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Addiction– A Loss of Plasticity of the Brain
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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Enzyme Finding Sheds Light On How Memories Are Made And What Goes Wrong In Brain Disorders
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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What ‘natural’ means in food regulations
‘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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Consumers’ views on natural and clean label terminology
‘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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Cartoon characters attract kids to junk food
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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Show of the Week July 5 2010
Synergistic effects of tea polyphenols and ascorbic acid on human lung adenocarcinoma SPC-A-1 cells
Blueberry Ameliorates Hepatic Fibrosis
Certain Proteins Extend Life Span in Worms by 30 Percent
‘Spoonful Of Sugar’ Makes The Worms’ Life Span Go Down
Avoiding Sweets May Spell A Longer Life, Study In Worms Suggests
Not So Sweet— Over-Consumption Of Sugar Linked To Aging
Synergistic effects of tea polyphenols and ascorbic acid on human lung adenocarcinoma SPC-A-1 cells.
Li W, Wu JX, Tu YY.–Department of Tea Science, Zhejiang–University, Hangzhou 310029, China.
Abstract
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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Blueberry Ameliorates Hepatic Fibrosis
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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Certain Proteins Extend Life Span in Worms by 30 Percent
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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‘Spoonful Of Sugar’ Makes The Worms’ Life Span Go Down
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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Avoiding Sweets May Spell A Longer Life, Study In Worms Suggests
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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Not So Sweet— Over-Consumption Of Sugar Linked To Aging
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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Glucose-To-Glycerol Conversion In Long-Lived Yeast Provides Anti-Aging Effects
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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Show of the Week July 9 2010
A New Effect of Caffeine Boosts Performance
Endurance Increase Recipe
New Zealand’s Prime Minister: Climate Change bill a “load of rubbish” and “hoax”
Researchers Find ‘Switch’ For Brain’s Pleasure Pathway
Sleep Seems to Fuel Energy Surge in Rats’ Brains
–ATP Remedies
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A New Effect of Caffeine Boosts Performance
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
Endurance Increase Recipe
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:
http://www.parliament.nz/en-NZ/PB/Debates/Debates/3/2/8/47HansD_20050510_00001115-Climate-Change-Response-Amendment-Bill-First.htm %5B6%5D
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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Researchers Find ‘Switch’ For Brain’s Pleasure Pathway
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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Understanding How Folic Acid Might Help Heal Brain and Spinal Cord Injuries
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.
ATP Remedies
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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Show of the Week July 12 2010
Supplement dialogue strengthens on Capitol Hill
FTC denied expansion of powers
Nutrient profiles reinstated in EU Parliament vote
Milestone In The Regeneration Of Brain Cells
New Source Discovered for Generation of Nerve Cells in Brain— Things that increase GABA
Forming New Brain Cells: Key Regulatory Peptide Discovered
Supplement dialogue strengthens on Capitol Hill
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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FTC denied expansion of powers
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.