Here are some things MSG can damage in you and how to offset t —do not go out of your way to consume this—–and remember if you have a weak heart this must be avoided at all cost-
Here are some things MSG can damage in you and how to offset t —do not go out of your way to consume this—–and remember if you have a weak heart this must be avoided at all cost-
Coffee Drinkers Have Lower Risk of Death- Study Suggests
A new study found that older adults who drank coffee — caffeinated or decaffeinated — had a lower risk of death overall than others who did not drink coffee.
ScienceDaily (May 19, 2012) — Older adults who drank coffee — caffeinated or decaffeinated — had a lower risk of death overall than others who did not drink coffee, according a study by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, and AARP.—Coffee drinkers were less likely to die from heart disease, respiratory disease, stroke, injuries and accidents, diabetes, and infections, although the association was not seen for cancer. These results from a large study of older adults were observed after adjustment for the effects of other risk factors on mortality, such as smoking and alcohol consumption. Researchers caution, however, that they can’t be sure whether these associations mean that drinking coffee actually makes people live longer. The results of the study were published in the May 17, 2012 edition of the New England Journal of Medicine.—Neal Freedman, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and his colleagues examined the association between coffee drinking and risk of death in 400,000 U.S. men and women ages 50 to 71 who participated in the NIH-AARP Diet and Health Study. Information about coffee intake was collected once by questionnaire at study entry in 1995-1996. The participants were followed until the date they died or Dec. 31, 2008, whichever came first.—The researchers found that the association between coffee and reduction in risk of death increased with the amount of coffee consumed. Relative to men and women who did not drink coffee, those who consumed three or more cups of coffee per day had approximately a 10 percent lower risk of death. Coffee drinking was not associated with cancer mortality among women, but there was a slight and only marginally statistically significant association of heavier coffee intake with increased risk of cancer death among men.–“Coffee is one of the most widely consumed beverages in America, but the association between coffee consumption and risk of death has been unclear. We found coffee consumption to be associated with lower risk of death overall, and of death from a number of different causes,” said Freedman. “Although we cannot infer a causal relationship between coffee drinking and lower risk of death, we believe these results do provide some reassurance that coffee drinking does not adversely affect health.”—The investigators caution that coffee intake was assessed by self-report at a single time point and therefore might not reflect long-term patterns of intake. Also, information was not available on how the coffee was prepared (espresso, boiled, filtered, etc.); the researchers consider it possible that preparation methods may affect the levels of any protective components in coffee.—“The mechanism by which coffee protects against risk of death — if indeed the finding reflects a causal relationship — is not clear, because coffee contains more than 1,000 compounds that might potentially affect health,” said Freedman. “The most studied compound is caffeine, although our findings were similar in those who reported the majority of their coffee intake to be caffeinated or decaffeinated.”—Story Source-The above story is reprinted from materials provided byNational Institutes of Health. –Journal Reference-Neal D. Freedman, Yikyung Park, Christian C. Abnet, Albert R. Hollenbeck, Rashmi Sinha. Association of Coffee Drinking with Total and Cause-Specific Mortality. New England Journal of Medicine, 2012; 366 (20): 1891 DOI: 10.1056/NEJMoa1112010
Potato Storage- Essential Oils as Antigerminants
ScienceDaily (Oct. 5, 2012) — One of the critical moments in the final quality of the potato occurs during its storage, as there exists the risk of sprouting or rotting due to pathogenic agents such as bacteria and fungi. In order to avoid this, agricultural engineer David Gómez Castillo carried out research for his PhD on the possibility of substituting the current use of chemical products by treating the tuber with essential oils of mint, caraway, coriander, eucalyptus and clove, “which have proved to be great potential inhibitors in the main problems detected.”—The chemical product Clorprofam (CIPC) is the most commonly used as a sprout suppressant on stored potatoes. Nevertheless, possible reductions in permitted dosages, market and consumer pressures seeking healthier and, moreover, more environmentally-friendly products, have made it necessary to find alternatives to these synthetic products, with the market, culinary and technological quality of the potato remaining unaltered.—This is the context of the research by David Gómez Castillo, who has evaluated alternative treatment using essential oils of mint, caraway, coriander, eucalyptus and clove. In concrete, he studied the effect of applying these oils with table-stock varieties of the potato (Agata and Monalisa) and industrial ones (Agria and Kennebec), and compared the results thereof with those that had been treated chemically.
A good alternative—The research analysed two parameters: the commercial quality (germination, texture and colour of the tuber) and the culinary and technological quality (colour and texture of slices of the potato, dry material, total soluble solids, reductor sugars and sensorial analysis). Evaluations at 10, 25, 40, 55 and 70 days in storage were also undertaken, the antimicrobial effect of essential oils being assessed for the principal phytopathogens (fungi and bacteria).—According to Mr Gómez, “we found a high antigerminant capacity with treatment using the essential oil of coriander for industrial crops, and with the essential oil of mint for both industrial and table-stock crops. These showed great inhibitory potential on the principal phytopathogenic problems studied and all this makes a good alternative to CPIC use for storage of potatoes.”—It was also shown that the essential oil of eucalyptus, for its high antigerminant capacity with table-stock potatoes, “could be another alternative for reducing post-harvest losses due to phytopathogenic problems, obtaining even better results if the treatment is accompanied by the essential oil of clove.”–In the opinion of this researcher, the use of treatment with essential oils in the storage of potatoes “can provide added value in the application of antigerminant treatment, due to its efficacy in controlling the progress of important phytopathogens.”—Story Source-The above story is reprinted from materials provided by Basque Research.
Recipe for AntiPhytopathegenic for Potato’s—take either a combination of peppermint and coriander add 2 drops each to either a Sprayer with water—make sure the Essential oils are dispersed well in the water—blend in a blender for about 2 minutes to mix—once done then spray the potatoes being stored—or take a vaporiser and add the oils into the vaporiser and allow it to mist the air as well—this will cause the components to be air borne and will reduce the break down—-this same principle can be done with other things as well or even utilize this principle to do a room or household to eliminate pathogens that might be airborne—keep the potatoes in a cool place for storage as well will reduce spoilage
Top 10 Foods Highest in Potassium
Potassium is an essential nutrient used to maintain fluid and electrolyte balance in the body. A deficiency in potassium causes fatigue, irritability, and hypertension (increased blood pressure). Overdose of potassium from natural sources is nearly impossible, however, it is possible to consume too much potassium via potassium salts which can lead to nausea, vomiting, and even heart attack. Potassium from natural food sources, like the ones listed below, are considered safe and healthy. The current percent daily value for potassium is a whopping 3.5 grams, below is a list of high potassium foods. For more foods high in potassium please see the lists of potassium rich foods, fruits high in potassium, and vegetables high in potassium.
#1: Dried Herbs
Long used for medicinal purposes, herbs are packed with nutrients and potassium is no exception. Dried Chervil contains the most potassium with 4.7g (135% DV) per 100g serving, or 95mg (3% DV) per tablespoon. It is followed by Dried Coriander (3% DV) per tblsp, Dried Parsley (2% DV), Dried Basil, Dried Dill, Dried Tarragon, Ground Turmeric, Saffron, and finally Dried Oregano with 50mg (1% DV).
Click to see complete nutrition facts
Avocados are great when made into guacamole or in a salad. 100 grams will provide 485mg of potassium or 14% of the DV. That is 1.1g (32% DV) in one cup pureed, and 975mg (28% DV) in a single avocado (201 grams).
Click to see complete nutrition facts || More Fruits High in Potassium
#3: Paprika and Red Chili Powder
Either paprika or red chili powder add a nice kick to any dish, and with all the potassium they provide you have good reason to start adding them. Paprika provides the most potassium with 2.3g (67% DV) per 100 gram serving, or 164mg (5% DV) per tablespoon. Chili powder will provide 1.9g (55% DV) per 100 gram serving or 153mg (4% DV) per tablespoon. Click to see complete nutrition facts
#4: Cocoa Powder and Chocolate
Dark chocolate is an excellent source of iron and zinc in addition to potassium. Pure cocoa powder without any fat, milk, or sugar, provides the most potassium with 1.5 grams (44% DV) in a 100g serving, or 1.3g (37% DV) per cup, and 76mg (2% DV) per tablespoon. Unsweetened baking chocolate provides 830mg (24% DV) per 100 gram serving or 241mg (7% DV) per square. Most sweetened milk chocolates will provide around 272mg (11% DV) per 100 gram serving, and 164mg (5% DV) per bar (1.5oz). Click to see complete nutrition facts
#5: Dried Apricots, Prunes, Zante Currants, and Raisins
Most common as a snack, dried apricots and prunes can also be chopped and served in a salad. A good source of fiber and many other vitamins, apricots provide 1.9g (53%DV) of potassium per 100g serving (about 20 dried apricots). Prunes provide 1g (30% DV) per 100g serving, or 1.4g (40% DV) per cup. Zante currants are really a type of grape and taste very similar to raisins. Zante currants provide 892mg (25% DV) of potassium per 100g serving, or 1.3g (37% DV) per cup. Raisins provide almost the same amount with 825mg (24% DV) per 100 gram serving, or 1.2g (24% DV) per cup. Click to see complete nutrition facts
#6: Pistachios and Other Nuts
Pistachios are a delicious snack, and a great addition to salads. 100 grams (~3/4cup) will provide 1g (30% DV) of potassium. Other nuts high in potassium include Beechnuts (29% DV per 100g), Ginko nuts (29% DV), Chestnuts (28% DV), Almonds (21% DV), Hazelnuts (19% DV), Cashews (18% DV), Pine nuts (17% DV), Coconuts (16% DV), and Walnuts (15% DV).
Click to see complete nutrition facts
#7: Seeds (Pumpkin, Squash, Sunflower, and Flax)
A popular food in the Middle East and East Asia pumpkin and squash seeds contain about 919mg (26% DV) of potassium per 100g serving, 588mg (17% DV) per cup. If you can’t find these in your local supermarket you will surely find them in Middle Eastern or East Asian specialty stores. Alternatively, you can also save any pumpkin and squash seeds you have and roast them in your oven. The seeds are typically eaten by cracking the outer shell and eating the seed inside. Sunflower seeds are also a good source of potassium, providing 850mg (24% DV) per 100 gram serving, or 1.1g (31% DV) per cup. Flax seeds provide 813mg (23% DV) of potassium per 100 gram serving, or 1.4g (39% DV) per cup, and 81mg (2% DV) per tablespoon.
Click to see complete nutrition facts. Buy Pumpkin Seeds from Amazon.com
#8: Fish (Pompano, Salmon, Halibut, Tuna)
Fish has many health benefits and is a great source of potassium. Pompano provides the most with 636mg (18% DV) per 100 gram serving, or 540mg (15% DV) per fillet (3 ounces, 85 grams). It is followed by Salmon which provides 534mg (15% DV) per 3 ounce serving, Halibut, Yellow Fin Tuna, Lingcod, Mackerel, Anchovies, Herring, Cod, Snapper, Rockfish, Tilefish, Grouper, and finally Trout with 394mg (11% DV) in a 3 ounce serinvg. Cooking fish with dry heat is the best way to preseve the potassium content. Click to see complete nutrition facts
White beans provide the most potassium with 561mg (16% DV) per 100 gram serving, 1g (29% DV) per cup cooked. White beans are followed by Adzuki Beans, Soy Beans, Lima Beans, Pinto Beans, Kidney Beans, Great Northern Beans, Navy Beans, Pigeon Peas, Cranberry (Roman) Beans, French Beans, Lentils, Split Peas, Black Beans, Hyancinth, and finally Yardlong Beans with 539mg (15% DV) per cup cooked.
Click to see complete nutrition facts
#10: Dates (Medjool)
Dates are great as a snack, as an addition to fruits salads, or even savory stews. Medjool dates provide 696mg (20% DV) per 100 gram serving, or 167mg (5% DV) in a single date.
Click to see complete nutrition facts
EFSA publishes initial review on GM maize and herbicide study
The European Food Safety Authority has concluded that a recent paper raising concerns about the potential toxicity of genetically modified (GM) maize NK603 and of a herbicide containing glyphosate is of insufficient scientific quality to be considered as valid for risk assessment.—EFSA’s initial review found that the design, reporting and analysis of the study, as outlined in the paper, are inadequate. To enable the fullest understanding of the study the Authority has invited authors Séraliniet al to share key additional information.–Such shortcomings mean that EFSA is presently unable to regard the authors’ conclusions as scientifically sound. The numerous issues relating to the design and methodology of the study as described in the paper mean that no conclusions can be made about the occurrence of tumours in the rats tested.—Therefore, based on the information published by the authors, EFSA does not see a need to re-examine its previous safety evaluation of maize NK603 nor to consider these findings in the ongoing assessment of glyphosate.—EFSA assessed the paper against recognised good scientific practices, such as internationally agreed study and reporting guidelines.—-Per Bergman, who led EFSA’s work, said: “Some may be surprised that EFSA’s statement focuses on the methodology of this study rather than its outcomes;however, this goes to the very heart of the matter. When conducting a study it is crucial to ensure a proper framework is in place. Having clear objectives and the correct design and methodology create a solid base from which accurate data and valid conclusions can follow. Without these elements a study is unlikely to be reliable and valid.”—The Director of Scientific Evaluation of Regulated Products added that the consideration of possible long-term effects of GMOs has been, and will continue to be, a key focus of EFSA’s work to protect animals, humans and the environment.—-EFSA’s preliminary review issued today is the first step in a two-stage process. A second analysis will be delivered by the end of October 2012. This will take into account any additional information from the study authors, who will be given an opportunity to supply study documentation and procedures to the Authority to ensure the broadest possible understanding of their work. It will also include an overview of Member State assessments of the paper and an analysis from the German authorities responsible for the assessment of glyphosate.
Main findings of Initial Review—The task force, whose members were drawn from the Authority’s GMO, pesticide and scientific assessment units, has outlined a list of issues about the paper that would need to be resolved before it could be viewed as well-conducted and properly-reported study.
- The strain of rat used in the two-year study is prone to developing tumours during their life expectancy of approximately two years. This means the observed frequency of tumours is influenced by the natural incidence of tumours typical of this strain, regardless of any treatment. This is neither taken into account nor discussed by the authors.
- The authors split the rats into 10 treatment sets but established only one control group. This meant there was no appropriate control for four sets – some 40% of the animals – all of whom were fed GM maize treated or not treated with a herbicide containing glyphosate.
- The paper has not complied with internationally-recognised standard methods – known as protocols – for setting up and carrying out experiments. Many of these procedures are developed by the OECD (Organisation for Economic Cooperation and Development).
- For a study of this type, the relevant OECD guideline specifies the need for a minimum of 50 rats per treatment group. Séralini et al used only 10 rodents per treatment set. The low number of animals used is insufficient to distinguish between the incidence of tumours due to chance rather than specific treatment effects.
- The authors have not stated any objectives, which are the questions a study is designed to answer. Research objectives define crucial factors such as the study design, correct sample size, and the statistical methods used to analyse data – all of which have a direct impact on the reliability of findings.
- No information is given about the composition of the food given to the rats, how it was stored or details of harmful substances – such as mycotoxins – that it might have contained.
- It is not possible to properly evaluate the exposure of the rats to the herbicide as intake is not clearly reported. The authors report only the application rate of the herbicide used to spray the plants and the concentration added to the rats’ drinking water but report no details about the volume of the feed or water consumed.
- The paper does not employ a commonly-used statistical analysis method nor does it state if the method was specified prior to starting the study. The validity of the method used is queried and there are questions over the reporting of tumour incidence. Important data, such as a summary of drop outs and an estimation of unbiased treatment effects have not been included in the paper.
- Many endpoints – what is measured in the study – have not been reported in the paper. This includes relevant information on lesions, other than tumours, that were observed. EFSA has called on the authors to report all endpoints in the name of openness and transparency.
- Review of the Séralini et al. (2012) publication on a 2-year rodent feeding study with glyphosate formulations and GM maize NK603
- Letter to Prof. Séralini regarding EFSA’s Review of the Séralini et al. (2012) publication on a 2-year rodent feeding trial with Glyphosate Formulations and GM maize NK603 as published online on 19 September 2012 in Food and Chemical Toxicology, 4 October 2012
Notes to editors:
EFSA set up a multi-disciplinary task force in response to an urgent request from the European Commission to evaluate a paper by Séralini et al to assess whether its findings could lead the Authority to reconsider its previous opinion on maize NK603. The two-year study, published in the journal Food and Chemical Toxicology on 19 September 2012, has suggested that consumption of the GM maize and a herbicide containing glyphosate at levels below officially-safe limits are linked to a reported increase in incidence of tumours in rats.
**************************************************************************Claims on many supplements don't comply with law, report saysThe structure function claims on many dietary supplement products do not comply with federal law,a government report released on WednesdayThe[U1] report recommends greater regulatorypowers for FDA to bring products into compliance[U2] .---Industry sources reacted negatively to the assertionthat FDA needs new statutory powers, but were more accommodating on the report’s suggestions on howthe claims notification process should be tightened up[U3] . The report, conducted by the Office of InspectorGeneral of the United States Department of Health and Human Services, looked at the claims on 127 dietary supplements in the weight loss and immune support The report looked at the label language and what kindof evidence was cited to back up the claims, to judge compliance with FDA-mandated notifications and disclaimersand to see how many claims trended over into prohibited disease claim territory. The report said that thepopularity of structure function claims is on the rise, and maintains that problems with the useof these claims is on the rise, too. Report cites thin supporting evidence The report’s broad conclusionswere these: Many claims were not backed by evidence from human studies[U4] . Of the human studiessupplied by manufacturers in response to HHS requests, few appeared to satisfy FDA recommendationsin every respect in terms of study design and relevance to the meaning of the claim[U5] . It also foundthat 20% of the supplements in the sample were making prohibited disease claims and that 7% lackedthe disclaimer that is supposed to accompany every structure function claim. The report went on torecommend that FDA should seek additional statutory authority to regulate label claims to make surethat suitable evidence exists to back up the claim, to make sure that proper label notifications arein place and to make sure companies are not making illegal disease claims In[U6] addition, it said FDAneeds to clean up its tracking of who is making what claims, and who has complied with the requirement of a 30-dayprior notification of the use of a claim on a product. Immediate reaction Report overreaches Reaction from tradegroups and industry observers was swift and decisive. The Office of Inspector General reviewed just 127 supplementsout of an estimated 29,000 products on the market. This small sample of supplements shouldn’t smear the entire industry,said John Shaw, executive director and CEO of the Natural Products Foundation. The president and CEO of theorganization, said, What’s most disappointing is that this was not a random sampling [of the industry].The vast majorityof the industry, including our members, is doing the right thing. These reports give good companies a black eye,he said.The small sample size and big conclusions also was an issue for Marc Ullman, who has worked with the" Natural Products Foundation’s Truth in Advertising industry self-regulation effort. They are recommended sweepingchanges to the law, the imposition of vast new regulatory burdens on FDA based on the fact that (a small number)of dietary supplements didn’t pass substantiation. To me it seems quite a reach, Ullman, an attorney with the NewYork-based firm Ullman, Shapiro Ullman, told a reporter. I cannot fathom the kind of broad generalizations theymade based on this kind of sample size. Nuanced response to report’s recommendations Regarding the recommendations,Mister said CRN was very supportive of FDA to do more, especially when it came keeping bettertrack of health claim notifications, which companies are supposed to send in 30 days prior to aproduct hitting the But the first recommendation, calling for FDA to ‘statutory authority to reviewsubstantiation for structure/function claims to determine whether they are truthful and notmisleading[U7] ,’ is a non-starter, he said.This sounds like pre-market approval to us, Mister said. I do hope thatFDA sees that some of this is targeted towards them, he added. The agency needs to manage the information theyalready have. Structure/function claims and registrations need to be catalogued to be accessible.The methodologyof the report divided up the supplements more or less equally between the weight loss and immune sectors, andalso about equally between supplements purchased in retail outlets on the Internet. This last detail interested TonyYoung, legal counsel for the American Herbal Products Association, especially in relation to the finding that 20% ofproducts were making disease claims. An interesting question would be whether those were products purchased off theInternet or in retail stores. We expect that there is a higher standard out there to get products on retail shelves andthat most of the major retailers don’t carry products that make that kind of claim, he said. No public health risk Atthe end of the day, Young said, there is no imminent public health risk in the report’s findings. Whether FDA shouldexpend substantial resources doing the kinds of things that were suggested is a decision that FDA would have to makewith regard to all of the other public health priorities,” he said.The report might go overboard in its enforcementrecommendations, Ullman said, but that doesn’t obviate legitimate questions about how some companies market theirproducts As an industry we need to recognize—and we do recognize—that there is a problem, he said, going on to cite NPF’sTruth in Advertising effort and CRN’s cooperation with the "http://www.bbb.org/us/national-advertising-division/"National Advertising Division as appropriate ways to self-police label claims.Everybody in our industry argues that thereshould be more enforcement with respect to unlawful disease claims so there is pretty much unanimity on that,Young said[U8] .
[U1]A new attack on supplements
[U2]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market—where the owners will surrender there companies and sell out
[U3]This is the HFI-health food industry caving in and surrendering—the industry should be looking after itself without gov’t interference—
[U4]This is the EFSA—european food and safe authority nonsence—this is the FDA compliance with the EFSA
[U6]Gov’t interference—again to debilitate the industry to a point where they either bail out or surrender—the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov’t
[U7]Is this not the dumbest thing you ever heard? The wolf guarding the hen house—the industry is going to ask the gov’t to monitor the competition??? What a deception here
[U8]This is really disappointing—the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
[U1]Smart Meter-Cell Phone—HAARP -Microwaves
[U2] A new attack on supplements
[U3]Drug Companies want to debilitate the industry further for easier acquisition of that health food industry market—where the owners will surrender there companies and sell out
[U4]This is the HFI-health food industry caving in and surrendering—the industry should be looking after itself without gov’t interference—
[U5]This is the EFSA—european food and safe authority nonsence—this is the FDA compliance with the EFSA
[U7]Gov’t interference—again to debilitate the industry to a point where they either bail out or surrender—the health food industry as well a the consumers need to collaborate and get rid of the common enemy Gov’t
[U8]Is this not the dumbest thing you ever heard? The wolf guarding the hen house—the industry is going to ask the gov’t to monitor the competition??? What a deception here
[U9]This is really disappointing—the big players what the FDA to do there dirty work for them so they can eliminate all competition and have it all under 1 umbrella this is what is really going on a destruction of a free enterprise effect and everyone has to comply and the independent is going to either be absorbed or eliminated from the market
Inactivation of human immunodeficiency virus by Betadine products & chlorhexidine.
Harbison MA, Hammer SM.
J Acquir Immune Defic Syndr . 1989;2(1):16-20.
Infectious Disease Section, New England Deaconess Hospital, Boston, Massachusetts.
Eleven povidone-iodine-containing products (Betadine) and chlorhexidine gluconate solution were tested for their ability to inactivate human immunodeficiency virus (HIV) in a cell culture system. All Betadine products completely inactivated the virus at povidone-iodine concentrations of greater than or equal to 0.5% (10- to 20-fold dilutions of stock) except for Betadine Lubricating Antiseptic Gel, which required 2.5% for efficacy (1:2 dilution).
The action of three antiseptics/disinfectants against enveloped and non-enveloped viruses.
Wood A, Payne D.
J Hosp Infect . 1998 Apr;38(4):283-95.
Results indicate that all products were effective in inactivating the enveloped viruses herpes simplex virus type 1 and human immunodeficiency virus type 1, whilst being ineffective in inactivating human coronavirusŠ..Four antiseptic/disinfectant solutions with chloroxylenol, benzalkonium chloride, cetrimide/chlorhexidine and povidone-iodine were also assessed for antiviral effect against human immunodeficiency virus in the presence of whole human blood. All four solutions proved to be effective within 1 min despite the cytotoxic nature of the compounds to the detection system. —Note from Mark Konlee: A few years ago I talked with 2 persons from different parts of the country who have been on an unusual diet for several years with striking similarities and results. They ate no meat and ate seafood, fish and or sea vegetables daily for several years. They were also both HIV positive and non-progressors and neither person had used prescribed antiviral drugs for HIV. Could the iodine and other trace minerals in the seafood they consumed have had something to do with their status as non-progressors? Could eating sea vegetables and ocean fish daily help stop HIV
HOW SMART METERS MAY CAUSE AUTISM AND CANCER
Andrew Goldsworthy July 2011
There is increasing evidence that wireless transmissions have biological effects, some of which are harmful, at levels that may be orders of magnitude below present safety guidelines. These guidelines were drawn up on the assumption that the radiation could only damage living tissues if it generated significant heat. It has since been shown that radiation at much lower levels has direct electrical effects. These are mainly on electrically charged cell membranes, where the low frequency pulses from the modulated microwaves make them vibrate and leak. This can give rise to many “modern illnesses” ranging from electromagnetic hypersensitivity to cancer and disorders of the immune system. The most dramatic increase in the incidence of autism due to damage to the developing brains of the fetus and young children. Modulated microwaves, such as those from cell phones, portable phones, WiFi, baby monitors and wireless smart meters are sources of potentially damaging radiation. The strength of the radiation appears to be less important than the duration and pattern of the exposure, with intermittent and repeated exposure being the most damaging. The strong regular transmissions from wireless smart meters are particularly harmful and more likely to lead to DNA damage, cancer and autism.
Sub-thermal effects of electromagnetic radiation.
There are thousands of scientific papers showing biological effects of non-ionizing electromagnetic radiation occurring well below the levels at which them can generate significant heat. Many of these have been reviewed at by expert scientist at www.bioinitiative.org andhttp://www.neilcherry.com/documents.php . They include harmful effects such as damage to DNA in living cells that can lead to cancer, loss of fertility, brain damage due to the disruption of the blood-brain barrier and neuronal hyperactivity leading to autism in children. Many of these effects can be attributed to the loss of structurally important calcium from cell membranes, which makes them leak. This can disrupt normal metabolism and also release DNase (which destroys DNA) from the internal structures (lysosomes) that normally recycle waste into the rest of the cell http://www.hese-project.org/hese-uk/en/papers/cell_phone_and_cell.pdf .
Prolonged and intermittent radiation causes more damage
The duration of the radiation seems to be more important than its strength, with the effects being cumulative as more and more cells are damaged. Interestingly, DNA damage from cell phone radiation is greater when the exposure is intermittent (5 minutes on, 10 minutes off) than when continuous (Diem et al 2005). This may be because the cells are constantly adapting and using energy to defend themselves; they drop their guard during the off period and are caught unawares when it goes on again. This constant switching uses more energy, which eventually leaves the cells less able to counteract the effects of the radiation.
Diem et al. (2005) also found that the effect on DNA damage was still greater if the microwaves were pulsed or modulated to carry information (modulation involves sudden stops and starts of the signal, which are even more damaging).
Smart meters, which operate 24/7 and radiate modulated microwaves intermittently, can therefore be expected to be particularly harmful to DNA.
Microwave radiation causes cancer
There is already evidence that heavy cell phone users are more prone to brain cancers. This has resulted in cell phones now being rated by the World Health Organisation as class 2B carcinogens. This rating may later be increased, since brain tumours normally take decades to develop and few people have been regularly using a cell phone for more than a single decade. Particularly worrying is the finding by Hardell and Carlberg (2009 ) that young people were about 5-times more likely to get brain cancer both from cordless and cell phones if they began using them before the age of 20. The regular transmissions from wireless smart meters can be expected to have much the same effect, with younger people being more at risk. This is possibly because their brain structure is still growing and developing and therefore more susceptible to damage leading to cancer.
The effect of microwaves on autism is far worse
The greatest damage from microwaves is when the brain is first developing in the foetus and the very young child, when it can lead to autism. Dr Dietrich Klinghardt has recently shown the relationship between microwaves and autism; a summary of his work can be found athttp://electromagnetichealth.org/media-stories/#Autism .
What is autism?
Autism is in fact a group of life-long disorders (autistic spectrum disorders or ASD) caused by brain malfunctions and is associated with subtle changes in brain anatomy (see Amaral et al. 2008 for a review). The core symptoms are an inability to communicate adequately with others and include abnormal social behaviour, poor verbal and non-verbal communication, unusual and restricted interests, and persistent repetitive behaviour. There are also non-core symptoms, such as an increased risk of epileptic seizures, anxiety and mood disorders. ASD has a strong genetic component, occurs predominantly in males and tends to run in families.
Genetic ASD may be caused by calcium entering neurons
It has been hypothesised that some genetic forms of ASD can be accounted for by known mutations in the genes for ion channels that result in an increased background concentration of calcium in neurons. This would be expected to lead to neuronal hyperactivity, the formation of sometimes unnecessary and inappropriate synapses, which in turn can lead to ASD (Krey and Dolmetsch 2007).
Electromagnetic fields let calcium into neurons too
There has been a 60-fold increase in ASD in recent years, which cannot be accounted for by improvements in diagnostic methods and can only be explained by changes in the environment. This increase corresponds in time to the proliferation of mobile telecommunications, WiFi, and microwave ovens as well as extremely low frequency fields (ELF) from mains wiring and domestic appliances. We can now explain this in terms of electromagnetically-induced membrane leakage leading to brain hyperactivity and abnormal brain development.
Non-ionising radiation makes cell membranes leak
The first effect of non-ionising electromagnetic radiation is to generate small alternating voltages across the cell membranes, which destabilize them and make them leak. This can have all sorts of consequences as unwanted substances diffuse into and out of cells unhindered, and materials in different parts of the cell that are normally kept separate, become mixed.
Why weak fields are more damaging than strong ones
We have known since the work of Suzanne Bawin and her co-workers (Bawin et al. 1975) that modulated radio-frequency electromagnetic radiation that is far too weak to cause significant heating can nevertheless remove calcium ions (positively charged calcium atoms) from cell membranes in the brain. Later, Carl Blackman showed that this also occurs with extremely low frequency electromagnetic radiation (ELF) but only within one or more “amplitude windows”, above and below which there is little or no effect (Blackman et al. 1982; Blackman 1990). A proposed molecular mechanism for this can be found in Goldsworthy (2010). In particular, it explains why weak electromagnetic fields can have a greater effect than strong ones and why prolonged exposure to weak fields (where cells are maintained in the unstable condition for longer) is potentially more damaging than relatively brief exposure to much stronger ones.
How calcium ions stabilize cell membranes
This loss of calcium is important because calcium ions bind to and stabilize the negatively charged membranes of living cells. They sit between the negatively charged components of the cell membrane and bind them together rather like mortar binds together the bricks in a wall. Loss of just some of these calcium ions destabilize the membrane and make it more inclined to leak, which can have serious metabolic consequences. Among these are the effects of membrane leakage on the neurons of the brain.
How membrane leakage affects neurons
Neurons transmit information between one another in the form of chemical neurotransmitters that pass across the synapses where they make contact. However, the release of these is normally triggered by a brief pulse of calcium entering the cell. If the membrane is leaky due to electromagnetic exposure, it will already have a high internal calcium concentration as calcium leaks in from the much higher concentration outside. The effect of this is to put the cells into hair-trigger mode so that they are more likely to release neurotransmitters and the brain as a whole may become hyperactive (Beason and Semm 2002; Krey and Dolmetsch 2007, Volkow et al. 2011). This may not be a good thing since the brain may become overloaded leading to a loss of concentration and what we now call attention deficit hyperactive disorder (ADHD).
How does this impact on autism?
Before and just after its birth, a child’s brain is essentially a blank canvas, and it goes through an intense period of learning to become aware of the significance of all of its new sensory inputs, e.g. to recognise its mother’s face, her expressions and eventually other people and their relationship to him/her (Hawley & Gunner 2000). During this process, the neurons in the brain make countless new connections, the patterns of which store what the child has learnt. However, after a matter of months, connections that are rarely used are pruned automatically (Huttenlocher & Dabholkar 1997) so that those that remain are hard-wired into the child’s psyche. The production of too many and often spurious signals due to electromagnetic exposure during this period will generate frequent random connections, which will also not be pruned, even though they may not make sense. It may be significant that autistic children tend to have slightly larger heads, possibly to accommodate unpruned neurons (Hill & Frith 2003).
Because the pruning process in electromagnetically-exposed children may be more random, it could leave the child with a defective hard-wired mind-set for social interactions, which may then contribute to the various autistic spectrum disorders. These children are not necessarily unintelligent; they may even have more brain cells than the rest of us and some may actually be savants. They may just be held back from having a normal life by a deficiency in the dedicated hard-wired neural networks needed for efficient communication.
Autism and the economy
The incidence of autism has increased 60-fold, in parallel with the increase in electromagnetic pollution over the last thirty years. The chance of having an autistic child may now be as high as one in fifty. Apart from the personal tragedies for the affected children and their families, autism is of enormous economic importance. In the UK alone, the annual cost to the Nation in care and lost production exceeds the annual tax revenue from the entire mobile phone industry, which is about 20billion UK pounds. http://www2.lse.ac.uk/newsAndMedia/news/archives/2009/05/MartinKnappAutism.aspx In theory the Government could close down the entire mobile phone industry and actually show a profit!
There are ways in which the modulation of the signal can be changed to avoid this, but in the meantime, the compulsory introduction of smart meters can only contribute further to autism on a grand scale. This will be a further burden on the economy and increase the National deficit. This will far outweigh any possible advantages from the use of these meters.
There is also a risk of legal complications for the utility companies. If it can be shown that that the consumer has taken reasonable precautions to minimise their microwave exposure by eliminating WiFi, cordless phones and wireless baby monitors from their house, the utility company could be held legally responsible for any autistic children that they may have.
In the UK, the lifetime cost of caring for an autistic child is in the region of one million pounds. It would be reasonable to claim compensation for this amount. In the United States, it may also be possible to claim punitive damages if it can be shown that the utility company knew of this risk when they installed or refused to remove a smart meter when requested.
Dr Andrew Goldsworthy
Lecturer in Biology (retired)
Imperial College London
Amaral DG, Schumann CM, Nordahl CW (2008), Neuroanatomy of Autism, Trends in Neurosciences 31: 137-145
Bawin SM, Kaczmarek KL, Adey WR (1975), Effects of modulated VHF fields on the central nervous system. Ann NY Acad Sci 247: 74-81
Beason RC, Semm P (2002), Responses of neurons to an amplitude modulated microwave stimulus. Neuroscience Letters 333: 175-178
Blackman CF (1990), ELF effects on calcium homeostasis. In: Wilson BW, Stevens RG, Anderson LE (eds) Extremely Low Frequency Electromagnetic Fields: the Question of Cancer. Battelle Press, Columbus, Ohio, pp 189-208
Blackman CF, Benane SG, Kinney LS, House DE, Joines WT (1982), Effects of ELF fields on calcium-ion efflux from brain tissue in vitro. Radiation Research 92: 510-520
Diem E, Schwarz C, Adlkofer F, Jahn O, Rudiger H (2005). Non-thermal DNA breakage by mobile-phone radiation (1800 MHz) in human fibroblasts and in transformed GFSH-R17 rat granulosa cells in vitro. Mutation Research 583: 178-183
Goldsworthy A (2010) , Witness Statement, http://mcs-america.org/june2010pg910111213141516.pdf
Hardell L, Carlberg M (2009), Mobile phones, cordless phones and the risk for brain tumours. Int J Oncology 35: 5-17 DOI: 10.3892/ijo_00000307
Hawley T, Gunner M (2000), How early experiences affect brain development. http://tinyurl.com/5u23ae
Hill EL, Frith U (2003), Understanding autism: insights from mind and brain. Phil Trans R Soc Lond B 358 281-289
Huttenlocher PR, Dabholkar AS (1997) Regional differences in synaptogenesis in human cerebral cortex. J Comparative Neurology 387 167-178
Krey JF, Dolmetsch RE (2007) Molecular mechanisms of autism: a possible role for Ca2+ signaling. Current Opinion in Neurobiology. 17: 112-119
Volkow ND, Tomasi D, Wang G, Vaska P, Fowler JS, Telang F, Alexoff D, Logan J, Wong C (2011), Effects of Cell Phone Radiofrequency Signal Exposure on Brain Glucose Metabolism. JAMA. 305 (8):808-813. doi: 10.1001/jama.2011.186
Aloe + Bioflavonoid ( Pectin )
Aloe vera in dermatology- a brief review.
Source–Department of Dermatology, Jondishapur University of Medical Sciences, Ahvaz, Iran. email@example.com
Abstract—Aloe vera Linne or aloe barbadensis Miller is a succulent from the Aloe family (400 different species), a tropical plant which is easily grown in hot and dry climates and widely distributed in Asia, Africa and other tropical areas. The use of aloe vera is being promoted for a large variety of conditions. The aim of this systematic review was to summarize all dermatology-oriented in vitro and in vivo experiments and clinical trials on aloe vera preparations. Extensive literature search were carried out to identify all in vitro and in vivo studies as well as clinical trials on the subject. Data were extracted from these in a predefined standardized manner. Forty studies were located. The results suggest that oral administration of aloe vera in mice is effective on wound healing, can decrease the number and size of papillomas and reduce the incidence of tumors and leishmania parasitemia by >90% in the liver, spleen, and bone marrow. Topical application of aloe vera is not an effective prevention for radiation-induced injuries and has no sunburn or suntan protection. It can be effective for genital herpes, psoriasis, human papilloma virus, seborrheic dermatitis, aphthous stomatitis, xerosis, lichen planus, frostbite, burn, wound healing and inflammation. It can also be used as a biological vehicle andan anti-microbial and antifungal agent and also as a candidate for photodynamic therapy of some kinds of cancer. Even though there are some promising results with the use of aloe vera for diverse dermatologic conditions, clinical effectiveness of oral and topical aloe vera is not sufficiently and meticulously explored as yet.
PARSLEY, THE NEW PREDNISONE?
Parsley has been used for years as a folk remedy for water retention, coughs, allergy, autoimmune, and chronic inflammatory disorders. Although it is one of the most potent disease-fighting plants little is known about how parsley works its magic….that is, until now. Recently, scientists set out to examine just one of the many wonders of parsley, its immune effects, in rigorous scientific detail. They looked at how parsley oil interacts with T-cells and B-cells (both types of white blood cells) and macrophages (cells that engulf and eliminate other cells). Conclusion: parsley oil acted in a similar way to drugs that suppress the immune system, like prednisone, but without the harmful side effects. As if that weren’t enough, other studies have shown that parsley has antitumor, antibacterial, and antioxidant properties.
Karimi MH et al. “Parsley and immunomodulation.” Expert Rev Clin Immunol. 2012 May;8(4):295-7. http://www.expert-reviews.com/doi/pdf/10.1586/eci.12.12
It is believed that parsley is one of the world’s seven most potent disease-fighting spices . Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant.
Throughout history, herbs have been utilized as an important constituent of foods, industry and folk medicine. One of the widely used vegetal species in various nations’ medicine is parsley (Petroselinum crispum), which has remedial effects as a powerful diuretic agent [1,2], an abortifacient [3–5] and an expectorant [6,7]. Parsley is a native herb of the central Mediterranean region (southern Italy, Algeria and Tunisia), which is in the Apiaceae family, and is a species of Petroselinum . It is believed that parsley is one of the world’s seven most potent disease-fighting spices . Although parsley has been used to treat allergy, autoimmune and chronic inflammatory disorders, the mechanism underlying its beneficial effects in these immune-mediated diseases have been rarely investigated. Of the various therapeutically beneficial aspects of parsley, we decided to examine the immunomodulatory effects of this plant. In our study, the effects of parsley essential oil on phytohemagglutinin (PHA)-stimulated splenocytes (T cells) and lipopolysaccharide (LPS)-stimulated B cells, as the main effector cells in adaptive immune system, was examined. In addition, the suppressive activity of different concentrations (0.01–100 μg/ml) of parsley essential oil on macrophages and LPS-stimulated macrophages for evaluation of nitric oxide (NO) was studied . The methyl tetrazolium method was performed to survey the proliferation of mitogen-stimulated splenocytes as well as the viability of pretreated macrophages . NO production of both macrophage groups was determined in the Griess reaction . Parsley essential oil suppressed the proliferation of PHA-stimulated splenocytes at all applied concentrations. Similarly, it had a suppressive effect on the unstimulated and LPS-stimulated splenocytes, but only at high concentrations (10 and 100 μg/ml).NO production by unstimulated and stimulated macrophages was reduced by parsley essential oil; although, in all concentrations, unstimulated ones produced lower amounts of NO compared to the control group. These results can propose the suppressive effect of parsley essential oil on macrophages, as the major cells involved in the innate immune system .–The use of immunosuppressive drugs to control unwanted immune responses such as allergies, autoimmune disease and transplant rejection has grown over the past few years. The disadvantages and side effects of any immunosuppressive treatment are a significant and growing anxiety . Some serious side effects including nephrotoxicity, hepatotoxicity, induction of diabetes, hypertension and neurotoxicity have been stated for various immunosuppressive drugs [10,11]. Thus, healthier and lower risk therapeutics are required. In this regard, more attention has been recently made on natural products. For example, the immunosuppressive activity of various herbal plants and ingredients including Achillea talagonica,  Plantago ovata , Boerhaavia diffusa ,Stachys obtsicrena , Pollen Typhae  and Silymarin  has been explored. Parsley has also been shown to possess other biological activities than these described here. Several studies have suggested anticancer potential of parsley. By means of ascorbic acid‑induced lipid peroxidation, the antilipoperoxidant activity of parsley extracts has been shown [10,17,18]. The antioxidant activity of parsley essential oil has been confirmed in other investigations. Wong et al. indicated that the phenolic compounds of parsley were responsible for its antibacterial and antioxidant activity . Zhang and his coworkers demonstrated the antioxidant activity of this herb in terms of b-carotene bleaching capacity and free radical scavenging activity . This concept was then supported by further studies . Parsley possesses several flavonoids such as apiin and luteolin, and its essential oil contains apiol and myristicin. These components are believed to be responsible for the therapeutic effects of parsley [17,21]. Kandaswami et al. indicated the direct and indirect effects of flavonoids on tumor cells. Their studies showed that the hydroxylation pattern of the B-ring of the flavons and flavonols, such as luteolin and quercetin, seemed to affect their angionesis and anticancer activity, especially the inhibition of protein kinase activity and antiproliferation . Robak and his coworkers believe that flavonoids are the superoxide anion scavengers of the media and this effect can also lead to their anti-inflammatory effects . Daly et al. observed bioactive phytochemicals, including carotenoids, in parsley. Carotenoids were shown to be associated with a low risk of several human chronic disorders including age-related macular degeneration and certain cancers. Matching the wide use of this vegetal species as a diuretic in folk medicine, natriuretic and hypotensive effects of parsley were demonstrated in studies by Kreydiyyeh and Usta, and de Campos et al. [1,2]. Further studies indicated more biological effects of parsley plants, such as provitamine A activity, and influencing the cell signaling pathways [22,23]. In summary, parsley is a plant with various biological activities. With respect to its immunomodulatory effects, we found that its inhibitory effect on PHA-stimulated splenocytes might be due to the production of cytokines such as IFN-g and IL-2, which are vital for T-cell proliferation or it may influence the signaling pathways. Our results indicated that parsley essential oil can modulate the activity of macrophages without exerting cytotoxic effect. The immunomodulatory effect of parsley essential oil and its modulatory effects on NO production and function of macrophages may identify it as a useful natural candidate to treat some autoimmune and allergic diseases; however, its further application needs more investigation.
1 Kreydiyyeh SI, Usta J. Diuretic effect and mechanism of action of parsley. J. Ethnopharmacol. 79, 353–357 (2002).
2 de Campos KE, Balbi APC, De Freitas Alves MJQ. Diuretic and hypotensive activity of aqueous extract of parsley seeds (Petroselinum sativum Hoffm.) in rats. Braz. J. Pharmacog. 19(1A), 41–45 (2009).
3 Tyler VE. The Honest Herbalist (3rd Edition). Pharmaceutical Products Press, London, UK, 235–236 (1993).
4 Anderson LA, Newall CA, Phillipson JDA. Guide for Health-care Professionals. The Pharmaceutical Press, London, UK, 203–204 (1996).
5 Robbers JE, Tyler VE. Tyler’s Herbs of Choice. The Therapeutic Use of Phytochemicals. Haworth Herbal Press, NY, USA, 92 (1999).
6 Daly T, Jiwan MA, O’Brein M, Aherne SA. Carotenoid content of commonly consumed herbs and assessment of their bioaccessibility using an in vitrodigestion model. Plant. Foods Hum. Nutrit. 65(2), 164–169 (2010).
7 Zhang H, Chen F, Wang X, Yao HY. Evaluation of antioxidant activity of parsley (Petroselinum crispum) essential oil and identification of its antioxidant constituents. Food Res. Int. 39(8), 833–839 (2006).
8 Lopez MG, Sanchez-Mendoza IR, Ochoa-Alejo N. Compartive study of volatile components and fatty acids of plants and in-vitro cultures of parsley (Petroselinum crispum [Mill] nym ex hill). J. Agric. Food Chem. 47, 3292–3296 (1999).
9 Yousofi A, Daneshmandi S, Soleimani N, Bagheri K, Karimi MH. Immunomodulatory effect of Parsley (Petroselinum crispum) essential oil on immune cells: mitogen-activated splenocytes and peritoneal macrophages. Immunopharmacol. Immunotoxicol. 34(2), 303–308 (2012).
10 Vial T, Descotes J. Immunosuppressive drugs and cancer. Toxicology 185(3), 229–240 (2003).
11 Qin F, Sun HX. Immunosuppressive activity of pollen typhae ethanol extract on the immune responses in mice. J. Ethnopharmacol. 102, 424–429 (2005).
12 Rezaeipoor R, Saeidnia S, Kamalinejad M. Immunosuppressive activity of Achillea talagonica on humoral immune responses in experimental animals. J. Ethnopharmacol. 65, 273–276 (1999).
13 Rezaeipoor R, Saeidnia S, Kamalinejad M. The effect of Plantago ovata on humoral immune responses in experimental animals. J. Ethnopharmacol. 72, 283–286 (2000).
14 Mehrotra S, Mishra KP, Maurya R, Srimal RC, Singh VK. Immunomodulation by ethanolic extract of Boerhaavia diffusa roots. Int. Immunopharmacol.2, 987–996 (2002).
15 Amirghofran Z, Bahmani M, Azadmehr A, Javidnia K. Immunomodulatory and apoptotic effects of Stachys obtusicrena on proliferative lymphocytes.Med. Sci. Monit. 13(6), BR145–BR150 (2007).
16 Gharagozloo M, Velardi E, Bruscoli S et al. Silymarin suppress CD4+ T cell activation and proliferation: effects on NF-kB activity and IL-2 production.Pharmacol. Res. 61(5), 405–409 (2010).
17 Mimica-Dukić N, Popović M. Apiaceae species. A promising sources of pharmacologically active compounds I: Petrosellinum crispum, Apium greveolensand Pastinaca sativa. In: Recent Progress in Medicinal Plants. Govil JN, Singh VK (Eds). Studium Press LLC, TX, USA (2007).
18 Fejes S, Blázovics A, Lemberkovics E, Petri G, Szöke E, Kéry A. Free radical scavenging and membrane protective effects of methanol extracts fromAnthriscus cerefolium L. (Hoffm.) and Petroselinum crispum (Mill.) Nym. ex A. W. Hill. Phytother. Res. 14(5), 362–365 (2000).
19 Wong PYY, Kitts DD. Studies on the dual antioxidant and anti bacterial properties of parsley (Petroselinum crispum) and cilantro (Coriandrum sativum) extracts. Food Chem. 97, 505–515 (2006).
20 Kolarovic J, Popovic M, Zlinská J, Trivic S, Vojnovic M. Antioxidant activities of celery and parsley juices in rats treated with doxorubicin. Molecules 15, 6193–6204 (2010).
21 Lombaert GA, Siemens KH, Pellaers P, Mankotia M, Ng W. Furanocoumarins in celery and parsnips: method and multiyear Canadian survey. J. AOAC Int. 84, 1135–1143 (2001).
22 Kandaswami C, Lee LT, Lee PP et al. The antitumor activities of flavonoids. In Vivo 19(5), 895–909 (2005).
23 Robak J, Rys Z, Gryglewski J. Flavonoids are scavengers of super oxide anions. Biochem. Pharm. 37, 837–841 (1998)
[U1]Again this information is somewhat outdated—since mercury is in most fish consumed today it is arguably that the mercury can further diminish your low iodine levels—so again an alternative maybe eating grass fed beef which will have iodine in them based on the feed and without the mercury or seek other sources of aquatic life that may feed on seaweed to obtain the iodine
[U2]Radishes can be goiterogenic so again if you do consume them not often and should be utilizing seaweed or watercress with it
[U3]These are the goiterogenic goods
[U4]Smart Meter-Cell Phone—HAARP -Microwaves
[U5]A bad source—you would need to take 650grams -1 lb 7oz-to get the equivalent 1 drop of lugols
[U6]The key word is EXCESS!!
[U7]AGAIN this is only if the pollution is low and fish all has some form of arsenic and mercury so if you eat fish make sure that it is marinated properly with anti mercury substances—so that when being consumed the toxins are neutralized
[U8]Now this is where it gets tricky—it does not say how long it will take—but it gives the feeling or perspective that it will be quick—this IS NOT SO—it will be contingent on health—how much you are lacking—and what other complimentary minerals or aminos you may be missing as well
[U9]Other then Watercress the rest of the foods mentioned will be determined in there geographical areas which will determine how much is in the soil And how much is absorbed if any—the iodine that is
[U10]ACTIVATE the Thyroid
[U11]Even this is to low way to low-1000mcgs = 1mg the suggested daily dose is 13 mgs to sustain adequate levels—and use more depending on life style and exposure to environments
How to Self-Test for an Iodine Deficiency
1. Dip a cotton ball into USP Tincture of Iodine.
2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
3. Wait. — If the yellowish stain disappears in less than an 4 hours; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, you iodine levels are fine.
Why check your iodine levels?—Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night’s sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling “blah,” you may want to perform this self-test.—Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong.
Why are iodine levels so important?–Low levels of iodine mean your thyroid may not be functioning properly. The thyroid needs iodine to function as it helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude.—-Women are naturally prone to iodine deficiencies. That’s because the thyroid gland in women is twice as large as in men — so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That’s an 83% decline.—-Two thirds of the body’s iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed -sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels. Incorporating seafood and fish into your diet can also help[U1] . Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, radishes[U2] , and watercress. Some foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips.—[U3] To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are needed so make sure that foods containing these nutrients are included in your diet. However, if you have the immune system deficiency called Hashimoto’s Thyroiditis, you should not supplement your diet with iodine as it may aggravate the condition.
List of factors that impairs thyroid function.
1. Aging linked to a gradual decline of both thyroid and adrenal hormones.
2. Alpha Lipoic Acid (does not affect everyone)
4. Chronic illness
5. Cigarette smoking
6. Diet factors. Soy products and cruciferous vegetables dose dependent (avoid large quantities). Studies in animals show soy impairs T4 to T3 conversion.
7. Drugs (Birth control pills, Lithium, Estrogens, Propranolol, Beta blockers, Dexamethasone, Methimazole and Propylthiouracil)
8. External radiation[U4]
9. Growth hormone deficiency
10. Heavy metal toxicity including mercury and lead, pesticides, sodium chloride as well as sodium fluoride in city water.
12. High Stress
13. Low adrenal states
14. Malnutrition (mineral deficiencies) consumption of trans fats and hydrogenated fats and a lack of good fats monounsaturated avocados, olive oil, palm, omega 3.
15. Mineral and vitamin deficiencies (selenium, Vitamin A, B6 and B12)
16. Postoperative state
17. Physical trauma.
Besides the above list research views that in a state of hypothyroidism, hydrocortisone production and metabolism is usually low. Hypothyroidism can be established by chronic low basal body temperature as measured by the Barnes method upon rising. Thus a direct link has been established between subnormal thyroid and inadequate adrenal production of hormones.
Toxemia or the buildup of toxins in the body and an impairment of the detoxification pathways can be a major cause of impaired thyroid function. Link by link, the health of one organ affects the health of another. The liver, the organ through which most detoxification occurs, has the greatest burden of all.
Today, I reasonably estimate that due to toxins in the diet, air pollution and contaminants in the water we drink and electromagnetic pollution, that the combined effect contributes to overworked adrenal and subnormal thyroid activity in at least a third or more of the population in the United States.
Degeneration of the Adrenal Glands may occur as a symptom of Choline deficiency. [more info]
Vitamin A concentrates in the Adrenal Glands and may improve the function of the Adrenal Glands. references
Vitamin B5 may activate the Adrenal Glands and may “revive” exhausted Adrenal Glands.
Vitamin C is essential for the function of the Adrenal Glands – the Adrenal Glands (especially the Adrenal Medulla) contain approximately 30 mg of Vitamin C – the second highest concentration of Vitamin C of any component of the body.
Vitamin E concentrates in the Adrenal Glands (within the Adrenal Cortex). The Adrenal Glands contain 132 mcg of Vitamin E per gram).
Adrenal Extract may improve the function of the Adrenal Glands in persons with impaired Adrenal Gland function.
Tyrosine may relieve excessive stress on the Adrenal Glands
Pregnenolone production (from Cholesterol) occurs primarily in the Adrenal Glands (but is also produced in smaller quantities in other areas of the body, including the Liver, Brain, Skin and Retina of the Eye).
Could painting a circle of iodine solution on the skin daily help get rid of the candida albicans, parasites, HHV-6, herpes, hepatitis and multiple other bacterial, fungal, parasitic and viral infections including HIV?
Exploring many uses for topical iodine solution
Iodine for HIV – to directly kill the virus
Iodine to treat opportunistic infections in AIDS
Iodine for chronic Candidiasis, EBV and CMV
Iodine for viral hepatitis A, B, C and D
Iodine for HHV-6 infection
Iodine for parasites
Iodine for herpes
Iodine for strep and staff infections
Iodine for sore joints and arthritis
Iodine for rheumatism
Iodine for the flu
Iodine for a sore throat
Iodine for almost any bacterial, fungal, parasitic or viral infection that exists.
Iodine to increase the thyroid’s production of thyroxin
Iodine to help restore normal body temperature
Iodine to prevent and treat metabolic syndrome (obesity, diabetes and heart disease)
Iodine is cheap, plentiful and safe to use.
Here is how to do iodine testing and use
1. Dip a cotton ball into USP Tincture of Iodine –Lugols will do as well
2. Paint a 2 inch circle of iodine on your soft skin, like the inner part of your thigh or upper arm.
3. Wait. — If the yellowish stain disappears in less than an hour; it means your body is lacking crucial iodine and has soaked it up. If the stain remains for more than 4-8 hours, your iodine levels are fine.
Why check your iodine levels? —Low iodine levels can zap your energy and make you feel tired, edgy and worn out. Low iodine levels can even prevent you from getting a good night’s sleep. Before you go to your doctor with complaints of tossing and turning all night, aches and pains, and just feeling “blah,” you may want to perform this self-test.
Because the symptoms of an iodine deficiency are classically identical to so many other illnesses (like depression, stress, chronic fatigue, or fibromyalgia,) many doctors either misdiagnose it or miss it completely and tell you there is nothing wrong. —About 60% of all iodine in the human body is stored in the thyroid gland at the base of the neck. A Goiter, an enlargement of the thyroid gland, can occur when iodine deficiency is prolonged over a period of time. Iodine is the most important mineral used by the thyroid gland to produce thyroxin, a hormone that regulates the metabolic rate of energy production in the cells. —Iodine deficiency and a resulting insufficient production of thyroxin is linked to a wide range of illness form chronic infection of all types including candidiasis, herpes, bacterial, fungal and viral infections. —Table salt is iodized and is a source of iodine[U5] . However, excess sodium intake from salt consumption is a toxin and impairs the production of energy in the cells. Excess sodium intake is linked to metabolic syndrome including obesity, high blood pressure, heart disease and cancer. [U6] The best sources of iodine are from sea vegetables and seafood including ocean fish[U7] . Unfortunately, most people do not consume iodine rich foods on a daily basis. Low body temperature and long term chronic infections may be directly linked to a deficiency of iodine and an impaired thyroid function.
How much iodine to consume —-Why are iodine levels so important? Low levels of iodine mean your thyroid isn’t functioning properly. The thyroid helps balance hormones, regulate heartbeats, stabilize cholesterol, maintain weight control, encourage muscle growth, keep menstrual cycles regular, provide energy, and even helps you keep a positive mental attitude. —Women are naturally prone to iodine deficiencies. That’s because the thyroid gland in women is twice as large as in men — so under normal circumstances, women need more iodine. However, when women are under stress, the need for iodine can double or triple. Yet the foods we eat contain less and less dietary iodine. For example, back in 1940, the typical American diet contained about 800 micrograms of iodine. By 1995, that amount plunged to just 135 micrograms. That’s an 83% decline. —-Two thirds of the body’s iodine is found in the thyroid gland. One of the best ways to boost your iodine levels is to add seaweed sea vegetables to your diet. Just one teaspoon of sea vegetables a day can help you regain normal iodine levels[U8] . Incorporating seafood and fish into your diet can also help. Other foods that contain iodine are eggs and dairy products, including milk, cheese and yogurt, onions, and watercress. Some[U9] foods, called goitrogens, should be omitted for awhile as they hinder iodine utilization. These included kale, cabbage, peanuts, radishes, soy flour, Brussels sprouts, cauliflower, broccoli, kohlrabi and turnips. —-To reactivate the thyroid gland, tyrosine, iodine, zinc, copper and selenium are[U10] needed so make sure that foods containing these nutrients are included in your diet. —Editor’s note: The RDA of iodine is 150 mcg. That is just too little, in my opinion. Ideally, the average daily intake of iodine should be closer to 1000 mcg daily and higher than that for stress conditions that rapidly deplete iodine levels[U11] . Persons with systemic infections will need higher amount of iodine as this trace mineral will be rapidly bound to the infectious agents (bacterial, fungal or viral) in the process of destroying them thus leaving less iodine for the thyroid to pick up. While most people have an under active thyroid, a few people have an overactive thyroid but there is no research linking this to excess iodine intake.
Inactivation of human viruses by povidone-iodine in comparison with other antiseptics.
Kawana R, Kitamura T, Nakagomi O, Matsumoto I, Arita M, Yoshihara N, Yanagi K, Yamada A, Morita O, Yoshida Y, Furuya Y, Chiba S.
Dermatology . 1997;195 Suppl 2:29-35.
Morioka Yuuai General Hospital, Japan.
Inactivation of a range of viruses, such as adeno, mumps, rota-, polio- (types 1 and 3), coxsackie-, rhino-, herpes simplex, rubella, measles, influenza and human immunodeficiency viruses, by povidone-iodine (PVP-I) and other commercially available antiseptics in Japan was studied in accordance with the standardized protocol in vitro. In these experiments, antiseptics such as PVP-I solution, PVP-I gargle, PVP-I cream, chlorhexidine gluconate, alkyldiaminoethyl-glycine hydrochloride, benzalkonium chloride (BAC) and benzethonium chloride (BEC) were used. —-PVP-I was effective against all the virus species tested. PVP-I drug products, which were examined in these experiments, inactivated all the viruses within a short period of time. Rubella, measles, mumps viruses and HIV were sensitive to all of the antiseptics, and rotavirus was inactivated by BAC and BEC, while adeno-, polio- and rhinoviruses did not respond to the other antiseptics. PVP-I had a wider virucidal spectrum, covering both enveloped and nonenveloped viruses, than the other commercially available antiseptics.
Show Of the Month October 8 2012
Black Seed Plus Sarsparilla-Liver Protection
Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
BMC Complement Altern Med. 2012;12:25
Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
Abstract BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U19] s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action. METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death. RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.—CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.—PMID: 22458551 [PubMed – indexed for MEDLINE]
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
Symptoms of chemtrail spraying
by OkanaganChemtrails @ 20.08.10 – 19:05:47
We’ve covered this before on this blog but I believe that one way to put an end to this is to educate people how they are being poisoned. Who in their right mind wouldn’t want spraying to cease once they realize their health is being compromised? So here’s a new article and a few links to refresh everyone.
by Claude-Michel Prévost
Over the past ten years, through research and the personal accounts of many individuals, it has become readily apparent that the aluminum and barium salt mixtures, polymer fibers, toxic chemicals and biologicals sprayed in the atmosphere are the irritants that are either directly or indirectly responsible for health problems on the rise in the United States and elsewhere.
These toxic particulates are rapidly absorbed from the respiratory system and / or the gastrointestinal tract and are deposited in the lungs, muscles, and bone.
This illegal aerial spraying is producing atmospheric and ground conditions detrimental to human and animal health but favorable to the growth of harmful molds / fungus.
This overview is a partial list of health problems reported by private citizens to Chemtrail researchers.
1.Nose and lung bleeds (the latter including several reports from nursing homes of elderly dying from lung bleed outs, we believe being directly attributable to atmospheric aerosols); 2.Asthma and allergies;
3.Allergic bronchopulmonary aspergillosis (ABPA) (fungus on the lungs in both infants and adults),
4.Flu, Bronchitis and Pneumonia (in epidemic proportions, with doctors commenting to their patients on the many weeks it sometimes takes to improve and the lack of effective antibiotics to treat, including reports of pets having the flu, whole families being decimated), meningitis (inflammation / infection of the brain);
5.Upper respiratory symptoms (wheezing, dry cough), including Pulmonary Distress Syndrome (PDS) (in newborns, infants and adults alike), Sudden Infant Death (SIDS), and increased nationwide reports of the sudden death of athletes (reported in the news media as having possibly been attributable directly to air particulates / pollution);
6.Deaths from black mold; black or red mold on food crops (farmers reporting pH changes of soil and water), in buildings and ventilation systems (including school buildings);
7.Arthritis-like symptoms and muscular pain (young and old alike, sometimes crippling, and in pets);
8.Gastrointestinal distress (young and old alike, and in pets);
9.Bladder and yeast infections (includes bed wetting, not just in infants but adults);
10.Extreme fatigue (young and old alike);
11.Ringing of the ears, dizziness (increasingly reported immediately preceding or after a storm or weather system);
12.Eye problems – pink eye, blurred and deteriorating vision / nervous tics after exposure to the air outdoors;
13.Dry / cracking skin and lips, rashes, sores and fungal infections, aging of the skin;
14.Mental confusion / slow thinking and / or the feeling of mentally “being in a fog” (young and old alike, increasingly reported after actually being in heavy mists and fog banks);
15.Autoimmune disorders (Lupus, Crohn’s, Addison’s Disease, Rheumatoid Arthritis, etc.)
Note: Some of the above symptoms / illnesses can be related to other physical / environmental factors such as dehydration.)
Excessive amounts of aluminum can result in symptoms of poisoning. The symptoms include constipation, colic, loss of appetite, nausea, skin ailments, twitching of leg muscles, excessive perspiration, and loss of energy. People with aluminum poisoning should discontinue the use of aluminum cookware and the drinking of tap water. Small quantities of soluble salts of aluminum present in the blood causes slow form of poisoning characterized by motor paralysis and areas of local numbness, with fatty degeneration of kidney and liver. There are also anatomical changes in the nerve centres and symptoms of gastro intestinal inflammation.
In the last few years there has been much publicity about aluminum, as well as a tentative connection of aluminum to Alzheimer Disease. According to Dr. Terry L. Franks the clinical picture is clear that Alzheimers is concurrently involved with aluminum toxicity and he also believe it is the major contributing factor to Alzheimers. It will progressively worsen in North America in the coming year because of the pervasive use of aluminum. Aluminum has the tendency to freeze up or irritate nerve endings, producing spasm and contracture. When someone is going through aluminum detoxification can actually look like an advanced case of Alzheimers Disease.
Cooking utensils, antacids, baking powders, antiperspirants, some soft water, aluminum foils, concrete and process foods contain aluminum (table salt, cheese slices individually wrapped), bleached flour, fluoridated water increases leaching of aluminum.
How Aluminum Affects Health
In animal studies, aluminum blocks the action potential or electrical discharge of nerve cells, reducing nervous system activity. Aluminum also inhibits important enzymes in the brain (Na-K-ATPase and hexokinase). Aluminum may also inhibit uptake of important chemicals by nerve cells (dopamine, norepinephrine, and 5-hydroxytryptamine).
Dementia resulting from kidney dialysis related to aluminum toxicity causes memory loss, loss of coordination, confusion and disorientation.
Symptoms of Aluminum Toxicity
Early symptoms of aluminum toxicity include: flatulence, headaches, colic, dryness of skin and mucous membranes, tendency for colds, burning pain in the head relieved by food, heartburn and an aversion to meat. Later symptoms include paralytic muscular conditions, loss of memory and mental confusion. Other symtpoms may include:
Alzheimer’s disease, amyotrophic lateral sclerosis, anaemia, haemolysis, leukocytosis, porphyra, colitis, dental cavities, dementia dialactica, hypo-parathyroidism, kidney dysfunction, neuromuscular disorder, osteomalacia, Parkinson’s disease, ulcers.
Aluminum reduces intestinal activity, and by doing so can cause colic.
Treatmnet of Toxicity
Decreasing contact with and use of aluminum-containing substances will reduce intake and allow more aluminum to leave the body. Oral chelating agents will also help clear aluminum more rapidly. Calcium disodium edetate (EDTA) binds and clears aluminum from the body; this substance is fairly nontoxic and used as the agent for “chelation therapy,: an intravenous treatment used to pull metals such as lead from the body, and more recently used in the treatment of atherosclerosis and cardiovascular diseases.
Deferoxamine, an iron chelator, also binds aluminum. In a study with Alzheimer’s patients, nearly 40 percent of the patients showed an improvement in symptoms with deferoxamine treatment. There is some evidence that intravenous chelation with EDTA helps Alzheimer’s patients. More research is needed to evaluate aluminum’s involvement with this disease. Recovery is excellent for removing heavy metals.
Has been found to bind aluminum. The average dose, if the patient is relatively comfortable, is about six grams a day. Up to twelve grams is not excessive. The average time on an aluminum detoxification is three to four weeks.
The best way to prevent aluminum buildup is to avoid the sources of aluminum. Eliminating foods that have aluminum additives is probably healthier overall. Not using common table salt is a positive health step as well. Some tap waters contain aluminum, this can be checked. Avoiding aluminum cookware and replacing it with stainless steel, ceramic, or glass is a good idea. Blocking skin and sweat pores with aluminum anti-perspirants.
< The possibility of barium poisoning is a reality among people working in and living near heavy industrial sites such as chemical plants, factories that produce rubber products and other such places. That is because barium is one of the components used in manufacturing the products created in these plants.
However, because many of these products end up in ordinary households, it is also possible for a person who does not work in or live near an industrial plant to experience barium poisoning. Rat poison, for instance, contains barium compounds. Some fluorescent bulbs have coatings made from barium oxide. Fish caught in waters near industrial sites may have absorbed barium from the water.
Given the considerable probability of a person becoming afflicted with barium poisoning, how would you know for sure if you or someone living with you ingested barium at toxic levels? If you find yourself or someone living in your household with symptoms of barium poisoning, then you should act immediately.
What Is Barium?
In order to understand how serious barium poisoning is, we need first to understand what barium is in the first place. Barium is a heavy metal that naturally occurs in the environment. It is silvery white in appearance.
Barium is valuable in many industries that make use of heavy metal because it can remove traces of oxygen in some chemical compounds. It also increases the luster of glass. However, barium is explosive and can react violently when mixed with water. Also, it cannot be digested by the body; barium can be poisonous if the amount the body contains exceeds tolerable levels.
Symptoms of Barium Poisoning to Look For
When barium accumulates in the body, it usually affects the functions of the nervous system. Barium poisoning displays symptoms that are similar to flu, which is why it is not strange to find the condition misdiagnosed as flu. Common symptoms of barium poisoning include:
1. Muscle weakness and tremors 2. Difficulty in breathing 3. Stomach irritations accompanied by diarrhea 4. Anxiety 5. Cardiac irregularities such as abnormally high blood pressure and rapid heartbeat 6. Paralysis
What to Do in Case of Barium Poisoning
In case someone in your household has just ingested something that contains barium, the first thing you need to do is to induce him or her to vomit. This will get some of the barium out of the victim’s system. You can also mix a tablespoon of Epsom salts (sodium sulfate or magnesium sulfate) with a glass of water and get the victim to drink it. Afterwards, you should bring the victim to the emergency room of the nearest hospital to make sure that he or she does not succumb to barium poisoning.
You can also prevent barium poisoning from happening in your home. For one, you should keep your rat poison or any other chemical substances in your house that contains barium out of reach of children. Make sure that you have labeled their containers properly.
You should also avoid eating fish that was caught near industrial sites and ascertain that the fish and seafood you eat does not contain barium or any other heavy metal. This will prevent you from accumulating barium in your system and suffer from barium poisoning later on.
[U1]East indian Sarsparilla-chinese Sarsparilla and Black seed-decoction would be a tea boiled down to a complete extract
[U2]The less healthy oils would be soy and vegetable and canola oils or anything hydrogenated—these are toxic and become more so when heated and literally cause Genetic damage to the body
[U3]This is outdated there is no such thing as good or bad cholesterol in fact this study shows that using these
Diet promotes sleep duration and quality.
Nutr Res. 2012 May;32(5):309-19–Authors: Peuhkuri K, Sihvola N, Korpela R
Abstract–Sleep, much like eating, is an essential part of life. The mechanisms of sleep are only partially clear and are the subject of intense research. There is increasing evidence showing that sleep has an influence on dietary choices. Both cross-sectional and epidemiologic studies have demonstrated that those who sleep less are more likely to consume energy-rich foods (such as fats or refined carbohydrates), to consume fewer portions of vegetables, and to have more irregular meal patterns. In this narrative review, we pose the opposite question: can ingested food affect sleep? The purpose of this review is to discuss the evidence linking diet and sleep and to determine whether what we eat and what kind of nutrients we obtain from the food consumed before bedtime matter. In addition, scientific evidence behind traditional sleep-promoting foods such as milk and some herbal products is briefly described. These are reviewed using data from clinical trials, mostly in healthy subjects. In addition, we discuss the possible mechanisms behind these observations. Lastly, we summarize our findings that emerging evidence confirms a link between diet and sleep. Overall, foods impacting the availability of tryptophan, as well as the synthesis of serotonin and melatonin, may be the most helpful in promoting sleep. Although there are clear physiological connections behind these effects, the clinical relevance needs to be studied further.—PMID: 22652369 [PubMed – indexed for MEDLINE]
Short Sleep Duration and Weight Gain– A Systematic Review
- 1Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University Hospitals Case Medical Center and Case Western Reserve University, Cleveland, Ohio, USA
- 2Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, Massachusetts, USA
- 3Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts, USA
- 4Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts, USA
Correspondence: Sanjay R. Patel ()
Received 18 April 2007; Accepted 19 July 2007; Published online 17 January 2008.
The recent obesity epidemic has been accompanied by a parallel growth in chronic sleep deprivation. Physiologic studies suggest sleep deprivation may influence weight through effects on appetite, physical activity, and/or thermoregulation. This work reviews the literature regarding short sleep duration as an independent risk factor for obesity and weight gain.
Methods and Procedures—A literature search was conducted for all articles published between 1966 and January 2007 using the search “sleep” and (“duration” or “hour” or “hours”) and (“obesity” or “weight”) in the MEDLINE database. Additional references were identified by reviewing bibliographies and contacting experts in the field. Studies reporting the association between sleep duration and at least one measure of weight were included.
Results—Thirty-six publications (31 cross-sectional, 5 prospective, and 0 experimental) were identified. Findings in both cross-sectional and cohort studies of children suggested short sleep duration is strongly and consistently associated with concurrent and future obesity. Results from adult cross-sectional analyses were more mixed with 17 of 23 studies supporting an independent association between short sleep duration and increased weight. In contrast, all three longitudinal studies in adults found a positive association between short sleep duration and future weight. This relationship appeared to wane with age.
Discussion–Short sleep duration appears independently associated with weight gain, particularly in younger age groups. However, major study design limitations preclude definitive conclusions. Further research with objective measures of sleep duration, repeated assessments of both sleep and weight, and experimental study designs that manipulate sleep are needed to better define the causal relationship of sleep deprivation on obesity.
Introduction—Over the past several decades, the prevalence of obesity has grown to epidemic proportions. Concurrent with this rise in weight there has been a similar epidemic of chronic sleep deprivation. According to annual surveys done by the National Sleep Foundation, by 1998 only 35% of American adults were obtaining 8 h of sleep and that number had fallen to 26% by 2005 (ref. 1[U12] ).—–Evidence has grown over the past decade supporting a role for short sleep duration as a novel risk factor for weight gain and obesity. A number of causal pathways linking reduced sleep with obesity have been posited based on experimental studies of sleep deprivation. Chronic partial sleep deprivation causes feelings of fatigue which may lead to reduced physical activity (2,3). Sleep deprivation may also have neurohormonal effects that increase caloric intake (4). Because of the rapidly accelerating prevalence of sleep deprivation, any causal association between short sleep durations and obesity would have substantial importance from a public health standpoint. We performed a systematic review of the literature to assess the present evidence suggesting that sleep deprivation may represent a novel risk factor for weight gain and obesity.
Methods and Procedures—-Relevant original articles were identified by searching the MEDLINE database (National Library of Medicine, Bethesda, MD) of articles published between 1966 and August 2006 examining the relationship between sleep duration and weight gain, obesity, or both. The primary search was performed using the keywords “sleep” and (“duration” or “hour” or “hours”) and (“obesity” or “weight”). A subsequent search was also performed using medical subheading terms. The searches were repeated in January 2007 to identify any new publications. Bibliographies of retrieved articles were reviewed, and experts in the field were contacted to further identify relevant works. Articles were restricted to studies conducted in humans presenting original research. Where data from the same cohort were presented in more than one article, only the report that most directly analyzed the sleep–weight association was included. All abstracts obtained from this search were screened. Relevant articles were obtained and evaluated for presentation of data regarding the association between sleep duration and at least one measure of weight (e.g., BMI, BMI z-score, and weight) either cross-sectionally or longitudinally. A meta-analysis was attempted, but the degree of heterogeneity among study designs, particularly with respect to the measure of association and the definition of short sleep duration, was prohibitive, and therefore a more qualitative assessment is presented. Greater weight is given to large studies, prospective cohort studies, and studies which objectively assessed sleep durations. Because of differences in the sleep requirements of children and adults, these groups are considered separately. Where results were presented graphically, authors were contacted to obtain the numeric data (3,5,6).
Results—The keyword search initially identified a total of 1,013 citations. After screening through abstracts for relevance, 36 articles of potential relevance were identified. The medical subheading search identified an additional five articles. Fifteen articles were excluded because, though both sleep duration and weight data were collected, the association between these two factors was not assessed. Another five articles were excluded for presentation of data overlapping with another report, leaving 21 articles. Ten investigations were added after the original extraction from review of references and expert contact. The updated search in January 2007 identified 44 additional citations, of which 5 were relevant for this synthesis. Thus 36 studies were included in this analysis. Of these, 31 are cross-sectional studies, 2 are prospective cohort studies, and 3 report both cross-sectional and prospective findings. No experimental studies with weight as an outcome were identified. There are 13 studies examining the association between sleep duration and weight in pediatric populations and 23 studies of adults.
Cross-sectional studies in children—Eleven studies were identified which assessed the cross-sectional association between sleep duration and weight in children (Table 1). All 11 works reported a positive association between short sleep duration and increased obesity. For the most part, obesity was defined by age-adjusted thresholds of BMI, which was directly measured, while sleep duration was typically obtained from questionnaires completed by parents. Because sleep requirements change through childhood, definitions of short sleep duration varied greatly based on the age of the cohort being studied.–The largest pediatric cohort to date is a Japanese birth cohort of 8,274 children assessed between the ages of 6 and 7 (ref. 7). Compared to children with a sleep duration of 10 h, the odds ratios (ORs) for obesity were 1.49, 1.89, and 2.89 for sleep durations of 9–10, 8–9, or <8 h, respectively. A study of 4,511 Portuguese school children aged 7–9 reported similar findings (8). Compared to a sleep duration of 11 h, the ORs for obesity were 2.27 and 2.56 for sleep durations of 9–10 and 8 h, respectively.—-Two studies have analyzed data from children undergoing health screens at school enrollment. A study of 6,645 German children aged 5–6 years found the ORs for obesity were 1.18 and 2.22 for sleep durations of 10.5–11.0 and <10.5 h, respectively, compared to 11.5 h (9). A similar study of 1,031 French 5-year-olds found the OR for obesity was 1.4 for a sleep duration <11 h (10).—Three smaller studies have examined a broader range of grade school children. A study of 422 Canadian children ages 5–10 found that compared to a sleep duration of 12 h, the ORs for obesity were 1.42 and 3.45 for sleep durations of 10.5–11.5 and 10 h (11). Two small case–control studies of children aged 6–10 years, one from Brazil and one from Tunisia, reported similar findings. Giugliano and Carneiro reported obese children had 31 min shorter sleep duration than normal weight children but no significant difference was found between overweight and normal weight children (12). Ben Slama et al. found 58% of obese children had a sleep duration <8 h compared to only 11% of nonobese children (13).
Four studies have examined the relationship between sleep duration and weight in adolescents. Two of these studies, though small, were notable for using objective measures of sleep habits. Measuring sleep duration with wrist actigraphy over a 24-h period in 383 children aged 11–16, Gupta et al. reported one of the strongest associations between short sleep duration and obesity, with the odds of obesity increasing five-fold for every hour reduction in sleep duration (14). Benefice et al., using an accelerometer worn near the hip to assess sleep over 3–4 days in 40 Senegalese girls aged 13–14 years, observed that sleep duration was reduced by 6.85 min for every 1 kg/m2 increase in BMI (15). This work was notable for demonstrating a sleep–weight relationship in a nonobese population—mean BMI was only 16.9 kg/m2. The other adolescent reports included one of 4,486 American teens (mean age 16.6 years), which found short self-reported sleep duration predicted both higher BMI z-score and overweight among boys. However, no relationship was found in girls (16). A study of 656 Taiwanese teenagers (mean age 15.0 years) found that the frequency of obtaining a sleep duration of at least 6–8 h was inversely correlated with obesity risk (17).
The consistent findings from studies spanning five continents suggest that the reported associations are independent of ethnicity, though no formal assessment of effect modification by race has been reported. Several studies suggest boys may be more susceptible to sleep loss than girls. Sekine et al. found the OR for obesity associated with a sleep duration <8 h compared to >10 h was 5.5 in boys and 2.1 in girls (7). Similarly, Chaput et al. found that the OR for obesity associated with a sleep duration of 10 h as opposed to 12 h was 5.7 in boys and 3.2 in girls (11). Knutson found the risk of being overweight increased 10% for each hour reduction in sleep duration among boys, while no significant effect was found among girls (16). A few studies have attempted to identify the causal pathway linking sleep duration to obesity. Von Kries et al. found no relationship between sleep habits and caloric intake obtained from a food frequency questionnaire (9). Gupta et al., using actigraphy, and Benefice et al., using accelerometry to estimate activity levels, each found no relationship between sleep duration and physical activity (14,15).
Cross-sectional Studies in adults—Nineteen studies have focused on the cross-sectional relationship between sleep duration and weight in adults. The findings have been less consistent than the pediatric literature. Eleven studies reported a clear association between short sleep duration and increased weight, and two studies reported mixed findings with an association found in one gender but not in the other. Five studies reported no association between short sleep duration and increased weight, while one found short sleep duration was associated with reduced weight. In addition, six studies have found evidence that long sleep durations are also associated with increased weight resulting in a U-shaped curve between sleep duration and weight. In general, obesity has been defined as a BMI 30 kg/m2 based on either measured or self-reported height and weight. Habitual sleep duration has been typically obtained through questionnaire.—-The largest studies reporting on the association between sleep duration and weight were designed as prospective cohort studies to examine the effects of a wide range of behaviors on health outcomes and were not specifically designed to study sleep duration (5,18,19,20). Furthermore, data on the cross-sectional association between sleep duration and weight in these cohorts were presented as part of analyses designed to assess sleep duration as a predictor of mortality and so focused on the potential of weight to confound the sleep–mortality association. As a result, only the marginal associations between sleep duration and BMI were computed. The largest of these studies was a survey by the American Cancer Society of over 1.1 million individuals (5). This study found a U-shaped association between sleep duration and BMI among women with the minimum at 7 h and a monotonic trend in men such that longer sleep durations were associated with a lower BMI. Comparing a sleep duration of 4–7 h, women had a 1.39 kg/m2 greater BMI and men had a 0.57 kg/m2 greater BMI. The next largest study was a Japanese cohort of over 100,000 individuals (19). This is the only study to find short sleep durations associated with reduced weight. Mean BMI in those with sleep durations 4, 5, 6, and 7 h were 22.2, 22.6, 22.9 and 22.7 kg/m2 for men and 22.6, 22.9, 22.9, and 22.9 kg/m2 for women. A second Japanese cohort of over 10,000 individuals found no association between sleep duration and weight (20). On the other hand, a Scottish study of 6,797 individuals found mean BMI was 0.3 kg/m2 greater among men with a sleep duration <7 h compared to 7–8 h (18). Two other studies considered weight as a secondary outcome. The Sleep Heart Health Study, in studying the association of sleep duration with hypertension, found a U-shaped association between sleep duration and weight with BMI 0.7 and 0.4 kg/m2 greater in those with sleep durations <6 and 6–7 h compared to 7–8 h (21). A Swedish study of sleep duration and diabetes found sleep duration was inversely correlated with both BMI (r = -0.06) and waist-to-hip ratio (r = -0.08) (ref. 22).
Two studies using population-based sampling techniques have directly assessed the relationship between short sleep duration and obesity in middle-aged populations. The larger studied 3,158 adults and found an inverse association between sleep duration and obesity with a minimum risk associated with a sleep duration of 8–9 h (23). Compared to this group, the ORs for obesity were 1.85, 1.49, 1.24, and 1.09 for sleep durations 5, 5–6, 6–7, and 7–8 h. A second study of 1,772 Spanish subjects found a similar association with the odds of obesity 39% greater in those with a sleep duration of 6 h compared to a sleep duration of 7 h.
Several studies have examined the sleep–weight association in working populations. A survey of 4,878 Brazilian truck drivers found a sleep duration <8 h per day was associated with a 24% greater odds of obesity (24). Similarly, a survey of 4,793 Hong Kong union members found an inverse correlation between sleep duration and BMI (r = -0.037, P = 0.02) (ref. 25). This relationship was almost exclusively observed in men. In contrast, a French study of 3,127 workers found that while no association between sleep duration and weight was found in men, among women, those with a sleep duration of 6 h had a 0.63 kg/m2 greater mean BMI than those with longer sleep durations (26). In a study of 1,024 government workers in Wisconsin, a U-shaped association was found using sleep duration based on sleep diaries (27). In multivariate modeling, the minimum BMI corresponded to a sleep duration of 7.7 h. A cross-sectional study of 990 employed adults in Iowa found that BMI was 0.42 kg/m2 greater for each hour reduction in sleep duration (28).
Analysis of a Canadian family-based cohort supports the presence of a U-shaped relationship between sleep duration and obesity (29). The ORs for obesity were 1.63 and 1.51 in women with sleep durations of 5–6 and 9–10 h compared to 7–8 h. The corresponding values in men were 1.72 and 1.18. Similar associations were found between sleep duration and waist-to-hip ratio, body fat mass, and skinfold thicknesses.
Two reports have specifically examined the association between sleep duration and weight in geriatric cohorts. Both were designed to define normative sleep habits in the elderly and considered weight as a predictor of sleep duration. The first study recruited 8,091 individuals over the age of 55 from seven European nations (30). Obesity did not predict being in the lowest 5th percentile of sleep durations. A study of 1,026 French subjects over 60 found those with a BMI >27 kg/m2 were 3.6 times more likely to report nocturnal sleep duration in the lowest 5th percentile than those with BMI of 20–25 kg/m2 (31). However, the obese were also more likely to report daytime naps so that no association existed between total sleep duration and obesity.–Only one study of adults has examined the sleep–weight relationship using an objective measure of sleep duration. Lauderdale et al. investigated predictors of sleep duration in 669 individuals and used 72-h actigraphy to assess average sleep duration (32). In multivariate analysis, the study found a weak inverse correlation between sleep duration and BMI that was not statistically significant.—Two studies have examined the association between sleep habits and weight in clinic populations. Among 924 Americans attending a primary care clinic, sleep duration was longest in those with BMI <25 kg/m2 (33). In a study of 453 Japanese clinic patients, the odds of obesity was nearly double in those with a sleep duration <6 h (34).—Overall, the cross-sectional data in adults suggest short sleepers are heavier though the findings are much less consistent than the pediatric data. Several reports have noted a U-shaped association between sleep duration and weight in adults with the lowest BMI associated with a sleep duration of 7–8 h (5,21,27,29). If this relationship is truly U-shaped, studies that force a linear relationship in modeling the sleep–weight association would underestimate the true effect of short sleep duration and might explain the negative findings in some studies. Ethnic differences in susceptibility to sleep deprivation may also explain the disparate findings, as two of the three Japanese studies were negative. Although no study has directly examined differential susceptibility by ethnicity, several studies have noted that both obesity and sleep deprivation are more common among African Americans than whites (23,32). Findings on differences in gender susceptibility have been mixed. While several studies suggested a greater vulnerability in women (5,26,29,33), at least two reports found an association between short sleep duration and obesity existed only in men (18,25).—In terms of understanding the mechanism of any sleep–weight association, four of the studies finding an association between short sleep duration and obesity found this association could not be explained by differences in physical activity (18,26,29,35). In addition, one of the negative studies also found no relationship between sleep duration and physical activity (32). None of the studies assessed caloric intake. However, two studies examined biomarkers that may be relevant to appetite. Short sleep durations were associated with suppressed leptin levels in both the Quebec Family Study and the Wisconsin Sleep Cohort Study after adjusting for obesity (27,29). Short sleep durations were also associated with elevated ghrelin levels in the Wisconsin cohort (27).
Cell tower regulations frustrate homeowners Towers under 15 metres tall avoid municipal scrutiny
Do you live near an unexpected cellphone tower?
Homeowners across Canada are discovering cellphone towers popping up in residential neighbourhoods that slip just under height regulations that would require the company to notify those living nearby. Oakville[U13] , Ont., resident Lisa Guglietti was in the midst of building her dream home when the mother of three noticed eight cellular network antennas strapped to the chimney of a Bell Canada building, a short distance from her son’s bedroom. “We were surprised that we weren’t notified,” she said. “We asked some of the neighbours. None of the neighbours had any clue that these cellular antenna had been put up.” Under federal regulations, cellphone companies must notify the municipality for towers at least 15 metres high, but many new installations are coming up short of the limit, at just 14.9 metres. Homeowners say the rule undermines their ability to weigh in on installations in the community. Though the antennas are an eyesore, Guglietti’s primary concern is possible health effects. Experts disagree on the impact caused by cell towers. The International Agency for Research on Cancer classifies radiofrequency electromagnetic fields, which are emitted by wireless phones and cell towers, as a possible human carcinogen. Health Canada states that radiofrequency fields given off by cellphone towers are safe as long as the facility adheres to federal regulatory requirements limiting human exposure. In an email to CBC News, a Bell spokesperson wrote that all its sites, including the Oakville, Ont., one near Guglietti’s house, “meet or exceed all federal safety and other operating requirements.”
City councillor struggles with issue—In June, construction began on a 14.9-metre cellphone tower in a Barrie, Ont. neighbourhood that triggered a backlash over potential health concerns for those living across the street and students walking to nearby schools. “Telecommunications companies are able to come in and put these things basically wherever they want: as close to any residents, as close to any schools, and as close to any community centre they want,” Barrie, Ont. city councillor John Brassard told CBC News. “Why not make it 14.99 metres?” he asked. Since the incident, the Barrie city councillor has begun working to change federal regulations to give Canadians a voice over the placement of cell towers in their neighbourhoods. “Authority and a large part of that decision making should be made by the municipality and in consultation with Industry Canada. Not just Industry Canada alone.”
Government, company response—CBC News requested government data on the number of towers under 15 metres erected across Canada, but Industry Canada said the department doesn’t keep a database of that information[U14] . In the last year, Ottawa has collected about $582 million in revenue from telecommunications companies rolling out their networks of cell towers[U15] . Industry Canada told CBC News that companies are required to consult with the municipality and public before installing antenna towers, unless the towers fall within a certain height. “Certain installations, including towers less than 15 metres, generally have minimal local impact and so may be excluded from municipal consultation,” an Industry Canada spokesperson said in a written statement to CBC News. After discovering the cell antennas on the large brick building next door to her new house, Guglietti contacted the federal agency. An Industry Canada official responded in an email to Guglietti on June 8, 2012 that “given that the installation at the Bell central office building on Balsam Street complies with all procedural and technical requirements, Industry Canada is not in a position to order Bell to relocate the facility.” Cell tower antennas were strapped to a chimney that was 13 metres away from the bedroom of Lisa Guglietti’s son[U16] . (Angela Gilbert/CBC) Guglietti also contacted Bell Canada, which owns the building next door, and says she was initially told it would try to find an alternative location. However, the eight cell antennas remain attached to the chimney next door.
‘Don’t want to be a guinea pig’ –The scientific uncertainty over the health impact of cellphone towers doesn’t sit well with Guglietti. “I’m supposed to be OK with that?” asked Guglietti. “I’m supposed to have my son exposed to these frequencies day in and day out and I have to wait. Maybe in 10 years from now I’m going to find out, ‘Oh yeah there is, there can be health hazards in living so close to a cell tower.’ ” “I don’t want to be a guinea pig,” said Guglietti. A Bell spokesperson said in an email to CBC News that cellphone towers are being installed to meet customer demand[U17] . Guglietti said she’s certain other homeowners are dealing with similar concerns. If you have any information on this story, or other cellphone tower stories, please contact us at . “I need to protect myself and I need to protect my family. I’m a mother and I’m sure anyone would do the same thing in our situation.” If you have any information on this story, or other cellphone tower stories, please contact us at .
Red wine and components flavonoids inhibit UGT2B17 in vitro.
BACKGROUND: -The metabolism and excretion of the anabolic steroid testosterone occurs by glucuronidation to the conjugate testosterone glucuronide which is then excreted in urine. Alterations in UGT glucuronidation enzyme activity could alter the rate of testosterone excretion and thus its bioavailability. The aim of this study is to investigate if red wine, a common dietary substance, has an inhibitory effect on UGT2B17.
METHODS-Testosterone glucuronidation was assayed using human UGT2B17 supersomes with quantification of unglucuronidated testosterone over time using HPLC with DAD detection. The selected red wine was analysed using HPLC and the inhibitory effects of the wine and phenolic components were tested independently in a screening assay. Further analyses were conducted for the strongest inhibitors at physiologically relevant concentrations. Control experiments were conducted to determine the effects of the ethanol on UGT2B17.
RESULTS-Over the concentration range of 2 to 8% the red wine sample inhibited the glucuronidation of testosterone by up to 70% over 2 hours[U18] . The ethanol content had no significant effect. Three red wine phenolics, identified by HLPC analyses, also inhibited the enzyme by varying amounts in the order of quercetin (72%), caffeic acid (22%) and gallic acid (9%); using a ratio of phenolic: testosterone of 1:2.5. In contrast p-coumaric acid and chlorogenic acid had no effect on the UGT2B17. The most active phenolic was selected for a detailed study at physiologically relevant concentrations, and quercetin maintained inhibitory activity of 20% at 2 M despite a ten-fold excess of testosterone.
CONCLUSION-This study reports that in an in vitro supersome-based assay, the key steroid-metabolising enzyme UGT2B17 is inhibited by a number of phenolic dietary substances and therefore may reduce the rate of testosterone glucuronidation in vivo. These results highlight the potential interactions of a number of common dietary compounds on testosterone metabolism. Considering the variety of foodstuffs that contain flavonoids, it is feasible that diet can elevate levels of circulating testosterone through reduction in urinary excretion. These results warrant further investigation and extension to a human trial to delineate the health implications.
Rhodiola Protects HPG Axis during Exercise or Physical Work
[Salidroside protects the hypothalamic-pituitary-gonad axis of male rats undergoing negative psychological stress in experimental navigation and intensive exercise].
[Article in Chinese]
Source-Department of Endocrinology, Nanjing University School of Medicine/Nanjing General Hospital of Nanjing Military Region, Nanjing, 210002 Jiangsu, China.
OBJECTIVE-To study the effects of salidroside on the function and ultramicro-pathological change of the hypothalamic-pituitary-gonadal (HPG) axis of male rats in experimental navigation and intensive exercise.
METHODS-Six-week SD rats were randomized into 3 groups: non-stress control (NC, n = 10), training control (TC, n = 12) and salidroside treatment (ST, n = 12) group. Blood samples were collected from the NC rats that did not receive any stimulus after a 7-day intragastric administration of saline. The TC rats underwent a 10-day running training with increasing load on the treadmill followed by a 7-day intragastric administration of saline. The ST rats were subjected to the same process of running training as the TC group and received intragastric administration of salidroside. Then blood samples were immediately obtained and the levels of testosterone (T), corticosterone (CORT), adrenocorticotropic hormone (ACTH), luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) measured by radioimmunoassay. The testis histopathology was observed by HE staining, and the ultrastructural changes of the pituitaries and testes investigated by electron microscopy.
RESULTS-The serum T level was significantly lower in the TC than in the NC group, but showed no significant difference between the ST and NC groups. HE staining revealed no significant difference in testis histopathology among the 3 groups. Ultramicro-pathology showed that the secretory granules of the pituitary cells were significantly reduced in the TC rats compared with the NC ones; the number of the granules significantly increased in the ST group compared with the TC rats; and mitochondrial swelling, increase of electron density and decrease/disappearance of mitochondrial cristae were observed in the Leydig cells of the TC rats. But no significant differences were found in the testicular cells between the ST and NC groups.
CONCLUSION-Negative psychological stress and intensive exercise can significantly suppress the function of the HPG axis in rats. Salidroside therapy has protective effect on the HPG axis.
Chlorophyll revisited- anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same
The U.S. Drug Enforcement Administration classifies ADHD drugs as Scheudle ll,
in the same class of highly addictive drugs as morphine, opium and cocaine.
A) Drug Agency Regulatory Warnings on Stimulants/ADHD drugs – There have 31 drug regulatory agency warnings from eight countries including warnings of stimulant induced heart problems, suicide, violence, depression, mania, psychosis, hallucinations and death. See Tab A
B) Drug Studies on Stimulants – There have been 119 studies in twelve countries on stimulant induced side effects including birth defects, heart problems, depression, suicidal ideation, violence, hallucinations, mania, psychosis, homicidal ideation and death. See Tab B
C) Adverse Reaction Reports filed with the US FDA – There have been 14,158 adverse reactions reported to the US FDA in connection with stimulants. See Tab C
Tab A) Stimulant Drug Warnings:
There have been 31 warnings from eight countries (United States, United Kingdom, Canada, Japan, Australia, New Zealand, France and Singapore) warning that stimulants cause harmful side effects, which include:
12 warnings on stimulants causing heart problems 8 warnings on stimulants causing mania/psychosis 8 warnings on stimulants causing death 3 warnings on stimulants causing hallucinations 2 warnings on stimulants causing depression 2 warnings on stimulants causing violence, hostility or aggression 2 warnings on stimulants causing seizures 1 warning on stimulants causing suicide risk/attempts 1 warning on stimulants causing anxiety Back to Top
Tab B) Stimulant Drug Studies:
There are 20 studies from four countries (United States, Australia, Denmark and Italy) showing that stimulants cause harmful side effects, including:
5 studies on stimulants causing medication abuse 3 studies on stimulants causing heart problems 2 studies on stimulants causing death 1 study on stimulants causing suicide risk/attempts 1 study on stimulants causing birth defects 1 study on stimulants causing violence 1 study on stimulants causing homicidal ideation 1 study on stimulants causing depression 1 study on stimulants causing mania, psychosis and hallucinations Back to Top
Tab C – Stimulant Drug Side Effects Reported to the FDA:
The Adverse Drug Reactions that have been reported to the FDA’s Adverse Event Reporting System (MedWatch), between 2004 and 2011 include:
871 cases of stimulants causing reactions related to suicide (completed suicides, suicide attempts, suicidal ideation and suicidal behavior) 636 cases of stimulants causing aggression 593 cases of stimulants causing hallucinations 499 cases of stimulants causing anxiety 495 cases of stimulants causing abnormal behavior 464 cases of stimulants causing depression 220 cases of stimulants causing death/sudden death 147 cases of stimulants causing mania 52 cases of stimulants causing homicidal ideation 44 cases of stimulants causing diabetes 30 cases of stimulants causing hostility 25 cases of stimulants causing coma 23 cases of stimulants causing physical Assault 21 cases of stimulants causing birth defects 13 cases of stimulants causing violence-related symptoms 12 cases of stimulants causing psychosis 11 cases of stimulants causing homicide 9 cases of stimulants causing sexual dysfunction 1 case of stimulants causing stillbirth
Modulation of apoptosis in human hepatocellular carcinoma (HepG2 cells) by a standardized herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizomes with anti- hepatocarcinogenic effects.
BMC Complement Altern Med. 2012;12:25
Authors: Samarakoon SR, Thabrew I, Galhena PB, Tennekoon KH
Abstract BACKGROUND: A standardized poly-herbal decoction of Nigella sativa seeds, Hemidesmus indicus roots and Smilax glabra rhizome[U1] s used traditionally in Sri Lanka for cancer therapy has been demonstrated previously, to have anti-hepatocarcinogenic potential. Cytotoxicity, antioxidant activity, anti-inflammatory activity, and up regulation of p53 and p21 activities are considered to be some of the possible mechanisms through which the above decoction may mediate its anti-hepatocarcinogenic action. The main aim of the present study was to determine whether apoptosis is also a major mechanism by which the decoction mediates its anti-hepatocarcinogenic action. METHODS: Evaluation of apoptosis in HepG2 cells was carried out by (a) microscopic observations of cell morphology, (b) DNA fragmentation analysis, (c) activities of caspase 3 and 9, as well as by (d) analysis of the expression of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins associated with cell death. RESULTS: The results demonstrated that in HepG2 cells, the decoction can induce (a) DNA fragmentation and (b) characteristic morphological changes associated with apoptosis (nuclear condensation, membrane blebbing, nuclear fragmentation and apoptotic bodies). The decoction could also, in a time and dose dependent manner, up regulate the expression of the pro-apoptotic gene Bax and down regulate expression of anti-apoptotic Bcl-2 gene (as evident from RT-PCR analysis, immunohistochemistry and western blotting). Further, the decoction significantly (p < .001) enhanced the activities of caspase-3 and caspase-9 in a time and dose dependent manner.—CONCLUSIONS: Overall findings provide confirmatory evidence to demonstrate that the decoction may mediate its reported anti-hepatocarcinogenic effect, at least in part, through modulation of apoptosis.—PMID: 22458551 [PubMed – indexed for MEDLINE]
Recipe for making this decoction of Black seed and Smilax ( sarsaparilla)—take equal parts of each herb and boil them down to at least half of the volume of water you put in— I.E 2 pint down to 1 pint or less ( 500mls for the metric to 250 mls)—and then use small amounts 1-2 oz increments 4-5 times daily
Sesame and Rice Bran Oil Lowers Blood Pressure, Improves Cholesterol
ScienceDaily (Sep. 18, 2012) — People who cooked with a blend of sesame and rice bran oils saw a significant drop in blood pressure and improved cholesterol levels, according to new research presented at the American Heart Association’s High Blood Pressure Research 2012 Scientific Sessions.—The researchers found cooking with a combination of these oils in a variety of ways worked nearly as well as a commonly prescribed high blood pressure medication, and that the use of the oil blend with medication yielded even more impressive results.—“Rice bran oil, like sesame oil, is low in saturated fat and appears to improve a patient’s cholesterol profile,” said Devarajan Sankar, M.D, Ph.D., a research scientist in the Department of Cardiovascular Disease at Fukuoka University Chikushi Hospital in Chikushino, Japan. “Additionally, it may reduce heart disease risk in other ways, including being a substitute for less healthy oils and fats in the diet[U2] .”–The 60-day study in New Delhi, India, divided 300 people with mild to moderately high blood pressure into three groups. One group was treated with a commonly used blood pressure lowering medication called a calcium-channel blocker (nifedipine). The second group was given the oil blend and told to use about an ounce each day in their meals.—The final group received the calcium channel blocker and the oil blend.—-All three groups, with approximately an equal number of men and women, average age of 57, saw drops in their systolic blood pressure. Systolic blood pressure is the top number in a blood pressure reading and measures the force of blood against your artery walls when the heart is pumping.—Systolic blood pressure dropped an average of 14 points for those using only the oil blend and 16 points for those taking medication. Those using both saw a 36-point drop.—Diastolic blood pressure also dropped significantly: 11 points for those eating the oil, 12 for those on medication and 24 for those using both. Diastolic blood pressure is the bottom number in a blood pressure reading that measures the force of blood against your artery walls when your heart is at rest between beats.—As for cholesterol, those using the oils saw a 26 percent drop in their LDL (“bad” cholesterol) and a 9.5 percent increase in the HDL (“good” cholesterol[U3] ), while no changes in cholesterol were observed for the patients who used only the calcium-channel blocker. Those who took the calcium channel blocker and the oils had a 27 percent drop in LDL levels and a 10.9 percent increase in the HDL[U4] . Healthier fatty acids and antioxidants, such as sesamin, sesamol, sesamolin and oryzanol, in the oil blends may be responsible for the results, Sankar said. These antioxidants, mono and poly unsaturated oils are compounds found in plants and have been linked with lower blood pressure and total cholesterol in earlier studies.–Additional studies are needed to determine if the oil blend is as beneficial as it seems. The combination was made specifically for this study, and there are no plans to market it commercially, Sankar said. Blending these oils yourself would not necessarily produce these effects.–Co-authors are.Ravinder Singh, M.B.B.S., and Biprabuddha Chatterjee, M.Sc.-Story Source-The above story is reprinted from materials provided by American Heart Association.
Chlorophyll revisited~~ anti-inflammatory activities of chlorophyll a and inhibition of expression of TNF-α gene by the same.
Inflammation. 2012 Jun;35(3):959-66
Authors: Subramoniam A, Asha VV, Nair SA, Sasidharan SP, Sureshkumar PK, Rajendran KN, Karunagaran D, Ramalingam K
Abstract–In view of the folklore use of green leaves to treat inflammation, the anti-inflammatory property of chlorophylls and their degradation products were studied. Chlorophyll a and pheophytin a (magnesium-free chlorophyll a) from fresh leaves showed potent anti-inflammatory activity against carrageenan-induced paw edema in mice and formalin-induced paw edema in rats.[U5] Chlorophyll a inhibited bacterial lipopolysaccharide-induced TNF-α (a pro-inflammatory cytokine) gene expression in HEK293 cells, but it did not influence the expression of inducible nitric acid synthase and cyclooxygenase-2 genes. Chlorophyll b only marginally inhibited both inflammation and TNF-α gene expression. But both chlorophyll a and chlorophyll b showed the same level of marginal inhibition on 12-O-tetradecanoyl-phorbol-13-acetate-induced NF-κB activation. Chlorophylls and pheophytins showed in vitro anti-oxidant activity. The study shows that chlorophyll a and its degradation products are valuable and abundantly available anti-inflammatory agents and promising for the development of phytomedicine or conventional medicine to treat inflammation and related diseases.—PMID: 22038065 [PubMed – indexed for MEDLINE]
Chlorophyll is a chemoprotein commonly known for its contribution to the green pigmentation in plants, and is related to protoheme, the red pigment of blood. It can be obtained from green leafy vegetables (broccoli, Brussel sprouts, cabbage, lettuce, and spinach), algae (Chlorella and Spirulina), wheat grass, and numerous herbs (alfalfa, damiana, nettle, and parsley).–Chlorophyll has been used traditionally to improve bad breath and other forms of body odor including odors of the urine, feces, and infected wounds. More recently chlorophyll has been used to aid in the removal of various toxins via the liver and remains a key compound for improving the function of essential detoxification pathways. Supportive evidence suggests it may be used as an anti-inflammatory agent for conditions, such as pancreatitis as well as exhibiting potent antioxidant and chemoprotective activities. Scientific research has demonstrated it may be an effective therapeutic agent in the treatment of herpes simplex, benign breast disease, chemoprevention, tuberculosis, and rheumatoid arthritis. Type 2 diabetes and obesity are also being explored as areas where chlorophyll can also be used.
Bacterial Cause Found for Skin Condition Rosacea
ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement[U6] . Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.[U7] –A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals[U8] , which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite[U9] and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. [U10] What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”[U11] —“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0
How LOW Cholesterol Can Harm Your Health Grain-Wheat-Chronic Poison Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism Myocardial infarction in relation to mercury and fatty acids from fish Supplement Your Stem Cells—how to look at this study ************************************************************************** How LOW Cholesterol Can Harm Your Health You’ve heard for decades about the dangers of high cholesterol, but did you know that LOW cholesterol can lead to violence towards self and other, and has been linked to premature aging, death and other adverse health effects?–In a world gone mad with anti-cholesterol anxiety, and where gobbling down pharmaceuticals designed to poison the body into no longer synthesizing it is somehow considered sane behavior, it is refreshing to look at some of the research on the health benefits of cholesterol, or conversely, the dangers of low cholesterol. Benefits of Cholesterol Cholesterol Is Needed To Prevent Aggression It has been known for almost 30 years that low serum cholesterol levels are associated with habitually violent tendencies of homicidal offenders under the influence of alcohol.[i] Since then, there are at least 8 other studies that have either confirmed or explored the cholesterol-violence link, including both violence towards self and other. One of the possible explanations for this association was discussed in an article published in the British Journal of Psychiatry in 1993: “One of the functions of serotonin in the central nervous system is the suppression of harmful behaviour impulses…Low membrane cholesterol decreases the number of serotonin receptors. Since membrane cholesterol exchanges freely with cholesterol in the surrounding medium, a lowered serum cholesterol concentration may contribute to a decrease in brain serotonin, with poorer suppression of aggressive behaviour”.[ii] Not surprisingly, several reports have now surfaced on cholesterol-lowering statin drugs contributing to irritability and/or aggression. Cholesterol Is Needed To Fight Cancer The inverse relationship between cholesterol levels and the risk for a variety of cancers, and mortality associated with cancer, has been known about since the late 80′s.[iii] Since then, the cholesterol-cancer connection has been confirmed over and over again. It is to be expected, therefore, that statin drug use would be linked with increased cancer incidence, which indeed it is.[iv] Even when you take so-called “bad” LDL-cholesterol and administer it to a culture of highly malignant, multi-drug resistant leukemia cells, the cells lose their resistance to chemotherapy. Cholesterol Is Needed To Prevent Hemorrhagic Stroke There are two types of stroke: 1) Ischemic, associated with lack of blood flow and oxygen to the brain 2) Hemorrhagic, associated with the rupture of a blood vessel in the brain, and bleeding. The risk for the former, in theory, could be raised in the presence of excessive oxidized cholesterol. However, it is the risk for the second, hemorrhagic stroke, which is increased when cholesterol levels are low. Noted as far back as 1994 in the British Medical Journal, in an article titled, “Assessing possible hazards of reducing serum cholesterol,” researchers found “The only cause of death attributable to low serum cholesterol concentration was haemorrhagic stroke.”[vi] Other studies can be viewed that confirm this association on our stroke-cholesterol link page. Cholesterol Is Needed for Memory Low HDL cholesterol has been identified as a risk factor for deficit and decline in memory in midlife. [vii] Even in Parkinson’s disease, higher total serum cholesterol concentrations are associated with slower clinical progression of the disease.[viii]Statin drugs, which inhibit the production of cholesterol, hence severely affecting the brain, are now required by the FDA to display the black box warning that they may adversely affect the memory.[ix] We have indexed over 50 studies from the National Library of Medicine’s bibliographic database, Medline, on the neurotoxicity of statin drugs, with six of these specifically addressing statin-induced memory impairment. Cholesterol is Needed for Longevity In a fascinating study published in PLoS in 2011, telomere length – the shoestring cap-like ends of the chromosomes which prevent DNA damage associated with cellular aging – was linked to higher LDL and total cholesterol levels. The longer the length of these protective caps, the higher the cholesterol.[x] Indeed, several studies indicate that lower cholesterol is associated with increased mortality. Cholesterol Helps Us Fight Infection It has been observed that a cholesterol-rich diet improves patients with tuberculosis, leading researchers to suggest “cholesterol should be used as a complementary measure in antitubercular treatment.”[xi] Cholesterol-lowering drugs, incidentally, exhibit immunosuppressive and potent immunotoxic properties, likely in part due to their cholesterol depleting effects. Given that cholesterol is essential for all animal life and that each cell is capable of synthesizing it from simpler molecules, we should not be surprised by examples provided above of cholesterol’s significant health benefits. Nor should it be surprising that cholesterol-lowering drugs have over 300 adverse health effects. For now, suffice it to say, that conventional medical practice would do well to receive instruction from basic principles of biology, rather than simply the drug-company marketing copy it increasingly falls prey to. Article Sources
**************************************************************************** Grain-Wheat-Chronic Poison (CBS News) Modern wheat is a “perfect, chronic poison,” according to Dr. William Davis, a cardiologist who has published a book all about the world’s most popular grain. -Davis said that the wheat we eat these days isn’t the wheat your grandma had: “It’s an 18-inch tall plant created by genetic research in the ’60s and ’70s,” he said on “CBS This Morning.” “This thing has many new features nobody told you about, such as there’s a new protein in this thing called gliadin. It’s not gluten. I’m not addressing people with gluten sensitivities and celiac disease. I’m talking about everybody else because everybody else is susceptible to the gliadin protein that is an opiate. This thing binds into the opiate receptors in your brain and in most people stimulates appetite, such that we consume 440 more calories per day, 365 days per year.”–Asked if the farming industry could change back to the grain it formerly produced, Davis said it could, but it would not be economically feasible because it yields less per acre. However, Davis said a movement has begun with people turning away from wheat – and dropping substantial weight. –“If three people lost eight pounds, big deal,” he said. “But we’re seeing hundreds of thousands of people losing 30, 80, 150 pounds. Diabetics become no longer diabetic; people with arthritis having dramatic relief. People losing leg swelling, acid reflux, irritable bowel syndrome, depression, and on and on every day.”–To avoid these wheat-oriented products, Davis suggests eating “real food,” such as avocados, olives, olive oil, meats, and vegetables. “(It’s) the stuff that is least likely to have been changed by agribusiness,” he said. “Certainly not grains. When I say grains, of course, over 90 percent of all grains we eat will be wheat, it’s not barley… or flax. It’s going to be wheat. –“It’s really a wheat issue.”–Some health resources, such as the Mayo Clinic, advocate a more balanced diet that does include wheat. But Davis said on “CTM” they’re just offering a poor alternative. –“All that literature says is to replace something bad, white enriched products with something less bad, whole grains, and there’s an apparent health benefit – ‘Let’s eat a whole bunch of less bad things.’ So I take…unfiltered cigarettes and replace with Salem filtered cigarettes, you should smoke the Salems. That’s the logic of nutrition, it’s a deeply flawed logic. What if I take it to the next level, and we say, ‘Let’s eliminate all grains,’ what happens then?—“That’s when you see, not improvements in health, that’s when you see transformations in health.” http://www.cbsnews.com/8301-505269_162-57505149/modern-wheat-a-perfect-chronic-poison-doctor-says/?tag=cbsnewsSectionContent.8 *********************************************************************** Nutritional Supplement Offers Promise in Treatment of Unique Form of Autism ScienceDaily (Sep. 6, 2012) — An international team of researchers, led by scientists at the University of California, San Diego and Yale University schools of medicine, have identified a form of autism with epilepsy that may potentially be treatable with a common nutritional supplement.–The findings are published in the Sept. 6, 2012 online issue of Science.–Roughly one-quarter of patients with autism also suffer from epilepsy, a brain disorder characterized by repeated seizures or convulsions over time. The causes of the epilepsy are multiple and largely unknown. Using a technique called exome sequencing, the UC San Diego and Yale scientists found that a gene mutation present in some patients with autism speeds up metabolism of certain amino acids. These patients also suffer from epileptic seizures. The discovery may help physicians diagnose this particular form of autism earlier and treat sooner.–The researchers focused on a specific type of amino acid known as branched chain amino acids or BCAAs. BCAAs are not produced naturally in the human body and must be acquired through diet. During periods of starvation, humans have evolved a means to turn off the metabolism of these amino acids. It is this ability to shut down that metabolic activity that researchers have found to be defective in some autism patients.—“It was very surprising to find mutations in a potentially treatable metabolic pathway specific for autism,” said senior author Joseph G. Gleeson, MD, professor in the UCSD Department of Neurosciences and Howard Hughes Medical Institute investigator. “What was most exciting was that the potential treatment is obvious and simple: Just give affected patients the naturally occurring amino acids their bodies lack.”—Gleeson and colleagues used the emerging technology of exome sequencing to study two closely related families that have children with autism spectrum disorder. These children also had a history of seizures or abnormal electrical brain wave activity, as well as a mutation in the gene that regulates BCAAs. In exome sequencing, researchers analyze all of the elements in the genome involved in making proteins.—In addition, the scientists examined cultured neural stem cells from these patients and found they behaved normally in the presence of BCAAs, suggesting the condition might be treatable with nutritional supplementation. They also studied a line of mice engineered with a mutation in the same gene, which showed the condition was both inducible by lowering the dietary intake of the BCAAs and reversible by raising the dietary intake. Mice treated with BCAA supplementation displayed improved neurobehavioral symptoms, reinforcing the idea that the approach could work in humans as well.–“Studying the animals was key to our discovery,” said first author Gaia Novarino, PhD, a staff scientist in Gleeson’s lab. “We found that the mice displayed a condition very similar to our patients, and also had spontaneous epileptic seizures, just like our patients. Once we found that we could treat the condition in mice, the pressing question was whether we could effectively treat our patients.”—Using a nutritional supplement purchased at a health food store at a specific dose, the scientists reported that they could correct BCAA levels in the study patients with no ill effect. The next step, said Gleeson, is to determine if the supplement helps reduce the symptoms of epilepsy and/or autism in humans.—“We think this work will establish a basis for future screening of all patients with autism and/or epilepsy for this or related genetic mutations, which could be an early predictor of the disease,” he said. “What we don’t know is how many patients with autism and/or epilepsy have mutations in this gene and could benefit from treatment, but we think it is an extremely rare condition.” Co-authors are Paul El-Fishawy, Child Study Center, Yale University School of Medicine; Hulya Kayserili, Medical Genetics Department, Istanbul University, Turkey; Nagwa A. Meguid, Rehab O. Khalil, Adel F. Hashish and Hebatalla S. Hashem, Department of Research on Children with Special Needs, National Research Centre, Cairo, Egypt; Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Neurogenetics Laboratory, Howard Hughes Medical Institute, Department of Neurosciences, UC San Diego; Majdi Kara, Pediatric Department, Tripoli Children’s Hospital, Libya; Tawfeq Ben-Omran, Clinical and Metabolic Genetics Division, Department of Pediatrics, Hamad Medical Corporation, Doha, Qatar; A. Gulhan Ercan-Sencicek, Stephan J. Sanders and Matthew W. State, Program on Neurogenetics, Child Study Center, Department of Psychiatry and Department of Genetics, Yale University School of Medicine; Abha R. Gupta, Child Study Center, Department of Pediatrics, Yale University School of Medicine; Dietrich Matern, Biochemical Genetics Laboratory, Department of Laboratory Medicine and Pathology, Mayo Clinic; Stacy Gabriel, Broad Institute of Harvard and Massachusetts Institute of Technology; Larry Sweetman, Institute of Metabolic Disease, Baylor Research Institute; Yasmeen Rahimi and Robert A. Harris, Roudebush VA Medical Center and Department of Biochemistry and Molecular Biology, Indiana University School of Medicine.–Funding for this research came, in part, from the National Institutes of Health (grants P1HD070494, R01NS048453, P30NS047101, RC2MH089956, K08MH087639, T32MH018268, U54HG003067), the Center for Inherited Disease Research, the Simons Foundation Research Initiative, Veterans Administration Merit Award, the German Research Foundation, the American Academy of Child and Adolescent Psychiatry Pilot Research Award/Elaine Schlosser Lewis Fund and the American Psychiatric Association/Lilly Research Fellowship.—Story Source-The above story is reprinted from materials provided by University of California, San Diego, via Newswise. –Journal Reference-Gaia Novarino, Paul El-Fishawy, Hulya Kayserili, Nagwa A. Meguid, Eric M. Scott, Jana Schroth, Jennifer L. Silhavy, Majdi Kara, Rehab O. Khalil, Tawfeg Ben-Omran, A. Gulhan Ercan-Sencicek, Adel F. Hashish, Stephan J. Sanders, Abha R. Gupta, Hebatalla S. Hashem, Dietrich Matern, Stacey Gabriel, Larry Sweetman, Yasmeen Rahimi, Robert A. Harris, Matthew W. State, and Joseph G. Gleeson. Mutations in BCKD-kinase Lead to a Potentially Treatable Form of Autism with Epilepsy. Science, 2012; DOI: 10.1126/science.1224631 ************************************************************************ Myocardial infarction in relation to mercury and fatty acids from fish: a risk-benefit analysis based on pooled Finnish and Swedish data in men1,2,3,4
Abstract Background: Exposure to methylmercury from fish has been associated with increased risk of myocardial infarction (MI) in some studies. At the same time, marine n−3 (omega-3) PUFAs[U1] are an inherent constituent of fish and are regarded as beneficial. To our knowledge, no risk-benefit model on the basis of data on methylmercury, PUFA, and MI risk has yet been presented. Objective: The objective of this study was to describe how exposure to both marine n−3 PUFAs and methylmercury relates to MI risk by using data from Finland and Sweden. Design: We used matched case-control sets from Sweden and Finland that were nested in population-based, prospective cohort studies. We included 361 men with MI from Sweden and 211 men with MI from Finland. MI risk was estimated in a logistic regression model with the amount of mercury in hair (hair-Hg) and concentrations of n−3 PUFAs (EPA and DHA) in serum (S-PUFA) as independent variables. Results: The median hair-Hg was 0.57 μg/g in Swedish and 1.32 μg/g in Finnish control subjects, whereas the percentage of S-PUFA was 4.21% and 3.83%, respectively. In combined analysis, hair-Hg was associated with higher (P = 0.005) and S-PUFA with lower (P = 0.011) MI risk. Our model indicated that even a small change in fish consumption (ie, by increasing S-PUFA by 1%) would prevent 7% of MIs, despite a small increase in mercury exposure. However, at a high hair-Hg, the modeled beneficial effect of PUFA on MI risk was counteracted by methylmercury. [U2] Conclusions: Exposure to methylmercury was associated with increased risk of MI, and higher [U3] S-PUFA concentrations were associated with decreased risk of MI. Thus, MI risk may be reduced by the consumption of fish high in PUFAs and low in methylmercury. [U4] ********************************************************************** Supplement Your Stem Cells—how to look at this study ScienceDaily (Apr. 7, 2010) — A nutritional supplement could stimulate the production of stem cells integral for repairing the body. Research published in BioMed Central’s open access Journal of Translational Medicine suggests that a commercially-available supplement can increase the blood circulation of hematopoietic stem cells, which can give rise to all blood cells, and endothelial progenitor cells, which repair damage to blood vessels.—Thomas E. Ichim from Medistem Incorporated, USA worked with a team of 13 researchers from industry and academia to further investigate whether this supplement, containing a cocktail of green tea, astralagus, goji berry extracts, ‘good’ bacteria Lactobacillus fermentum, antioxidant ellagic acid, immune enhancer beta 1,3 glucan and vitamin D3, was able to increase the number of stem cells circulating in the blood. They recruited 18 healthy adults aged between 20 and 72 who stopped any other dietary supplements 4-5 days [U5] before starting a two-week course of this supplement, taking it twice daily. The researchers took blood from the participants before they started the course and on days 1, 2, 7 and 14 to test for signs of stem cell activity by looking for cells expressing the genetic stem cell markers CD133, CD34 and KDR. They then confirmed whether taking the supplement changed the overall levels of hematopoietic stem cells and endothelial progenitor cells in the blood by using HALO (Hematopoietic Assay via Luminescent Output) and colony forming assays respectively.—Hematopoietic stem cells and endothelial progenitor cells increased after taking the nutritional supplement, suggesting that the supplement may be a useful stimulator for both types of stem cells. In this study, the levels of these stem cells peaked at 2-7 days and started to drop at 14 days, suggesting that this supplement could be used for continuous treatment for conditions associated with decreases in these stem cells such as Alzheimer’s Disease. Other therapeutic treatments used to recruit hematopoietic stem cells are not viable as long-term solutions due to costs and increased health risks caused by the extremely high levels of stem cells that these treatments maintain in the blood.—“To our knowledge, this is the first study demonstrating profound mobilization effect with possible clinical significance by a food supplement-based approach,” say the authors, adding, “Indeed it may be possible that our supplement could be beneficial in conditions associated with reduced progenitor cells such as diabetes or in smokers which possess lower baseline values as compared to controls.” Although they are quick to add, “However, given commercial pressures associated with this largely unregulated field, we propose detailed scientific investigations must be made before disease-associated claims are made by the scientific community.”–Story Source-The above story is reprinted from materials provided by BioMed Central, via EurekAlert!, a service of AAAS. –Journal Reference-Nina A Mikirova, James A Jackson, Ron Hunninghake, Julian Kenyon, Kyle WH Chan, Cathy A Swindlehurst, Boris Minev, Amit N Patel, Michael P Murphy, Leonard Smith, Famela Ramos, Doru T Alexandrescu, Thomas E Ichim and Neil H Riordan. Nutraceutical augmentation of circulating endothelial progenitor cells and hematopoietic stem cells in human subjects. Journal of Translational Medicine, (in press) [link]
COPPER AND ZINC SALICYLATES Bacterial Cause Found for Skin Condition Rosacea Aqueous garlic extract and its phytochemical profile– special reference to antioxidant status Hexavalent chromium and its effect on health: possible protective role of garlic Scientists Pursue Connection between Infectious Disease Afflicting Cattle and MorgellonsDisease Affecting Humans ************************************************************************** COPPER AND ZINC SALICYLATES—-Two Excellent Inflammation Fighters
By Walter Last
Copper is an essential trace mineral. All tissues of the body need it for normal metabolic functions. Sometimes there is too much of the inorganic form in drinking water (acid water flowing through copper pipes). It can then gradually accumulate in the body and lead to toxicity symptoms with signs of zinc deficiency, over-stimulation, psychosis and liver damage.However, in organic form as chelates or copper complexes it is excellent for reducing inflammations, strengthening connective tissue, restoring hair colour and the oxidative energy metabolism as well as fighting parasites and cancer and may sometimes improve brain and liver functions.—If you give animals a choice between drinking normal water and water in which a copper pipe has been immersed, they will reportedly prefer the high copper water. This helps to keep them free of parasites. Copper armbands are well known to reduce arthritis. Copper serum levels are elevated up to threefold above normal with inflammations and with many chronic and infectious diseases, apparently because the body mobilises all tissue stores of copper to fight the condition. During remissions the copper levels return back to normal.—The most effective anti-inflammatory agents are copper complexes. Commonly these are related to salicylic acid. In addition, copper ascorbate has strong anti-viral properties. Copper salicylate has a better anti-inflammatory effect than cortisone but without the side effects. In addition it has also good anti-cancer, anti-tremor and anti-convulsive properties, suitable for treatment of epilepsy and possibly Parkinson’s disease. Children with severe copper deficiency constantly have convulsive seizures. Another feature of severe copper deficiency is degeneration of the central nervous system. There are at least 6 important copper-dependent enzymes in the brain. One of these is required for the conversion of tyrosine into dopamine which is lacking in Parkinson’s disease. A copper enzyme is also needed for the synthesis of adrenalin (epinephrine).–In experiments copper salicylate prevented chemically induced skin cancers. Furthermore, a single application resulted in a 55% reduction in experimental animal tumours in 20 weeks. The main metabolic defect of cancer cells, according to Dr Johanna Budwig and other researchers, is a deficiency of the enzyme cytochrome oxidase. This causes a blockage in the cellular respiration or oxidative energy production of the affected cells. Budwig claims that plenty of linseed oil and sulphur amino acids (L-cysteine and especially L-methionine) help to correct this situation.—Cytochrome oxidase is a copper dependent enzyme and additional copper might be of further benefit. In the final stages of this oxidative energy production electrons are transferred to copper (II) and iron (III) in the cytochrome oxidase to form copper (I) and iron (II). In the last step these electrons are then transferred to oxygen, which now can attract hydrogen ions to form water. In cancer cells this transfer of electrons to oxygen is blocked and energy is being produced very inefficiently by converting glucose into lactic acid.–However, practical experience has shown that copper is more important to prevent cancer or a regrowth of tumours and possibly with dormant tumours. If growing tumours are present, then copper is needed to form new blood vessels. Taking high amounts of zinc creates a relative copper deficiency and helps to prevent the formation of new blood vessels.—Copper salicylates have a similar action as superoxide dismutase (SOD) to protect cells from free radicals. Dr John R.J. Sorenson at the University of Arkansas has done most of the research work on copper complexes. In one of his publications he states that with the exception of Wilson’s disease, there are no chronic degenerative diseases in man known to result from non-industrial exposure to copper.–Dr Werner Hangerter, head of medicine at the University of Kiel, successfully used copper salicylates for over 20 years with more than 1100 patients with rheumatoid arthritis and other inflammatory conditions. Of 620 patients with rheumatoid arthritis 65% became symptom free and another 23% improved significantly, only 12% remained unchanged. With acute rheumatic fever 100% became symptom free. Also neuromuscular problems such as sciatica, neuralgia and cervical spine-shoulder problems responded very well. Even short-term treatment of rheumatoid arthritis resulted in long-term remissions or improvements.—The therapeutic potency and safety of the copper complexes of aspirin (acetyl-salicylic acid) and salicylic acid is much better than for aspirin itself or for inorganic copper. These complexes are 5 to 8 times more effective than aspirin but less toxic. The therapeutic index (the margin between effectiveness and toxic effects) has been stated as being significantly greater than for other anti-inflammatory drugs. While aspirin causes or aggravates peptic ulcers, the copper complexes have a better ulcer-healing effect than commonly used anti-inflammatory ulcer drugs. Harmful effects of aspirin, salicylic acid and similar drugs apparently arise because they bind copper in the body and cause a localised copper deficiency in the tissues.—Unfortunately, copper salicylate or other effective copper complexes are not normally available or only in very low doses, presumably because they cannot be patented. However, they are relatively easy to make for someone who wants to experiment. Order salicylic acid through a cooperating pharmacist and dissolve 2 g or about half a teaspoonful in half a litre of hot water.–Use covered glassware and distilled or de-ionised water and several pieces of copper with a large surface area immersed in it. Keep it warm, between 60º and 90ºC or just below boiling. Add more water as required and adjust the final volume to 500 ml. At first a light yellow-greenish colour develops, but at one point the colour considerably deepens. This may happen after 15 to 20 hours of heating and you may now let it cool and fill into a glass bottle.—Near the end of the heating process and during storage black copper oxide starts forming and slowly accumulates at the bottom. This is due to copper being converted from the original one-valent copper (I) salicylate to two-valent copper (II) salicylate. With this, the salicylic acid binds only half of the dissolved copper and the rest becomes copper oxide. The effectiveness of the solution does not seem to be affected by this and the amount of copper in the complex is not related to its potency. From time to time you may decant the solution from any settled copper oxide and crystals or filter it through tissue paper.—Copper (I) salicylate is a strong antioxidant and also appears to have good anti-inflammatory qualities, but all the published papers are on copper (II) salicylate. However the only data for a Cu (I) complex that I could find (penicillamine) showed it to have even stronger anti-inflammatory activity than the corresponding Cu (II) complex. Initially copper (I) will dominate in the self-prepared copper salicylate but the more copper oxide precipitates the more will copper (II) gain the upper hand. While salicylic acid only dissolves in hot water, copper (II) salicylate is easily soluble in cold water and is very stable and generally well tolerated when taken orally.Copper salicylate is also excellent for external use as packs or rubs on sites of tumours and inflammation, also rubbing it on skin prone to skin cancer. To improve its skin absorption you may mix it with some aloe vera gel or follow the copper salicylate rub with some aloe vera.—For internal use with generalised inflammations or other indications 60 mg of copper salicylate have been used in clinical trials once or twice and up to four times daily. Try a teaspoonful (approximately 25 mg of copper salicylate) three times daily in liquids with meals, preferably under professional supervision. For short-term use you may also double this amount. When it produces the desired effect, cut back to a maintenance dose of 1 teaspoonful a day or interrupt the intake after 2 weeks to see what happens.—Copper (I) salicylate is a strong antioxidant and may interfere with oxygen therapy. Therefore, it is advisable to alternate periods of taking high doses of copper salicylate with periods of intensive oxygen therapy. However, external application of copper salicylate should still be fine during oxygen therapy.—Another possibility of making copper salicylate yourself is by ingesting sodium salicylate and a copper chelate together. Copper salicylate then appears to form in the stomach. In some countries sodium salicylate is available as tablets, in others it may be obtained from a friendly chemist/pharmacist as a crystallised powder. Copper chelate, commonly as amino acid chelate or gluconate, may be available from a health food shop or over the Internet. Taking a 650 mg tablet of sodium salicylate together with 5 mg of copper in chelated form has reportedly eliminated severe arthritic pain. As maintenance dose a 350 mg tablet of sodium salicylate together with 2.5 mg of copper have been taken up to three times a day. If the sodium salicylate is available as powder, you may assume that a level teaspoonful is about 4 g. By dividing this into 6 equal portions you will have about 650 mg per portion.—You also find a source of copper salicylate tablets on the Internet or you may be able to obtain copper (II) salicylate crystals from a supplier of laboratory or fine chemicals. In this case you could divide a rounded teaspoonful into 100 equal parts, each part would then be approximately 50 mg.——–For a potent anti-viral remedy you may produce copper ascorbate. This is not difficult either. The only problem is that ascorbic acid easily becomes oxidised in contact with metal. Therefore, it is best to exclude all air. Bring some distilled or de-ionised water to boiling and, as hot as possible, fill a 500 ml glass or hard plastic container nearly to the top. Immerse a piece of copper and add 4 to 5 g or about one teaspoon of ascorbic acid powder. Keep refrigerated and remove the copper after a few days. After part of it has been used minimise the air space by filling it into a smaller bottle or jar. As an infection fighter try a teaspoonful several times a day for up to 2 weeks.—Copper salicylate is a very stable complex and most of it appears to be excreted unchanged. Therefore, it may be regarded more as a remedy rather than a food supplement. Nevertheless, when taking this or other copper complexes, colloids or chelates over a longer period it is advisable to take additional zinc, about 30 mg a day, in order to avoid a zinc deficiency from developing.—Finally I want to stress that the use of copper salicylate and ascorbate, especially when you make these yourself, is strictly experimental and no one can take any responsibility for what you are doing. If in doubt, then use it only externally. Individuals who are sensitive to salicylates need to be extra careful but I believe that even then it will generally be well tolerated. Handle copper salicylate with care, it stains garments.–I believe that colloidal copper has similar beneficial properties as copper salicylate and you might alternate using both with some longer breaks in-between. You can make colloidal copper in the same way as colloidal silver, just use two strips of copper instead of silver electrodes. However, the use of colloidal copper is experimental as well and you have to find out by yourself how much to take and how beneficial it is for you.—The Schweitzer Formula—Zinc has strong anti-inflammatory and antibiotic properties as well but can become deficient with a high copper intake. Therefore, it is usually best to increase the intake of both minerals together.[U1] With a high copper intake, also a high zinc supplementation should be used. This may be best in the form of Schweitzer Formula, a complex formed by zinc (oxide or carbonate), boron (boric acid) and salicylic acid. This is an excellent antibiotic, disinfectant, fungicide, anti-inflammatory and healing remedy.—-The Schweitzer Formula was developed 1915 in Germany and sold worldwide since 1920. In addition to any kind of infection or inflammation, it has been used in cancer treatment, to improve the immune response and blood oxygenation. Applied externally it helps to heal injuries and skin diseases, including acne, scarring varicose veins and varicose ulcers.—You can easily make the Schweitzer Formula yourself. Dissolve 9.2 g of salicylic acid, 2.1 g of boric acid and 2.7 g of zinc oxide or 4 g of zinc carbonate in 2 litres of hot water. You may get these ingredients from a pharmacist or supplier of fine chemicals and have exact quantities weight out. However, it is sufficient to use approximate amounts. You may use 2 level teaspoons of salicylic acid and half a teaspoon each of boric acid and zinc oxide or one level teaspoon of zinc carbonate.—-However, in Australia boric acid has now been scheduled as a prescription poison. Apparently eating large amounts of boric acid mixed with castor sugar that the parents had used to eliminate ants poisoned some infants. If you cannot obtain boric acid from a friendly chemist, you may use borax instead. This introduces some additional sodium ions. While this is not desirable, I do not expect this to significantly reduce the healing qualities of the Schweitzer Formula. To get the same amount of boron you may use about 30% more borax than boric acid.—-Use distilled or de-ionised water and a non-metal container. Heat for about an hour and stir occasionally with a non-metal spoon until no more of the zinc oxide or zinc carbonate at the bottom of the container seems to dissolve. Then decant or filter into a glass container and store in a dark and cool place. Any surplus of zinc oxide or carbonate that remains undissolved shows that all the boric acid and salicylic acid have been used up. However, any surplus of boric acid would be beneficial and just supply additional boron.–As a biochemist I do not see a difference between using this solution directly and letting it crystallise and then dissolving the crystals. However, I have not been able to verify this in a clinical trial. If you do want to crystallise the complex, then let the water evaporate very slowly in a flat non-metal tray covered with fine gauze. As a general rule, the slower the crystallisation, the bigger the crystals. Therefore, keep the tray undisturbed in a cool place. For quick crystallisation and smaller crystals you may expose the tray to direct sunlight. For use you may then dissolve the crystals again in 2 litres of hot water.—–As with copper salicylate, there are no exact guidelines on how much to take. A tablespoonful has been taken 3 times daily with liquid or meals for extended periods. For shorter periods this dose has been doubled. It is also good to rub onto the skin, especially where there are any problems.—You may take this at the ratio of one tablespoon of Schweitzer Formula to one teaspoon of copper salicylate[U2] . For long-term use I would take one spoonful of each daily. I believe that long-term use of copper or zinc should be balanced by taking the other mineral as well, be it as salicylate complex, colloid or conventional remedy. I also believe that copper and zinc as complexes or colloids are safer and more effective than the long-term use of aspirin or other anti-inflammatory drugs.—-One tablespoonful of Schweitzer contains about 15 mg of zinc, 15 mg of boric acid or 2.5 mg of boron and 70 mg of salicylic acid. As with copper salicylate, most of these can be expected to be eliminated from the body as a complex. Therefore, Schweitzer Formula cannot be regarded as a zinc or boron supplement and these may need to be additionally supplemented in a different form. However, to assess any potential toxicity, we may assume that the complex completely disintegrates in the body. This would then supply only relatively low levels of the individual ingredients. Twice these amounts of zinc and boron are recommended as being beneficial and much higher amounts have been used in nutritional therapy. Therefore, I cannot see any possible toxicity at least up to 3 tablespoons daily.—Also many commonly used foods are quite high in salicylates. Some individuals, especially hyperactive children are sensitive to salicylates and get a reaction from it. However, I believe that this is due to the chelating effect of salicylic acid, which may cause zinc and copper deficiency in the body. Therefore, in the form of zinc and copper complexes, salicylates may not normally cause a reaction in susceptible individuals.–After a period of use, it is advisable to interrupt using these remedies for a while and observe any effects., I want to stress again, that the use of these remedies over long periods or in high doses is experimental and you must be prepared to take responsibility for any side effects yourself. *************************************************************************************** Bacterial Cause Found for Skin Condition Rosacea ScienceDaily (Aug. 28, 2012) — Scientists are closer to establishing a definitive bacterial cause for the skin condition rosacea. This will allow more targeted, effective treatments to be developed for sufferers, according to a review published in the Journal of Medical Microbiology.—Rosacea is a common dermatological condition that causes reddening and inflammation of the skin mostly around the cheeks, nose and chin. In severe cases skin lesions may form and lead to disfigurement[U3] . Rosacea affects around 3% of the population — usually fair-skinned females aged 30-50 and particularly those with weak immune systems. The condition is treated with a variety of antibiotics, even though there has never been a well-established bacterial cause.[U4] –A new review carried out by the National University of Ireland concludes that rosacea may be triggered by bacteria that live within tiny mites that reside in the skin.–The mite species Demodex folliculorum is worm-like in shape and usually lives harmlessly inside the pilosebaceous unit which surrounds hair follicles of the face. They are normal inhabitants of the face and increase in number with age and skin damage — for example, following exposure to sunlight. The numbers of Demodex mites living in the skin of rosacea patients is higher than in normal individuals[U5] , which has previously suggested a possible role for the mites in initiating the condition.—More recently, the bacterium Bacillus oleronius was isolated from inside a Demodex mite[U6] and was found to produce molecules provoking an immune reaction in rosacea patients. Other studies have shown patients with varying types of rosacea react to the molecules produced by this bacterium — exposing it as a likely trigger for the condition. [U7] What’s more, this bacterium is sensitive to the antibiotics used to treat rosacea.—Dr Kevin Kavanagh who conducted the review explained, “The bacteria live in the digestive tracts of Demodex mites found on the face, in a mutually beneficial relationship. When the mites die, the bacteria are released and leak into surrounding skin tissues — triggering tissue degradation and inflammation.”[U8] —“Once the numbers of mites increase, so does the number of bacteria, making rosacea more likely to occur. Targeting these bacteria may be a useful way of treating and preventing this condition,” said Dr Kavanagh. “Alternatively we could look at controlling the population of Demodex mites in the face.. Some pharmaceutical companies are already developing therapies to do this, which represents a novel way of preventing and reversing rosacea, which can be painful and embarrassing for many people.”—-Story Source-The above story is reprinted from materials provided by Society for General Microbiology, via AlphaGalileo. —Journal Reference-Stanisław Jarmuda, Niamh O’Reilly, Ryszard Żaba, Oliwia Jakubowicz, Andrzej Szkaradkiewicz and Kevin Kavanagh. The potential role of Demodex folliculorum mites and bacteria in the induction of rosacea. Journal of Medical Microbiology, 2012 DOI: 10.1099/jmm.0.048090-0 ************************************************************************** Aqueous garlic extract and its phytochemical profile– special reference to antioxidant status. Int J Food Sci Nutr. 2012 Jun;63(4):431-9—Authors: Rasul Suleria HA, Sadiq Butt M, Muhammad Anjum F, Saeed F, Batool R, Nisar Ahmad A Abstract—Garlic (Allium sativum L) has distinct nutritional profile with special reference to its bioactive components and is used in different diet-based therapies to cure various lifestyle-related disorders. For this purpose, characterization and extraction of garlic were carried out followed by antioxidant assays. Different solvents (50% aqueous ethanol, 50% aqueous methanol and water) at different time intervals (4, 5 and 6 h) at 60°C were used to optimize aqueous extraction efficiency of garlic. Among the solvents, water extract resulted in better extraction yield (31.85 ± 2.09 g/25 g) at 5 h. The antioxidant potential of all these solvents was estimated through in vitro studies. In this context, it was observed that higher amount of total phenolic contents was present in aqueous methanol 71.87 ± 1.69% at 45 min. Antiradical (1,1-diphenyl-2-picrylhydrazyl assay) and antioxidant activity showed that the maximum value was 73.80 ± 3.69 and 83.83 ± 0.16%, respectively, in methanolic extract at 45 min while glucose diffusion and ferric reducing antioxidant power were 97.00 ± 0.20 and 32.66 ± 0.72% at p < 0.05, respectively. Aqueous garlic extract was selected as the best treatment on the basis of percentage yield and safety modulation in human body absorption. Aqueous garlic extract was subjected to pH, acidity, total soluble solids (TSS) and colour. It was observed that the pH of aqueous garlic extract decreased with the passage of time while acidity increased. It was also concluded that storage affected the value of TSS and colour significantly. L* values for colour on 0 day were 34.18 ± 0.08, whereas those on 28th day were 38.84 ± 0.03. It was predicted that 28 days storage resulted in significant increase in L* value, while a* value decreased from 4.31 ± 0.01 to 0.32 ± 0.01 at the end of storage study.—PMID: 22098476 [PubMed – indexed for MEDLINE] ********************************************************************** Hexavalent chromium and its effect on health- possible protective role of garlic (Allium sativum Linn). J Basic Clin Physiol Pharmacol. 2011;22(1-2):3-10—Authors: Das KK, Dhundasi SA, Das SN Abstract—Hexavalent chromium or chromium (VI) is a powerful epithelial irritant and a confirmed human carcinogen. This heavy metal is toxic to many plants, aquatic animals, and bacteria. Chromium (VI) which consists of 10%-15% total chromium usage, is principally used for metal plating (H2Cr2O7), as dyes, paint pigments, and leather tanning, etc. Industrial production of chromium (II) and (III) compounds are also available but in small amounts as compared to chromium (VI). Chromium (VI) can act as an oxidant directly on the skin surface or it can be absorbed through the skin, especially if the skin surface is damaged. The prooxidative effects of chromium (VI) inhibit antioxidant enzymes and deplete intracellular glutathione in living systems and act as hematotoxic, immunotoxic, hepatotoxic, pulmonary toxic, and nephrotoxic agents. In this review, we particularly address the hexavalent chromium-induced generation of reactive oxygen species and increased lipid peroxidation in humans and animals, and the possible role of garlic (Allium sativum Linn) as a protective antioxidant.–PMID: 22865357 [PubMed – indexed for MEDLINE] **************************************************************************** http://www.thecehf.org/morgellons-disease-research-update-august-2012.html Morgellons Disease Research Update August 2012 Research Update … Scientists Pursue Connection between Infectious Disease Afflicting Cattle and Morgellons Disease Affecting Humans Progress moves forward as more research shows Morgellons disease has a physiologic (physical not mental) basis. ——- The Morgellons break through started with the research publication, Filament Formation Associated with Spirochetal Infection: a comparative approach to Morgellons Disease by Marianne Middelveen, a Canadian veterinary microbiologist and Raphael Stricker, MD. The CEHF first announced this news last fall when this peer reviewed publication appeared in the November, 2011 issue of Clinical, Cosmetic and Investigational Dermatology.
Why is this important? —-In November, 2011, Middelveen and Stricker reported to have found evidence of a veterinary analog to Morgellons (MD). BDD, an infectious disease which has plagued cattle for decades, has fibers/filaments within their tissue and lesions that were recognized as a match to those found in the controversial disease known as Morgellons (MD) in humans. Studies on fibers/filaments from cattle with the bovine hoof disease and those found in MD suffers provided startling evidence challenging the dermatologists’ unfounded assumption that MD is a psychiatric disorder called “Delusions of Parasitosis”. Anyone who suffers from Morgellons knows how real these symptoms are and how disheartening it is to be told it is all in your head. Although the publication stated that the etiology (cause) of MD was not yet known, the findings by Middelveen and Stricker provided corroborative evidence to support a physiological and, perhaps, infectious etiology, lending a new direction for further research. Second Study Announced by the CEHF on May 16, 2012 –Morgellon Fibres http://www.omicsonline.org/2155-9554/2155-9554-3-140.pdf Indeed, their second study, Morgellons Disease: A Chemical and Light Microscopic Study, published May, 2012 in the peer reviewed publication, Journal of Clinical & Experimental Dermatology Research, continued this BDD and MD comparison in greater detail. Researchers were able to conduct a more in-depth analysis of dermatological specimens from three Morgellons patients and biopsies from cattle with proliferative late stage BDD. Examinations were conducted by light microscopy, by chemical experiments and by immunohistological testing. Results of the Study … These findings confirmed that filaments/fibers from both bovine and human samples were similar in formation at the cellular level and had the chemical and physical properties of keratin. The composition of MD filaments from humans was confirmed to be keratin by immunohistological staining with antibodies specific for human keratins. Fibers from three human patients were found to be biological in origin and are produced by keratinocytes in epithelial and follicular tissues. —An interesting side note is that researchers Middelveen and Stricker found filaments/fibers associated with MD beneath unbroken skin as well as in lesions, thus, demonstrating they are not self-implanted. This confirms previous research from Dr. Randy Wymore at the OSU-Center for the Investigation of Morgellons Disease. Why is this important? —-The original premise–that MD is physiological is holding up to the test of scientific scrutiny. Morgellons Study Cited by Faculty of 1000 http://www.thecehf.org/morgellons-study-cited-by-faculty-of-1000.html The quality and importance of this research is highlighted in Faculty of 1000 Award. Faculty of 1000 (F1000) is a global community of over 10,000 experts who select, rate and evaluate the very best articles in biology and medicine. The core mission of the F1000 is to identify and evaluate the most important articles in biology and medical research publications. The organization highlights and brings awareness to significant new research. The selection of Morgellons Disease: A Chemical and Light Microscopic Study places the work in this work in the top 2% of published articles in these fields. It classifies the study as “must read” and is certainly an honor for the entire research team. More information can be accessed at the F1000 website (http://f1000.com/716597867). Thank You and Congratulations to Our Researchers!! —-No one can apply to be considered for this. This research was chosen and recognized on its merits and for the importance it holds worldwide. Everyone at The Charles E. Holman Foundation and from the Morgellons community wish to express our congratulations to Marianne Middelveen, Elizabeth Rasmussen, Douglas Kahn, and Raphael Stricker for this recognition. The award was indeed serendipity. We now have documented, peer reviewed evidence published, corroborating MD is not Delusions of Parasitosis. MD, like BBD, has a true physical cause. “ … Because BDD is a disease in which spirochetes have been identified as primary etiologic agents, and spirochetal sero-reactivity has been associated with MD, it is reasonable to assume that spirochetal infection plays an important role in MD… Further immunohistological and electron microscopy studies are needed to solve the mystery of Morgellons …” (Middelveen and Stricker). This points the way to the next step in our research. To paraphrase Paul Harvey, stay tuned in and signed up for the next edition of Keeping You in the Loop …for the “rest of the story.”
Rosmarinic acid induces melanogenesis – through protein kinase A activation signaling
Silver bullet for cancer: Metal can kill some tumours better than chemotherapy with fewer side effectsSilver can kill some cancers as effectively as chemotherapy and with potentially fewer side effects, new research claims.–Scientists say that old wives tales about the precious metal being a ‘silver bullet’ to beat the Big C could be true.–The metal already has a wide range of medicinal uses and is a common antiseptic, antibiotic and means of purifying water in the third world. —Good news: Silver can kill some cancers as effectively as chemotherapy and with potentially fewer side effects, new research has claimed—And British researchers now say that silver compounds are as effective at killing certain cancer cells as a leading chemotherapy drug, but with potentially far fewer side-effects. —They compared it to Cisplatin, currently used to treat a wide variety of cancers, but known to have harsh side effects including nausea, vomiting and even kidney damage.—Silver is used already in everyday products such as deodorant with no known side-effects, and could make for a potentially cheaper alternative to platinum-based Cisplatin. –Researchers from the University of Leeds conducted lab tests which exposed breast and colon cancer cells to various silver-based chemicals over a six day period. –Results, published in journal Dalton Transactions, showed that these silver-compounds were ‘as effective as Cisplatin’ at killing cancer with potentially fewer side effects. –While the team are still unsure about how exactly silver battles cancer, they think its effectiveness may be caused by the structure surrounding silver atoms, known as its ligand. –Way forward: Researchers from the University of Leeds found that silver could be used to help defeat breast cancer –They think this may help release the silver ion into cells when it enters the body, killing any cancer. —Study author Dr Charlotte Willans plans to spend the next year looking closely at what effect silver has on both cancerous and healthy cells, and whether it could be a safe and effective new anti-cancer drug.–She said: ‘It’s certainly an exciting discovery, although I think we have a lot of work to do in the future. It opens the doors in terms of what we can do and investigate.—‘Getting these results also gives us the opportunity we need to apply for funding to take the research further.–‘This could lead to a cheaper, less toxic alternative to current treatments for cancer.‘–Explaining the research in greater detail, Dr Willans added: ‘As many are unfortunately aware, chemotherapy can be a very gruelling experience for the patient. —‘Finding effective, yet non-toxic drugs is an ongoing problem, but these preliminary results are an important step in solving it.–‘Our research has looked at the structure which surrounds a central silver atom. This “shrubbery” is what determines how reactive it is and what it will interact with. ‘Our research has used different types of these ligands to see which is the most effective against cancer cells.’
A School Nurse has written the info below—- Please share – because it really works!
“Apply a glob of liquid soap to a cotton ball. Cover the tick with the soap-soaked cotton ball and swab it for a few seconds (15-20); the tick will come out on its own and be stuck to the cotton ball when you lift it away.—–This technique has worked every time I’ve used it (and that was frequently), and it’s much less traumatic for the patient and easier for me..” —“Unless someone is allergic to soap, I can’t see that this would be damaging in any way. —I even had my doctor’s wife call me for advice because she had one stuck to her back and she couldn’t reach it with tweezers. She used this method and immediately called me back to say, “It worked
Stop the GM Apple! Take Action before June 3.
A small BC company called Okanagan Specialty Fruits has just submitted a request to Health Canada and the Canadian Food Inspection Agency for approval of a genetically modified (GM, also called genetically engineered) “non-browning” apple. Contamination from GM apples threatens the future of our apples, and the farmers who grow them.—
1. Send your comments to the Canadian Food Inspection Agency before June 3, 2012 at <http://active.inspection.gc.ca/eng/plaveg/bio/subs/biocome.asp> Tell the government that you don’t want to eat a GM apple!—- Consumers don’t want GM apples. – The GM “non-browning” apple will mislead consumers by presenting an apple that looks freshly cut or unbruised when it is not. – BC apple growers have already rejected the GM apple. – Contamination from GM apple trees is a risk to Canadian apple producers. – The CFIA and Health Canada should not be wasting public funds reviewing a GM apple that no one wants. – The government should consult with farmers and consumers before approving any new GM crop. —You can see the notice of the submission for approval of the GM apple at: <http://inspection.gc.ca/plants/plants-with-novel-traits/notices-of-submission/okanagan-specialty-fruits-inc-/eng/1335141426301/1335142810470>
This is just the first of many actions needed to stop the GM apple.
2. You can also sign a petition created by the British Columbia NDP here: <https://spreadsheets.google.com/spreadsheet/viewform?formkey=dEVua2pOc0ZjWjZNeVFhd1FRMmNwVGc6MQ>
3. For more information and to get more involved see http://www.cban.ca/apple
Background–The genetically modified (GM) ?non-browning? apple is engineered to keep from going brown after being cut. This apple is designed for fast food companies and other companies that use pre-cut apples. The technology was developed in Australia and was licensed by small BC company Okanagan Specialty Fruits.—Okanagan Specialty Fruits asked for approval in the US in March 2010 and has just asked for approval in Canada. The GM apple has not yet been approved anywhere in the world. BC apple growers stopped the GM apple from being field tested in Canada in 2001. The federal agricultural research station in Summerland in the Okanagan valley, an important fruit growing area, was preparing to start field trials but BC growers who were concerned about contamination stopped them from happening.—Many apple grower associations in Canada and the US oppose the GM apple, including the BC Fruit Tree Association.– This action alert was issued on May 18 2012 by Bee SAFE, the Canadian Biotechnology Action Network, GE Free BC, Okanagan Greens Society, True Food Foundation and Vigilance OGM.
Lucy Sharratt, Coordinator Canadian Biotechnology Action Network (CBAN) Collaborative Campaigning for Food Sovereignty and Environmental Justice Suite 206, 180 Metcalfe Street Ottawa, Ontario, Canada, K2P 1P5 Phone: 613 241 2267 ext. 25 Fax: 613 241 2506 firstname.lastname@example.org www.cban.ca
Stop the GM Apple: http://www.cban.ca/apple
Rosmarinic acid induces melanogenesis through protein kinase A activation signaling.
Source–Biospectrum Life Science Institute, SK Ventium 101-701, Dangjung Dong, Gunpo City, 436-776 Kyunggi-do, Republic of Korea.
Abstract–Melanogenesis is a physiological process that results in the synthesis of melanin pigments, which play a crucial protective role against skin photocarcinogenesis. In order to determine the effects of rosmarinic acid on melanogenesis and elucidate the molecular events of melanogenesis induced by rosmarinic acid, several experiments were performed in B16 melanoma cells. In this study, we showed that the melanin content and tyrosinase expression were increased by rosmarinic acid in a concentration-dependent manner. In addition, after the melanin content was increased by rosmarinic acid, it was reduced by H-89 and KT 5720, protein kinase A (PKA) inhibitors, but not by SB203580, a p38(mapk) inhibitor, or Ro-32-0432, a PKC inhibitor, which suggests the involvement of PKA in rosmarinic acid-induced melanogenesis. Consistent with this, rosmarinic acid induced the phosphorylation of CRE-binding protein (CREB), but had no effect on the phosphorylation of p38(mapk) or the inhibition of Akt phosphorylation. Additionally, rosmarinic acid induced the activation of cAMP response element (CRE) without having any effect on cAMP production, which suggests that rosmarinic acid-induced melanogenesis is mediated by PKA, which occurs downstream of cAMP production. This result was further confirmed by the fact that rosmarinic acid-induced phosphorylation of CREB was inhibited by H-89, but not by PD98059, a MEK1 inhibitor, or by LY294002, a phosphatidylinositol-3-kinase (PI3K) inhibitor. Rosmarinic acid-induced expression of tyrosinase protein was attenuated by H-89. Based on these results, we report for the first time that rosmarinic acid induces melanogenesis through PKA activation signaling.
Recipe—take the essential oil of rosemary-4 drops to an ounce of a carrier oil shake and or percuss and apply to skin—
Makinga Wash with a combination of these herbs and then filtering and bottling –can be used as a rince—a skin toner—
Making A tea out of Perilla as well with sage and peppermint is another method
When making the teas go 1:1 ration and make at the least a 2 pint of water in a pot—bring to boil then simmer it down to about half and pour several oz and drink
Pure rosmarinic acid is a cream colored powder. Rosmarinic acid belongs to the group of polyphenols.
Rosmarinic acid has antioxidant, anti-inflammatory and antimicrobial activities. -The antioxidant activity of rosmarinic acid is stronger than that of vitamin E. Rosmarinic acid helps to prevent cell damage caused by free radicals, thereby reducing the risk for cancer and atherosclerosis. Rosmarinic acid has anti-inflammatory properties. Perilla, rich in rosmarinic acid, is used for its anti-allergic activity. A study by Sanbongi C and colleagues (Clinical and Experimental Allergy, June 2004) have shown that the oral administration of rosmarinic acid is an effective intervention for allergic asthma. Another study by Youn J and colleagues (Journal of Rheumatology, June 2003) demonstrated that rosmarinic acid suppressed synovitis in mice and that it may be beneficial for the treatment of rheumatoid arthritis. Unlike antihistamines, rosmarinic acid prevents the activation of immune responder cells, which cause swelling and fluid formation. –Rosmarinic acid is also used for food preservation. In Japan the perilla extracts, rich in rosmarinic acid, is used the garnish and improve the shelf life of fresh seafood.–Rosmarinic acid is used to treat peptic ulcers, arthritis, cataract, cancer, rheumatoid arthritis and bronchial asthma. —Synonyms—Ros A, [[3-(3,4-Dihydroxyphenyl)-1-oxo-2E-propenyl]oxy]-3,4-dihydroxy- benzenepropanoic acid
Some laboratory mice were given specially engineered insuling-producing genes. These genes were then remotely activated using radio waves. This could mean a whole new field of medical procedures in which we turn genes on and off at will.[U1] —This breakthrough is the work of geneticists at New York’s Rockefeller University. It’s a pretty circuitous path from the initial burst of radio waves to the activation of the gene, and there’s still a lot of refinement and improvement that needs to be made before this can be used in medical treatments, but still – we’re talking about the ability to modify the behavior of genes without ever going inside a patient’s body.[U2] That’s a potentially colossal advance.–Admittedly, while the treatment itself is totally non-invasive, the researchers did first have to inject some nanoparticles onto the mice’s cells in order to affect their genes.[U3] It’s a bit of a complex process, but Nature has a good explanation of just what was involved—Friedman and his colleagues coated iron oxide nanoparticles with antibodies that bind to a modified version of the temperature-sensitive ion channel TRPV1, which sits on the surface of cells. They injected these particles into tumours grown under the skins of mice, then used the magnetic field generated by a device similar to a miniature magnetic-resonance-imaging machine to heat the nanoparticles with low-frequency radio waves. In turn, the nanoparticles heated the ion channel to its activation temperature of 42 °C. Opening the channel allowed calcium to flow into cells, triggering secondary signals that switched on an engineered calcium-sensitive gene that produces insulin. After 30 minutes of radio-wave exposure, the mice’s insulin levels had increased and their blood sugar levels had dropped.—The radio waves are ideal for this sort of remote manipulation because they can pass through thick layers of tissue, and they can be easily focused by the TRPV1 channel to affect only the desired target[U4] . Lead researcher Jeffrey Friedman says that, although this particular treatment had to do with insulin production, this isn’t actually meant specifically as a diabetes treatment. That’s a good thing, considering this treatment is massively more inefficient than many diabetes treatments currently available. Instead, this is just meant as a general proof of concept, and insulin production happens to be one of the easier gene activities to manipulate.–Even better, the researchers have already developed a way to achieve similar, albeit weaker, results without having to inject nanoparticles at all. They have developed cells that can grow their own required nanoparticles, meaning there would be no need to give patients strange chemicals or molecules. However, as Nature explains, this would still require growing tumors inside humans to actually get these cell cultures in place, which means the treatment isn’t yet ethically permissible in humans. It’s definitely early days yet, but this is one seriously intriguing line of research