.---"The problem is, we have all these crop plants--wheat and corn and barley and so on--that didn't evolve or get developed on aluminum-toxic soils," study leader and professor of biochemistry Paul Larsen says. "They don't have natural resistance or tolerance to aluminum." Plant breeders are working on developing strains that can cope better with toxic aluminum, but they have only been able to make incremental improvements, Larsen says.---[U1]In a study in Current Biology, Larsen and his colleague Megan Rounds have uncovered a simple mutation to a single gene that makes plants thrive in spite of levels of aluminum that would normally be toxic.[U2] Larsen and Rounds found the gene, called AtATR, by combing through mutants of Arabidopsis, a member of the mustard family that's commonly used in plant-genetics studies. The gene is related to a family of proteins known to help with finding and responding to DNA damage in nearly all multicellular organisms.---Toxic aluminum ions are known to damage DNA, and the new study suggests that plants respond by shutting down growth of cells in the tips of their roots when they accumulate too much DNA damage. Plants may have evolved this response to help them, over generations, cope with aluminum's toxic effects, Larsen speculates. But in the short run, it means that the plants are less healthy and are stunted and more vulnerable to stressors such as droughts.---But the newly identified mutation inactivates the AtATR protein, so cells don't respond to DNA damage by shutting down cell division, thereby bypassing that checkpoint, Larsen says. "The plant is effectively blind to what's happening in the cell." So the mutant plants can maintain high levels of growth in the presence of toxic levels of aluminum, even if they sustain some DNA damage. ---It is not yet clear how much DNA damage the plants sustain, Larsen says. But the strategy could work to promote short-term growth even if it would sacrifice the plants' DNA. To avoid DNA damage accumulating over generations of growing on aluminum-rich soils, farmers could obtain seeds from mutant plants grown on aluminum-free soil.[U3] This would mirror how farmers in industrialized countries use hybrid seeds from agribusinesses rather than saving their own seeds for planting further generations of crops.---"The work provides the first compelling evidence for a mechanism that explains the toxic effect of [aluminum] on root growth," says plant biologist Manny Delhaize of the Commonwealth Scientific and Industrial Research Organisation Plant Industry Center, in Canberra, Australia. "There have been numerous theories about how aluminum arrests root growth, and this work provides convincing evidence regarding the molecular process involved." Delhaize says that another method of keeping the growth rates high, while limiting any DNA damage, might be to engineer plants so that their root tips express molecules that would inactivate AtATR.---However, such a targeted approach may not be necessary, Larsen argues. Even after growing the mutant plants on aluminum-containing soils for several generations, there are "no obvious deleterious effects on growth, viability, [or] seed production," he says
[U1]It is a Possibility---an opinion from me---That maybe these plants have not immunity to them because they would carry enough of the metal to be transferred to whatever was being fed and would wind up with aluminum contamination not to mention the re absorption of the metal back into the ground
[U2]How did this change ??? the genetics in the plant was altered but not the environment---so how does this make it safe---it just makes it not die as a result of the poison environment---the plant is still loaded with these elements-Back to being pseudo science
[U3]MORE GMO SEED to be sold and entrench the farmers into a unfair trade with the corporations
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ScienceDaily (July 16, 2010) — Research is giving scientists new insight into why a restricted diet can lead to a longer lifespan and reduced incidence of age-related diseases for a wide variety of animals. Scientists have known for some time that a restricted diet can extend the lifespan of certain animals but this work shows how it affects ageing mechanisms -- and significantly has also shown that the effects occur even if the restricted diet is adopted later in life.---The work could help scientists to better understand, and ultimately, prevent a range of age-related diseases in humans.---The research is being presented at the conference of the British Society for Research on Ageing (BSRA) in Newcastle. It was conducted by scientists at the BBSRC Centre for Integrated Systems Biology of Ageing and Nutrition (CISBAN) at Newcastle University.---Working with the theory that cell senescence -- the point at which a cell can no longer replicate -- is a major cause of ageing the researchers set out to investigate what effect a restricted diet had on this process. By looking at mice fed a restricted diet the team found that they had a reduced accumulation of senescent cells in their livers and intestines. Both organs are known to accumulate large numbers of these cells as animals age.--Alongside this the CISBAN scientists also found that the telomeres of the chromosomes of the mice on restricted diets were better maintained despite their ageing. Telomeres are the protective 'ends' of chromosomes that prevent errors, and therefore diseases, occurring as DNA replicates throughout an organisms lifetime but they are known to become 'eroded' over time.---The adult mice were fed a restricted diet for a short period of time demonstrating that it may not be necessary to follow a very low calorie diet for a lifetime to gain the benefits the scientists found.---Chunfang Wang, the lead researcher on this project at CISBAN, said: "Many people will have heard of the theory that eating a very low calorie diet can help to extend lifespan and there is a lot of evidence that this is true. However, we need a better understanding of what is actually happening in an organism on a restricted diet. Our research, which looked at parts of the body that easily show biological signs of ageing, suggests that a restricted diet can help to reduce the amount of cell senescence occurring and can reduce damage to protective telomeres. In turn this prevents the accumulation of damaging tissue oxidation which would normally lead to age-related disease."---Professor Thomas von Zglinicki, who oversaw the research, said: "It's particularly exciting that our experiments found this effect on age-related senescent cells and loss of telomeres, even when food restriction was applied to animals in later life. We don't yet know if food restriction delays ageing in humans, and maybe we wouldn't want it. But at least we now know that interventions can work if started later. This proof of principle encourages us at CISBAN in our search for interventions that might in the foreseeable future be used to combat frailty in old patients."---CISBAN is one of the six BBSRC Centres for Integrative Systems Biology. The centres represent a more than £40M investment by the Biotechnology and Biological Sciences Research Council (BBSRC) to support the development of systems biology in the UK. The centres are also supported by the Engineering and Physical Sciences Research Council.---Systems biology uses the study of a whole, interconnected system -- a cell, an organism or even an ecosystem -- with computer modelling to better make the outputs of biology more useful to scientists, policymakers and industry.---Prof Douglas Kell, BBSRC Chief Executive and keynote speaker at the BSRA Conference, said: "As lifespan continues to extend in the developed world we face the challenge of increasing our 'healthspan', that is the years of our lives when we can expect to be healthy and free from serious or chronic illness. By using a systems biology approach to investigate the fundamental mechanisms that underpin the ageing process the CISBAN scientists are helping to find ways to keep more people living healthy, independent lives for longer."---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Biotechnology and Biological Sciences Research Council (BBSRC), via AlphaGalileo
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Study found that dogs on a diet lived on average 1.8 years longer than those with a greater calorie intake. ---ScienceDaily (Apr. 20, 2007) — Changes caused to bugs in the gut by restricting calorie intake may partly explain why dietary restriction can extend lifespan, according to new analysis from a life-long project looking at the effects of dietary restriction on Labrador Retriever dogs.---Bugs in the gut are known as gut microbes and they live symbiotically in human and animal bodies, playing an important role in metabolism. Abnormalities in some types of gut microbes have recently been linked to diseases such as diabetes and obesity[U1].---Today's research, published in the Journal of Proteome Research, was based on a study in which 24 dogs were paired, with one dog in each pair given 25% less food than the other. Those with a restricted intake of calories lived, on average, about 1.8 years longer than those with a greater intake and they had fewer problems with diseases such as diabetes and osteoarthritis, plus an older median age for onset of late-life diseases.[U2]---The researchers, from Imperial College London, Nestlé Research Center (NRC) and Nestlé-Purina, found long-term differences in the metabolism of the dietary-restricted and non-dietary-restricted dogs. Metabolic profile plays a key role in determining animals' response to illness and their susceptibility to disease.---The scientists believe that differences in the makeup of gut microbes between the two sets of dogs could partly explain their metabolic differences. The dogs that were not on a restricted diet had increased levels of potentially unhealthy aliphatic amines in their urine. These reflect reduced levels of a nutrient that is essential for metabolising fat, known as choline, indicating the presence of a certain makeup of gut microbe in the dogs. This makeup of gut microbes has been associated in recent studies with the development of insulin resistance and obesity.---Professor Jeremy Nicholson from Imperial College London said: "This fascinating study was primarily focused on trying to find optimised nutritional regimes to keep pet animals such as dogs healthy and as long-lived as possible. However these types of life-long studies can help us understand human diseases and ageing as well, and that is the added bonus of being able to do long-term non-invasive metabolic monitoring."---The researchers suggest that part of the healthier metabolic profiles of dogs on a restricted diet is related to their changed gut microbial activity, which in turn contributes to their generally improved health and longer lifespan. However, they also found that the overall effects of ageing on restricted and non-restricted animals exerted a greater effect on the metabolic profile than dietary restriction. This in itself is interesting as the lifelong metabolic trajectories of large animals had never been studied in this detail before and such information might be of relevance to ageing humans and their diseases. The team believes that one important outcome of this work will be the ability to improve the design of products' nutritional properties that mimic the health benefits of dietary restriction in pet dogs.---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Imperial College London.
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ScienceDaily (Sep. 19, 2006) — A new study directed by Mount Sinai School of Medicine extends and strengthens the research that experimental dietary regimens might halt or even reverse symptoms of Alzheimer's Disease (AD). The study entitled "Calorie Restriction Attenuates Alzheimer's Disease Type Brain Amyloidosis in Squirrel Monkeys" which has been accepted for publication and will be published in the November 2006 issue of the Journal of Alzheimer's Disease, demonstrates the potential beneficial role of calorie restriction in AD type brain neuropathology in non-human primates. Restricting caloric intake may prevent AD by triggering activity in the brain associated with longevity. ---"The present study strengthens the possibility that CR may exert beneficial effects on delaying the onset of AD- amyloid brain neuropathology in humans, similar to that observed in squirrel monkey and rodent models of AD," reported Mount Sinai researcher Dr. Pasinetti and his colleagues, who published their study, showing how restricting caloric intake based on a low-carbohydrate diet may prevent AD in an experimental mouse model, in the July 2006 issue of the Journal of Biological Chemistry. ---"This new breakthrough brings great anticipation for further human study of caloric restriction, for AD investigators and for those physicians who treat millions of people suffering with this disease" says Giulio Maria Pasinetti, M.D., Ph.D., Professor of Psychiatry and Neuroscience, Director of the Neuroinflammation Research Center at Mount Sinai School of Medicine and lead author of the study. "The findings offer a glimmer of hope that there may someday be a way to prevent and stop this devastating disease in its tracks." --AD is a rapidly growing public health concern with potentially devastating effects. An estimated 4.5 million Americans have AD. Presently, there are no known cures or effective preventive strategies. While genetic factors are responsible in early-onset cases, they appear to play less of a role in late-onset-sporadic AD cases, the most common form of AD. --In this new study, Dr. Pasinetti at Mount Sinai School of Medicine, in collaboration with Dr. Donald Ingram at the Laboratory of Experimental Gerontology, National Institute on Aging, NIH, maintained the Squirrel Monkeys on calorie restrictive or normal diets throughout their entire lifespan until they died of natural causes. The researchers found that ~30% calorie restriction resulted in reduced AD type amyloid neuropathology in the temporal cortex relative to control fed monkeys. The decreased AD type neuropathology correlated with increased longevity of related protein SIRT1, located in the same brain region that influences a variety of functions including aging related diseases. ---Collectively, the study suggests that the investigation of calorie restriction in non-human primates may be a valuable approach towards understanding the role of calorie restriction in human AD pathology. The present study strengthens the possibility that calorie restriction may exert beneficial effects in delaying the onset of AD. The findings also elucidate the important relationship between the expression of longevity genes like SIRT1 in calorie restriction dietary regimens and mechanisms associated with the prevention of AD.---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by The Mount Sinai Hospital / Mount Sinai School of Medicine, via EurekAlert!, a service of AAAS.
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ScienceDaily (Dec. 6, 2009) — Getting the correct balance of proteins in our diet may be more important for healthy ageing than reducing calories, new research funded by the Wellcome Trust and Research into Ageing suggests.--The research may help explain why 'dietary restriction' (also known as calorie restriction) -- reducing food intake whilst maintaining sufficient quantities of vitamins, minerals and other important nutrients -- appears to have health benefits. In many organisms, such as the fruit fly (drosophila), mice, rats and the Rhesus monkey, these benefits include living longer. Evidence suggests that dietary restriction can have health benefits for humans, too, though it is unclear whether it can increase longevity.--Dietary restriction can have a potentially negative side effect, however: diminished fertility.[U3] For example, the female fruit fly reproduces less frequently on a low calorie diet and its litter size is reduced, though its reproductive span lasts longer. This is believed to be an evolutionary trait: in times of famine, essential nutrients are diverted away from reproduction and towards survival.---To understand whether the health benefits of dietary restriction stem from a reduction in specific nutrients or in calorie intake in general, researchers at the Institute of Healthy Ageing, UCL (University College London), measured the effects of manipulating the diet of female fruit flies. The results of the study are published December 3 in the journal Nature.---The fruit flies were fed a diet of yeast, sugar and water, but with differing amounts of key nutrients, such as vitamins, lipids and amino acids. The researchers found that varying the amount of amino acids in the mixture affected lifespan and fertility; varying the amount of the other nutrients had little or no effect.---In fact, when the researchers studied the effect further, they found that levels of a particular amino acid known as methionine were crucial to maximising lifespan without decreasing fertility. Adding methionine to a low calorie diet boosted fertility without reducing lifespan; likewise, reducing methionine content in a high calorie diet prolonged lifespan. Previous studies have also shown that reducing the intake of methionine in rodents can help extend lifespan.--"By carefully manipulating the balance of amino acids in the diet, we have been able to maximise both lifespan and fertility," explains Dr Matthew Piper, one of the study authors. "This indicates that it is possible to extend lifespan without wholesale dietary restriction and without the unfortunate consequence of lowering reproductive capacity."---Amino acids are the building blocks of life as they form the basis of proteins. Methionine is one of the most important amino acids at it is essential to the formation of all proteins. Whilst proteins are formed naturally in the body, we also consume proteins from many different food types, including meat and dairy products, and pulses. The relative abundance of methionine differs depending on the food type in question; it occurs in naturally high levels in foods such as sesame seeds, Brazil nuts, wheat germ, fish and meats.--"In the past, we have tended to think that the amount of protein is what is important to our diet," says Dr Piper. "We've shown here that in flies -- and this is likely to be the case for other organisms -- the balance of amino acids in the diet can affect health later in life. If this is the case for humans, then the type of protein will be more important.---"It's not as simple as saying 'eat less nuts' or 'eat more nuts' to live longer -- it's about getting the protein balance right, a factor that might be particularly important for high protein diets, such as the Atkins diet or body builders' protein supplements."--Because the effects of dietary restriction on lifespan appears to be evolutionarily conserved -- occurring in organisms from yeast to monkeys -- scientists believe that the mechanisms may also be conserved. This opens up the possibility of using these organisms as models to study how dietary restriction works.--Although the human genome has around four times the number of genes as the fruit fly genome, there is a close relationship between many of these genes. Since it is easy to create mutants and carry out experiments on fruit flies, the functions of many fly genes have been established and newly discovered human genes can often be matched against their fly counterparts. Therefore, even though the fruit fly does not on the surface resemble humans, many findings about its basic biology can be interpreted for human biology. ---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Wellcome Trust.--Journal References:--Grandison et al. Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila. Nature, December 3, 2009; DOI: 10.1038/nature08619----Grandison et al. Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila. Nature, December 3, 2009; DOI: 10.1038/nature08619
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Methionine---Methionine lowers circulating levels of Acetaldehyde following Alcohol (ethanol) ingestion. -Minerals---Methionine lowers elevated serum Copper levels.----Methionine binds (chelates) with and facilitates the excretion of many Toxic Minerals (toxic heavy metals) research including:-Aluminium -Arsenic -Cadmium -Lead -Mercury ----Neurotransmitters----Methionine helps to detoxify excessive Histamine and helps to lower elevated Histamine levels. ---- Pharmaceutical Drugs----Methionine is an effective antidote for Paracetamol poisoning----Methionine lowers circulating levels of Acetaldehyde following Alcohol (ethanol) ingestion---- It and cysteine are the only sulfur containing amino acids that are coded for by DNA (Homocysteine is an amino acid and contains sulfur, but is a product of S-adenosylmethionine 1 carbon metabolism and is not coded for by DNA). Methionine is a methyl donor as S-adenosyl methionine (SAM). It is incorporated into the N-terminal position of all proteins in eukaryotes and archaea, though it may be removed by post-translational modification (bacteria incorporate N-formyl methionine instead). Methionine can also occur at other positions in the protein. It plays a role in cysteine, carnitine and taurine synthesis by the transsulfuration pathway, lecithin production, the synthesis of phosphatidylcholine and other phospholipids. Improper conversion of methionine can lead to atherosclerosis. Methionine is a chelating agent.
Recipe—Combining Vitamin C with MSM is one way to utilize these 2 supplements ---MSM converts to Methionine---Consuming Foods rich in this amino acid as well will increase the impact-- Cheese – Cottage-Yogurt—Eggs-Chicken Eggs-- Brazil Nuts—Seafood—Sardines-Seeds- Pumpkin Seeds-Sesame Seeds- cereals (esp. couscous, millet and oatmeal),—Garlic---Capsicum (Red)---Onion-- Meat, yeast, Fish, algae, plankton, seal blubber-- Methionine (used as an adjunct to Cimetidine) accelerates the healing of Duodenal Ulcers. ---Methionine helps to prevent Gallstones. Methionine is useful for the prevention and treatment of (chronic) Pancreatitis (due to its Antioxidant properties that protect the Pancreas from the excessive generation of Free Radicals that are speculated to cause Pancreatitis).
Eyes/Vision---Methionine deficiency can cause Cataracts and Methionine supplementation helps to prevent the development of Cataracts.
Hair--Methionine (ingested orally) improves Hair Condition
****Suspect increased risk of collagen or skeletal
disorders if:--Low methionine, lysine ---then • Supplement with appropriate amino acids
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Special Report
Harassment By Health Canada On a health food store!!
Progressive Pharmacy Draws Attention
Marigold Compounding and Natural Pharmacy in Courtenay, BC is the first of its kind. It is one of the most progressive pharmacies in North America as far as the scope and the mode of its operation. It is the true integration of pharmacy, homeopathy, Chinese medicine, Ayurvedic medicine and other modalities at a professional level. --It has been recently caught in the controversy that is affecting the delivery of natural health care and natural products in Canada.
On June 14, four inspectors from Health Canada, accompanied by two RCMP officers, and inspectors from the College of Pharmacists of BC raided the pharmacy and seized products without NPN's (Natural Product Number) and ordered the closure of the store.---The total value of the products taken away by Health Canada was $146,290.85 (valued at cost)
How is Marigold different? ---Marigold is no ordinary pharmacy. First of all, the philosophy is based on Vis Curatio Intentio (to heal as nature intended). They do not carry regular drugstore items such as Tylenol, Nyquil, not even Band-aids. Instead, you will find a wide selection of the best quality vitamins and supplements, including professional lines such as Thorne, Seroyal, Metagenics, AOR, and Waiora. They carry functional foods, medicinal mushrooms, Ayurvedic medicine, Traditional Chinese Medicine, homeopathy, tissue salts and chemical free dermatological preparations. They also have their own line of products which are prepared in the compounding pharmacy.
What is the Natural Health Products Directorate (NHPD)? -
The NHPR (Natural Health Products Regulations) came into full effect in January 2010. It is federal legislation through which Health Canada would legislate the sale of natural health products as it does “drugs” through the Food and Drug Act and the Food and Drugs Regulation. With the classification as drugs, the intent is to have all natural products develop a body of evidence based on science. The fact that natural ingredients can not be patented poses a dilemma for manufacturers. Natural ingredients can be isolated and purified and even chemically altered, but does this change the properties? Are they still natural? ---For the quarterly reporting periods (2008/2009 and the first three quarters of 2009/2010) which represents 37.9% of the product licensing applications received since the start of the NHPR in 2004, a total of 19,402 applications have been processed of which 11,195 were licensed, 2,493 were withdrawn and 5,714 were refused. (Source: Clash of the Regulatory Bodies by Andrew Waldie, Integrated health Practitioner, Special Report, Vol 10-2) This represents just a small fraction of natural products on the market. These are products already currently on the shelves, and does not count products in development. Already, many suppliers have stopped shipping to Canada and many small companies who cannot afford to comply are waiting in anticipation of what will happen.
Health Canada has far-reaching powers and in protecting the public interest can enter any private or business property and enforce the Act. Since 2004, there has been a growing backlog of applications and the CHFA (Canadian Health Food Association) has described the backlog as alarming. Bill C-36 will further enhance the ability of Health Canada to enforce their powers.---In January 2010, NAPRA, the National Association of Pharmacy Regulatory Authorities, of which the College of Pharmacists of BC is a member, issued a position statement advising pharmacies to stop selling any products that do not have a DIN ( Drug Identification Number), an NPN ( Natural Product Number) or a DIN-HM (Homeopathic Medicine DIN). This has been adopted by some provincial College of Pharmacists and is now being implemented through the removal of products at the retail level.
Where does Marigold fit in?
Marigold does not fit in neatly into any category. Although we are a full service pharmacy with prescription services, we are very different from a traditional drugstore. Our expertise is in natural medicine, but we also understand the language and complexity of pharmaceutical drugs. Since we are not a health food store, Health Canada sees us as falling under the auspices of the College of Pharmacists. --Marigold Compounding and Natural Pharmacy creates its own line of chemical- free products. In our formulations, we consciously and carefully select natural ingredients and avoid toxic chemicals. As much as possible, we try to stay close to the natural state of the medicine. We avoid using parabens, petroleum distillates, artificial colours, triethanolamine, magnesium stearate, butylated hydroxyanisole, butylated hydroxytoluene, PABA, sodium lauryl sulfate, artificial flavours and clay fillers. We formulate our capsules using alfalfa as the filler, rather than lactose or magnesium stearate.---Authorities from Health Canada have advised us in the past that as a compounding pharmacy, we have the ability to prepare products without an NPN registration as long as it fulfills the following criteria:
1. It is prepared in a proper laboratory with good manufacturing processes.
2. It is delivered directly to the end-user, the patient.
3. There exists a professional relationship between a health practitioner and the patient.
Our ability to deliver professional advice is unparalleled in the industry. We have the following ten accredited practitioners on our staff:
Janette Cormier, AA, RH, R.Ac. Registered Herbalist, Registered Acupuncturist
Michel Duhaime, R.Ac,, DTCM Registered Acupuncturist, Transformation Acupuncture, EFT
Raje Harwood Registered Reflexologist, Auricular Therapy
Dr. Erika Kneeland, B.Sc., ND Naturopathic Physician with a specialty in obstetrics, pediatrics and women’s health
Dr. Lise Maltais, FCAH, ND Naturopathic Physician, Registered Homeopathic Physician, Bowen Practitioner
Charlese Nan, RMT Registered Massage Therapist, Injury Specialist
Kira Neumann, RNCP Registered Holistic Nutritionist, Nutrition Consultant
Sharon Niscak, M.Sc., RH Registered Herbalist
Carol Smith, BA Reiki Master
Rudy Sanchez, B.Sc. Pharm. Consulting Pharmacist, Formulator
Raid by Health Canada and the College of Pharmacists:
On June 14, 2010, the store was inspected by four inspectors from Health Canada, two inspectors from the College of Pharmacists, accompanied by two RCMP officers. Products that did not contain NPN’s were removed from the shelves and taken away. ---The store was closed and has been closed since, as we comply with the requirements set out by the College and Health Canada. ---Here are some of the products that were removed from the shelves:
All Natural Sunscreens containing zinc oxide in various concentrations
Buttspackle containing calendula, peru balsam and zinc oxide
Arthrotopik Cream for inflammation, containing devil’s claw, calendula and arnica
Jocamu Ointment containing arnica and Rhus tox
Wild Oregano Oil, pure oil
Arnica Ointment 10%
Shatavari Ayurvedic Powder
Oil of Lavender pure essential oil
Grapefruit Seed Extract, pure
Colloidal Silver
Goldenseal Powder in Manuka 16+ Medicinal Honey
Health Canada has seized inventory which does not bear NPN’s. Part of this inventory are products that we make based on our own formulas. Part of this inventory is from suppliers who have not complied with NPN regulations. The store is closed by the College of Pharmacists of BC pending compliance with regulations.
These are the steps that are being done at this time:
1. Institution of individualized professional practitioner consultations prior to sale of products without NPN. This will require that we record patient name, date of purchase and practitioner information, This will allow us to sell these products and continue preparing them if needed.
2. Installation of a service counter to remove public access to Marigold Products.
3. Initiation of the procedure to register a site license for Marigold and allow us eventually to file for NPN’s for our products.
4. Meeting the compliance issues set out by the College of Pharmacists of BC
regarding labeling, compounding registers, etc.
We are using this opportunity to input our inventory into a POS system and make these improvements to allow us to continue serving your health needs.
Marigold is a very unique and progressive pharmacy that happens to be right here in Courtenay. We appreciate your support during this period and ask you to participate as much as you can in the protection of natural health not just for this store, but for all natural health retailers and practitioners. ---1. For more information about Health Canada regulations regarding the requirement of NPN’s, please go to the website for NHPPA (Natural Health Products Protection Association) and watch some of the videos of Shawn Buckley, constitutional lawyer and advocate for protection of natural health products. nhppa.org
2. Visit the site of CHFA (Canadian Health Food Association) and click on regulations to get information of the NHPD. chfa.ca
3. If you want to write a letter of support for Marigold, (especially if you have had a chance to use our services and have a story you want to share about outcomes), please send emails to:
marigoldgrassroots@gmail.com
4. All media enquiries are directed to :
250 338 9623 or marigoldgrassroots@gmail.com
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[U1]The concept her eis that something would be disrupting the gut flora---with child obesity it would be something that they would be definiting eating such as a genetically modifief grown food or even soy—chemicals and artificial food additives and plastics would also contribute to the diminishing of the flora as well as alcohol from starches that may not be digestible or be broken down
[U2]Remember one year in dog years is 7 so that would equate to almost 14 years!!!
[U3]Not sure I would call this a bad thing for some of us getting Older
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1-Chinese medicinal herb Radix Astragali suppresses cardiac contractile dysfunction and inflammation in a rat model of autoimmune myocarditis.
Toxicol Lett. 2008 Nov 10;182(1-3):29-35--Authors: Zhao P, Su G, Xiao X, Hao E, Zhu X, Ren J
Radix Astragali, a Chinese medicinal herb, consists of polysaccharides and flavonoids as its main active ingredients. It has been widely used for treatment of cardiovascular diseases such as heart failure, angina pectoris, myocardial infarction and stroke in Asian countries. This study was designed to evaluate the effect of Radix Astragali on myocardial dysfunction, cardiac remodeling and morphological alteration in an experimental model of autoimmune myocarditis, a clinical condition often resulting in dilated cardiomyopathy. Experimental autoimmune myocarditis was established with a subcutaneous injection of porcine cardiac myosin into rear footpad in Lewis rats. Radix Astragali treatment was delivered via an intravenous injection (0.2 ml/100g body weight, daily) for 3 weeks. Results from transthoracic echocardiography indicated that experimental autoimmune myocarditis led to impaired myocardial contractile function which was reconciled by Radix Astragali. The experimental autoimmune myocarditis triggered profound inflammation and fibrosis in myocardium as assessed by hematoxylin and eosin (H and E) and Masson's trichrome staining. Interestingly, Radix Astragali significantly attenuated autoimmune myocarditis-induced myocardial inflammation and fibrosis. Similarly, Radix Astragali treatment alleviated autoimmune myocarditis-triggered overt lymphocyte proliferation. Furthermore, Radix Astragali significantly attenuated elevated levels of the Th1 cytokines (IFN-gamma and IL-2), and increased the Th2 cytokines (IL-4 and IL-10) in autoimmune myocarditis. Collectively, our data revealed that Radix Astragali effectively protected against cardiac functional and morphological aberrations in experimental autoimmune myocarditis.----PMID: 18782607 [PubMed - indexed for MEDLINE]
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2-Novel herbal flavonoids promote apoptosis but differentially induce cell cycle arrest in human colon cancer cell.
Invest New Drugs. 2009 Jan 13;--Authors: Auyeung KK, Ko JK
Formononetin is a novel herbal isoflavonoid isolated from Astragalus membranaceus, a medicinal plant that possesses antitumorigenic property. We attempted to compare the anticarcinogenic mechanism of formononetin with that of the known proapoptotic flavonoid isoliquiritigenin (ISL) in human cancer cells. We first evaluated the effects of formononetin and ISL on HCT 116 colon cancer cell viability. Immunofluorescence staining was then performed to observe the morphological changes of cancer cells undergoing apoptosis, which had been substantiated using Annexin V-FITC/propidium iodide staining. Western immunoblotting and flow cytometry were also employed to study parameters associated with apoptosis and cell proliferation. Our data show that formononetin and ISL both inhibited the growth of colon cancer cells and promoted apoptosis. These processes were accompanied by caspase activation and downregulation of the antiapoptotic proteins Bcl-2 and Bcl-x(L). Besides, the novel proapoptotic protein NSAID-activated gene (NAG-1) and its upstream regulator were overexpressed in drug-treated cells. Nevertheless, only ISL was found to induce a G2 arrest. These findings exemplify that both formononetin and ISL could cause growth inhibition and facilitate apoptosis in colon cancer cells, while only ISL is capable of inducing phase-specific cell cycle arrest. This suggests that the anticarcinogenic activities of different herbal flavonoids may involve both common and differential mechanisms of action, which could be developed as potential anticancer drugs.PMID: 19139819 [PubMed - as supplied by publisher
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3-Astragalus polysaccharides inhibited diabetic cardiomyopathy in hamsters depending on suppression of heart chymase activation.
J Diabetes Complications. 2010 May-Jun;24(3):199-208--Authors: Chen W, Li YM, Yu MH
Diabetic cardiomyopathy is associated with high morbidity and mortality of heart failure. Overactivation of the local chymase-Ang II system plays a dominant role in diabetic cardiomyopathy. Astragalus polysaccharide (APS) is used in traditional Chinese medicine to boost immunity. To study the effect of APS on local system of chymase-Ang II in diabetic cardiomyopathy, we investigated APS/normal saline (NS)-administrated streptozotocin-induced diabetic hamsters. After APS/NS administration at a dose of 1 g/kg per day for 10 weeks, hemodynamic parameters, levels of insulin (INS), C-peptide (C-P), glycosylated serum protein (GSP), lipoproteins, myocardial enzymes, and Ang II (plasma and myocardial) were tested; myocardial collagen (type I and III), myocardial ultrastructure, and activities of matrix metalloproteinase (MMPs) were measured; activities and expression of cardiac chymase and ACE were detected by using quantitative real-time RT-PCR and RIA; protein expression of cardiac phosphoric extracellular signal-regulated kinase 1/2 (p-ERK1/2) was measured by Western blot. AP-administrated diabetic hamsters had lower levels of GSP, lipoproteins, myocardial enzymes, myocardial Ang II, expression of collagen I and I/ III, activities of pro-MMP-2 and MMP-2, activities and expression of chymase, and expression of p-ERK1/2 than NS-administrated diabetic hamsters and could better protect the myocardial ultrastructure. There was no difference in hemodynamic parameters between two groups. These results indicate that APS could inhibit diabetic cardiomyopathy in hamsters depending on the suppression of the local cardiac chymase-Ang II system.---PMID: 19230716 [PubMed - indexed for MEDLINE]
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– An Update
Denver Office Chicago Office Washington D.C. Office
P.O. Box 3469 444 North Michigan Avenue 1301 Pennsylvania Avenue, N.W.
Englewood, CO 80155 Chicago, Illinois 60611 Suite #300
(303) 694-0305 (312) 467-5520 Washington, DC 20004
(202) 347-0228 11-424 1995.0
Conjugated linoleic acid (CLA), a natural derivative of the fatty acid linoleic acid, has received increasing attention in recent years. Starting with anticarcinogenic effects, the potential benefits of this unique fatty acid have extended to antiatherogenic properties, anti-diabetic properties, enhanced immune response and positive effects on energy partitioning and growth.--These effects have been documented in numerous reviews (1-4) as well as in extensive scientific literature that has grown exponentially since the late 1980’s (5). As a naturally occurring compound in foods from--ruminant animal sources, CLA’s anticarcinogenic properties are unique. Of the vast number of naturally occurring substances, demonstrated to have anti-carcinogenic activity, all but a very few are of plant origin (1).
Chemistry/Structure
CLA is a collective term used to describe a mixture of positional and geometric isomers/forms of linoleic acid. Linoleic acid is an 18-carbon unsaturated fatty acid with two double bonds in positions 9 and 12, both
in the “cis” (on same side) configuration. Thus, the “chemical name” of linoleic acid is cis-9, cis-12-octadecadienoic acid. In contrast, the two double bonds in CLA are primarily in positions 9 and 11, and 10 and 12 along the carbon chain with the designation of a conjugated-diene. In addition to these “positional” changes of the double bonds, there can also be geometric changes (cis(c) or trans(t) [on opposite sides] configuration). Thus, at least eight different CLA isomers of linoleic--acid have been identified. Of these isomers, the c9, t11 form is believed to be the most common natural form of CLA, with biological activity. However, in recent years, biological activity has been proposed for--other forms, especially the t10, c12 isomer. Although not widely accepted, the name “rumenic acid” has been proposed as a “common name” for the major CLA isomer found in natural products (6). For a comparison of these CLA isomer “forms” with linoleic acid. Additional potentially active isomers are also being identified and studied (2,7). Figure 1. Chemical Structures of Linoleic Acid and Two Isomers of Conjugated Linoleic Acid (CLA). * Linoleic acid (c-9, c-12) Conjugated linoleic acid Conjugated linoleic acid octadecadienoic acid c-9, t-11 isomer t-10, c-12 isomer [U1]* Adapted from: Steinhart, C. Conjugated Linoleic Acid The Good News about Animal Fat. J.Chem.Educ. 73:A302; 1996. 2 Table 1. Representative/Relative Concentrations of CLA in Uncooked Foods [adapted from Chin et al. (12)].
Total CLA c9, tll-isomer
Food (mg/g fat) (%)
Meat
Fresh ground beef 4.3 85
Beef round 2.9 79
Beef frank 3.3 83
Beef smoked sausage 3.8 84
Veal 2.7 84
Lamb 5.6 92
Pork 0.6 82
Poultry
Chicken 0.9 84
Fresh ground turkey 2.5 76
Seafood
Salmon 0.3 n.d.*
Lake trout 0.5 n.d.
Shrimp 0.6 n.d.
Dairy Products
Homogenized milk 5.5 92
Butter 4.7 88
Sour cream 4.6 90
Plain yogurt 4.8 84
Ice cream 3.6 86
Sharp cheddar cheese 3.6 93
Mozzarella cheese 4.9 95
Colby cheese 6.1 92
Cottage cheese 4.5 83
Reduced fat swiss 6.7 90
Am. Processed cheese 5.0 93
Cheez whizTM 5.0 92
Vegetable Oils
Safflower 0.7 44
Sunflower 0.4 38
Canola 0.5 44
Corn 0.2 39
* n.d. => not detectable
History/Identification/Sources
CLA is a naturally occurring fatty acid found in food products from ruminants (cattle and sheep). Although identified much earlier, increased interest in CLA occurred when it was isolated and identified by Pariza
and coworkers as an anticarcinogenic substance from grilled ground beef (8-10). It was also found to be present in a variety of dairy products (11).--The total CLA content in foods may vary widely. Representative and relative concentrations of CLA in a variety of foods are summarized in Table 1. CLA concentrations are highest in foods from ruminants (including beef, lamb and dairy products). Seafoods, pork, most poultry products and vegetable oils are not notable sources of CLA (12). CLA has been found in triglycerides, lipoproteins and cell membrane phospholipids in various tissues of rodents, rabbits and humans (2). As a normal isomerization product of linoleic acid metabolism by rumen bacteria, CLA is synthesized from free linoleic acid through biohydrogenation pathways and enzymatic isomerization. Early studies suggested that CLA content could be increased in foods that are heat processed (dairy pasteurization, pan frying of meats, etc.) (11). However, later studies (13) suggest that CLA is not increased by cooking, but rather with water loss, CLA remains constant on a per gram of fat basis. Additionally, CLA is stable and not destroyed by cooking or storage. Foods from ruminant sources (beef and dairy) generally have CLA levels in the range of 3-7 mg/g fat; although, recent studies have shown it may be possible to increase these “naturally” occurring levels (4,14-16). Multisite Anticarcinogen – Cell and Animal Studies Following the initial identification of CLA as a modulator of mutagenensis and carcinogenesis, research interest accelerated. Additional studies confirmed this anticarcinogen effect in a variety of tissues, especially skin and forestomach. Continuing work with a wide variety of cell cultures and cancer cell lines (including malignant melanoma, colorectal cancer, breast/mammary cancer, lung adenocarcinoma, prostate cancer, leukemia, ovarian and liver cancers) have demonstrated inhibition by CLA (3,17-20). In contrast, linoleic acid did not inhibit the growth of any cell line and in some cases stimulated tumor growth and metastasis (18,21). Perhaps the most significant early anticarcinogenic effects of CLA were described by Ip and co-workers (22,23) where CLA prevented mammary cancer in rodents given CLA in the diet, prior to administration of a carcinogen. This contrasted with earlier studies that used acute dosing by direct contact, gavage, or via cell culture additions. These dietary studies found a dose-dependent protection at levels of 1% CLA and below, but no further beneficial effect was evident at levels above 1%. In studies with dietary CLA at 0.05, 0.1, 0.25 and 0.5%, as little as 0.1% CLA was sufficient to cause a significant reduction in mammary tumors. This confirmed CLA as a powerful anticarcinogen, which could be administered safely via the diet to achieve cancer protection, in an animal model. To put in perspective, the effect of CLA (an animal fat) in cancer prevention is specific and is more powerful than for any other fatty acid in modulating tumor development (1). For instance, unlike linoleic acid (a 3 close relative of CLA) which sometimes stimulates carcinogenesis (21), CLA is inhibitory. Also, the n-3 fatty acids of fish oil, which generally are responsible for tumor suppression, require in excess of 10% in the diet to elicit the same tumor suppression responses. In contrast, CLA at levels as low as 0.1% in the diet produce a significant reduction in mammary tumor yield in animal studies. Further work by Ip and co-workers has shown that the timing of CLA feeding can be critical. For instance, when CLA is given during the time the mammary tissue is actively developing, you see a lasting protective effect. If CLA is given after carcinogen administration, a continual supply of CLA is needed for a preventive effect. CLA appears to have a major impact on the mammary gland, making the tissue less susceptible to tumor formation (4,23,24). Work continues to determine the exact mechanism by which CLA may effect carcinogen metabolism, activation or detoxification (2,3,25). Studies with mice given CLA, prior to administration of the heterocyclic amine IQ, have shown varying reductions in IQ-DNA adducts in the liver, lung, large and small intestine, kidneys and colon (26,27). CLA at levels equivalent to 0.5% of the diet, exerted inhibitory effects on the process of colon carcinogenesis (27). Other Beneficial Effects of CLA Antiatherogenic and
Hypocholesterolemic
Based on the possibility that CLA would exhibit antioxidant activity, both in vivo and in vitro (22,28), studies were initiated to examine the effect of CLA on experimental atherogenesis in rabbits (29). When CLA, was
added at 0.5% to an atherogenic diet, for 12 weeks, the aortas of the CLA fed rabbits exhibited less atherosclerosis. Also, LDL (low-density lipoprotein) cholesterol and triglycerides (TG) were lower in the CLA fed group (29). This observation was later supported by studies in hamsters
where CLA feeding resulted in lower plasma total and LDL cholesterol and TG levels (30). The CLA fed animals also had less aortic streak formation.
Fat Partitioning and Metabolism
One of the most interesting effects of CLA appears to be its influence on body fat levels and the proportion of lean to fat, especially in young growing animals. CLA induces a relative decrease in body fat levels and an increase in lean muscle. This observation has been noted in several studies with mice, rats, chicks and pigs (4,31-33). In a study with growing pigs, the results were quite dramatic. Backfat thickness was reduced up to 27% in CLA fed pigs and there was a 6.8% increase in percent lean (33). Such results have generated considerable interest as to whether humans will experience similar fat reductions and increases in proportion of muscle mass if CLA is consumed in the diet. Studies in humans are currently underway (4). Effects on Immune Response and Bone Formation The effects of CLA on fat partitioning may be at least partially the result of modulation of the immune system. Ordinarily, stimulation of the immune system produces cytokines (proteins released by a cell, upon contact with an antigen, acts as a mediator) which can cause breakdown of muscle cells. CLA can modulate (decrease) the production of cytokines and thus prevent muscle degradation. Experiments in chicks, rats, and mice show that CLA increases feed efficiency and counteracts immune-induced cachexia or malnutrition--(4,31,34). Through this effect on cytokines, CLA may also have positive effects on bone health (4,35,36). Diets rich in fats containing CLA, compared to soybean oil, caused a greater rate of bone formation (4).
Anti-diabetic Effects
CLA has been found to help normalize or reduce blood glucose levels and possibly prevent diabetes (37). Using a laboratory animal model for diabetes, CLA was found to prevent the onset of diabetes. CLA appears to
work as well as a new class of diabetes-fighting drugs (thiazolidinediones) and may provide the added advantage of weight reduction, as drug treatments often result in weight gain. These initial findings with diabetic
rats are very encouraging and are the basis for continuing studies in human diabetics.
Other Human Studies – Epidemiology/ BREAST MILK IN WOMEN
Epidemiological studies support the hypothesis that there is some factor in whole milk that exerts a protective effect against breast cancer and coronary heart disease (4,38,39). Lower incidences of these diseases were
related to greater consumption of whole milk but not to intakes of low fat milk. The presence of CLA in milkfat may be a protective factor. In a recent report the incidence of breast cancer was significantly lower in women with higher breast tissue levels of CLA (40). It is clear that the CLA content of blood serum and breast milk can be modified by diet (41-43). In earlier studies in Australia, it had been found that breast milk from women of the Hare Krishna religious sect contained twice as much CLA as milk from Australian mothers on conventional diets (11.2 vs. 5.8 mg/g) (44). This 4 was attributed to the large amount of butter and ghee -(a clarified butter) consumed by the Hare Krishna. Park and coworkers (43) have also confirmed that CLA levels in human milk can be enhanced by increasing the CLA content of the maternal diet. Effective Intake/Dose Levels For any compound that produces the dramatic effects noted for CLA, an immediate question concerns the minimally effective dose level. Does it vary for different health and disease conditions, tissue sites and response levels? Is a “chronic” dose level required, or can an “acute” dose be effective and if so, when should it be consumed? Are food sources adequate or are supplemental sources required? If only some of the isomers of CLA are biologically effective, which ones are they? If so, dose levels of CLA should be “corrected” for the active isomer. Whether from food sources or supplements, any comparisons of effects should be sure to equate levels of the active isomer. These are just some of the many questions about CLA which require further research. Usual Dietary Intakes Current measures of usual or actual dietary intakes of CLA are very limited, most being only estimates. A listing of published reports based on estimates and data analysis is presented in Table 2. (10,45-49).--A variety of factors can influence estimates of CLA intake. Food composition and frequency of intake of particular foods affect dietary intake of any food component. For CLA, there may be the added variable of level of the biologically active form/isomer of CLA consumed. Also, men usually consume more meat than women do; dairy foods generally provide a higher percentage of dietary CLA than beef; and individuals may be beef or dairy users or non-users. In addition, intake estimates may be based on assumptions of dietary proportions, such as in the German studies of meat/meat products (40/60) and pork/beef (80/20) (47). In another study (48), available data on CLA content of foods has been applied to consumption data from the USDA CSFII 94-96 (Continuing Survey of Food Intake of Individuals). Based on intake data from this large dataset it is estimated that approximately 36% of total CLA intake is from beef and approximately 52% from dairy products. Dietary Beef as a Source Can a reasonable diet, containing beef, provide beneficial levels of CLA, considering that the minimal effective dose response is still unknown? At present, the answer would be “probably”, but more studies are needed to determine minimally effective levels of CLA. Animal studies have shown benefits at dietary levels as---low as 0.1-0.5%. Also, the potential for CLA enhanced, (but still “natural”), dietary sources of beef and dairy products is just now being explored (4). It has been shown that a number of dietary components for cattle can increase CLA levels in milk and beef. These include: plants consumed in pasture, forage in feeds, and unsaturated plant oils (with sunflower oil resulting in the most CLA). CLA concentrations in milk have been increased up to four fold by various dietary manipulations (4,14). Increases in the CLA content of beef tissue--is currently being explored, with preliminary indications that elevations in CLA content are possible via feeding practices (16). Table 2. Estimates of CLA Intake in Humans. Reference Population Studied Males Females All mg/day 10 Not specified — — “several hundred mg/day” 45 Australian (not specified) — 500-1500 46 German men 310
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Daily supplements of CLA (conjugated linoleic acids) may improve the airway hyper-reactivity in asthmatics, suggests a new study.
A daily dose of 4.5 grams of CLA produced significant reduction in airway hyper-responsiveness as well as favorable effects on body weight and adipokine levels – cytokines produced in fat tissue – according to findings published in this month’s journal Clinical & Experimental Allergy. ---CLA (conjugated linoleic acid) is a fatty acid naturally present in ruminant meat and dairy products. Due to changes in the Western diet, average intake of CLA has fallen[U2]; if the fat is removed from a dairy product to make a low fat version that will be acceptable to consumers, CLA is removed along with it. ---The researchers used Cognis’ Tonalin branded CLA, and the study was funded by Cognis. The CLA oil used is a mixture of isomers: cis-9, trans-11 (36.4 percent) and trans-10, cis-12 (37.0 percent). ---A significant body of science supports the potential of the ingredient to enhance lean body mass and aid in body sculpting. The new study, by scientists from the University of British Columbia in Vancouver, is the first to report that the ingredient may also have benefits for overweight asthmatics. ---. ---Commenting on the potential mechanism, the researchers note two possibilities: “Whether the improvement in AHR was due to direct effects on airway inflammation (likely cis-9, trans-11 mediated) or perhaps related to altered body composition and adipocytokine levels (likely trans-10, cis-12 mediated) in our overweight population is not clear,” they stated. ---Indeed, talking to NutraIngredients-USA at the IFT Annual Meeting and Expo in Chicago, David Cai, PhD, science and regulatory manager, North America and Asia for Cognis concurred that it was too early to make conclusions.
Study details
The researchers recruited 28 overweight mild asthmatics aged between 19 and 40 to participate in their prospective, randomized, double-blind, placebo-controlled study. Subjects were randomly assigned to receive either 4.5 grams per day of CLA or placebo for 12 weeks. --At the end of the study the researchers noted significant improvements in airway hyper-responsiveness (AHR) and this was accompanied by a significant improvement in their ability to tolerate strenuous exercise. ---In addition, subjects in the CLA group experienced significant improvements in the BMI, with an average reduction of 0.5 kg/m2, compared to a 0.8 kg/m2 increase in the placebo group.
Potential asthma alternative
The authors stressed however that care should be taken in extending the results to other sections of the population. “However, we believe our demonstrated efficacy is such that additional studies in these groups are warranted,” they said. ---“A huge number of asthma patients seek complementary therapies, and a wide array of products are marketed as ‘asthma treatments’, frequently with no evidence. CLA is safe, clinically effective and may be considered for overweight mild asthmatics seeking natural remedies as part of their asthma management plan,” wrote the researchers. “We encourage further studies to elucidate the role of CLA in a broader asthma population,” they concluded.
Source:
Clinical & Experimental Allergy
July 2010, Volume 40, Pages 1071-1078
“Conjugated linoleic acid improves airway hyper-reactivity in overweight mild
asthmatics”--Authors: R. MacRedmond, G. Singhera[1], S. Attridge, M. Bahzad,
C. Fava, Y. Lai, T. S. Hallstrand, D. R. Dorscheid
Recipe—Make your own CLA---all you need is butter---take it and put ½ pd ( 225 grams) in a frying pan or pot ---at low heat warm up this butter til the cream separates Spoon out the cream and you have butter oil which has now had an elevated level of CLA Add 1 drop of the essential oil of Rosemary or Sage or both and this will preserve this
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Low dose supplementation of creatine could help combat fatigue, according to the results of a new study.
Published in the journal Nutrition, the study set out to test whether low dose creatine supplements could improve muscle function. ---Creatine, an amino acid-like compound, was first identified in 1832 for its presence in muscle. It has been the subject of about 70 randomized, controlled trials over the last 12 years or so, with the majority investigating creatine’s performance-enhancing benefits. --However, according to the authors of the current study, there was a gap in the literature regarding the effects of low-dose creatine ingestion on high-intensity exercise performance and body composition when dosing was based on body size and administered over a period of time that would allow sufficient muscle uptake.
Tests
The trial involved twenty health men and women, who were randomized to receive creatine supplements or placebo. Participants were given 0.03 g of creatine (provided by NutraSense Company, Shawnee Mission, KS, USA) or placebo per kilogram of body weight per day for 6 weeks (range 1.7–2.9 g/d). Before supplementation participants were tested twice for anthropometric/body composition, muscle strength, and muscle fatigue, and they also provided blood samples to test plasma creatine concentration. They were then tested again after supplementation.
Results
At the end of the
six week period, researchers found that the supplementation did not result in
any significant differences in body mass, fat-free mass, fat mass, body fat
---percentage, total body water, or maximal strength[U3].
--However,
plasma creatine increased significantly in the creatine group.
In addition, this group was found to be more resistant to fatigue in some of the
tests. ---“Our data indicate that the ingestion of
approximately
2.3g of creatine per day for six weeks can increase body creatine retention and
enhance fatigue resistance during repeated sets of high-intensity contractions
with no increase in body mass,”
wrote the researchers.
“An additional unique finding of the present study is the absence of
weight gain or increases in total body water[U4].
These may be viewed as beneficial effects in athletic populations for whom
weight gain is undesirable. Future research should examine the effects of
different doses of creatine supplementation with body composition and muscle
function outcomes assessed at multiple time points in an effort to determine the
minimal effective dose,”
they concluded. ---Source: Low-dose creatine supplementation enhances fatigue
resistance in the absence of weight gain--Nutrition (2010),
--doi:10.1016/j.nut.2010.04.001
Authors : Rawson ES, et al.
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Fibromyalgia patients have significantly lower levels of Creatine than healthy people (and supplemental Creatine Monohydrate may help to restore endogenous Creatine levels to normal in Fibromyalgia patients) - studies to determine whether supplemental Creatine Monohydrate could alleviate Fibromyalgia have not yet been performed.
Creatine concentrates in the Muscles (and supplemental forms of Creatine concentrate in the Muscles):
Creatine improves the condition of Muscle Fibers.
95% of the body’s Creatine reserves are stored in Skeletal Muscles.
Muscular Dystrophy patients often excrete excessive amounts of Creatine (a condition known as Creatinuria) in their Urine - this indicates that supplemental Creatine may alleviate Muscular Dystrophy.
Rheumatoid Arthritis patients have significantly lower levels of Creatine than healthy people (and supplemental Creatine Monohydrate may help to restore endogenous Creatine levels to normal in Rheumatoid Arthritis patients) - studies to determine whether supplemental Creatine Monohydrate could alleviate Rheumatoid Arthritis have not yet been performed. research
Nervous System---Some of the body’s Creatine pool is stored in the Brain
Creatine may reduce
homocysteine levels
Homocysteine has been recognized as an important independent risk factor of
heart disease, more so than cholesterol levels according to some studies.
Creatine biosynthesis has been postulated as a major effector of homocysteine
concentrations,2 and oral creatine supplements may reduce levels of homocysteine.
Many studies have found that methyl donors (such as trimethylglycine (TMG)
reduce levels of homocysteine, which also reduces the risk of heart disease.
Conversely, pathways that demand large amounts of methyl groups may hinder the
body’s ability to reduce homocysteine levels. The methylation of
guanidinoacetate to form creatine consumes more methyl groups than all other
methylation reactions combined in the human body. Researchers have postulated
that increasing or decreasing methyl demands on the body may increase or
decrease homocysteine levels. In one study researchers fed rats either
guanidinoacetate- or creatine-supplemented diets for two weeks.3 According to
the researchers “plasma homocysteine was significantly increased (~50%) in rats
maintained on guanidinoacetate-supplemented diets, whereas rats maintained on
creatine-supplemented diets exhibited a significantly lower (~25%) plasma
homocysteine level.” These results suggest that homocysteine metabolism is
sensitive to methylation demand imposed by physiological substrates such as
creatine.
Creatine and chronic fatigue/fibromyalgia
Because of creatine’s apparent abilities to improve the symptoms of other
pathologies involving a lack of high energy compounds (e.g., congestive heart
failure, etc.) as well as the aforementioned afflictions outlined in the
introduction to this article, it has been suggested that creatine may help with
chronic fatigue syndrome and fibromyalgia (some researchers now post that they
are in fact the same syndrome). Although the causes of both pathologies is still
being debated, a lack of high energy compounds (e.g. ATP) at the level of the
mitochondria and general muscle weakness exists. For example, people with
fibromyalgia have lower levels of creatine phosphate and ATP levels compared to
controls.4 No direct studies exist at this time showing creatine supplementation
improves the symptomology of either chronic fatigue or fibromyalgia.
Considering, however, the other data that finds that creatine supplementation
increases creatine and ATP levels consistently in other pathologies where low
levels of creatine and ATP are found, it stands to reason that people suffering
from either syndrome may want to peruse the use of creatine. Another similar
syndrome to chronic fatigue and fibromyalgia, is Multiple Chemical Sensitivity
Syndrome, which may also be potentially improved by the use of creatine
supplements, though more research is clearly needed.
Recipe-How to take Creatine---best way I have seen to take it is in either a Hot beverage like coffee or tea or to use a glycocarb ( sugar based carbohydrate ) found in health food stores using about 25 grams to a 5 gram dose( warning this can offset insulin and pancreas) if training and using this for recovery and increase ATP then this would be a good way to utilize this---But for those who are working and living a life of long hours and work this can be used at a 3-5 gram dose everyday in a warm beverage---add a sweetner like honey or maplesyrup to the warm beverage---this will bee seen to be effective in about 3 weeks at this dose—USED to have everyone do a 20 gram dose for 5 days---all it did for most is give everyone a bloated stomach at that dose---unless you were deficient in this.---This kind of dosing was designed to sell more product especially at that time when it was introduced—it never lived up to the hype on performance but it has been used therapeutically and it appears to have a strengthening effect especially among the elderly---it can be used with CLA ( above ) to increase Health –Strenght_ and Energy.
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[U1]These are the Isomers You want to SEE if they are not on here then leave it on the shelf
[U2]Wonder why---the Food pyramid has been changed so that the things that would up build the body are now at the other end and instead of getting the fats from butter or animal protein high in this you are eating grains that are loaded with cancer causing properties due to the starchy sugars further exasperating an already chronic condition for those with intestinal and respiratory issues
[U3]Again 30 mg does is not enough to do anything---if the studies were at the least 3 gram dose then there would have been a significant effect again depending if there was fist a deficiency to begin with---vegetarians would see a significant impact with a dose of 3 grams or even less due to the fact that they would be deficient in the 3 aminos making creatine
[U4]This true---and at this dose this will work and again taking it a coffee or tea will also make it more absorbable due to the fact this will dissolve more readily when it is warm---
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ScienceDaily (Feb. 6, 2008) — Four days' exposure to a REM sleep deprivation procedure reduces cell proliferation in the part of the forebrain that contributes to long-term memory of rats, according to a new study.---The study, authored by Dennis McGinty, PhD, of the V.A. Greater Los Angeles Healthcare System, focused on male Sprague-Dawley rats. REM sleep deprivation was achieved by a brief treadmill movement initiated by automatic online detection of REM sleep. A yoked-control (YC) rat was placed in the same treadmill and experienced the identical movement regardless of the stage of the sleep-wake cycle.---According to the results, REM sleep was reduced by 85 percent in REM sleep deprived rats and by 43 percent in YC rats. Cell proliferation was reduced by 63 percent in REM sleep deprived rats compared with YC rats. Across all animals, cell proliferation exhibited a positive correlation with the percentage of REM sleep.--"Several studies have shown that sleep contributes to brain plasticity in general, and to adult neurogenesis, in particular," said Dr. McGinty. "Neurogenesis is a concrete example of brain plasticity, suppression of adult neurogenesis is thought to be important in pathologies such as depression. One current question has to do with the relative contribution of the two sleep states, non-REM and REM, which have very different, even opposite, physiological properties. This study showed that REM sleep has a critical role in facilitating brain plasticity. The study does not exclude an equally important role for non-REM sleep. In other recent work, we have shown that sleep fragmentation can also suppress adult neurogenesis. How sleep affects the molecular mechanisms underlying neurogenesis remains to be explored."---The article "Rapid eye movement sleep deprivation contributes to reduction of neurogenesis in the hippocampal dentate gyrus of the adult rat" was published in the February 1 issue of the journal Sleep.Story Source: The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by American Academy of Sleep Medicine.--
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ScienceDaily (July 21, 2010) — A combination of nutrients called NT-020 promoted adult neural stem cell proliferation in aged rats and boosted their memory performance, reported University of South Florida researchers studying natural therapeutic approaches to promoting the health of neurons in the aging brain.--Researchers from the USF Department of Neurosurgery and Brain Repair tested two groups of aged laboratory rats; one group received NT-020 and another, the control group, did not. In the NT-020 group, the process by which neurons are generated -- called neurogenesis -- increased.--The study was published in the current issue of Rejuvenation Research (Vol. 13 No. 5, June, 2010). The NT-020 formula was patented by USF and licensed to Natura Therapeutics, Inc.--"Aging has been linked to oxidative stress, and we have previously shown that natural compounds made from blueberries, green tea, and amino acids, such as carnosine, are high in antioxidants and have anti-inflammatory and anti-oxidative activity," said Sandra Acosta, MS, the study's lead author and a PhD student in the USF Center of Excellence in Aging and Brain Repair . "The combination of these nutrients, called NT-020, creates a synergistic effect that promotes the proliferation of stem cells in the aged animals."--Acosta and colleagues compared the NT-020 group to the control group by evaluating their performance on a variety of behavioral and memory tests, including a spatial navigation test. The NT-020 group demonstrated increased adult neural stem cell proliferation in the two main stem cell niches in the brains and improvement in learning and memory.--In past studies, NT-020 has been shown to have beneficial effects on animals with simulated stroke. NT-020 has also been shown to encourage the proliferation of adult stem cells, which have the potential to develop into tissue and bone cells and also migrate to areas of damage to help with repair.---That increased stem cell proliferation coincided with better cognitive performance is significant.--"The notion that aging is a stem cell disease has been gaining popularity," said study senior author Paula Bickford, PhD, professor of neurosurgery and brain repair at USF and a senior research career scientist at the James A. Haley Veterans' Hospital (Tampa). "Our hypothesis is that aging alters the local environment in the brain and other organs and can promote an environment that retards the growth of stem cells. For example, high glucose, which would be seen with diabetes, excessive alcohol and oxidative stress, can lead to reduced neurogenesis."--The researchers concluded that increased inflammation in the brains of the aged animals led to reduced production of stem cells, but that stem cell renewal created a rejuvenating effect. They found that NT-020 treated animals had fewer activated inflammatory cells in the brain, reflecting a decrease in factors that reduced the production of stem cells.---"NT-020 may have not only a positive effect on the stem cell niche," concluded Bickford. "NT-020 may have far-reaching effects on organ function beyond the replacement of injured cells, as demonstrated by cognitive improvement in the NT-020 group."--Disclaimer statement: Paula Bickford and Paul Sanberg are co-founders of Natura Therapeutics, Inc.---Story Source:---The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of South Florida (USF Health). The original article was written by Randolph Fillmore, USF Center of Excellence for Aging and Brain Repair.---Journal Reference:---S. Acosta, J. Jernberg, C.D. Sanberg, P.R. Sanberg, Brent J. Small, Carmelina Gemma, Paula C. Bickford. NT-020, a Natural Therapeutic Approach to Optimize Spatial Memory Performance and Increase Neural Progenitor Cell Proliferation and Decrease Inflammation in the Aged Rat. Rejuvenation Research, 2010; 100629131832013 DOI: 10.1089/rej.2009.1011
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ScienceDaily (Mar. 28, 2008) — There is new promise on the horizon for those who suffer from REM Sleep Behaviour Disorder (RBD) according to researchers at the University of Toronto.--RDB, a neurological disorder that causes violent twitches and muscle contractions during rapid eye-movement (REM) sleep, can lead to serious injuries. John Peever, Assistant Professor at the University of Toronto, discovered that an inhibitory brain chemical called glycine is responsible for actively suppressing muscle twitches in REM sleep.---Deficiency in glycine levels in the brain cells that control muscles (motoneurons) was found to cause the violent muscle contractions that mimic the primary symptom of RBD.---"This study shows the mechanism that suppresses muscles twitches in REM sleep and this will lead to better treatments and potential cures for this disorder," says Peever. "Treating REM sleep disorder may have much broader implications, since within five to eight years of being diagnosed with this disorder, 60-80% of individuals eventually develop Parkinson's disease."---The study findings are published in the March 26th edition of the Journal of Neuroscience.---Story Source:--The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by University of Toronto, via EurekAlert!, a service of AAAS
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3 protein fragments may drive immune response to gluten in those with genetic predisposition to the disorder----WEDNESDAY, July 21 (HealthDay News) -- Scientists believe they've identified the molecular triggers of celiac disease, a finding they say could lead to the first drugs to tame the chronic, painful gut disorder[U1].---People with celiac disease are intolerant to the protein gluten, which is found in wheat, barley and rye[U2]. Consuming these foods triggers an immune reaction that damages the lining of the small intestine, which can prevent the body from absorbing essential vitamins and nutrients.---Currently, the only treatment for celiac disease is adoption of a gluten-free diet, which means avoiding many types of bread, pasta, cereal and other foods. But gluten contamination in many foods makes it difficult to avoid and leads to long-lasting intestinal damage in some patients, said study senior author Robert Anderson, head of the celiac disease research laboratory at the Walter and Eliza Hall Institute of Medical Research in Parkville, Australia.---Regulating the aberrant immune response to gluten with a drug "would be a much more efficient way of dealing with celiac disease," [U3]Anderson said, but an incomplete understanding of how the immune system responds to gluten has prevented researchers from developing such therapies.---Gluten actually consists of many different protein components, and it's been unclear which of these fragments induces the immune response seen in celiac disease.---"You can't design drugs for celiac disease until you know the parts of the gluten that are driving the condition," Anderson explained.---During their investigation, he and his colleagues analyzed immune responses in the blood of more than 200 celiac disease patients after they had consumed meals containing gluten.---The researchers screened the blood samples for responses to thousands of different protein fragments (peptides) found in gluten, and they found that the patients' immune systems seemed to be responding negatively to only three of them.---That suggests that "a very precise trigger is driving the immune response," Anderson said. "The problem is not so much gluten, it's really these three peptides."---The authors also noted that most of the immune response to gluten appears tied to a single type of immune system cell, called the T cell.---The results are published in the July 21 issue of Science Translational Medicine.--According to Dr. Alessio Fasano of the University of Maryland School of Medicine in Baltimore, the evidence is indeed strong that these three protein fragments trigger the celiac immune response, but "I'm not sure that it's the end of the story," he added. It remains possible that the screen didn't catch all the gluten components involved in the immune response, Fasano said.---The findings will also not be relevant to everyone with celiac disease, Anderson added, since his team studied patients with a particular genetic susceptibility to the disease. Although most people with the disease show this genetic background, some do not. Anderson and his colleagues are currently working to identify which gluten proteins induce the immune response in the remainder of celiac patients.---Through Anderson's company, Nexpep, based in Ivanhoe, Australia, the researchers are also conducting phase I clinical trials on a drug based on the three gluten protein fragments they identified. The aim of the drug is to desensitize celiac patients to the offending proteins by presenting them in very controlled amounts[U4]. They expect results within the next couple of months.---The current study received funding from Nexpep, the Australian National Health and Medical Research Council, Coeliac UK, the Coeliac Research Fund, and others.---SOURCES: Robert Anderson, Ph.D., head, celiac disease research laboratory, Walter and Eliza Hall Institute, Parkville, Australia; Alessio Fasano, M.D., professor of pediatrics, medicine, and physiology and director of the Mucosal Biology Research Center, University of Maryland School of Medicine, Baltimore; July 21, 2010, Science Translational Medicine
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Recipe—Sleep Remedies—Glycine ( 500 mgs ) + Niacinamide ( 500mgs)-Inositol (500mgs) + Glycine ( 500mgs )—Glycine ( 500mgs) + Magnesium ( 100-200 mgs ) Creatine 3 grams + Magnesium ( 100-200 mgs )- Taurine ( 500 mgs) + Magnesium ( 100-200 mgs) --Gaba 500mgs ) + Niacinamide ( 500 mgs )- Tryptophan ( 500 mgs before bed ) + niacin ( 20 mgs )- Honey ( 1 tsp ) and Cocoa ( ½ tsp )- Melatonin ( 3 mgs-10 mgs )- Chamomile + St John’s Wort ( 1:1 ratio in 2 pint pot ) – Lavender Tea ( 1 tablespoon per 2 pint pot )- Passion Flower with any of the previous mentioned herbs again 1:1 will induce a solid state of sleep
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[U1]Again they are going to use a drug to suppress the real problem---Genetic disposition did not come til we had GMO foods –the real problem here is that the grains are GMO and as a result are causing this intolerance not because people are eating wheat but because the wheat has been tampered and the food processing as well
[U2]The research on this is that the gluten has been genetically altered and as a result there is excess amount of proline and Glutamates –which will cause a high histamine release—an allergic response
[U3]Again Not a cure –just allowing the damage to be present while the person is unaware of the furthering damage of the colon
[U4]Desensitizing someone does not mean it will be safe---again this is all smoke and mirrors to get people to consume more of the eugenics foods that are being sold